TY - JOUR T1 - The fluidity of DOPC bilayers and membrane fractions prepared from murine plasmacytoma cells is unchanged after incorporation of pristane (2,6,10,14-tetramethylpentadecane) as assessed by fluorescence polarization analysis. AN - 75517009; 1343851 AB - The nature of the plasmacytomagenic activity of pristane (2,6,10,14-tetramethylpentadecane) is poorly defined. However, evidence for tumor promoting properties of pristane has recently come forward that includes direct cellular effects on B lymphocytes; i.e., the plasmacytoma precursor cell. Bly et al. (Cancer Biochem. Biophys. 11, 1990, 145-154) observed changed membrane fluidities in lymphocytes after administration of pristane in vivo. We measured steady-state fluorescence polarization using DPH (1,6-diphenyl-1,3,5-hexatriene) and APCL (1-acyl-2-[12-(9-anthryl)-11-trans-dodecenoyl]-sn-glycero-3- phosphocholine) as probes in DOPC (L-alpha-dioleoylphosphatidylcholin) model membranes and membrane fractions derived from plasmacytoma cells after incorporation of pristane in vitro. In a previous investigation, we verified the in vitro uptake of pristane into DOPC bilayers under the conditions employed here (Gawrisch and Janz, Biochim. Biophys. Acta 1070, 1991, 409-418). However, neither in DOPC bilayers nor in plasmacytoma membrane fractions could we detect changes in fluorescence polarization after in vitro incorporation of pristane within reasonable error limits. Therefore, we suggest that the observed alterations in membrane fluidity in lymphocytes from pristane-treated animals are the indirect result of the in vivo treatment but not a direct effect of pristane on membrane fluidity. JF - Cancer biochemistry biophysics AU - Janz, S AU - Krumbiegel, M AU - Gawrisch, K AD - Laboratory of Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Md 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 85 EP - 92 VL - 13 IS - 2 SN - 0305-7232, 0305-7232 KW - Carcinogens KW - 0 KW - Lipid Bilayers KW - Phosphatidylcholines KW - Terpenes KW - Diphenylhexatriene KW - 1720-32-7 KW - pristane KW - 26HZV48DT1 KW - 1,2-oleoylphosphatidylcholine KW - H026DM5V6U KW - Index Medicus KW - Animals KW - Solubility KW - Tumor Cells, Cultured -- metabolism KW - Fluorescence Polarization KW - Tumor Cells, Cultured -- drug effects KW - Cell Membrane -- drug effects KW - Phosphatidylcholines -- chemistry KW - Mice KW - Lipid Bilayers -- chemistry KW - Cell Membrane -- metabolism KW - Terpenes -- toxicity KW - Terpenes -- administration & dosage KW - Plasmacytoma -- metabolism KW - Carcinogens -- administration & dosage KW - Plasmacytoma -- chemically induced KW - Membrane Fluidity -- physiology KW - Membrane Fluidity -- drug effects KW - Carcinogens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75517009?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+biochemistry+biophysics&rft.atitle=The+fluidity+of+DOPC+bilayers+and+membrane+fractions+prepared+from+murine+plasmacytoma+cells+is+unchanged+after+incorporation+of+pristane+%282%2C6%2C10%2C14-tetramethylpentadecane%29+as+assessed+by+fluorescence+polarization+analysis.&rft.au=Janz%2C+S%3BKrumbiegel%2C+M%3BGawrisch%2C+K&rft.aulast=Janz&rft.aufirst=S&rft.date=1992-11-01&rft.volume=13&rft.issue=2&rft.spage=85&rft.isbn=&rft.btitle=&rft.title=Cancer+biochemistry+biophysics&rft.issn=03057232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-03-25 N1 - Date created - 1994-03-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - D2 dopamine receptor genotype and cerebrospinal fluid homovanillic acid, 5-hydroxyindoleacetic acid and 3-methoxy-4-hydroxyphenylglycol in alcoholics in Finland and the United States. AN - 73455172; 1283042 AB - If a genetic association between the D2 dopamine receptor genotype and alcoholism is mediated by altered dopamine function, then a stronger association might be found in alcoholics who are deviant in indices of dopamine function and by comparing alcoholics to nonalcoholics matched for ethnic origin. Therefore, we evaluated the D2/TaqI polymorphism in 29 impulsive violent alcoholic Finns, 17 nonimpulsive violent alcoholic Finns and 36 Finnish controls free of mental disorders, alcoholism and substance abuse. In 37 of the alcoholics, we measured cerebrospinal fluid (CSF) homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA) and 3-methoxy-4-hydroxyphenylglycol. There was no relationship between D2/Taq 1 genotype and concentrations of these monoamine metabolites in this group, which exhibits lower CSF HVA and 5-HIAA as compared to controls. There was also no genotypic difference between Finnish alcoholics and nonalcoholic controls. The lack of relationship between D2/Taq1 genotype and HVA concentration was replicated in 24 Caucasian alcoholics in the United States. JF - Acta psychiatrica Scandinavica AU - Goldman, D AU - Dean, M AU - Brown, G L AU - Bolos, A M AU - Tokola, R AU - Virkkunen, M AU - Linnoila, M AD - Laboratory of Neurogenetics, National Cancer Institute, Frederick, Maryland. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 351 EP - 357 VL - 86 IS - 5 SN - 0001-690X, 0001-690X KW - Receptors, Dopamine KW - 0 KW - Methoxyhydroxyphenylglycol KW - 534-82-7 KW - Hydroxyindoleacetic Acid KW - 54-16-0 KW - Homovanillic Acid KW - X77S6GMS36 KW - Index Medicus KW - United States KW - Genotype KW - Alleles KW - Methoxyhydroxyphenylglycol -- cerebrospinal fluid KW - Finland KW - Ethnic Groups KW - Polymorphism, Genetic -- genetics KW - Humans KW - Adult KW - Hydroxyindoleacetic Acid -- cerebrospinal fluid KW - Male KW - Homovanillic Acid -- cerebrospinal fluid KW - Alcoholism -- cerebrospinal fluid KW - Receptors, Dopamine -- genetics KW - Alcoholism -- genetics KW - Receptors, Dopamine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73455172?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Acta+psychiatrica+Scandinavica&rft.atitle=D2+dopamine+receptor+genotype+and+cerebrospinal+fluid+homovanillic+acid%2C+5-hydroxyindoleacetic+acid+and+3-methoxy-4-hydroxyphenylglycol+in+alcoholics+in+Finland+and+the+United+States.&rft.au=Goldman%2C+D%3BDean%2C+M%3BBrown%2C+G+L%3BBolos%2C+A+M%3BTokola%2C+R%3BVirkkunen%2C+M%3BLinnoila%2C+M&rft.aulast=Goldman&rft.aufirst=D&rft.date=1992-11-01&rft.volume=86&rft.issue=5&rft.spage=351&rft.isbn=&rft.btitle=&rft.title=Acta+psychiatrica+Scandinavica&rft.issn=0001690X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-17 N1 - Date created - 1993-02-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pseudomonas exotoxin: recombinant conjugates as therapeutic agents. AN - 73447722; 1487051 JF - Biochemical Society transactions AU - FitzGerald, D J AU - Pastan, I AD - Department of Health and Human Services, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 731 EP - 734 VL - 20 IS - 4 SN - 0300-5127, 0300-5127 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Immunotoxins KW - Recombinant Fusion Proteins KW - Recombinant Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Animals KW - Humans KW - Recombinant Fusion Proteins -- therapeutic use KW - Recombinant Proteins -- therapeutic use KW - Bacterial Toxins -- metabolism KW - Bacterial Toxins -- therapeutic use KW - Exotoxins -- metabolism KW - Immunotoxins -- therapeutic use KW - Immunotoxins -- metabolism KW - Pseudomonas aeruginosa KW - Exotoxins -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73447722?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+Society+transactions&rft.atitle=Pseudomonas+exotoxin%3A+recombinant+conjugates+as+therapeutic+agents.&rft.au=FitzGerald%2C+D+J%3BPastan%2C+I&rft.aulast=FitzGerald&rft.aufirst=D&rft.date=1992-11-01&rft.volume=20&rft.issue=4&rft.spage=731&rft.isbn=&rft.btitle=&rft.title=Biochemical+Society+transactions&rft.issn=03005127&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-24 N1 - Date created - 1993-02-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dying to be equal: women, alcohol, and cardiovascular disease. AN - 73363496; 1458038 AB - This data note explores the relationship of gender, alcohol consumption and premature death from cardiovascular disease (MCVD). Data on the 8164 deaths attributed to MCVD from the National Mortality Followback Study (NMFS) were analyzed controlling for gender and consumption. Women who are heavy drinkers die young at a rate equal to that of men who drink heavily. In light of this, we recommend that future research and preventive efforts in this area include females as subjects and alcohol as a major risk factor. JF - British journal of addiction AU - Hanna, E AU - Dufour, M C AU - Elliott, S AU - Stinson, F AU - Harford, T C AD - National Institute on Alcohol Abuse and Alcoholism, (NIAAA), Rockville, MD 20857. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 1593 EP - 1597 VL - 87 IS - 11 SN - 0952-0481, 0952-0481 KW - Index Medicus KW - Mortality KW - Attitude to Health KW - Humans KW - Adult KW - Health Promotion -- trends KW - Aged KW - Middle Aged KW - Male KW - Female KW - Cardiovascular Diseases -- mortality KW - Cardiovascular Diseases -- etiology KW - Women's Health KW - Cardiovascular Diseases -- classification KW - Alcoholism -- prevention & control KW - Alcoholism -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73363496?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+addiction&rft.atitle=Dying+to+be+equal%3A+women%2C+alcohol%2C+and+cardiovascular+disease.&rft.au=Hanna%2C+E%3BDufour%2C+M+C%3BElliott%2C+S%3BStinson%2C+F%3BHarford%2C+T+C&rft.aulast=Hanna&rft.aufirst=E&rft.date=1992-11-01&rft.volume=87&rft.issue=11&rft.spage=1593&rft.isbn=&rft.btitle=&rft.title=British+journal+of+addiction&rft.issn=09520481&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-08 N1 - Date created - 1993-01-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The treatment of Wegener's granulomatosis with glucocorticoids and methotrexate. AN - 73335088; 1445449 AB - To identify alternatives to daily low-dose cyclophosphamide (CYC) in the treatment of Wegener's granulomatosis (WG). An open-label pilot study of weekly low-dose methotrexate (MTX) plus glucocorticoids (GC) for treatment of patients with WG was performed. Twenty-nine patients who did not have immediately life-threatening disease were included. Outcome was determined by clinical characteristics, pathologic findings, course of illness, laboratory and radiographic findings, and successful withdrawal of GC therapy. Weekly administration of MTX (at a mean stable dosage of 20 mg) and GC resulted in marked improvement in 76% of the 29 patients. Remission was achieved in 69% of the patients, 7% improved but had intermittent smoldering disease that precluded total withdrawal of GC, and 17% had progressive disease within 2-6 months of starting the study treatment. Two patients who initially achieved remission later had relapses after GC was discontinued. Of those who remain in remission (mean followup time 14.5 months), 72% have not required GC for a mean period of 10 months. Although standard therapy for WG (daily CYC and GC) has dramatically improved outcome in this often-fatal disease, treatment morbidity has led to attempts to identify effective interventions that have less toxicity. Weekly low-dose MTX was shown in this study to be a feasible alternative to CYC in patients whose illness was not immediately life-threatening or in whom prior CYC treatment was ineffective or produced serious toxicity. Although these results are preliminary, they are encouraging and justify further studies in which MTX, CYC, and other alternative therapeutic approaches are compared concurrently. JF - Arthritis and rheumatism AU - Hoffman, G S AU - Leavitt, R Y AU - Kerr, G S AU - Fauci, A S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 1322 EP - 1329 VL - 35 IS - 11 SN - 0004-3591, 0004-3591 KW - Antibodies, Antineutrophil Cytoplasmic KW - 0 KW - Autoantibodies KW - Glucocorticoids KW - Methotrexate KW - YL5FZ2Y5U1 KW - Abridged Index Medicus KW - Index Medicus KW - Drug Therapy, Combination KW - Treatment Failure KW - Prospective Studies KW - Humans KW - Adult KW - Autoantibodies -- analysis KW - Aged KW - Pilot Projects KW - Middle Aged KW - Recurrence KW - Male KW - Female KW - Remission Induction KW - Granulomatosis with Polyangiitis -- immunology KW - Methotrexate -- therapeutic use KW - Glucocorticoids -- therapeutic use KW - Granulomatosis with Polyangiitis -- drug therapy KW - Granulomatosis with Polyangiitis -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73335088?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Arthritis+and+rheumatism&rft.atitle=The+treatment+of+Wegener%27s+granulomatosis+with+glucocorticoids+and+methotrexate.&rft.au=Hoffman%2C+G+S%3BLeavitt%2C+R+Y%3BKerr%2C+G+S%3BFauci%2C+A+S&rft.aulast=Hoffman&rft.aufirst=G&rft.date=1992-11-01&rft.volume=35&rft.issue=11&rft.spage=1322&rft.isbn=&rft.btitle=&rft.title=Arthritis+and+rheumatism&rft.issn=00043591&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-07 N1 - Date created - 1992-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cholera toxin pretreatment protects against tumor necrosis factor lethality without compromising tumor response to therapy. AN - 73318779; 1444796 AB - Antitumor therapy with tumor necrosis factor is limited by systemic toxic effects. We studied whether cholera toxin, a bacterial exotoxin that adenosine diphosphate-ribosylates the alpha-subunit of Gs proteins, could separate the lethal from the antitumor effects of tumor necrosis factor. A single dose of intravenous cholera toxin protected non-tumor-bearing mice from a lethal dose of Escherichia coli endotoxin administered 6 or 24 hours later. On the basis of these results, tumor-bearing mice were randomized to receive either cholera toxin or saline, followed 6 hours later by either human tumor necrosis factor (400 micrograms/kg) or saline. Tumor-bearing mice pretreated with cholera toxin had (1) reduced treatment-related mortality (0/11 vs 5/11 for saline controls) and (2) tumor regression similar to that of controls. In a separate experiment in tumor-bearing mice, intravenous human tumor necrosis factor treatment induced an increase in serum levels of murine tumor necrosis factor to a peak of 500 pg/mL at 1 hour in saline-pretreated controls, while a similar increase could not be detected in those mice pretreated with cholera toxin. These results suggest that pretreatment with cholera toxin can reduce the endogenous tumor necrosis factor response to administered tumor necrosis factor and separate the lethal from the antitumor effects. Cholera toxin may prove to be a useful tool for investigating the mechanisms underlying the varied effects of tumor necrosis factor. JF - Archives of surgery (Chicago, Ill. : 1960) AU - Block, M I AU - Alexander, H R AU - Norton, J A AD - Surgical Metabolism Section, National Cancer Institute, National Institutes of Health, Bethesda, Md. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 1330 EP - 1334 VL - 127 IS - 11 SN - 0004-0010, 0004-0010 KW - Endotoxins KW - 0 KW - Tumor Necrosis Factor-alpha KW - Cholera Toxin KW - 9012-63-9 KW - Abridged Index Medicus KW - Index Medicus KW - Drug Therapy, Combination KW - Animals KW - Survival Rate KW - Infusions, Intravenous KW - Mice, Inbred C57BL KW - Escherichia coli KW - Endotoxins -- adverse effects KW - Disease Models, Animal KW - Mice KW - Drug Evaluation, Preclinical KW - Female KW - Sarcoma, Experimental -- drug therapy KW - Tumor Necrosis Factor-alpha -- administration & dosage KW - Cholera Toxin -- pharmacology KW - Cholera Toxin -- administration & dosage KW - Tumor Necrosis Factor-alpha -- adverse effects KW - Sarcoma, Experimental -- pathology KW - Sarcoma, Experimental -- mortality KW - Cholera Toxin -- therapeutic use KW - Tumor Necrosis Factor-alpha -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73318779?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+surgery+%28Chicago%2C+Ill.+%3A+1960%29&rft.atitle=Cholera+toxin+pretreatment+protects+against+tumor+necrosis+factor+lethality+without+compromising+tumor+response+to+therapy.&rft.au=Block%2C+M+I%3BAlexander%2C+H+R%3BNorton%2C+J+A&rft.aulast=Block&rft.aufirst=M&rft.date=1992-11-01&rft.volume=127&rft.issue=11&rft.spage=1330&rft.isbn=&rft.btitle=&rft.title=Archives+of+surgery+%28Chicago%2C+Ill.+%3A+1960%29&rft.issn=00040010&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-08 N1 - Date created - 1992-12-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of MgCl2 on the release and recycling of heparan sulfate proteoglycans in a rat parathyroid cell line. AN - 73294301; 1416969 AB - Divalent cations, such as Mg2+, Ba2+, and Co2+, are known to mimic the effects of Ca2+ in parathyroid cells, but it is not clear whether the mechanism of their action is the same as that of Ca2+. We have shown that extracellular Ca2+ concentration ([Ca2+]e) regulates the distribution and recycling of cell-surface heparan sulfate (HS) proteoglycans in a rat parathyroid cell line; at normal to high [Ca2+]e (e.g., 2 mM) HS proteoglycans are primarily localized intracellularly, while at low [Ca2+]e (0.05 mM) they are translocated to the cell surface and rapidly recycle (Takeuchi, Y., Sakaguchi, K., Yanagishita, M., Aurbach, G. D., and Hascall, V. C., 1990, J. Biol. Chem. 265, 13661-13668). We now show that a high concentration of Mg2+ (8 mM) reduces the amount of recycling HS proteoglycans in low [Ca2+]e. However, the primary effects of high Ca2+ and high Mg2+ on the recycling HS proteoglycans are different. High [Ca2+]e causes translocation of HS proteoglycans to intracellular compartments, while high Mg2+ stimulates cleavage of their core proteins and subsequent shedding of HS proteoglycans into the medium, thereby depleting the recycling molecules. However, high Mg2+ does not induce shedding of HS proteoglycans in high [Ca2+]e. The effects of Ba2+ and Co2+ were similar to those of Mg2+, but Sr2+ showed no significant effects on HS proteoglycan translocation. Otherwise, 8 mM Mg2+ did not alter biosynthesis or intracellular catabolism of HS proteoglycans. These observations suggest that the recycling of HS proteoglycans in parathyroid cells is sensitive only to [Ca2+]e, whereas several other divalent cations can deplete the recycling HS proteoglycans by a distinctly different mechanism. Thus, the mechanism by which Ca2+ regulates the amounts of the recycling HS proteoglycans may be more physiological and play a functional role in parathyroid cells. JF - Archives of biochemistry and biophysics AU - Takeuchi, Y AU - Yanagishita, M AU - Hascall, V C AD - Bone Research Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/11/01/ PY - 1992 DA - 1992 Nov 01 SP - 371 EP - 379 VL - 298 IS - 2 SN - 0003-9861, 0003-9861 KW - Cations, Divalent KW - 0 KW - Heparan Sulfate Proteoglycans KW - Proteoglycans KW - Sulfates KW - Sulfur Radioisotopes KW - Magnesium Chloride KW - 02F3473H9O KW - Tritium KW - 10028-17-8 KW - Heparitin Sulfate KW - 9050-30-0 KW - Leucine KW - GMW67QNF9C KW - Calcium Chloride KW - M4I0D6VV5M KW - Glucosamine KW - N08U5BOQ1K KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Electrophoresis, Polyacrylamide Gel KW - Chromatography, Ion Exchange KW - Rats KW - Sulfates -- metabolism KW - Kinetics KW - Leucine -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Glucosamine -- metabolism KW - Calcium Chloride -- pharmacology KW - Cell Line KW - Cations, Divalent -- pharmacology KW - Proteoglycans -- biosynthesis KW - Heparitin Sulfate -- metabolism KW - Proteoglycans -- metabolism KW - Parathyroid Glands -- metabolism KW - Magnesium Chloride -- pharmacology KW - Proteoglycans -- isolation & purification KW - Heparitin Sulfate -- isolation & purification KW - Heparitin Sulfate -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73294301?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+biochemistry+and+biophysics&rft.atitle=Effects+of+MgCl2+on+the+release+and+recycling+of+heparan+sulfate+proteoglycans+in+a+rat+parathyroid+cell+line.&rft.au=Takeuchi%2C+Y%3BYanagishita%2C+M%3BHascall%2C+V+C&rft.aulast=Takeuchi&rft.aufirst=Y&rft.date=1992-11-01&rft.volume=298&rft.issue=2&rft.spage=371&rft.isbn=&rft.btitle=&rft.title=Archives+of+biochemistry+and+biophysics&rft.issn=00039861&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-13 N1 - Date created - 1992-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Changes in T-helper cell function in human immunodeficiency virus-infected children during didanosine therapy as a measure of antiretroviral activity. AN - 73281636; 1421391 AB - Didanosine has shown activity against the human immunodeficiency virus (HIV) in both children and adults. We prospectively assessed T-helper cell (Th) function as determined by in vitro interleukin-2 (IL-2) production in response to a panel of T-cell stimuli in 22 HIV-infected children before and during didanosine therapy and we correlated the incidence of opportunistic and recurrent bacterial infections with changes in p24 antigen and CD4 counts. Didanosine (270, 360, or 540 mg/m2/d) was administered orally for periods ranging from 8 to 40 weeks (mean, 24 weeks). Five of six asymptomatic patients (Centers for Disease Control P-1) compared with 6 of 16 symptomatic (P-2) patients exhibited improved Th function (greater than threefold increase in IL-2 production to at least 2 of the 4 stimuli) during therapy. Of 12 patients without infections during therapy, 9 (75%) showed improvement in Th function, compared with only 2 of 10 patients with infections (P = .03). Notably, the incidence of infections was not correlated with improvements in CD4 count or decreases in p24 antigen. Improvement in Th function during didanosine therapy is correlated with decreased incidence of infections. Assessment of Th function may provide an additional measurement of immunologic response to antiretroviral therapy. JF - Blood AU - Clerici, M AU - Roilides, E AU - Butler, K M AU - DePalma, L AU - Venzon, D AU - Shearer, G M AU - Pizzo, P A AD - Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/11/01/ PY - 1992 DA - 1992 Nov 01 SP - 2196 EP - 2202 VL - 80 IS - 9 SN - 0006-4971, 0006-4971 KW - Interleukin-2 KW - 0 KW - Didanosine KW - K3GDH6OH08 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Infant KW - Reference Values KW - Cells, Cultured KW - Humans KW - Adult KW - Interleukin-2 -- biosynthesis KW - Follow-Up Studies KW - Child KW - Adolescent KW - Male KW - Female KW - Child, Preschool KW - Didanosine -- toxicity KW - Didanosine -- therapeutic use KW - HIV Infections -- immunology KW - HIV Infections -- drug therapy KW - T-Lymphocytes, Helper-Inducer -- drug effects KW - T-Lymphocytes, Helper-Inducer -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73281636?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Blood&rft.atitle=Changes+in+T-helper+cell+function+in+human+immunodeficiency+virus-infected+children+during+didanosine+therapy+as+a+measure+of+antiretroviral+activity.&rft.au=Clerici%2C+M%3BRoilides%2C+E%3BButler%2C+K+M%3BDePalma%2C+L%3BVenzon%2C+D%3BShearer%2C+G+M%3BPizzo%2C+P+A&rft.aulast=Clerici&rft.aufirst=M&rft.date=1992-11-01&rft.volume=80&rft.issue=9&rft.spage=2196&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-07 N1 - Date created - 1992-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Recombinant toxins containing the variable domains of the anti-Tac monoclonal antibody to the interleukin-2 receptor kill malignant cells from patients with chronic lymphocytic leukemia. AN - 73277002; 1421405 AB - We have previously shown that the variable domains of the monoclonal antibody anti-Tac [anti-Tac(Fv)] can be fused to derivatives of Pseudomonas exotoxin (PE) or diphtheria toxin (DT) to produce recombinant immunotoxins that kill interleukin-2 (IL-2) receptor-bearing cells. We now report that two of these single-chain recombinant immunotoxins, anti-Tac(Fv)-PE40KDEL and DT388-anti-Tac(Fv), are cytotoxic toward peripheral blood mononuclear cells (PBMCs) from patients with chronic lymphocytic leukemia (CLL). In anti-Tac(Fv)-PE40KDEL, anti-Tac(Fv) is genetically fused to the amino terminus of PE40KDEL, a recombinant form of PE which contains amino acids 253-608 of PE and the -KDEL mutation at the carboxyl terminus. In DT388-anti-Tac(Fv), anti-Tac(Fv) is fused to the carboxyl terminus of the first 388 amino acids of DT. PBMCs from 14 patients were incubated with the recombinant toxins for 60 hours, and [3H]-leucine incorporation was measured. Anti-Tac(Fv)-PE40KDEL was cytotoxic to 7 of the 14 patient samples, with half-maximal inhibition of protein synthesis (IC50) achieved at 1.2 to 9 ng/mL (1.8 to 13 x 10(-11) mol/L). DT388-anti-Tac(Fv) was cytotoxic to 11 of the 14 samples, with IC50s ranging from less than 1 to 250 ng/mL. DT388-IL-2, in which the first 388 amino acids of DT are attached to IL-2, was marginally cytotoxic toward only 4 of 13 CLL samples tested with IC50s ranging from 100 to 550 ng/mL. Trypan blue staining of cells from several patients indicated that inhibition of protein synthesis correlated with cell death. Binding assays using [3H]-anti-Tac indicated that the CLL cells from nine of the patients contained between 400 and 2,500 sites per cell. Cells from another patient, which were resistant to both anti-Tac(Fv)-PE40KDEL and DT388-anti-Tac(Fv), had less than 100 sites per cell. We conclude that anti-Tac(Fv)-PE40KDEL and DT388-anti-Tac(Fv) can kill CLL cells which have low numbers of IL-2 receptors, and should be investigated further for therapy of this disease. JF - Blood AU - Kreitman, R J AU - Chaudhary, V K AU - Kozak, R W AU - FitzGerald, D J AU - Waldman, T A AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/11/01/ PY - 1992 DA - 1992 Nov 01 SP - 2344 EP - 2352 VL - 80 IS - 9 SN - 0006-4971, 0006-4971 KW - Antibodies, Monoclonal KW - 0 KW - Bacterial Toxins KW - Exotoxins KW - Immunotoxins KW - Receptors, Interleukin-2 KW - Recombinant Fusion Proteins KW - Recombinant Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Abridged Index Medicus KW - Index Medicus KW - Recombinant Proteins -- pharmacology KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - Humans KW - Recombinant Fusion Proteins -- pharmacology KW - Aged KW - Middle Aged KW - Antibodies, Monoclonal -- pharmacology KW - Pseudomonas aeruginosa KW - Male KW - Female KW - Exotoxins -- genetics KW - Exotoxins -- pharmacology KW - Leukemia, Lymphocytic, Chronic, B-Cell -- blood KW - Monocytes -- pathology KW - Monocytes -- drug effects KW - Immunotoxins -- pharmacology KW - Receptors, Interleukin-2 -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73277002?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Blood&rft.atitle=Recombinant+toxins+containing+the+variable+domains+of+the+anti-Tac+monoclonal+antibody+to+the+interleukin-2+receptor+kill+malignant+cells+from+patients+with+chronic+lymphocytic+leukemia.&rft.au=Kreitman%2C+R+J%3BChaudhary%2C+V+K%3BKozak%2C+R+W%3BFitzGerald%2C+D+J%3BWaldman%2C+T+A%3BPastan%2C+I&rft.aulast=Kreitman&rft.aufirst=R&rft.date=1992-11-01&rft.volume=80&rft.issue=9&rft.spage=2344&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-07 N1 - Date created - 1992-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Occupational risk factors for multiple myeloma among Danish men. AN - 73264400; 1420859 AB - A large population-based case-control study evaluated occupational exposures in 1,098 Danish males diagnosed with multiple myeloma from 1970 to 1984 and in 4,169 age- and gender-matched controls alive at the time of case-diagnosis. Industrial histories were obtained from the Supplementary Pension Fund which, since 1964, has recorded employments of adult Danes; occupation came from subjects' most recent tax records. Four industrial hygienists created a job-exposure matrix for 47 substances based on 15,000 unique industry/occupation combinations in subjects' histories. Risk of myeloma was significantly elevated among road and railroad workers, precision metalworkers, and workers in the transportation and communication industries. Risk increased significantly with duration of employment in: production of synthetic yarns, plastic packaging, and miscellaneous chemical compounds; fabricating structural metal and stationary tanks; body factories; electrical plants; and retail sale of paint and wallpaper. Risks of myeloma were elevated, though statistically nonsignificantly, in all categories of exposure to gasoline and engine exhausts. Risks rose with likelihood and duration of exposure to phthalates, and were statistically significant and nearly fivefold with probable exposure to vinyl chloride for five or more years. After adjusting for multiple exposures and disregarding exposures within 10 years of diagnosis (or selection as a control), probable exposure to vinyl chloride was associated with increased risk of myeloma, which rose to fivefold with longer exposure. Associations with gasoline, engine exhausts, and phthalates persisted, but were inconsistent with duration and probability of exposure. Previously reported associations with agriculture were not confirmed by these data. JF - Cancer causes & control : CCC AU - Heineman, E F AU - Olsen, J H AU - Pottern, L M AU - Gomez, M AU - Raffn, E AU - Blair, A AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 10892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 555 EP - 568 VL - 3 IS - 6 SN - 0957-5243, 0957-5243 KW - Gasoline KW - 0 KW - Phthalic Acids KW - Smoke KW - phthalic acid KW - 6O7F7IX66E KW - Vinyl Chloride KW - WD06X94M2D KW - Index Medicus KW - Odds Ratio KW - Age Factors KW - Humans KW - Communication KW - Aged KW - Transportation KW - Aged, 80 and over KW - Risk Factors KW - Military Personnel KW - Case-Control Studies KW - Denmark -- epidemiology KW - Incidence KW - Middle Aged KW - Occupations KW - Time Factors KW - Chemical Industry KW - Male KW - Occupational Exposure KW - Multiple Myeloma -- epidemiology KW - Occupational Diseases -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73264400?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+causes+%26+control+%3A+CCC&rft.atitle=Occupational+risk+factors+for+multiple+myeloma+among+Danish+men.&rft.au=Heineman%2C+E+F%3BOlsen%2C+J+H%3BPottern%2C+L+M%3BGomez%2C+M%3BRaffn%2C+E%3BBlair%2C+A&rft.aulast=Heineman&rft.aufirst=E&rft.date=1992-11-01&rft.volume=3&rft.issue=6&rft.spage=555&rft.isbn=&rft.btitle=&rft.title=Cancer+causes+%26+control+%3A+CCC&rft.issn=09575243&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-18 N1 - Date created - 1992-12-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Partial characterization, progressive development and correlations of some neoplastic characters in 20-methylcholanthrene-induced transformed murine embryonal fibroblasts. AN - 73308605; 1423239 AB - Non-trypsinized primary fibroblast cells from 20-day-old Swiss mouse embryo was transformed by 20-methylcholanthrene (MCA) and was designated as CNCI-PM-20. The progressive development of some transformation related characters such as morphological alterations, reduced population doubling time, increased saturation density, reduced serum requirement, increased plating efficiency, loss of density dependent growth inhibition, anchorage-independent growth and tumorigenicity in mice clearly demonstrated the multistep process of carcinogenesis as well as the neoplastic nature of the cell line. Furthermore, the association of reduced requirement of serum and loss of density-dependent growth inhibition with tumorigenicity were also observed. Finally, anchorage-independent growth, greater malignant nature of transformed foci and increased number of giant cells may be required for tumorigenicity of this cell line. JF - Cancer letters AU - Mukherjee, P AU - Das, S K AD - Department of Tissue Culture, Chittaranjan National Cancer Institute (Research Unit), Calcutta, India. Y1 - 1992/10/30/ PY - 1992 DA - 1992 Oct 30 SP - 1 EP - 12 VL - 67 IS - 1 SN - 0304-3835, 0304-3835 KW - Methylcholanthrene KW - 56-49-5 KW - Index Medicus KW - Animals KW - Cell Count KW - Mice KW - Pregnancy KW - Neoplasm Transplantation KW - Fibroblasts -- pathology KW - Cells, Cultured KW - Blood Physiological Phenomena KW - Embryo, Mammalian KW - Female KW - Male KW - Cell Division KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73308605?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+letters&rft.atitle=Partial+characterization%2C+progressive+development+and+correlations+of+some+neoplastic+characters+in+20-methylcholanthrene-induced+transformed+murine+embryonal+fibroblasts.&rft.au=Mukherjee%2C+P%3BDas%2C+S+K&rft.aulast=Mukherjee&rft.aufirst=P&rft.date=1992-10-30&rft.volume=67&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Cancer+letters&rft.issn=03043835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-15 N1 - Date created - 1992-12-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - N-acetylaspartylglutamate acts as an agonist upon homomeric NMDA receptor (NMDAR1) expressed in Xenopus oocytes. AN - 73229693; 1356833 AB - The electrophysiological effects of N-acetylaspartylglutamate (NAAG), an endogenous peptide restrictively distributed in the central nervous system, were studied using Xenopus oocytes injected with RNAs transcribed from cloned glutamate receptor cDNAs. NAAG induced an inward current, dose dependently, in oocytes injected with RNA for an N-methyl-D-aspartate receptor subunit (NMDAR1). In contrast, the oocytes injected with RNAs for AMPA-selective glutamate receptors (GluR1, GluR3, GluR1+GluR2 and GluR2+GluR3) scarcely responded to NAAG, and the oocytes injected with RNA for kainate receptor (GluR6) did not respond to NAAG. The half-maximal response (ED50) value of NAAG on expressed NMDAR1 was 185 microM, which shows that NAAG is about 115-times less potent than L-glutamate (Glu), the ED50 of which value was 1.6 microM. The maximal current amplitude induced by NAAG was about 70% of that by Glu. NAAG-induced current in NMDAR1-injected oocytes was potentiated by glycine, dose-dependently antagonized by DL-2-amino-5-phosphonovaleric acid, and blocked by magnesium ions in a voltage-dependent fashion. These results suggest that NAAG is one of the endogenous agonists selective for NMDAR1. JF - FEBS letters AU - Sekiguchi, M AU - Wada, K AU - Wenthold, R J AD - Laboratory of Neurochemistry, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/10/26/ PY - 1992 DA - 1992 Oct 26 SP - 285 EP - 289 VL - 311 IS - 3 SN - 0014-5793, 0014-5793 KW - Dipeptides KW - 0 KW - Glutamates KW - Receptors, N-Methyl-D-Aspartate KW - Recombinant Proteins KW - isospaglumic acid KW - 1W8M12WXYL KW - Glutamic Acid KW - 3KX376GY7L KW - N-Methylaspartate KW - 6384-92-5 KW - 2-Amino-5-phosphonovalerate KW - 76726-92-6 KW - Kainic Acid KW - SIV03811UC KW - Index Medicus KW - Animals KW - Recombinant Proteins -- drug effects KW - Kainic Acid -- pharmacology KW - Dose-Response Relationship, Drug KW - Transcription, Genetic KW - Cloning, Molecular KW - Xenopus laevis KW - 2-Amino-5-phosphonovalerate -- pharmacology KW - Recombinant Proteins -- metabolism KW - Glutamates -- pharmacology KW - N-Methylaspartate -- pharmacology KW - Kinetics KW - Membrane Potentials -- drug effects KW - Female KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Oocytes -- drug effects KW - Oocytes -- physiology KW - Receptors, N-Methyl-D-Aspartate -- genetics KW - Dipeptides -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73229693?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+letters&rft.atitle=N-acetylaspartylglutamate+acts+as+an+agonist+upon+homomeric+NMDA+receptor+%28NMDAR1%29+expressed+in+Xenopus+oocytes.&rft.au=Sekiguchi%2C+M%3BWada%2C+K%3BWenthold%2C+R+J&rft.aulast=Sekiguchi&rft.aufirst=M&rft.date=1992-10-26&rft.volume=311&rft.issue=3&rft.spage=285&rft.isbn=&rft.btitle=&rft.title=FEBS+letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-25 N1 - Date created - 1992-11-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Angiogenin is a cytotoxic, tRNA-specific ribonuclease in the RNase A superfamily. AN - 73242915; 1400510 AB - Angiogenin is a 14.4-kDa human plasma protein with 65% homology to RNase A that retains the key active site residues and three of the four RNase A disulfide bonds. We demonstrate that recombinant angiogenin functions as a cytotoxic tRNA-specific RNase in cell-free lysates and when injected into Xenopus oocytes. Inhibition of protein synthesis by angiogenin correlates with degradation of endogenous oocyte tRNA. Exogenous, radiolabeled tRNA is also hydrolyzed by angiogenin, whereas oocyte rRNA and mRNA are not detectably degraded by angiogenin. Protein synthesis was restored to angiogenin-injected oocytes by injecting the RNase inhibitor RNasin plus total Xenopus or calf liver tRNAs, thereby demonstrating that the tRNA degradation induced by angiogenin was the sole cause of cytotoxicity. A similar tRNA-reversible inhibition of protein synthesis was seen in rabbit reticulocyte lysates. Angiogenin therefore appears to be a specific cellular tRNase, whereas five homologues in the RNase A superfamily lack angiogenin's specificity for tRNA. One of these homologues purified from human eosinophils, eosinophil-derived neurotoxin, nonspecifically degrades oocyte RNA similar to RNase A and is also cytotoxic at very low concentrations. JF - The Journal of biological chemistry AU - Saxena, S K AU - Rybak, S M AU - Davey, R T AU - Youle, R J AU - Ackerman, E J AD - Genetics and Biochemistry Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10/25/ PY - 1992 DA - 1992 Oct 25 SP - 21982 EP - 21986 VL - 267 IS - 30 SN - 0021-9258, 0021-9258 KW - Cytotoxins KW - 0 KW - Proteins KW - RNA, Transfer KW - 9014-25-9 KW - Ribonucleases KW - EC 3.1.- KW - angiogenin KW - EC 3.1.27.- KW - Ribonuclease, Pancreatic KW - EC 3.1.27.5 KW - Index Medicus KW - Protein Biosynthesis KW - Animals KW - Cattle KW - Blotting, Northern KW - Sequence Alignment KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Substrate Specificity KW - Sequence Homology, Amino Acid KW - Cell Survival KW - Cytotoxins -- classification KW - Cytotoxins -- metabolism KW - RNA, Transfer -- metabolism KW - Proteins -- classification KW - Ribonucleases -- genetics KW - Cytotoxins -- genetics KW - Ribonucleases -- metabolism KW - Ribonuclease, Pancreatic -- metabolism KW - Proteins -- metabolism KW - Proteins -- genetics KW - Ribonucleases -- classification KW - Ribonuclease, Pancreatic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73242915?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Angiogenin+is+a+cytotoxic%2C+tRNA-specific+ribonuclease+in+the+RNase+A+superfamily.&rft.au=Saxena%2C+S+K%3BRybak%2C+S+M%3BDavey%2C+R+T%3BYoule%2C+R+J%3BAckerman%2C+E+J&rft.aulast=Saxena&rft.aufirst=S&rft.date=1992-10-25&rft.volume=267&rft.issue=30&rft.spage=21982&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-25 N1 - Date created - 1992-11-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Niacinamide blocks 3-acetylpyridine toxicity of cerebellar granule cells in vitro. AN - 73403985; 1361407 AB - 3-Acetylpyridine (3AP) is a potent neurotoxin when administered to laboratory animals. However, its neurotoxic effects have not been investigated extensively in vitro. Cultured cerebellar granule cells are killed by concentrations of 3AP of 0.1-1 mM (ED50 = 220 microM) but not by its 2-acetyl and 4-acetyl analogues. The toxicity of 3AP is enhanced by preexposure to subtoxic concentrations of N-methyl-D-aspartate (NMDA) and is unaffected by the NMDA receptor antagonists MK-801 or APV, as well as by deprenyl, mazindol, or tetrahydrofolic acid. However, 3AP toxicity is completely blocked by preincubating cerebellar granule cells with low concentrations of niacinamide. These data lead us to suggest that 3AP toxicity is due to the substitution of 3AP for niacinamide in the formation of niacinamide adenine dinucleotides (NAD(P)). JF - Brain research AU - Weller, M AU - Marini, A M AU - Paul, S M AD - Section on Molecular Pharmacology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1992/10/23/ PY - 1992 DA - 1992 Oct 23 SP - 160 EP - 164 VL - 594 IS - 1 SN - 0006-8993, 0006-8993 KW - Excitatory Amino Acid Antagonists KW - 0 KW - Glutamates KW - Pyridines KW - Tetrahydrofolates KW - 3-acetylpyridine KW - 00QT8FX306 KW - Niacinamide KW - 25X51I8RD4 KW - Selegiline KW - 2K1V7GP655 KW - Glutamic Acid KW - 3KX376GY7L KW - 5,6,7,8-tetrahydrofolic acid KW - 43ZWB253H4 KW - N-Methylaspartate KW - 6384-92-5 KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - 2-Amino-5-phosphonovalerate KW - 76726-92-6 KW - Mazindol KW - C56709M5NH KW - Index Medicus KW - Rats KW - Animals KW - Selegiline -- pharmacology KW - Rats, Sprague-Dawley KW - Mazindol -- pharmacology KW - 2-Amino-5-phosphonovalerate -- pharmacology KW - N-Methylaspartate -- pharmacology KW - Tetrahydrofolates -- pharmacology KW - Glutamates -- toxicity KW - Drug Synergism KW - Dizocilpine Maleate -- pharmacology KW - Niacinamide -- pharmacology KW - Cerebellum -- cytology KW - Pyridines -- toxicity KW - Neurons -- drug effects KW - Cerebellum -- drug effects KW - Pyridines -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73403985?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Niacinamide+blocks+3-acetylpyridine+toxicity+of+cerebellar+granule+cells+in+vitro.&rft.au=Weller%2C+M%3BMarini%2C+A+M%3BPaul%2C+S+M&rft.aulast=Weller&rft.aufirst=M&rft.date=1992-10-23&rft.volume=594&rft.issue=1&rft.spage=160&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-27 N1 - Date created - 1993-01-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dietary retinoids are essential for skin papilloma formation induced by either the two-stage or the complete tumorigenesis model in female SENCAR mice. AN - 73408606; 1451104 AB - Our previous work has shown that dietary retinoic acid (RA) is necessary for skin tumor formation induced by the two-stage protocol with the initiator 7,12-dimethylbenz[a]anthracene (DMBA) and the promoter 12-O-tetradecanoyl phorbol-13-acetate (TPA) (De Luca et al., Cancer Res., 36 (1976) 2334-2339). Here we report that retinoids are required for tumorigenesis by the two-stage as well as by the complete tumorigenesis protocol. Mice were treated with a single dose of DMBA (20 micrograms), followed by 20 applications of TPA (2 micrograms), or by 20 applications of DMBA (25 micrograms for 2 weeks and 51 micrograms thereafter). Regardless of the tumor induction protocol, tumor formation was inhibited by vitamin A-deficiency, while RA (3 micrograms/g of diet) or retinyl palmitate (RP, 6 micrograms/g) supplementation permitted the appearance of tumors. In addition, in comparison to the purified diets and regardless of their RA levels, the non-purified Purina chow diet enhanced tumor yield especially in the two-stage tumorigenesis protocol. This effect was less striking in mice with tumors induced by the complete tumorigenesis protocol. In summary, dietary retinoids are essential for skin tumor formation induced either by the two-stage or the complete tumorigenesis protocol. JF - Cancer letters AU - De Luca, L M AU - Sly, L AU - Jones, C S AU - Chen, L C AD - Differentiation Control Section, Laboratory of Cellular Carcinogenesis and Tumor Promotion National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/10/21/ PY - 1992 DA - 1992 Oct 21 SP - 233 EP - 239 VL - 66 IS - 3 SN - 0304-3835, 0304-3835 KW - Vitamin A KW - 11103-57-4 KW - retinol palmitate KW - 1D1K0N0VVC KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Vitamin A Deficiency -- physiopathology KW - Body Weight -- drug effects KW - Mice KW - Diet KW - Time Factors KW - Female KW - Tetradecanoylphorbol Acetate -- toxicity KW - Vitamin A -- analogs & derivatives KW - Vitamin A -- administration & dosage KW - Papilloma -- pathology KW - 9,10-Dimethyl-1,2-benzanthracene -- toxicity KW - Vitamin A -- toxicity KW - Skin Neoplasms -- chemically induced KW - Vitamin A -- pharmacology KW - Skin Neoplasms -- pathology KW - Papilloma -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73408606?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+letters&rft.atitle=Dietary+retinoids+are+essential+for+skin+papilloma+formation+induced+by+either+the+two-stage+or+the+complete+tumorigenesis+model+in+female+SENCAR+mice.&rft.au=De+Luca%2C+L+M%3BSly%2C+L%3BJones%2C+C+S%3BChen%2C+L+C&rft.aulast=De+Luca&rft.aufirst=L&rft.date=1992-10-21&rft.volume=66&rft.issue=3&rft.spage=233&rft.isbn=&rft.btitle=&rft.title=Cancer+letters&rft.issn=03043835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-07 N1 - Date created - 1993-01-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Not myositis. A series of chance encounters. AN - 73261734; 1404746 JF - JAMA AU - Plotz, P H AD - Connective Tissue Diseases Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Md 20892. Y1 - 1992/10/21/ PY - 1992 DA - 1992 Oct 21 SP - 2074 EP - 2077 VL - 268 IS - 15 SN - 0098-7484, 0098-7484 KW - Phosphofructokinase-1 KW - EC 2.7.1.11 KW - Abridged Index Medicus KW - Index Medicus KW - Diagnosis, Differential KW - Myxedema -- diagnosis KW - Humans KW - Phosphofructokinase-1 -- deficiency KW - Neuromuscular Diseases -- diagnosis KW - Aged KW - Arteritis -- pathology KW - Muscles -- blood supply KW - Arteritis -- diagnosis KW - Muscular Diseases -- diagnosis KW - Muscular Diseases -- chemically induced KW - Adult KW - Middle Aged KW - Muscles -- pathology KW - Female KW - Myositis -- diagnosis KW - Myositis -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73261734?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=proceeding&rft.jtitle=JAMA&rft.atitle=Not+myositis.+A+series+of+chance+encounters.&rft.au=Plotz%2C+P+H&rft.aulast=Plotz&rft.aufirst=P&rft.date=1992-10-21&rft.volume=268&rft.issue=15&rft.spage=2074&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-04 N1 - Date created - 1992-11-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Construction of a new universal vector for insertional mutagenesis by homologous recombination. AN - 73242182; 1327975 AB - We describe here the construction of a vector (pSSC-9) which can be used for the insertional mutagenesis of any gene for which genomic sequences have been cloned. This vector contains a neomycin-resistance-encoding gene (neoR) which is driven by a modified thymidine kinase (tk) promoter for positive selection. Flanking neoR are two tk genes driven by their own promoters for negative selection of nonhomologous insertions. The neoR and tk cassettes are separated by four unique cloning sites on the right-hand side of the neoR cassette and three unique sites on the left-hand side. The vector also includes two SfiI sites, one on each side of the tk cassettes, for the excision of the cloned genomic DNA fragments along with the selectable markers. Electroporation of pSSC-9 into mouse embryonic stem (ES) cells and cultured diploid mouse adrenal Y-1 cells conferred resistance to G418 and sensitivity to ganciclovir in both cell lines. These results illustrate the expression of the positive and negative selectable markers in two different cell lines and thus suggest that the vector could be used in ES cells, as well as in cultured somatic cells. JF - Gene AU - Chauhan, S S AU - Gottesman, M M AD - Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/10/21/ PY - 1992 DA - 1992 Oct 21 SP - 281 EP - 285 VL - 120 IS - 2 SN - 0378-1119, 0378-1119 KW - neoR KW - tk KW - Recombinant Proteins KW - 0 KW - Phosphotransferases KW - EC 2.7.- KW - Thymidine Kinase KW - EC 2.7.1.21 KW - Kanamycin Kinase KW - EC 2.7.1.95 KW - Ganciclovir KW - P9G3CKZ4P5 KW - Index Medicus KW - Phosphotransferases -- analysis KW - Phosphotransferases -- genetics KW - Animals KW - Thymidine Kinase -- metabolism KW - Mice KW - Phosphotransferases -- metabolism KW - Base Sequence KW - Promoter Regions, Genetic KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - Recombinant Proteins -- metabolism KW - Thymidine Kinase -- analysis KW - Molecular Sequence Data KW - Recombinant Proteins -- analysis KW - Cell Line KW - Thymidine Kinase -- genetics KW - Ganciclovir -- pharmacology KW - Genetic Vectors KW - Recombination, Genetic KW - Mutagenesis, Insertional UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73242182?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene&rft.atitle=Construction+of+a+new+universal+vector+for+insertional+mutagenesis+by+homologous+recombination.&rft.au=Chauhan%2C+S+S%3BGottesman%2C+M+M&rft.aulast=Chauhan&rft.aufirst=S&rft.date=1992-10-21&rft.volume=120&rft.issue=2&rft.spage=281&rft.isbn=&rft.btitle=&rft.title=Gene&rft.issn=03781119&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-25 N1 - Date created - 1992-11-25 N1 - Date revised - 2017-01-13 N1 - Gene symbol - neoR; tk N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Risk of suicide among persons with AIDS. A national assessment. AN - 73230569; 1404744 AB - We sought to describe the rate, risk, trends, methods, and distribution of suicide among persons with the acquired immunodeficiency syndrome (AIDS) in the United States. We used National Center for Health Statistics multiple-cause mortality data from 1987 through 1989 to identify suicides among persons with AIDS (PWAs) and public-access AIDS surveillance data to determine person-years of observation of PWAs. Residents of the United States with death certificates indicating suicide. Death certificates indicating both AIDS and suicide. In 1987 through 1989, a total of 165 suicides among PWAs occurred in 45 states and the District of Columbia. All but one case were male. Among males the rate was 165 per 100,000 person-years of observation, 7.4-fold higher than among demographically similar men in the general population. Self-poisoning with drugs was both the most common method (35%) and the method with the highest standardized mortality ratio (35). Suicide risk for PWAs decreased significantly (P < .05) from 1987 to 1989. Persons with AIDS have an increased risk of suicide, and assessment of such risk should be a standard practice in their care. These assessments should be carefully considered when potentially lethal medications are prescribed. The declining trend in suicide rates between 1987 and 1989 is encouraging; possible causes include emerging therapies for human immunodeficiency virus/AIDS, better psychiatric care for these patients, and lessened social stigma against PWAs. JF - JAMA AU - Coté, T R AU - Biggar, R J AU - Dannenberg, A L AD - National Cancer Institute, Viral Epidemiology Section, Rockville, Md 20852. Y1 - 1992/10/21/ PY - 1992 DA - 1992 Oct 21 SP - 2066 EP - 2068 VL - 268 IS - 15 SN - 0098-7484, 0098-7484 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Risk Factors KW - Humans KW - Adult KW - Middle Aged KW - Adolescent KW - United States -- epidemiology KW - Male KW - Acquired Immunodeficiency Syndrome -- epidemiology KW - Suicide -- trends KW - Suicide -- statistics & numerical data KW - Suicide -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73230569?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=JAMA&rft.atitle=Risk+of+suicide+among+persons+with+AIDS.+A+national+assessment.&rft.au=Cot%C3%A9%2C+T+R%3BBiggar%2C+R+J%3BDannenberg%2C+A+L&rft.aulast=Cot%C3%A9&rft.aufirst=T&rft.date=1992-10-21&rft.volume=268&rft.issue=15&rft.spage=2066&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-04 N1 - Date created - 1992-11-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: JAMA. 1993 Jun 9;269(22):2847-8 [8497086] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - High-performance liquid chromatographic separation of purine deoxyribonucleoside monophosphate-benzo[a]pyrene adducts. AN - 73401054; 1460077 AB - Chromatographic methods that allow the separation of adducts of purine nucleoside 3'-phosphates with the pure enantiomers of the anti-dihydrodiol epoxide of benzo[a]pyrene are developed. The optimization procedure includes evaluation of the effect of buffer molarity, the pH of the buffer, and the role of organic modifiers. The method can be utilized to prepare standards with known absolute configuration that can be further used in the Randerath 32P-postlabeling procedure. JF - Journal of chromatography AU - Peltonen, K AU - Canella, K AU - Dipple, A AD - Chemistry of Carcinogenesis Laboratory, NCI-Frederick Cancer Research and Development Center, MD 21702. Y1 - 1992/10/16/ PY - 1992 DA - 1992 Oct 16 SP - 247 EP - 254 VL - 623 IS - 2 KW - Acetonitriles KW - 0 KW - Furans KW - Nucleotides KW - Purine Nucleosides KW - Benzo(a)pyrene KW - 3417WMA06D KW - tetrahydrofuran KW - 3N8FZZ6PY4 KW - acetonitrile KW - Z072SB282N KW - Index Medicus KW - Stereoisomerism KW - Acetonitriles -- analysis KW - Nucleotides -- analysis KW - Furans -- analysis KW - Benzo(a)pyrene -- analysis KW - Chromatography, High Pressure Liquid -- methods KW - Purine Nucleosides -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73401054?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+chromatography&rft.atitle=High-performance+liquid+chromatographic+separation+of+purine+deoxyribonucleoside+monophosphate-benzo%5Ba%5Dpyrene+adducts.&rft.au=Peltonen%2C+K%3BCanella%2C+K%3BDipple%2C+A&rft.aulast=Peltonen&rft.aufirst=K&rft.date=1992-10-16&rft.volume=623&rft.issue=2&rft.spage=247&rft.isbn=&rft.btitle=&rft.title=Journal+of+chromatography&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-12 N1 - Date created - 1993-01-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Preferential activation of [3H]phorbol-12,13-dibutyrate binding by AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) in neonatal striatal cell cultures. AN - 73355532; 1280525 AB - Activation of excitatory amino acid receptors increased [3H]phorbol-12,13-dibutyrate ([3H]PdBu) binding in four week cultures of striatal cells from postnatal day 7 rat pups (PN7), and in PN7 cells co-cultured the fourth week with striatal cells from postnatal day 1 rat pups. Kainate (KA), trans-1-amino-cyclopentyl-1,3-dicarboxylate (ACPD), and N-methyl-D-aspartate (NMDA) increased [3H]PdBu binding equally in both types of cultures, but alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) increased binding by 3-fold in the co-cultures. Thus, [3H]PdBu binding in these two types of striatal cultures offers a simple model system for studying the regulation of AMPA/KA receptor responses. JF - Brain research AU - McMillian, M AU - Hong, J S AU - Pennypacker, K R AD - Neuropharmacology Section, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, NC 27709. Y1 - 1992/10/16/ PY - 1992 DA - 1992 Oct 16 SP - 307 EP - 310 VL - 593 IS - 2 SN - 0006-8993, 0006-8993 KW - Glial Fibrillary Acidic Protein KW - 0 KW - Neurotoxins KW - Cycloleucine KW - 0TQU7668EI KW - 1-amino-1,3-dicarboxycyclopentane KW - 111900-32-4 KW - Ibotenic Acid KW - 2552-55-8 KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - N-Methylaspartate KW - 6384-92-5 KW - alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid KW - 77521-29-0 KW - Phosphopyruvate Hydratase KW - EC 4.2.1.11 KW - Kainic Acid KW - SIV03811UC KW - Index Medicus KW - Animals KW - Kainic Acid -- pharmacology KW - Cycloleucine -- pharmacology KW - Cycloleucine -- analogs & derivatives KW - Neurotoxins -- pharmacology KW - Binding Sites KW - Rats KW - Animals, Newborn KW - Rats, Inbred F344 KW - Phosphopyruvate Hydratase -- analysis KW - Cells, Cultured KW - N-Methylaspartate -- pharmacology KW - Glial Fibrillary Acidic Protein -- analysis KW - Neurons -- metabolism KW - Phorbol 12,13-Dibutyrate -- metabolism KW - Ibotenic Acid -- analogs & derivatives KW - Neurons -- drug effects KW - Corpus Striatum -- metabolism KW - Neurons -- cytology KW - Ibotenic Acid -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73355532?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Preferential+activation+of+%5B3H%5Dphorbol-12%2C13-dibutyrate+binding+by+AMPA+%28alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic+acid%29+in+neonatal+striatal+cell+cultures.&rft.au=McMillian%2C+M%3BHong%2C+J+S%3BPennypacker%2C+K+R&rft.aulast=McMillian&rft.aufirst=M&rft.date=1992-10-16&rft.volume=593&rft.issue=2&rft.spage=307&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-06 N1 - Date created - 1993-01-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Neural computing in cancer drug development: predicting mechanism of action. AN - 73257154; 1411538 AB - Described here are neural networks capable of predicting a drug's mechanism of action from its pattern of activity against a panel of 60 malignant cell lines in the National Cancer Institute's drug screening program. Given six possible classes of mechanism, the network misses the correct category for only 12 out of 141 agents (8.5 percent), whereas linear discriminant analysis, a standard statistical technique, misses 20 out of 141 (14.2 percent). The success of the neural net indicates several things. (i) The cell line response patterns are rich in information about mechanism. (ii) Appropriately designed neural networks can make effective use of that information. (iii) Trained networks can be used to classify prospectively the more than 10,000 agents per year tested by the screening program. Related networks, in combination with classical statistical tools, will help in a variety of ways to move new anticancer agents through the pipeline from in vitro studies to clinical application. JF - Science (New York, N.Y.) AU - Weinstein, J N AU - Kohn, K W AU - Grever, M R AU - Viswanadhan, V N AU - Rubinstein, L V AU - Monks, A P AU - Scudiero, D A AU - Welch, L AU - Koutsoukos, A D AU - Chiausa, A J AD - Laboratory of Mathematical Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/10/16/ PY - 1992 DA - 1992 Oct 16 SP - 447 EP - 451 VL - 258 IS - 5081 SN - 0036-8075, 0036-8075 KW - Alkylating Agents KW - 0 KW - Antineoplastic Agents KW - Growth Inhibitors KW - Index Medicus KW - Tumor Cells, Cultured -- drug effects KW - Neural Networks (Computer) KW - Humans KW - In Vitro Techniques KW - Databases, Factual KW - Drug Evaluation, Preclinical KW - Antineoplastic Agents -- classification KW - Drug Design UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73257154?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft.atitle=Neural+computing+in+cancer+drug+development%3A+predicting+mechanism+of+action.&rft.au=Weinstein%2C+J+N%3BKohn%2C+K+W%3BGrever%2C+M+R%3BViswanadhan%2C+V+N%3BRubinstein%2C+L+V%3BMonks%2C+A+P%3BScudiero%2C+D+A%3BWelch%2C+L%3BKoutsoukos%2C+A+D%3BChiausa%2C+A+J&rft.aulast=Weinstein&rft.aufirst=J&rft.date=1992-10-16&rft.volume=258&rft.issue=5081&rft.spage=447&rft.isbn=&rft.btitle=&rft.title=Science+%28New+York%2C+N.Y.%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-25 N1 - Date created - 1992-11-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mik-beta 1(Fv)-PE40, a recombinant immunotoxin cytotoxic toward cells bearing the beta-chain of the IL-2 receptor. AN - 73250491; 1401913 AB - Mik-beta 1 is a mAb that binds to the beta subunit of the IL-2R. We have constructed a recombinant single chain immunotoxin Mik-beta 1(Fv)-PE40 by genetically fusing the H and L V domains of Mik-beta 1 to each other via a peptide linker, and then to PE40, a derivative of Pseudomonas exotoxin. Mik-beta 1(Fv)-PE40 was selectively cytotoxic for cells expressing high levels of IL-2R beta (p75) subunit. Mik-beta 1(Fv)-PE40 was cytotoxic to the NK cell line YT-S, which expresses p75 but not p55 subunits, with an IC50 of 6 ng/ml. The ATL line HUT-102 was less sensitive, with an IC50 of 200 ng/ml. However, the IC50 could be lowered to 11 ng/ml when Mik-beta 1(Fv)-PE40 was allowed to bind to HUT-102 cells at 4 degrees C for 4 h before overnight incubation at 37 degrees C. An excess of Mik-beta 1 but not of anti-Tac, the anti-p55 mAb, prevented the cytotoxicity of Mik-beta 1(Fv)-PE40. We constructed a more active version of Mik-beta 1(Fv)-PE40, designated Mik-beta 1(Fv)-PE40KDEL, by converting the carboxyl-terminus of the toxin from -REDLK to -KDEL. Mik-beta 1(Fv)-PE40KDEL showed an IC50 of 2 ng/ml toward YT-S cells and 35 ng/ml toward HUT-102 cells. Binding studies using radioiodinated Mik-beta 1 showed that Mik-beta 1(Fv)-PE40 bound to the p75 receptor subunit with 11% of the affinity of the native Mik-beta 1 antibody. Mik-beta 1(Fv)-PE40 may be a useful reagent to study cells that express IL-2R, and it deserves further study as a possible treatment for cancers in which the malignant cells express high numbers of p75 subunit. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Kreitman, R J AU - Schneider, W P AU - Queen, C AU - Tsudo, M AU - Fitzgerald, D J AU - Waldmann, T A AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/10/15/ PY - 1992 DA - 1992 Oct 15 SP - 2810 EP - 2815 VL - 149 IS - 8 SN - 0022-1767, 0022-1767 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Immunotoxins KW - Receptors, Interleukin-2 KW - Recombinant Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Abridged Index Medicus KW - Index Medicus KW - Protein Biosynthesis KW - Base Sequence KW - Recombinant Proteins -- pharmacology KW - Humans KW - Temperature KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Cell Line KW - Immunotoxins -- chemistry KW - Exotoxins -- pharmacology KW - Immunotoxins -- genetics KW - Immunotoxins -- pharmacology KW - Receptors, Interleukin-2 -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73250491?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Mik-beta+1%28Fv%29-PE40%2C+a+recombinant+immunotoxin+cytotoxic+toward+cells+bearing+the+beta-chain+of+the+IL-2+receptor.&rft.au=Kreitman%2C+R+J%3BSchneider%2C+W+P%3BQueen%2C+C%3BTsudo%2C+M%3BFitzgerald%2C+D+J%3BWaldmann%2C+T+A%3BPastan%2C+I&rft.aulast=Kreitman&rft.aufirst=R&rft.date=1992-10-15&rft.volume=149&rft.issue=8&rft.spage=2810&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-13 N1 - Date created - 1992-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Targeting of the T-cell receptor zeta-chain gene in embryonic stem cells: strategies for generating multiple mutations in a single gene. AN - 73247261; 1409721 AB - The T-cell receptor zeta chain is a member of a family of related proteins that play a critical role in coupling cell-surface receptors to intracellular signaling pathways. To study the role of zeta chain in T-cell ontogeny, we generated targeted mutations of the zeta-chain gene in murine embryonic stem cells. The mutant alleles are predicted to result either in a null phenotype or in the synthesis of a truncated protein capable of supporting T-cell-receptor surface expression but deficient in transmembrane signaling. Both of these targeting events were recovered in a single electroporation experiment with either coelectroporation or a combination deletion/truncation construct. Our results suggest that similar approaches could be used to generate multiple single mutations, modifications of more than one site within a gene, or subtle alterations that rely upon coconversion with the selectable marker gene. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Love, P E AU - Tremblay, M L AU - Westphal, H AD - Laboratory of Mammalian Genes and Development, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/10/15/ PY - 1992 DA - 1992 Oct 15 SP - 9929 EP - 9933 VL - 89 IS - 20 SN - 0027-8424, 0027-8424 KW - Membrane Proteins KW - 0 KW - Oligodeoxyribonucleotides KW - Receptors, Antigen, T-Cell KW - antigen T cell receptor, zeta chain KW - Index Medicus KW - Animals KW - Base Sequence KW - Genes KW - Tumor Cells, Cultured KW - Transfection KW - Oligodeoxyribonucleotides -- chemistry KW - Restriction Mapping KW - Recombination, Genetic KW - In Vitro Techniques KW - Molecular Sequence Data KW - Mice KW - Teratoma KW - Sequence Deletion KW - DNA Mutational Analysis -- methods KW - Membrane Proteins -- genetics KW - Receptors, Antigen, T-Cell -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73247261?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Targeting+of+the+T-cell+receptor+zeta-chain+gene+in+embryonic+stem+cells%3A+strategies+for+generating+multiple+mutations+in+a+single+gene.&rft.au=Love%2C+P+E%3BTremblay%2C+M+L%3BWestphal%2C+H&rft.aulast=Love&rft.aufirst=P&rft.date=1992-10-15&rft.volume=89&rft.issue=20&rft.spage=9929&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-17 N1 - Date created - 1992-11-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1975 Apr;72(4):1441-5 [1055416] Proc Natl Acad Sci U S A. 1984 May;81(10):3153-7 [6328502] Cell. 1992 Jan 10;68(1):83-95 [1531041] Cell. 1991 May 3;65(3):443-9 [1673361] Cell. 1991 Mar 8;64(5):891-901 [1705867] Proc Natl Acad Sci U S A. 1991 Dec 1;88(23):10730-4 [1720548] Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3084-7 [1826563] Proc Natl Acad Sci U S A. 1991 May 1;88(9):3837-41 [1827205] Cell. 1991 Mar 8;64(5):875-8 [1848158] Mol Cell Biol. 1991 May;11(5):2769-77 [1850104] Mol Cell Biol. 1991 Sep;11(9):4509-17 [1875936] Cell. 1991 Sep 6;66(5):1051-66 [1909605] Cell. 1991 Feb 22;64(4):693-702 [1997203] Proc Natl Acad Sci U S A. 1991 May 15;88(10):4294-8 [2034673] Cell. 1991 Jun 28;65(7):1153-63 [2065352] Science. 1990 Jun 8;248(4960):1227-30 [2112266] Nature. 1990 Aug 30;346(6287):847-50 [2202907] Cell. 1990 Sep 21;62(6):1073-85 [2205396] Annu Rev Cell Biol. 1990;6:403-31 [2275818] Nature. 1990 May 3;345(6270):78-80 [2330056] Science. 1990 Jul 13;249(4965):174-7 [2371564] Nature. 1989 Sep 14;341(6238):159-62 [2528695] Nature. 1989 Dec 14;342(6251):803-5 [2532305] EMBO J. 1989 Dec 1;8(12):3651-6 [2583115] Science. 1989 Jun 16;244(4910):1288-92 [2660260] Trends Genet. 1989 Mar;5(3):70-6 [2660363] Proc Natl Acad Sci U S A. 1989 Nov;86(22):8932-5 [2682666] Nature. 1989 Nov 23;342(6248):435-8 [2685607] Annu Rev Genet. 1989;23:199-225 [2694931] J Biol Chem. 1989 Aug 5;264(22):13252-7 [2787796] Cell. 1987 Nov 6;51(3):503-12 [2822260] Cell. 1989 Jan 27;56(2):313-21 [2912572] Proc Natl Acad Sci U S A. 1988 Nov;85(22):8583-7 [3186749] Cell. 1988 Jan 15;52(1):85-95 [3278811] Nucleic Acids Res. 1988 Feb 11;16(3):1215 [3344216] Nature. 1987 Mar 19-25;326(6110):292-5 [3821905] J Embryol Exp Morphol. 1985 Jun;87:27-45 [3897439] Mol Cell Biol. 1985 Apr;5(4):659-66 [3990687] Curr Opin Biotechnol. 1991 Dec;2(6):823-9 [1367955] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of src-family cDNAs reveals distinct mechanisms underlying focus formation in transfected fibroblasts. AN - 73231993; 1383216 AB - Despite the intensive study of both cellular transformation and src-family protein-tyrosine kinases, there have been no direct comparisons of transforming potency for normal members of this gene-family. In this study, the focus-forming activity of normal c-src, fyn, and lck cDNAs were compared in NIH 3T3 cell transfection assays. Focus formation was studied quantitatively, and individual foci were analyzed for phosphotyrosine content and expression of appropriate translational products. Each foci arising from c-src transfectants had a marked increase in phosphotyrosine content, and the majority of these foci expressed a c-src protein with an aberrant carboxyl terminus. Foci derived from lck transfectants also had a marked increase in phosphotyrosine content, and some foci expressed a lck protein with an aberrant carboxyl terminus. In contrast, foci from fyn-transfected cells were not distinguished from G418-selected mass cultures in terms of total phosphotyrosine content or expression of p59fyn. These studies support the previously published concept that overexpression of the normal fyn protein contributes to focus formation in transfected NIH 3T3 cells but suggest that the focus-forming activity observed after c-src or lck transfections is frequently attributable to mutational events. Because lck mutations have not been previously described in transformed foci, we characterized the lck transcript expressed in two foci and identified a novel point mutation that encodes a lck protein with increased in vivo kinase and focus-forming activity. JF - The Journal of biological chemistry AU - Sartor, O AU - McLellan, C A AU - Chiueh, T AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/10/15/ PY - 1992 DA - 1992 Oct 15 SP - 21044 EP - 21051 VL - 267 IS - 29 SN - 0021-9258, 0021-9258 KW - c-src KW - fyn KW - lck KW - src KW - v-src KW - Oligodeoxyribonucleotides KW - 0 KW - Proto-Oncogene Proteins KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - FYN protein, human KW - EC 2.7.10.2 KW - Fyn protein, mouse KW - Lymphocyte Specific Protein Tyrosine Kinase p56(lck) KW - Oncogene Protein pp60(v-src) KW - Proto-Oncogene Proteins c-fyn KW - Proto-Oncogene Proteins pp60(c-src) KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - 3T3 Cells KW - Chickens KW - Base Sequence KW - Transfection KW - Humans KW - Molecular Sequence Data KW - Gene Expression KW - Mice KW - Proto-Oncogene Proteins pp60(c-src) -- isolation & purification KW - Genes, src KW - Multigene Family KW - Proto-Oncogene Proteins -- isolation & purification KW - Proto-Oncogene Proteins pp60(c-src) -- genetics KW - Proto-Oncogene Proteins pp60(c-src) -- biosynthesis KW - Protein-Tyrosine Kinases -- isolation & purification KW - Proto-Oncogenes KW - Oncogene Protein pp60(v-src) -- biosynthesis KW - Proto-Oncogene Proteins -- biosynthesis KW - Protein-Tyrosine Kinases -- genetics KW - Protein-Tyrosine Kinases -- biosynthesis KW - Oncogene Protein pp60(v-src) -- isolation & purification KW - Proto-Oncogene Proteins -- genetics KW - Cell Transformation, Neoplastic KW - Oncogene Protein pp60(v-src) -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73231993?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Comparison+of+src-family+cDNAs+reveals+distinct+mechanisms+underlying+focus+formation+in+transfected+fibroblasts.&rft.au=Sartor%2C+O%3BMcLellan%2C+C+A%3BChiueh%2C+T&rft.aulast=Sartor&rft.aufirst=O&rft.date=1992-10-15&rft.volume=267&rft.issue=29&rft.spage=21044&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-18 N1 - Date created - 1992-11-18 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-src; fyn; lck; src; v-src N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Thapsigargin defines the roles of cellular calcium in secretagogue-stimulated enzyme secretion from pancreatic acini. AN - 73231684; 1383205 AB - In the present study we used thapsigargin (TG), an inhibitor of microsomal calcium ATPase, to evaluate the roles of free cytoplasmic calcium and intracellular stored calcium in secretagogue-stimulated enzyme secretion from rat pancreatic acini. Using microspectrofluorimetry of fura-2-loaded pancreatic acini, we found that TG caused a sustained increase in free cytoplasmic calcium by mobilizing calcium from inositol 1,4,5-trisphosphate-sensitive intracellular stores and by increasing influx of extracellular calcium. TG also caused a small increase in basal amylase secretion, inhibited the stimulation of amylase secretion caused by secretagogues that increase inositol 1,4,5-trisphosphate, and potentiated the stimulation of amylase secretion caused by 12-O-tetradecanoylphorbol-13-acetate or secretagogues that increase cyclic adenosine 3',5'-monophosphate. Bombesin, which like TG increased free cytoplasmic calcium, also potentiated the stimulation of amylase secretion caused by secretagogues that increase cyclic adenosine 3',5'-monophosphate, but did not inhibit the stimulation of amylase secretion caused by secretagogues that increase inositol 1,4,5-trisphosphate. Finally, TG inhibited the sustained phase of cholecystokinin-stimulated amylase secretion and potentiated the time course of vasoactive intestinal peptide-stimulated amylase secretion. The present findings indicate that stimulation of amylase secretion by secretagogues that increase inositol 1,4,5-trisphosphate does not depend on increased free cytoplasmic calcium per se. In contrast, TG-induced potentiation of the stimulation of secretagogues that increase cellular cyclic adenosine 3',5'-monophosphate appears to result from increased free cytoplasmic calcium per se. JF - The Journal of biological chemistry AU - Metz, D C AU - Patto, R J AU - Mrozinski, J E AU - Jensen, R T AU - Turner, R J AU - Gardner, J D AD - Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10/15/ PY - 1992 DA - 1992 Oct 15 SP - 20620 EP - 20629 VL - 267 IS - 29 SN - 0021-9258, 0021-9258 KW - Terpenes KW - 0 KW - Secretin KW - 1393-25-5 KW - 8-Bromo Cyclic Adenosine Monophosphate KW - 23583-48-4 KW - Vasoactive Intestinal Peptide KW - 37221-79-7 KW - Calcimycin KW - 37H9VM9WZL KW - Thapsigargin KW - 67526-95-8 KW - Carbachol KW - 8Y164V895Y KW - Amylases KW - EC 3.2.1.- KW - Calcium-Transporting ATPases KW - EC 3.6.3.8 KW - Sincalide KW - M03GIQ7Z6P KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Bombesin KW - PX9AZU7QPK KW - Calcium KW - SY7Q814VUP KW - Fura-2 KW - TSN3DL106G KW - Index Medicus KW - Vasoactive Intestinal Peptide -- pharmacology KW - Animals KW - Spectrometry, Fluorescence KW - Calcimycin -- pharmacology KW - 8-Bromo Cyclic Adenosine Monophosphate -- pharmacology KW - Sincalide -- pharmacology KW - Rats KW - Rats, Sprague-Dawley KW - Cytoplasm -- metabolism KW - Kinetics KW - In Vitro Techniques KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Secretin -- pharmacology KW - Bombesin -- pharmacology KW - Carbachol -- pharmacology KW - Male KW - Calcium -- metabolism KW - Pancreas -- cytology KW - Calcium-Transporting ATPases -- antagonists & inhibitors KW - Terpenes -- pharmacology KW - Pancreas -- enzymology KW - Amylases -- secretion KW - Pancreas -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73231684?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Thapsigargin+defines+the+roles+of+cellular+calcium+in+secretagogue-stimulated+enzyme+secretion+from+pancreatic+acini.&rft.au=Metz%2C+D+C%3BPatto%2C+R+J%3BMrozinski%2C+J+E%3BJensen%2C+R+T%3BTurner%2C+R+J%3BGardner%2C+J+D&rft.aulast=Metz&rft.aufirst=D&rft.date=1992-10-15&rft.volume=267&rft.issue=29&rft.spage=20620&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-18 N1 - Date created - 1992-11-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of Ras by insulin in 3T3 L1 cells does not involve GTPase-activating protein phosphorylation. AN - 73223895; 1328223 AB - Insulin-induced differentiation of 3T3 L1 cells to adipocytes can be mimicked by the expression of transfected ras oncogenes but not of the tyrosine-kinase oncogenes src and trk. Expression of two different transfected, dominant inhibitory ras mutants resulted in significant inhibition of insulin-induced differentiation, suggesting that endogenous Ras proteins are mediators of insulin signaling in these cells. Exposure of untransfected 3T3 L1 cells to insulin resulted in significant formation of the active Ras.GTP complex, at levels comparable with those resulting from exposure to platelet-derived growth factor. However, whereas exposure of the same cells to platelet-derived growth factor resulted in significant tyrosine phosphorylation of the p21ras GTPase-activating protein (GAP), insulin-treated cells did not show any detectable levels of de novo GAP tyrosine phosphorylation. Interestingly, insulin caused tyrosine phosphorylation of the p62 polypeptide coprecipitated with GAP by anti-GAP antibodies. Insulin-induced activation of cytosolic MAP kinase activity in untransfected 3T3 L1 cells was also mimicked by Ras expression (in the absence of insulin) in the same cells transfected with an inducible ras construct. These results confirm that Ras proteins participate in insulin signaling pathways in these mammalian cells and indicate that activation of cytosolic MAP kinases is an early event occurring downstream from Ras activation. However, tyrosine phosphorylation of GAP appears not to be a significant upstream regulatory event in the activation of Ras by insulin. JF - The Journal of biological chemistry AU - Porras, A AU - Nebreda, A R AU - Benito, M AU - Santos, E AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10/15/ PY - 1992 DA - 1992 Oct 15 SP - 21124 EP - 21131 VL - 267 IS - 29 SN - 0021-9258, 0021-9258 KW - ras KW - src KW - trk KW - v-src KW - Ethers, Cyclic KW - 0 KW - GTPase-Activating Proteins KW - Insulin KW - Platelet-Derived Growth Factor KW - Proteins KW - Proto-Oncogene Proteins KW - ras GTPase-Activating Proteins KW - Guanosine Diphosphate KW - 146-91-8 KW - Okadaic Acid KW - 1W21G5Q4N2 KW - Dexamethasone KW - 7S5I7G3JQL KW - Guanosine Triphosphate KW - 86-01-1 KW - Protein Kinases KW - EC 2.7.- KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Receptor, trkA KW - Glycogen Synthase Kinase 3 KW - EC 2.7.11.26 KW - Phosphoprotein Phosphatases KW - EC 3.1.3.16 KW - Index Medicus KW - Animals KW - Platelet-Derived Growth Factor -- metabolism KW - Guanosine Diphosphate -- metabolism KW - Dexamethasone -- pharmacology KW - Platelet-Derived Growth Factor -- pharmacology KW - Genes, src -- drug effects KW - Guanosine Triphosphate -- metabolism KW - Phosphorylation KW - Adipose Tissue -- drug effects KW - Gene Expression Regulation -- drug effects KW - Adipose Tissue -- enzymology KW - Phosphoprotein Phosphatases -- antagonists & inhibitors KW - 3T3 Cells KW - Adipose Tissue -- cytology KW - Cell Differentiation KW - Mice KW - Ethers, Cyclic -- pharmacology KW - Protein Binding KW - Protein Kinases -- metabolism KW - Transfection KW - Proto-Oncogenes -- drug effects KW - Proto-Oncogene Proteins -- biosynthesis KW - Protein-Tyrosine Kinases -- genetics KW - Genes, ras -- drug effects KW - Protein-Tyrosine Kinases -- biosynthesis KW - Insulin -- pharmacology KW - Proto-Oncogene Proteins -- genetics KW - Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73223895?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Activation+of+Ras+by+insulin+in+3T3+L1+cells+does+not+involve+GTPase-activating+protein+phosphorylation.&rft.au=Porras%2C+A%3BNebreda%2C+A+R%3BBenito%2C+M%3BSantos%2C+E&rft.aulast=Porras&rft.aufirst=A&rft.date=1992-10-15&rft.volume=267&rft.issue=29&rft.spage=21124&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-18 N1 - Date created - 1992-11-18 N1 - Date revised - 2017-01-13 N1 - Gene symbol - ras; src; trk; v-src N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential irreversible insertion of protein kinase C into phospholipid vesicles by phorbol esters and related activators. AN - 73223822; 1400402 AB - Incubation of protein kinase C (PKC) alpha with phorbol 12,13-dibutyrate and phospholipid vesicles promoted a time-dependent irreversible insertion of the enzyme into the vesicles and the generation of a calcium-independent kinase activity. Calcium neither caused insertion nor influenced the insertion induced by the phorbol ester. The effect was strongly dependent on the phosphatidylserine concentration in the vesicle and could also be supported by other anionic phospholipids. An analysis of the structure-activity relations of PKC activators for the calcium-independent kinase activity revealed marked relative differences in potencies for binding and for insertion. Compounds such as phorbol 13-myristate 12-acetate and mezerein were very efficient at inducing insertion. In contrast, 12-deoxyphorbol esters and diacylglycerol were relatively inefficient at inducing insertion, requiring higher concentrations than expected from their binding affinities. The insertion of PKC alpha depended substantially on the length of the aliphatic esters in the 12- and 13-positions of the phorbol derivatives, and once again, potencies for insertion and binding were not directly proportional. Our findings suggest two different sites for ligand interaction on the molecule of PKC alpha with different structure-activity requirements. We speculate that the differential ability of compounds to promote insertion could contribute to the documented marked differences in the biological behavior of PKC activators. JF - The Journal of biological chemistry AU - Kazanietz, M G AU - Krausz, K W AU - Blumberg, P M AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/10/15/ PY - 1992 DA - 1992 Oct 15 SP - 20878 EP - 20886 VL - 267 IS - 29 SN - 0021-9258, 0021-9258 KW - Liposomes KW - 0 KW - Phorbol Esters KW - Phospholipids KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats KW - Animals KW - Models, Structural KW - Phorbol 12,13-Dibutyrate -- metabolism KW - Enzyme Activation KW - Kinetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Calcium -- pharmacology KW - Protein Binding KW - Structure-Activity Relationship KW - Binding Sites KW - Protein Kinase C -- metabolism KW - Phorbol Esters -- pharmacology KW - Brain -- enzymology KW - Phospholipids -- pharmacology KW - Protein Kinase C -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73223822?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Differential+irreversible+insertion+of+protein+kinase+C+into+phospholipid+vesicles+by+phorbol+esters+and+related+activators.&rft.au=Kazanietz%2C+M+G%3BKrausz%2C+K+W%3BBlumberg%2C+P+M&rft.aulast=Kazanietz&rft.aufirst=M&rft.date=1992-10-15&rft.volume=267&rft.issue=29&rft.spage=20878&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-18 N1 - Date created - 1992-11-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sequence specificity of aflatoxin B1-induced mutations in a plasmid replicated in xeroderma pigmentosum and DNA repair proficient human cells. AN - 73200930; 1394191 AB - The mutagenic spectrum induced by aflatoxin-DNA lesions in DNA repair deficient and repair proficient human cells was investigated. The reactive metabolite aflatoxin B1-8,9-epoxide was synthesized and reacted in vitro with the shuttle vector plasmid pS189. Plasmids were transfected into human fibroblasts and allowed to replicate, and the recovered plasmids were screened in indicator bacteria for plasmid survival and mutations in the supF marker gene. Sequence data were obtained from 71 independently arising mutants recovered from DNA repair deficient xeroderma pigmentosum (XP) cells [XP12BE(SV40)] and 60 mutants recovered from a DNA repair proficient cell line (GM0637). Plasmid survival was lower and mutation frequency higher with the XP cells, and the mutation hotspots differed substantially for the 2 cell lines. Most mutations (> 90%) were base substitutions at G:C pairs, only about one-half of which were G:C-->T:A transversions, the expected predominant mutation. One-third of the mutations at GG sites and none of those at isolated Gs were G:C-->A:T transitions. Tandem base substitutions also occurred only at GG sites and were found only with XP cells. The location of mutation hotspots with either cell line did not correlate with the level of modification within the sequence as assessed by a DNA polymerase stop assay. These results suggest that the DNA repair deficiency associated with XP can influence not only the overall frequency of mutations but also the distribution of mutations within a gene. The finding of transition mutations exclusively at GG sites may be of predictive value in attempts to link dietary aflatoxin exposure to cancers associated with specific mutations in the c-ras oncogene and the p53 tumor suppressor gene. JF - Cancer research AU - Levy, D D AU - Groopman, J D AU - Lim, S E AU - Seidman, M M AU - Kraemer, K H AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/10/15/ PY - 1992 DA - 1992 Oct 15 SP - 5668 EP - 5673 VL - 52 IS - 20 SN - 0008-5472, 0008-5472 KW - X-gal KW - lac KW - supF KW - DNA-Binding Proteins KW - 0 KW - Aflatoxin B1 KW - 9N2N2Y55MH KW - Index Medicus KW - Genetic Vectors -- drug effects KW - Base Sequence -- drug effects KW - Mutagenicity Tests KW - Humans KW - Molecular Sequence Data KW - DNA-Binding Proteins -- genetics KW - DNA-Binding Proteins -- toxicity KW - Cell Line, Transformed KW - Xeroderma Pigmentosum -- pathology KW - Mutation -- drug effects KW - DNA Repair KW - Xeroderma Pigmentosum -- genetics KW - Aflatoxin B1 -- toxicity KW - Plasmids -- drug effects KW - Aflatoxin B1 -- genetics KW - DNA Replication -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73200930?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Sequence+specificity+of+aflatoxin+B1-induced+mutations+in+a+plasmid+replicated+in+xeroderma+pigmentosum+and+DNA+repair+proficient+human+cells.&rft.au=Levy%2C+D+D%3BGroopman%2C+J+D%3BLim%2C+S+E%3BSeidman%2C+M+M%3BKraemer%2C+K+H&rft.aulast=Levy&rft.aufirst=D&rft.date=1992-10-15&rft.volume=52&rft.issue=20&rft.spage=5668&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-10 N1 - Date created - 1992-11-10 N1 - Date revised - 2017-01-13 N1 - Gene symbol - X-gal; lac; supF N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Quinolinic acid in culture media used for in vitro neurotoxicology studies. AN - 73449387; 1465223 AB - Serum from several species is frequently added to the incubation media of cells in vitro. The excitotoxin and N-methyl-D-aspartate receptor agonist quinolinic acid was found to be present in serum in concentrations ranging from 59 to 4895 nM. Some neuronal systems are reported to be particularly sensitive to the neurotoxic effects of quinolinic acid. Therefore, quinolinic acid in serum should be considered as a potentially confounding variable in neurotoxicology studies in vitro. JF - Neuroscience letters AU - Heyes, M P AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1992/10/12/ PY - 1992 DA - 1992 Oct 12 SP - 234 EP - 235 VL - 145 IS - 2 SN - 0304-3940, 0304-3940 KW - Culture Media KW - 0 KW - Quinolinic Acid KW - F6F0HK1URN KW - Index Medicus KW - Swine KW - Rats KW - Animals KW - Chickens KW - Cattle KW - Goats KW - Sheep KW - Humans KW - Horses KW - Rabbits KW - Mice KW - Quinolinic Acid -- blood KW - Quinolinic Acid -- toxicity KW - Nervous System Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73449387?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+letters&rft.atitle=Quinolinic+acid+in+culture+media+used+for+in+vitro+neurotoxicology+studies.&rft.au=Heyes%2C+M+P&rft.aulast=Heyes&rft.aufirst=M&rft.date=1992-10-12&rft.volume=145&rft.issue=2&rft.spage=234&rft.isbn=&rft.btitle=&rft.title=Pediatric+Annals&rft.issn=00904481&rft_id=info:doi/10.3928%2F00904481-20131022-11 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-19 N1 - Date created - 1993-01-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Processing of hepatocyte growth factor to the heterodimeric form is required for biological activity. AN - 73221554; 1383032 AB - Hepatocyte growth factor is a plasminogen-like molecule with diverse biological effects. Although it is synthesized as a single chain polypeptide, it was originally purified as a disulfide-linked heterodimer which was generated by an internal proteolytic event. Subsequent work indicated that preparations consisting largely of the monomeric form also exhibited potent activity. By using a combination of protease inhibition and site-directed mutagenesis, we established that conversion of the single chain polypeptide to the heterodimer occurred during the bioassay and was required for mitogenic and motogenic activity. JF - FEBS letters AU - Gak, E AU - Taylor, W G AU - Chan, A M AU - Rubin, J S AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/10/12/ PY - 1992 DA - 1992 Oct 12 SP - 17 EP - 21 VL - 311 IS - 1 SN - 0014-5793, 0014-5793 KW - Recombinant Proteins KW - 0 KW - Hepatocyte Growth Factor KW - 67256-21-7 KW - Aprotinin KW - 9087-70-1 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - Base Sequence KW - Recombinant Proteins -- biosynthesis KW - Aprotinin -- pharmacology KW - Molecular Sequence Data KW - Biological Assay KW - Protein Conformation KW - Protein Processing, Post-Translational -- drug effects KW - Hepatocyte Growth Factor -- pharmacology KW - Hepatocyte Growth Factor -- genetics KW - Hepatocyte Growth Factor -- metabolism KW - Cell Division -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73221554?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+letters&rft.atitle=Processing+of+hepatocyte+growth+factor+to+the+heterodimeric+form+is+required+for+biological+activity.&rft.au=Gak%2C+E%3BTaylor%2C+W+G%3BChan%2C+A+M%3BRubin%2C+J+S&rft.aulast=Gak&rft.aufirst=E&rft.date=1992-10-12&rft.volume=311&rft.issue=1&rft.spage=17&rft.isbn=&rft.btitle=&rft.title=FEBS+letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-20 N1 - Date created - 1992-11-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Long-term proliferation of mouse primordial germ cells in culture. AN - 73270367; 1383830 AB - Primordial germ cells (PGCs) are first identifiable as a population of about eight alkaline phosphatase-positive cells in the 7.0 days postcoitum mouse embryo. During the next 6 days of development they proliferate to give rise to the 25,000 cells that will establish the meiotic population. Steel factor is required for PGC survival both in vivo and in vitro and together with leukaemia inhibitory factor stimulates PGC proliferation in vitro. In feeder-dependent culture, PGCs will proliferate for up to 7 days, but their numbers eventually decline and their proliferative capacity is only a fraction of that seen in vivo. Here we report a further factor that stimulates PGC proliferation in vitro, basic fibroblast growth factor (bFGF). Furthermore, bFGF, in the presence of steel factor and leukaemia inhibitory factor, stimulates long-term proliferation of PGCs, leading to the derivation of large colonies of cells. These embryonic germ cells resemble embryonic stem cells, pluripotent cells derived from preimplantation embryos, or feeder-dependent embryonal carcinoma cells, pluripotent stem cells of PGC-derived tumours (teratomas and teratocarcinomas). To our knowledge, these results provide the first system for long-term culture of PGCs. JF - Nature AU - Resnick, J L AU - Bixler, L S AU - Cheng, L AU - Donovan, P J AD - Mammalian Genetics Laboratory, ABL-Basic Research Program, NCI-FCRDC, Frederick, Maryland 21702-1201. Y1 - 1992/10/08/ PY - 1992 DA - 1992 Oct 08 SP - 550 EP - 551 VL - 359 IS - 6395 SN - 0028-0836, 0028-0836 KW - Growth Inhibitors KW - 0 KW - Hematopoietic Cell Growth Factors KW - Interleukin-6 KW - Leukemia Inhibitory Factor KW - Lif protein, mouse KW - Lymphokines KW - Stem Cell Factor KW - Fibroblast Growth Factor 2 KW - 103107-01-3 KW - Index Medicus KW - Fibroblast Growth Factor 2 -- pharmacology KW - Animals KW - Cells, Cultured KW - Lymphokines -- pharmacology KW - Growth Inhibitors -- pharmacology KW - Mice KW - Hematopoietic Cell Growth Factors -- pharmacology KW - Time Factors KW - Immunoenzyme Techniques KW - Cell Division KW - Germ Cells -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73270367?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature&rft.atitle=Long-term+proliferation+of+mouse+primordial+germ+cells+in+culture.&rft.au=Resnick%2C+J+L%3BBixler%2C+L+S%3BCheng%2C+L%3BDonovan%2C+P+J&rft.aulast=Resnick&rft.aufirst=J&rft.date=1992-10-08&rft.volume=359&rft.issue=6395&rft.spage=550&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-13 N1 - Date created - 1992-11-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Nature. 1992 Oct 8;359(6395):482-3 [1406966] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of mitogen-induced c-fos expression in melanoma cells by retinoic acid involves the serum response element. AN - 73241672; 1400313 AB - To investigate the mechanism(s) by which all-transretinoic acid (RA) inhibits cell growth, we studied its effect on the expression of c-fos and c-jun in B16 melanoma cells. RA differentially inhibited proto-oncogene induction by mitogens, such as phorbol 12-myristate 13-acetate and serum. Suppression of c-fos was achieved with doses of RA as low as 10(-10) M and required pretreatment of cells with RA for a minimum of 2 h. In contrast, inhibition of c-jun required pretreatment for greater than 16 h with at least 10(-8) M RA and coincided with the observed decrease in cell growth. RA blocked c-fos induction by inhibiting transcription. This inhibition of transcription occurs through the serum response element (SRE), since the SRE alone was sufficient to confer down-regulation by RA to a minimal c-fos promoter construct. Thus, the SRE plays a critical role in the suppression of c-fos transcription by RA. JF - The Journal of biological chemistry AU - Busam, K J AU - Roberts, A B AU - Sporn, M B AD - Laboratory of Chemoprevention, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10/05/ PY - 1992 DA - 1992 Oct 05 SP - 19971 EP - 19977 VL - 267 IS - 28 SN - 0021-9258, 0021-9258 KW - c-fos KW - c-jun KW - DNA-Binding Proteins KW - 0 KW - Mitogens KW - Nuclear Proteins KW - Serum Response Factor KW - Tretinoin KW - 5688UTC01R KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Melanoma, Experimental KW - Cell Division -- drug effects KW - Mice KW - Transcription, Genetic KW - Plasmids KW - Precipitin Tests KW - Promoter Regions, Genetic KW - Tumor Cells, Cultured KW - Down-Regulation KW - Genes, jun -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Tretinoin -- pharmacology KW - Regulatory Sequences, Nucleic Acid KW - Genes, fos KW - Gene Expression Regulation -- drug effects KW - Mitogens -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73241672?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Inhibition+of+mitogen-induced+c-fos+expression+in+melanoma+cells+by+retinoic+acid+involves+the+serum+response+element.&rft.au=Busam%2C+K+J%3BRoberts%2C+A+B%3BSporn%2C+M+B&rft.aulast=Busam&rft.aufirst=K&rft.date=1992-10-05&rft.volume=267&rft.issue=28&rft.spage=19971&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-16 N1 - Date created - 1992-11-16 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-fos; c-jun N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Studies on p40, the leucine zipper motif-containing protein encoded by the first open reading frame of an active human LINE-1 transposable element. AN - 73232453; 1328181 AB - Full-length human LINE-1 retrotransposons encode p40 proteins with varying electrophoretic mobilities under denaturing conditions. The p40 expressed from the first open reading frame in the LINE-1 copy designated L1.2A co-electrophoreses with the endogenous p40 in human teratocarcinoma cells. This finding is consistent with previous data indicating that L1.2A is an active element. The amino acid sequence in the central region of the L1.2A p40 accounts, at least in part, for its characteristic mobility. This region includes sequences which can, in principle, form a leucine zipper. JF - The Journal of biological chemistry AU - Holmes, S E AU - Singer, M F AU - Swergold, G D AD - Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10/05/ PY - 1992 DA - 1992 Oct 05 SP - 19765 EP - 19768 VL - 267 IS - 28 SN - 0021-9258, 0021-9258 KW - DNA Transposable Elements KW - 0 KW - DNA-Binding Proteins KW - Oligonucleotides KW - Peptides KW - Proteins KW - L1Hs-encoded protein p40, human KW - 148349-28-4 KW - Index Medicus KW - Teratoma -- metabolism KW - Protein Biosynthesis KW - Blotting, Western KW - Base Sequence KW - Tumor Cells, Cultured KW - Open Reading Frames KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Leucine Zippers -- genetics KW - Peptides -- genetics KW - Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73232453?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=Inhibition+of+HIVa1+Replication+by+Novel+Multitarget+Ribozymes&rft.au=CHEN%2C+CHANGaJIE%3BBanerjea%2C+Akhil+C%3BHaglund%2C+Karl%3BHarmison%2C+George+G%3BSchubert%2C+Manfred&rft.aulast=CHEN&rft.aufirst=CHANGaJIE&rft.date=1992-10-01&rft.volume=660&rft.issue=1&rft.spage=271&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/10.1111%2Fj.1749-6632.1992.tb21081.x LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-16 N1 - Date created - 1992-11-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Calcium ionophore A23187 induces expression of the growth arrest and DNA damage inducible CCAAT/enhancer-binding protein (C/EBP)-related gene, gadd153. Ca2+ increases transcriptional activity and mRNA stability. AN - 73227601; 1400365 AB - gadd153 is a CCAAT/enhancer-binding protein (C/EBP)-related gene whose expression is induced in response to growth arrest and DNA damage. This investigation explored the possibility that Ca2+ might play a role in regulating expression of gadd 153. We have demonstrated that treatment of HeLa cells with the calcium ionophores A23187 and ionomycin leads to the induction of gadd153 mRNA. The induction was rapid; increases in mRNA were detected by 90 min of treatment, and near maximum levels were achieved within 5-h exposure to A23187. Elevated mRNA levels resulted from both an increase in the rate of gadd153 transcription and an increase in the stability of the gadd153 mRNA. The response was not dependent on protein kinase C nor was it coupled to c-fos expression. Buffering intracellular and extracellular Ca2+ by combined treatment with BAPTA-AM (acetoxymethyl ester form of bis(aminophenoxy)ethane N,N'-tetraacetic acid) and EGTA prevented the induction of gadd153 mRNA by A23187. In addition, these treatments prevented the induction of gadd153 mRNA in response to the DNA damaging agent methyl methanesulfonate. We conclude that intracellular Ca2+ plays a role in regulating gadd153 expression. More specifically, Ca2+ likely plays a role in the induction of gadd153 mRNA following DNA damage. JF - The Journal of biological chemistry AU - Bartlett, J D AU - Luethy, J D AU - Carlson, S G AU - Sollott, S J AU - Holbrook, N J AD - Laboratory of Molecular Genetics, National Institute on Aging, Baltimore, Maryland 21224. Y1 - 1992/10/05/ PY - 1992 DA - 1992 Oct 05 SP - 20465 EP - 20470 VL - 267 IS - 28 SN - 0021-9258, 0021-9258 KW - CCAAT-Enhancer-Binding Proteins KW - 0 KW - Cations, Divalent KW - DNA-Binding Proteins KW - Nuclear Proteins KW - Oligonucleotides KW - RNA, Messenger KW - 1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester KW - 139890-68-9 KW - Calcimycin KW - 37H9VM9WZL KW - Egtazic Acid KW - 526U7A2651 KW - DNA KW - 9007-49-2 KW - Methyl Methanesulfonate KW - AT5C31J09G KW - Protein Kinase C KW - EC 2.7.11.13 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Gene Expression -- drug effects KW - Egtazic Acid -- analogs & derivatives KW - HeLa Cells KW - Humans KW - Transcription, Genetic KW - RNA, Messenger -- genetics KW - Egtazic Acid -- chemistry KW - Methyl Methanesulfonate -- pharmacology KW - Protein Kinase C -- metabolism KW - Base Sequence KW - Kinetics KW - Molecular Sequence Data KW - Cell Division KW - Nuclear Proteins -- genetics KW - DNA Damage KW - DNA-Binding Proteins -- genetics KW - DNA-Binding Proteins -- biosynthesis KW - Calcium -- physiology KW - Nuclear Proteins -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73227601?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Calcium+ionophore+A23187+induces+expression+of+the+growth+arrest+and+DNA+damage+inducible+CCAAT%2Fenhancer-binding+protein+%28C%2FEBP%29-related+gene%2C+gadd153.+Ca2%2B+increases+transcriptional+activity+and+mRNA+stability.&rft.au=Bartlett%2C+J+D%3BLuethy%2C+J+D%3BCarlson%2C+S+G%3BSollott%2C+S+J%3BHolbrook%2C+N+J&rft.aulast=Bartlett&rft.aufirst=J&rft.date=1992-10-05&rft.volume=267&rft.issue=28&rft.spage=20465&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-16 N1 - Date created - 1992-11-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Localized mutagenesis and evidence for post-transcriptional regulation of MAK3. A putative N-acetyltransferase required for double-stranded RNA virus propagation in Saccharomyces cerevisiae. AN - 73220003; 1339437 AB - The MAK3 gene of Saccharomyces cerevisiae is necessary for the propagation of the L-A double-stranded RNA virus and its satellites, such as M1 that encodes a killer toxin. We cloned the MAK3 gene based on its genetic map position using physically mapped lambda-clones covering nearly all of the yeast genome. The minimal sequence necessary to complement the mak3-1 mutation contained 3 open reading frames (ORFs). Only one (ORF3) was necessary to complement mak3-1. A deletion insertion mutant of ORF3 grew slowly on nonfermentable carbon sources, an effect not due simply to its loss of L-A. Although ORF3 alone is sufficient for MAK3 activity when expressed from an expression vector, in its native context an additional 669 base pairs 3' to the ORF and complementary to the gene for a non-histone protein are necessary for expression, but not for normal steady state transcript levels. This suggests a post-transcriptional control of MAK3 expression by the 3' region. The MAK3 protein has substantial homology with several N-acetyltransferases with consensus patterns h..h.h. . . Y..[HK]GI[AG][KR].Lh. . .h and h.h[DE]. . . .N..A. . .Y . . .GF. . . .. . . .Y . . [DE]G, (h = hydrophobic). Mutation of any of the underlined conserved residues (94GI----AA, 123N----A, 130Y----A, 134GF----SL, 144Y----A, and 149G----A) inactivated the gene, supporting the hypothesis that MAK3 encodes an N-acetyltransferase. JF - The Journal of biological chemistry AU - Tercero, J C AU - Riles, L E AU - Wickner, R B AD - Section on Genetics of Simple Eukaryotes, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10/05/ PY - 1992 DA - 1992 Oct 05 SP - 20270 EP - 20276 VL - 267 IS - 28 SN - 0021-9258, 0021-9258 KW - DNA, Fungal KW - 0 KW - Fungal Proteins KW - RNA, Double-Stranded KW - RNA, Messenger KW - Saccharomyces cerevisiae Proteins KW - Arylamine N-Acetyltransferase KW - EC 2.3.1.5 KW - MAK3 protein, S cerevisiae KW - EC 2.3.1.88 KW - Index Medicus KW - Virus Replication KW - Chromosome Walking KW - Open Reading Frames KW - Amino Acid Sequence KW - Plasmids KW - Chromosome Mapping KW - Cloning, Molecular KW - Base Sequence KW - RNA, Messenger -- metabolism KW - Restriction Mapping KW - Molecular Sequence Data KW - Sequence Homology, Amino Acid KW - Saccharomyces cerevisiae -- genetics KW - Gene Expression Regulation, Fungal KW - Fungal Proteins -- metabolism KW - RNA Viruses -- physiology KW - Saccharomyces cerevisiae -- enzymology KW - Fungal Proteins -- genetics KW - Arylamine N-Acetyltransferase -- metabolism KW - Mutagenesis KW - Arylamine N-Acetyltransferase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73220003?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Localized+mutagenesis+and+evidence+for+post-transcriptional+regulation+of+MAK3.+A+putative+N-acetyltransferase+required+for+double-stranded+RNA+virus+propagation+in+Saccharomyces+cerevisiae.&rft.au=Tercero%2C+J+C%3BRiles%2C+L+E%3BWickner%2C+R+B&rft.aulast=Tercero&rft.aufirst=J&rft.date=1992-10-05&rft.volume=267&rft.issue=28&rft.spage=20270&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-16 N1 - Date created - 1992-11-16 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - D11151; GENBANK; M93405; D11150; M95912; D11149; D10348; D10347; M96626; M95771; L05565 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of HIVa1 Replication by Novel Multitarget Ribozymes AN - 875089930; 14716928 AB - Abstract not available. JF - Annals of the New York Academy of Sciences AU - CHEN, CHANGaJIE AU - Banerjea, Akhil C AU - Haglund, Karl AU - Harmison, George G AU - Schubert, Manfred AD - Laboratory of Viral and Molecular Pathogenesis National Institute of Neurological Disorders and Stroke National Institutes of Health Bethesda, Maryland 20892 Y1 - 1992/10// PY - 1992 DA - Oct 1992 SP - 271 EP - 273 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 USA VL - 660 IS - 1 SN - 0077-8923, 0077-8923 KW - Biotechnology and Bioengineering Abstracts KW - Human immunodeficiency virus KW - Replication KW - Ribozymes KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/875089930?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=Inhibition+of+HIVa1+Replication+by+Novel+Multitarget+Ribozymes&rft.au=CHEN%2C+CHANGaJIE%3BBanerjea%2C+Akhil+C%3BHaglund%2C+Karl%3BHarmison%2C+George+G%3BSchubert%2C+Manfred&rft.aulast=CHEN&rft.aufirst=CHANGaJIE&rft.date=1992-10-01&rft.volume=660&rft.issue=1&rft.spage=271&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/10.1111%2Fj.1749-6632.1992.tb21081.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Replication; Ribozymes; Human immunodeficiency virus DO - http://dx.doi.org/10.1111/j.1749-6632.1992.tb21081.x ER - TY - JOUR T1 - Specific Inhibition of Oncogene Expression in Vitro and in Vivo by Antisense Oligonucleotides AN - 875053905; 14716900 AB - Abstract not available. JF - Annals of the New York Academy of Sciences AU - Neckers, Len AU - Rosolen, Angelo AU - Fahmy, Brigid AU - Whitesell, Luke AD - Clinical Pharmacology Branch National Institutes of Health National Cancer Institute Bethesda, Maryland 20892 Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 37 EP - 44 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 USA VL - 660 IS - 1 SN - 0077-8923, 0077-8923 KW - Biotechnology and Bioengineering Abstracts; Oncogenes & Growth Factors Abstracts KW - Antisense oligonucleotides KW - Oncogenes KW - B 26660:Miscellaneous Oncogenes & Growth Factors KW - W 30940:Products UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/875053905?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=Specific+Inhibition+of+Oncogene+Expression+in+Vitro+and+in+Vivo+by+Antisense+Oligonucleotides&rft.au=Neckers%2C+Len%3BRosolen%2C+Angelo%3BFahmy%2C+Brigid%3BWhitesell%2C+Luke&rft.aulast=Neckers&rft.aufirst=Len&rft.date=1992-10-01&rft.volume=660&rft.issue=1&rft.spage=37&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/10.1111%2Fj.1749-6632.1992.tb21055.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2011-11-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Antisense oligonucleotides; Oncogenes DO - http://dx.doi.org/10.1111/j.1749-6632.1992.tb21055.x ER - TY - JOUR T1 - Focal transcranial magnetic stimulation and response bias in a forced-choice task. AN - 85264797; pmid-1431962 AB - The effects of transcranial magnetic stimulation were studied on the performance of a warned, forced-choice response time task by normal adults. The task consisted of extension of the index finger in response to the click produced by the discharge of the magnetic coil (go-signal). The subjects were asked to choose the right or left finger only after the go-signal was delivered. Single magnetic stimuli were delivered to the prefrontal or motor area, and in the control situation, away from the head. Magnetic stimulation affected hand preference only when it was delivered to the motor area. With stimulation of this area, subjects more often chose the hand contralateral to the site stimulated with response times that were mainly less than 200 ms. With longer response times (between 200 and 1100 ms), magnetic stimulation had no effect on hand preference regardless of the site stimulated. Stimulation of prefrontal areas yielded results similar to the control situation. These results suggest that response bias in this paradigm is caused by an effect of magnetic stimulation on neural structures within, or closely related to, the motor areas of the brain. Although the response bias was clear and predictable, the subjects were unaware of its existence. It is possible to influence endogenous processes of movement preparation externally without disrupting the conscious perception of volition. JF - Journal of Neurology, Neurosurgery, and Psychiatry AU - Brasil-Neto, J P AU - Pascual-Leone, A AU - Valls-Solé J AU - Cohen, L G AU - Hallett, M AD - Human Cortical Physiology Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 964 EP - 966 VL - 55 IS - 10 SN - 0022-3050, 0022-3050 KW - Reference Values KW - Human KW - Prefrontal Cortex KW - Dominance, Cerebral KW - Motor Cortex KW - Choice Behavior KW - Adult KW - Psychomotor Performance KW - Bias (Epidemiology) KW - Laterality KW - Attention KW - Male KW - Female KW - Reaction Time KW - Electromagnetic Fields UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85264797?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Neurology%2C+Neurosurgery%2C+and+Psychiatry&rft.atitle=Focal+transcranial+magnetic+stimulation+and+response+bias+in+a+forced-choice+task.&rft.au=Brasil-Neto%2C+J+P%3BPascual-Leone%2C+A%3BValls-Sol%C3%A9+J%3BCohen%2C+L+G%3BHallett%2C+M&rft.aulast=Brasil-Neto&rft.aufirst=J&rft.date=1992-10-01&rft.volume=55&rft.issue=10&rft.spage=964&rft.isbn=&rft.btitle=&rft.title=Journal+of+Neurology%2C+Neurosurgery%2C+and+Psychiatry&rft.issn=00223050&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Role of inferior temporal neurons in visual memory. II. Multiplying temporal waveforms related to vision and memory. AN - 85239839; pmid-1432085 AB - 1. In the companion paper we reported on the activity of neurons in the inferior temporal (IT) cortex during a sequential pattern matching task. In this task a sample stimulus was followed by a test stimulus that was either a match or a nonmatch. Many of the neurons encoded information about the patterns of both current and previous stimuli in the temporal modulation of their responses. 2. A simple information processing model of visual memory can be formed with just four steps: 1) encode the current stimulus; 2) recall the code of a remembered stimulus; 3) compare the two codes; 4) and decide whether they are similar or different. The analysis presented in the first paper suggested that some IT neurons were performing the comparison step of visual memory. 3. We propose that IT neurons participate in the comparison of temporal waveforms related to vision and memory by multiplying them together. This product could form the basis of a crosscorrelation-based comparison. 4. We tested our hypothesis by fitting a simple multiplicative model to data from IT neurons. The model generated waveforms in separate memory and visual channels. The waveforms arising from the two channels were then multiplied on a point by point basis to yield the output waveform. The model was fitted to the actual neuronal data by a gradient descent method to find the best fit waveforms that also had the lowest total energy. 5. The multiplicative model fit the neuronal responses quite well. The multiplicative model made consistently better predictions of the actual response waveforms than did an additive model. Furthermore, the fit was better when the actual relationship between the responses and the sample and test stimuli were preserved than when that relationship was randomized. 6. We infer from the superior fit of the multiplicative model that IT neurons are multiplying temporally modulated waveforms arising from separate visual and memory systems in the comparison step of visual memory. JF - Journal of Neurophysiology AU - Eskandar, E N AU - Optican, L M AU - Richmond, B J AD - Laboratory of Sensorimotor Research, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 1296 EP - 1306 VL - 68 IS - 4 SN - 0022-3077, 0022-3077 KW - Models, Psychological KW - Support, U.S. Gov't, P.H.S. KW - Animal KW - Decision Making KW - Cognition KW - Mathematics KW - Memory KW - Vision KW - Neurons KW - Pattern Recognition, Visual KW - Temporal Lobe KW - Macaca mulatta KW - Models, Neurological KW - Male KW - Female UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85239839?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Neurophysiology&rft.atitle=Role+of+inferior+temporal+neurons+in+visual+memory.+II.+Multiplying+temporal+waveforms+related+to+vision+and+memory.&rft.au=Eskandar%2C+E+N%3BOptican%2C+L+M%3BRichmond%2C+B+J&rft.aulast=Eskandar&rft.aufirst=E&rft.date=1992-10-01&rft.volume=68&rft.issue=4&rft.spage=1296&rft.isbn=&rft.btitle=&rft.title=Journal+of+Neurophysiology&rft.issn=00223077&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Genetic aspects of idiopathic speech and language disorders. AN - 85203542; pmid-1408200 AB - At the outset of this article, we posed the question of whether or not the current evidence from genetic studies of DLD and stuttering indicate that it would be fruitful to conduct studies aimed at determining the gene location for each of these disorders. As we pointed out, because these are behavioral development disorders, phenotypic variations and changes in characteristics through the life span pose problems when attempting to determine who is and is not affected. Further, because these disorders can be either idiopathic or secondary to a variety of causes, any genetic study must rule out or take account of cases secondary to other factors. Few studies conducted thus far have taken these problems into account, and the results must be considered tentative. Given these reservations, the results certainly point to a genetic component in both disorders, although the data collected thus far on DLD suggest a mendelian form of transmission. If further more intensive studies continue to support this model for DLD, linkage studies on this disorder are likely to be productive. JF - Otolaryngologic Clinics of North America AU - Ludlow, Christy L AU - Dooman, A G AD - Laryngeal and Speech Section, National Institute of Neurological Disorders and Stroke PY - 1992 SP - 979 EP - 994 VL - 25 IS - 5 SN - 0030-6665, 0030-6665 KW - Speech Disorders KW - Human KW - Language Development Disorders KW - Articulation Disorders KW - Stuttering UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85203542?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Otolaryngologic+Clinics+of+North+America&rft.atitle=Genetic+aspects+of+idiopathic+speech+and+language+disorders.&rft.au=Ludlow%2C+Christy+L%3BDooman%2C+A+G&rft.aulast=Ludlow&rft.aufirst=Christy&rft.date=1992-10-01&rft.volume=25&rft.issue=5&rft.spage=979&rft.isbn=&rft.btitle=&rft.title=Otolaryngologic+Clinics+of+North+America&rft.issn=00306665&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Neurotransmission in the auditory system. AN - 85203490; pmid-1357616 AB - Neurotransmitters and neuromodulators thought to be active on neurons in the cochlea, CN, and SOC have been reviewed. The variety of neurotransmitters and neuromodulators present and likely colocalized in these neurons are the chemical substrates that link morphologically and physiologically diverse neurons to process sound information. The impact of the limited number of neurotransmitters and neuromodulators in the auditory system is magnified by their interaction with structurally diverse receptors; thus great functional diversity is possible. Moreover, the effects of neurotransmitters and neuromodulators are not limited to synaptic transmission but serve as trophic agents for the establishment of neuronal circuitry during development and the rearrangement of synapses as a result of sensory experience or injury. An understanding of the neurochemical aspects of sensory processing at these diverse synapses then is of fundamental importance in understanding the organization of the auditory system. JF - Otolaryngologic Clinics of North America AU - Hunter, C AU - Doi, K AU - Wenthold, R J AD - Laboratory of Neurochemistry, National Institute on Deafness and other Communication Disorders, National Institutes of Health, Bethesda, Maryland. PY - 1992 SP - 1027 EP - 1052 VL - 25 IS - 5 SN - 0030-6665, 0030-6665 KW - Cochlea KW - Auditory Pathways KW - Human KW - Brain Stem KW - Neurotransmitters KW - Synaptic Transmission UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85203490?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Otolaryngologic+Clinics+of+North+America&rft.atitle=Neurotransmission+in+the+auditory+system.&rft.au=Hunter%2C+C%3BDoi%2C+K%3BWenthold%2C+R+J&rft.aulast=Hunter&rft.aufirst=C&rft.date=1992-10-01&rft.volume=25&rft.issue=5&rft.spage=1027&rft.isbn=&rft.btitle=&rft.title=Otolaryngologic+Clinics+of+North+America&rft.issn=00306665&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Strategies for constructing a guinea pig organ of Corti cDNA library and its potential use. AN - 85200706; pmid-1408189 AB - Mutations of genes common to several tissues or organs can lead to cellular damage, which may result in hearing impairment as part of a syndromic disorder. Mutations of genes that are unique to the organ of Corti would have a high probability of causing nonsyndromic hearing impairment. It is expected that such genes are involved in auditory transduction as well as in maintaining specific hair cell and supporting cell functions in the organ of Corti. Cloning and describing genes involved with nonsyndromic hearing impairment thus require the construction of a guinea pig cDNA library of the organ of Corti. JF - Otolaryngologic Clinics of North America AU - Wilcox, E R AD - National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland. PY - 1992 SP - 1011 EP - 1016 VL - 25 IS - 5 SN - 0030-6665, 0030-6665 KW - RNA, Messenger KW - Hearing Disorders KW - Guinea Pigs KW - Animal KW - DNA KW - Escherichia coli KW - Amino Acid Sequence KW - Mutation KW - Gene Amplification KW - Organ of Corti KW - Gene Library UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85200706?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Otolaryngologic+Clinics+of+North+America&rft.atitle=Strategies+for+constructing+a+guinea+pig+organ+of+Corti+cDNA+library+and+its+potential+use.&rft.au=Wilcox%2C+E+R&rft.aulast=Wilcox&rft.aufirst=E&rft.date=1992-10-01&rft.volume=25&rft.issue=5&rft.spage=1011&rft.isbn=&rft.btitle=&rft.title=Otolaryngologic+Clinics+of+North+America&rft.issn=00306665&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Single motor unit activity of human intrinsic laryngeal muscles during respiration. AN - 85175083; pmid-1416638 AB - Individual motor units in the thyroarytenoid (TA) and cricothyroid (CT) muscles were studied in 10 normal human volunteers during quiet respiration. Both tonic and phasic firing patterns were found in both TA and CT units. The rate of firing was higher during inhalation than during exhalation in phasic TA units and in tonic CT units. Tonically active units had a higher firing frequency than phasically active units in both TA and CT muscles. Phasically active units corresponded with the respiratory cycle, with firing associated with inhalation in both the TA and CT muscles. A variety of firing patterns were found between units in both the TA and CT muscles, and in one subject, units recorded from the same muscle had very different firing patterns. The results suggest that although laryngeal motoneurons are modulated by the respiratory cycle, they do not respond uniformly to respiration. JF - The Annals of Otology, Rhinology, and Laryngology AU - Chanaud, C M AU - Ludlow, C L AD - Voice and Speech Section, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 832 EP - 840 VL - 101 IS - 10 SN - 0003-4894, 0003-4894 KW - Laryngeal Muscles KW - Humans KW - Respiration KW - Adult KW - Electromyography KW - Action Potentials KW - Middle Aged KW - Female KW - Male KW - Motor Neurons UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85175083?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Annals+of+Otology%2C+Rhinology%2C+and+Laryngology&rft.atitle=Single+motor+unit+activity+of+human+intrinsic+laryngeal+muscles+during+respiration.&rft.au=Chanaud%2C+C+M%3BLudlow%2C+C+L&rft.aulast=Chanaud&rft.aufirst=C&rft.date=1992-10-01&rft.volume=101&rft.issue=10&rft.spage=832&rft.isbn=&rft.btitle=&rft.title=The+Annals+of+Otology%2C+Rhinology%2C+and+Laryngology&rft.issn=00034894&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Practical approach to diagnosis and management of hereditary hearing impairment (HHI). AN - 85155009; pmid-1425370 JF - Ear, Nose, and Throat Journal AU - Grundfast, K M AU - Lalwani, A K AD - Laboratory of Molecular Biology, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland. PY - 1992 SP - 479 EP - 84, 487 VL - 71 IS - 10 SN - 0145-5613, 0145-5613 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85155009?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Ear%2C+Nose%2C+and+Throat+Journal&rft.atitle=Practical+approach+to+diagnosis+and+management+of+hereditary+hearing+impairment+%28HHI%29.&rft.au=Grundfast%2C+K+M%3BLalwani%2C+A+K&rft.aulast=Grundfast&rft.aufirst=K&rft.date=1992-10-01&rft.volume=71&rft.issue=10&rft.spage=479&rft.isbn=&rft.btitle=&rft.title=Ear%2C+Nose%2C+and+Throat+Journal&rft.issn=01455613&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Prophylaxis and therapy for Pneumocystis pneumonia--where are we? AN - 75533410; 1344666 AB - The armamentarium of drugs to treat and to prevent Pneumocystis pneumonia has expanded substantially over the past decade. In all patient populations trimethoprim-sulfamethoxazole is the preferred regimen for both acute treatment and prophylaxis. Clindamycin-primaquine and atovaquone are both effective agents for acute therapy but there are no data yet suggesting that they are preferable to trimethoprim-sulfamethoxazole. Corticosteroid therapy is now standard for severe AIDS-associated Pneumocystis pneumonia, and should probably be used in other patient populations with severe pneumocystis pneumonia as well. JF - Infectious agents and disease AU - Masur, H AD - Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 270 EP - 278 VL - 1 IS - 5 SN - 1056-2044, 1056-2044 KW - Adrenal Cortex Hormones KW - 0 KW - Antifungal Agents KW - Naphthoquinones KW - Clindamycin KW - 3U02EL437C KW - Trimethoprim, Sulfamethoxazole Drug Combination KW - 8064-90-2 KW - Primaquine KW - MVR3634GX1 KW - Atovaquone KW - Y883P1Z2LT KW - Index Medicus KW - AIDS/HIV KW - AIDS-Related Opportunistic Infections -- drug therapy KW - Naphthoquinones -- therapeutic use KW - Antifungal Agents -- adverse effects KW - Humans KW - Trimethoprim, Sulfamethoxazole Drug Combination -- therapeutic use KW - Clinical Trials as Topic KW - AIDS-Related Opportunistic Infections -- prevention & control KW - Trimethoprim, Sulfamethoxazole Drug Combination -- adverse effects KW - Antifungal Agents -- therapeutic use KW - Drug Tolerance KW - Adrenal Cortex Hormones -- therapeutic use KW - Primaquine -- therapeutic use KW - Clindamycin -- therapeutic use KW - Pneumonia, Pneumocystis -- prevention & control KW - Pneumonia, Pneumocystis -- drug therapy KW - Pneumonia, Pneumocystis -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75533410?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Pesticides+and+non-Hodgkin%27s+lymphoma.&rft.au=Zahm%2C+S+H%3BBlair%2C+A&rft.aulast=Zahm&rft.aufirst=S&rft.date=1992-10-01&rft.volume=52&rft.issue=19+Suppl&rft.spage=5485s&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-05-13 N1 - Date created - 1994-05-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenicity of combined ultraviolet B radiation and psoralen plus ultraviolet A irradiation treatment of mice. AN - 75518825; 1342188 AB - Psoralen plus ultraviolet A (PUVA) therapy and UVB phototherapy are frequently used in the treatment of psoriasis and other skin diseases. Both treatments are thought to be carcinogenic, but little is known about their interaction in the induction of skin cancer. Tumors induced in mice treated with both PUVA and UVB, either given sequentially or concurrently, seemed to be more antigenic as a group than tumors treated by PUVA alone, as determined by their lower frequency of growth when transplanted into naive mice. In this study, we treated C3H mice with a subcarcinogenic dose of UVB radiation for 4 weeks, followed by PUVA treatment for 41 weeks (sequential experiment) or with both UVB radiation (minimal carcinogenic dose) and PUVA for 41 weeks (concurrent experiment) and monitored the development of skin cancers. Although a few tumors appeared earlier in the groups treated with both UVB and PUVA in both experiments, no significant differences were observed in the rate of tumor development in mice treated with UVB and PUVA versus those treated with PUVA alone. JF - Photodermatology, photoimmunology & photomedicine AU - Granstein, R D AU - Morison, W L AU - Kripke, M L AD - National Cancer Institute, Frederick Research Facility, Maryland. PY - 1992 SP - 198 EP - 202 VL - 9 IS - 5 SN - 0905-4383, 0905-4383 KW - Carcinogens KW - 0 KW - Methoxsalen KW - U4VJ29L7BQ KW - Index Medicus KW - Radiation Dosage KW - Probability KW - Animals KW - Carcinoma, Squamous Cell -- etiology KW - Germ-Free Life KW - Neoplasms, Radiation-Induced -- etiology KW - Thymectomy KW - Fibrosarcoma -- pathology KW - Mice KW - Fibrosarcoma -- etiology KW - Neoplasm Transplantation KW - Mice, Inbred Strains KW - X-Rays KW - Neoplasms, Radiation-Induced -- pathology KW - Carcinoma, Squamous Cell -- pathology KW - Mice, Inbred C3H KW - Female KW - Methoxsalen -- adverse effects KW - PUVA Therapy -- adverse effects KW - Skin Neoplasms -- etiology KW - Skin Neoplasms -- chemically induced KW - Ultraviolet Rays -- adverse effects KW - Skin Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75518825?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Photodermatology%2C+photoimmunology+%26+photomedicine&rft.atitle=Carcinogenicity+of+combined+ultraviolet+B+radiation+and+psoralen+plus+ultraviolet+A+irradiation+treatment+of+mice.&rft.au=Granstein%2C+R+D%3BMorison%2C+W+L%3BKripke%2C+M+L&rft.aulast=Granstein&rft.aufirst=R&rft.date=1992-10-01&rft.volume=9&rft.issue=5&rft.spage=198&rft.isbn=&rft.btitle=&rft.title=Photodermatology%2C+photoimmunology+%26+photomedicine&rft.issn=09054383&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-02-10 N1 - Date created - 1994-02-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pardaxin-stimulated calcium uptake in PC12 cells is blocked by cadmium and is not mediated by L-type calcium channels. AN - 75515192; 1285007 AB - Pardaxin is an excitatory neurotoxin which triggers neurotransmitter release as a result of voltage-dependent pore formation within the neuronal membrane. We have used several pharmacological manipulations of calcium influx to characterize pardaxin pore activity in PC12 cells in culture. Pardaxin stimulates the uptake of radioactive calcium into PC12 cells in a dose dependent fashion (ED50 of 0.4 microM). This stimulation is partially inhibited by nifedipine, a blocker of L-type calcium channels. Effective blockade of pardaxin stimulation was produced by the inorganic calcium channel blockers cadmium (IC50 of 10 microM) and nickel (2 mM). Homologous down regulation of L-calcium channels by the agonist Bay K-8644, inhibited the subsequent stimulation of calcium uptake by this drug, but not by pardaxin. A fluorometric analysis of pardaxin pore formation in unilamellar large liposomes indicates pardaxin pores are blocked by cadmium (10-200 microM). These data distinguish between pardaxin pores and L-type calcium channels in PC12 cells. We suggest pardaxin as a pharmacological ionophore tool to modulate neuronal calcium homeostasis and neurotransmitter release. JF - Journal of basic and clinical physiology and pharmacology AU - Nikodijevic, B AU - Nikodijevic, D AU - Lazarovici, P AD - Section on Growth Factors, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. PY - 1992 SP - 359 EP - 370 VL - 3 IS - 4 SN - 0792-6855, 0792-6855 KW - Calcium Channels KW - 0 KW - Calcium Radioisotopes KW - Fish Venoms KW - Liposomes KW - Cadmium KW - 00BH33GNGH KW - pardaxin KW - 67995-63-5 KW - 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester KW - 71145-03-4 KW - Nickel KW - 7OV03QG267 KW - Nifedipine KW - I9ZF7L6G2L KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Nifedipine -- pharmacology KW - Animals KW - Spectrometry, Fluorescence KW - Nickel -- pharmacology KW - Porosity KW - Liposomes -- metabolism KW - 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester -- pharmacology KW - Down-Regulation -- drug effects KW - Models, Biological KW - PC12 Cells KW - Calcium -- metabolism KW - Cadmium -- pharmacology KW - Calcium Channels -- metabolism KW - Fish Venoms -- antagonists & inhibitors KW - Calcium Channels -- drug effects KW - Fish Venoms -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75515192?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+basic+and+clinical+physiology+and+pharmacology&rft.atitle=Pardaxin-stimulated+calcium+uptake+in+PC12+cells+is+blocked+by+cadmium+and+is+not+mediated+by+L-type+calcium+channels.&rft.au=Nikodijevic%2C+B%3BNikodijevic%2C+D%3BLazarovici%2C+P&rft.aulast=Nikodijevic&rft.aufirst=B&rft.date=1992-10-01&rft.volume=3&rft.issue=4&rft.spage=359&rft.isbn=&rft.btitle=&rft.title=Journal+of+basic+and+clinical+physiology+and+pharmacology&rft.issn=07926855&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-20 N1 - Date created - 1993-10-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Analysis of human cytochrome P450 catalytic activities and expression. AN - 73533950; 1306334 AB - Cytochromes P450 are a large group of membrane-associated heme protein monooxygenases, most of which are responsible for metabolizing foreign compounds. Chemical carcinogens, which are ingested or absorbed into the body as inert forms, are metabolically activated by P450s to electrophilic metabolites capable of binding to and mutating DNA. Different P450 forms are responsible for activation of the various classes of chemical carcinogens including the arylamines, polycyclic aromatic hydrocarbons, nitrosamines and aflatoxins. Thus, the cellular constituency and levels of P450s could determine the fate of a particular carcinogen and the risk of humans to exposure. To study the catalytic activities of human P450s, human P450 cDNAs were cloned and expressed into active enzymes using cultured cells. By both transient and stable cDNA expression systems, several human P450s were found to be capable of metabolically-activating the human hepatocarcinogen aflatoxin B1. These cDNA expression systems can also be used to determine whether an unknown chemical will be activated by a human P450 and thus be toxic or mutagenic in humans. To assess the extent of interindividual variation in P450 expression, probes developed from P450 cDNAs are being used to quantify levels of P450 mRNAs in various human tissues. Studies using RNase protection revealed that the closely related CYP2B6 and CYP2B7 mRNAs could be independently quantified in liver and lung, respectively. This procedure can be used to examine expression of different P450 genes in banks of human tissue specimens. JF - The Tohoku journal of experimental medicine AU - Gonzalez, F J AU - Crespi, C L AU - Czerwinski, M AU - Gelboin, H V AD - Laboratory of Molecular Carcinogenesis, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 67 EP - 72 VL - 168 IS - 2 SN - 0040-8727, 0040-8727 KW - CYP2B KW - RNA, Messenger KW - 0 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Ribonucleases KW - EC 3.1.- KW - Index Medicus KW - Sensitivity and Specificity KW - Reproducibility of Results KW - Multigene Family KW - Humans KW - Organ Specificity -- physiology KW - DNA -- genetics KW - Catalysis KW - Liver -- enzymology KW - RNA, Messenger -- metabolism KW - Cytochrome P-450 Enzyme System -- genetics KW - Liver -- metabolism KW - Cytochrome P-450 Enzyme System -- metabolism KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Lung -- enzymology KW - Lung -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73533950?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Tohoku+journal+of+experimental+medicine&rft.atitle=Analysis+of+human+cytochrome+P450+catalytic+activities+and+expression.&rft.au=Gonzalez%2C+F+J%3BCrespi%2C+C+L%3BCzerwinski%2C+M%3BGelboin%2C+H+V&rft.aulast=Gonzalez&rft.aufirst=F&rft.date=1992-10-01&rft.volume=168&rft.issue=2&rft.spage=67&rft.isbn=&rft.btitle=&rft.title=The+Tohoku+journal+of+experimental+medicine&rft.issn=00408727&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-05 N1 - Date created - 1993-08-05 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CYP2B N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evaluation of Telazol-xylazine as an anesthetic combination for use in Syrian hamsters. AN - 73397064; 1460851 AB - The availability of safe parenteral anesthetics for use in Syrian hamsters is limited. We evaluated the effects of Telazol-xylazine (TZX) combinations with respect to anesthetic efficacy and potential for tissue damage. Two dose levels of the combination were administered by both the intraperitoneal (IP) and intramuscular (IM) routes. TZX by the IM route failed to consistently produce anesthesia and caused gross and histopathologic muscle lesions. IP administration of 20 mg/kg Telazol combined with 10 mg/kg xylazine was adequate for restraint purposes. IP administration of 30 mg/kg Telazol combined with 10 mg/kg xylazine produced a safe, reliable level of surgical anesthesia without evidence of gross or histopathologic lesions. There was no nephrotoxicity at either concentration of the anesthetic. A dose level of TZX that provides safe parenteral anesthesia in Syrian hamsters was determined. JF - Laboratory animal science AU - Forsythe, D B AU - Payton, A J AU - Dixon, D AU - Myers, P H AU - Clark, J A AU - Snipe, J R AD - Comparative Medicine Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 497 EP - 502 VL - 42 IS - 5 SN - 0023-6764, 0023-6764 KW - Drug Combinations KW - 0 KW - tiletamine, zolazepam drug combination KW - Xylazine KW - 2KFG9TP5V8 KW - Tiletamine KW - 2YFC543249 KW - Zolazepam KW - G1R474U58U KW - Index Medicus KW - Muscular Diseases -- pathology KW - Animals KW - Rodent Diseases -- chemically induced KW - Muscular Diseases -- chemically induced KW - Injections, Intraperitoneal -- veterinary KW - Respiration -- drug effects KW - Injections, Intramuscular -- veterinary KW - Muscular Diseases -- veterinary KW - Rodent Diseases -- pathology KW - Female KW - Cricetinae KW - Xylazine -- administration & dosage KW - Anesthesia, General -- veterinary KW - Zolazepam -- toxicity KW - Zolazepam -- administration & dosage KW - Xylazine -- toxicity KW - Mesocricetus KW - Tiletamine -- toxicity KW - Tiletamine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73397064?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Laboratory+animal+science&rft.atitle=Evaluation+of+Telazol-xylazine+as+an+anesthetic+combination+for+use+in+Syrian+hamsters.&rft.au=Forsythe%2C+D+B%3BPayton%2C+A+J%3BDixon%2C+D%3BMyers%2C+P+H%3BClark%2C+J+A%3BSnipe%2C+J+R&rft.aulast=Forsythe&rft.aufirst=D&rft.date=1992-10-01&rft.volume=42&rft.issue=5&rft.spage=497&rft.isbn=&rft.btitle=&rft.title=Laboratory+animal+science&rft.issn=00236764&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-14 N1 - Date created - 1993-01-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Charybdotoxin, dendrotoxin and mast cell degranulating peptide block the voltage-activated K+ current of fibroblast cells stably transfected with NGK1 (Kv1.2) K+ channel complementary DNA. AN - 73356956; 1280351 AB - The blocking actions of the K+ channel toxins charybdotoxin, dendrotoxin and mast cell degranulating peptide were studied in B82 mouse fibroblast cells transformed to express NGK1 (Kv1.2) K+ channels. All three toxins were potent blockers of the K+ current in these cells, with KD values of 1.7, 2.8 and 185 nM, respectively. The toxin block exhibited a weak voltage-dependence with the degree of inhibition decreasing at positive membrane potentials. For charybdotoxin and dendrotoxin, reducing [K+]i did not increase the fractional block, demonstrating that the relief of block at positive membrane potentials is not due to displacement of the toxin molecules by outward flow of K+ ions. A voltage-jump protocol was used to determine the rates of binding and unbinding of dendrotoxin and mast cell degranulating peptide; binding of charybdotoxin was too rapid to be quantitatively evaluated in this manner. The binding rates (dendrotoxin, approximately 5 x 10(7)/M per s; mast cell degranulating peptide, approximately 0.8 x 10(7)/M per s) were largely voltage-independent, suggesting that association of the toxin molecules with the channel is diffusion limited. The rates of unbinding (dendrotoxin, approximately 0.3/s; mast cell degranulating peptide, approximately 3/s at +60 mV) of both toxins increased e-fold per approximately 40 mV change in membrane potential, thus accounting for the voltage-dependence of the equilibrium block. Internal perfusion with the three toxins failed to affect the K+ current (in contrast to internal tetraethylammonium which strongly blocked the current), indicating that the toxins exert their blocking action by binding to extracellular sites. JF - Neuroscience AU - Werkman, T R AU - Kawamura, T AU - Yokoyama, S AU - Higashida, H AU - Rogawski, M A AD - Neuronal Excitability Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 935 EP - 946 VL - 50 IS - 4 SN - 0306-4522, 0306-4522 KW - Elapid Venoms KW - 0 KW - Peptides KW - Potassium Channels KW - Scorpion Venoms KW - Charybdotoxin KW - 115422-61-2 KW - mast cell degranulating peptide KW - 32908-73-9 KW - dendrotoxin KW - 74811-93-1 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Fibroblasts -- drug effects KW - Mice KW - Fibroblasts -- metabolism KW - Ampicillin Resistance -- genetics KW - Transfection KW - Cells, Cultured KW - Extracellular Space -- metabolism KW - DNA -- genetics KW - Restriction Mapping KW - Membrane Potentials -- drug effects KW - Extracellular Space -- drug effects KW - Elapid Venoms -- pharmacology KW - Potassium Channels -- metabolism KW - Scorpion Venoms -- pharmacology KW - Potassium Channels -- drug effects KW - Peptides -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73356956?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience&rft.atitle=Charybdotoxin%2C+dendrotoxin+and+mast+cell+degranulating+peptide+block+the+voltage-activated+K%2B+current+of+fibroblast+cells+stably+transfected+with+NGK1+%28Kv1.2%29+K%2B+channel+complementary+DNA.&rft.au=Werkman%2C+T+R%3BKawamura%2C+T%3BYokoyama%2C+S%3BHigashida%2C+H%3BRogawski%2C+M+A&rft.aulast=Werkman&rft.aufirst=T&rft.date=1992-10-01&rft.volume=50&rft.issue=4&rft.spage=935&rft.isbn=&rft.btitle=&rft.title=Neuroscience&rft.issn=03064522&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-29 N1 - Date created - 1992-12-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of chronic consumption of methylparathion on rat brain regional acetylcholinesterase activity and on levels of biogenic amines. AN - 73356783; 1455421 AB - Wistar rat pups (female) were exposed to methylparathion (MPTH) by gastric intubation in single doses, or in a chronic regimen of different durations. A single dose of 1 mg MPTH/kg body weight in 15-day-old pups caused a significant decrease of acetylcholinesterase (AChE) activity in cerebellum (CE), motor cortex (MC) and brain stem (BS). The effect began to appear in about 20 min after administration, the peak effect was attained in 120 min and later on this waned off completely by 24 h. The effect was similar in young (15 days) and in adult (70 days) rats. A single dose of 0.2 mg MPTH/kg in 15 day old pups caused a reduction of AChE activity only in the BS, while a 0.1 mg MPTH/kg single dose given to 15-day-old pups caused no effect even in seven regions of the brain examined. Effect of low dose chronic administration of MPTH on AChE activity was also studied in CE, MC, BS, hippocampus (HI), striatum-accumbens (SA), spinal cord (SC) and also in the hypothalamus (HY). Administration of 0.1 mg MPTH/kg from second day to 15 days of age caused significant reduction of AChE activity in only 2 of the 7 brain regions studied. Administration of double the dose (0.2 mg MPTH/kg) and for a longer duration (2nd day to 150 days of age), caused a depression in all the brain regions studied. In all these regions, the levels of NA, DA and 5HT did practically not change. The results suggest that chronic consumption of MPTH leads to a moderate decrease of AChE activity in several brain regions. JF - Toxicology AU - Kumar, M V AU - Desiraju, T AD - Department of Neurophysiology, National Institute of Mental Health and Neurosciences, Bangalore, India. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 13 EP - 20 VL - 75 IS - 1 SN - 0300-483X, 0300-483X KW - Biogenic Amines KW - 0 KW - Cholinesterase Inhibitors KW - Serotonin KW - 333DO1RDJY KW - Methyl Parathion KW - 41BCL2O91D KW - Acetylcholinesterase KW - EC 3.1.1.7 KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Aging -- metabolism KW - Animals KW - Central Nervous System -- metabolism KW - Drug Administration Schedule KW - Rectum KW - Body Temperature -- drug effects KW - Dose-Response Relationship, Drug KW - Dopamine -- metabolism KW - Aging -- physiology KW - Rats KW - Norepinephrine -- metabolism KW - Rats, Wistar KW - Serotonin -- metabolism KW - Time Factors KW - Female KW - Methyl Parathion -- toxicity KW - Brain -- enzymology KW - Biogenic Amines -- metabolism KW - Cholinesterase Inhibitors -- toxicity KW - Brain -- drug effects KW - Acetylcholinesterase -- metabolism KW - Brain -- metabolism KW - Acetylcholinesterase -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73356783?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology&rft.atitle=Effect+of+chronic+consumption+of+methylparathion+on+rat+brain+regional+acetylcholinesterase+activity+and+on+levels+of+biogenic+amines.&rft.au=Kumar%2C+M+V%3BDesiraju%2C+T&rft.aulast=Kumar&rft.aufirst=M&rft.date=1992-10-01&rft.volume=75&rft.issue=1&rft.spage=13&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-31 N1 - Date created - 1992-12-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - CONF T1 - U.S.-Japan seminar on "genomic instability during carcinogenesis and tumor progression". AN - 73353857; 1360469 JF - Japanese journal of cancer research : Gann AU - Harris, C C AU - Hirohashi, S Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1108 EP - 1111 VL - 83 IS - 10 KW - Index Medicus KW - International Cooperation KW - Genes, Tumor Suppressor -- genetics KW - Humans KW - Mutation KW - Gene Amplification KW - Genome, Human KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73353857?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=Japanese+journal+of+cancer+research+%3A+Gann&rft.atitle=U.S.-Japan+seminar+on+%22genomic+instability+during+carcinogenesis+and+tumor+progression%22.&rft.au=Harris%2C+C+C%3BHirohashi%2C+S&rft.aulast=Harris&rft.aufirst=C&rft.date=1992-10-01&rft.volume=83&rft.issue=10&rft.spage=1108&rft.isbn=&rft.btitle=&rft.title=Japanese+journal+of+cancer+research+%3A+Gann&rft.issn=09105050&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-31 N1 - Date created - 1992-12-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The LEC rat--an animal model for human hepatitis and hepatocellular carcinoma. AN - 73353781; 1333464 JF - Japanese journal of cancer research : Gann AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 VL - 83 IS - 10 SN - 0910-5050, 0910-5050 KW - c-fos KW - c-jun KW - c-myc KW - hts KW - Copper KW - 789U1901C5 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Mutant Strains KW - Humans KW - Copper -- metabolism KW - Hepatitis KW - Liver Neoplasms, Experimental -- genetics KW - Liver Neoplasms, Experimental -- etiology KW - Carcinoma, Hepatocellular -- etiology KW - Carcinoma, Hepatocellular -- genetics KW - Hepatitis, Animal -- genetics KW - Disease Models, Animal KW - Hepatitis, Animal -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73353781?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Japanese+journal+of+cancer+research+%3A+Gann&rft.atitle=The+LEC+rat--an+animal+model+for+human+hepatitis+and+hepatocellular+carcinoma.&rft.au=Thorgeirsson%2C+S+S&rft.aulast=Thorgeirsson&rft.aufirst=S&rft.date=1992-10-01&rft.volume=83&rft.issue=10&rft.spage=inside+front+cover&rft.isbn=&rft.btitle=&rft.title=Japanese+journal+of+cancer+research+%3A+Gann&rft.issn=09105050&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-31 N1 - Date created - 1992-12-31 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-fos; c-jun; c-myc; hts N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Therapy of patients with metastatic breast cancer with 5-fluorouracil, leucovorin and carboplatin. AN - 73349683; 1450439 AB - Thirty-four women with metastatic breast cancer were treated at the National Cancer Institute of the National Institutes of Health, with a regimen of leucovorin (L), 500 mg/m2 i.v. over 30 min, followed in 1 h by 5-fluorouracil (5-FU), 375 mg/m2 i.v. bolus on days 1-5, and carboplatin (CBDCA), 50-100 mg/m2 i.v. bolus on days 2-4, every 28 days. All patients had received previous combination chemotherapy with at least one regimen (29 patients with 5-FU-containing regimens). CBDCA, 100 mg/m2 on days 2-4, resulted in grade 4 neutropenia in 10 out of 11 patients associated with sepsis in all 10 patients. CBDCA, 75 mg/m2 (seven patients) and 50 mg/m2 (15 patients), resulted in grade 4 neutropenia in six and eight patients, and neutropenic sepsis in five and two cases, respectively. Grade 4 thrombocytopenia occurred in 10, five and two patients receiving 100, 75 and 50 mg/m2 of CBDCA, respectively. Other toxicities included grade 3/4 mucositis in 18 patients and grade 3/4 diarrhea in 10 patients. Twenty nine patients were evaluable for response, with one pathologic complete response (3%), two partial responses (6%), 18 stable disease (53%) and eight (24%) progressive disease. Sites of response included bone, viscera and soft tissue. The median time from entry on study to progression, for responders, was 15 months. When platinum-DNA adduct formation in peripheral white blood cells was analyzed in 27 patients at 24 h after drug administration, a significant correlation between adduct level and CBDCA cumulative dose was found.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Anti-cancer drugs AU - Pai, L H AU - Swain, S M AU - Venzon, D J AU - Reed, E AU - Poirier, M C AU - Gupta-Burt, S AU - Denicoff, A M AU - Allegra, C J AD - National Cancer Institute, National Institute of Health, Bethesda, MD 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 463 EP - 469 VL - 3 IS - 5 SN - 0959-4973, 0959-4973 KW - DNA, Neoplasm KW - 0 KW - Carboplatin KW - BG3F62OND5 KW - Leucovorin KW - Q573I9DVLP KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - DNA, Neoplasm -- blood KW - Dose-Response Relationship, Drug KW - Humans KW - Leucovorin -- administration & dosage KW - Aged KW - Carboplatin -- administration & dosage KW - DNA, Neoplasm -- drug effects KW - Fluorouracil -- administration & dosage KW - Adult KW - Leukocytes, Mononuclear -- metabolism KW - Middle Aged KW - Carboplatin -- blood KW - Female KW - Breast Neoplasms -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Breast Neoplasms -- blood KW - Breast Neoplasms -- secondary UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73349683?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Anti-cancer+drugs&rft.atitle=Therapy+of+patients+with+metastatic+breast+cancer+with+5-fluorouracil%2C+leucovorin+and+carboplatin.&rft.au=Pai%2C+L+H%3BSwain%2C+S+M%3BVenzon%2C+D+J%3BReed%2C+E%3BPoirier%2C+M+C%3BGupta-Burt%2C+S%3BDenicoff%2C+A+M%3BAllegra%2C+C+J&rft.aulast=Pai&rft.aufirst=L&rft.date=1992-10-01&rft.volume=3&rft.issue=5&rft.spage=463&rft.isbn=&rft.btitle=&rft.title=Anti-cancer+drugs&rft.issn=09594973&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-06 N1 - Date created - 1993-01-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of the cyclic adenosine 3',5'-monophosphate response element in efficient expression of the rat thyrotropin receptor promoter. AN - 73343691; 1333054 AB - The "minimal" promoter region of the TSH receptor gene, -195 to -39 basepairs (bp), exhibits basal promoter activity, thyroid specificity, and negative regulation by TSH via its cAMP signal. In FRT thyroid cells and by comparison to pTRCAT5'-199, 5'-deletion mutants of chloramphenicol acetyltransferase (CAT) constructs from -199 to -150 bp of the minimal promoter decrease basal CAT activity by 50%, whereas continued deletion to -146 bp increases activity more than 4-fold. Continued deletion to -131 bp results in basal activity less than that of the -199 bp construct. An octameric cAMP response element (CRE)-like sequence, TGAGGTCA, is within -146 to -131 bp and starts at -139 bp. Its mutation to a consensus CRE (TGACGTCA) or AP1 (TGAGTCA) site or mutation of several residues flanking its 3'-terminus can improve promoter activity as much as 8-fold compared to pTRCAT5'-199. A nonpalindromic mutation to CGAGGACA decreases basal promoter activity to the level of the 199-bp minimal promoter. The CRE-like sequence between -139 and -132 bp is a constitutive enhancer of promoter activity in FRT thyroid cells, since, ligated to a simian virus-40-promoter-driven CAT gene, it increases CAT activity in the absence of forskolin in proportion to copy number and independent of direction or position. It can, however, function as a cAMP-responsive CRE, as evidenced by the fact that forskolin increases the activity of the same simian virus-40-promoter-driven CAT gene constructs in Buffalo rat liver (BRL) cells. DNAase-I footprinting shows that the CRE region is protected by a purified binding region peptide of the CRE-binding protein, activating transcription factor-2, and recombinant AP1 (human c-jun) as well as by BRL, FRT, and FRTL-5 rat thyroid cell nuclear extracts. Gel mobility shift analyses show that multiple CRE-binding proteins in the BRL, FRT, and FRTL-5 cell nuclear extracts form complexes with the CRE-like site, that one of these is CRE-binding protein, and that all form complexes with mutant sequences of the CRE-like site in a manner that exactly parallels their effects on constitutive enhancer function in FRT thyroid cells. We show, therefore, that the CRE-like site in the minimal TSH receptor promoter functions as a constitutive enhancer of promoter activity in FRT thyroid cells yet is a cAMP-responsive CRE.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Molecular endocrinology (Baltimore, Md.) AU - Ikuyama, S AU - Shimura, H AU - Hoeffler, J P AU - Kohn, L D AD - Laboratory of Biochemistry and Metabolism, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1701 EP - 1715 VL - 6 IS - 10 SN - 0888-8809, 0888-8809 KW - Oligodeoxyribonucleotides KW - 0 KW - Receptors, Thyrotropin KW - Recombinant Proteins KW - Thyrotropin KW - 9002-71-5 KW - Cyclic AMP KW - E0399OZS9N KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - Animals KW - Cell Nucleus -- metabolism KW - Thyroid Gland KW - Chloramphenicol O-Acetyltransferase -- metabolism KW - Binding Sites KW - Mutagenesis, Site-Directed KW - Rats KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Base Sequence KW - Transfection KW - Recombinant Proteins -- metabolism KW - Enhancer Elements, Genetic KW - Molecular Sequence Data KW - Cell Line KW - Sequence Deletion KW - Promoter Regions, Genetic KW - Thyrotropin -- pharmacology KW - Gene Expression Regulation KW - Cyclic AMP -- physiology KW - Receptors, Thyrotropin -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73343691?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.atitle=Role+of+the+cyclic+adenosine+3%27%2C5%27-monophosphate+response+element+in+efficient+expression+of+the+rat+thyrotropin+receptor+promoter.&rft.au=Ikuyama%2C+S%3BShimura%2C+H%3BHoeffler%2C+J+P%3BKohn%2C+L+D&rft.aulast=Ikuyama&rft.aufirst=S&rft.date=1992-10-01&rft.volume=6&rft.issue=10&rft.spage=1701&rft.isbn=&rft.btitle=&rft.title=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.issn=08888809&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-24 N1 - Date created - 1992-12-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effect of alcohol withdrawal on serum concentrations of Lp(a), apolipoproteins A-1 and B, and lipids. AN - 73336430; 1332524 AB - Moderate alcohol consumption is associated with a decreased risk of coronary artery disease. The mechanism of the putative protective effect of alcohol intake, however, remains elusive. Recent studies suggest that a ratio of apolipoprotein A-I/apolipoprotein B and Lp(a) are better indicators of the risk of atherosclerosis than total cholesterol and high density lipoprotein cholesterol. To assess the effect of alcohol on these analytes, we determined the concentration of Lp(a), apolipoprotein A-I, apolipoprotein B, total cholesterol, and high-density lipoprotein cholesterol, and calculated low-density lipoprotein cholesterol in serum of 12 patients meeting DSM-III-R criteria for alcohol dependence at the time of admission for treatment of alcohol withdrawal (before). The analyses were repeated after 4 weeks of supervised abstinence on a locked research unit (after). With abstinence, there was a significant increase in the concentration of Lp(a), the atherogenic index and the ratio of low-density to high-density lipoprotein cholesterol but a significant decrease in total cholesterol, high-density lipoprotein cholesterol, apolipoprotein A-I, and the apolipoprotein A-I/B ratio. Apolipoprotein B and low-density lipoprotein cholesterol showed no significant changes before and after alcohol abstinence. Thus, decreased Lp(a) and increased high-density lipoprotein cholesterol and apolipoprotein A-I may be factors mediating the putative protective effect of alcohol in coronary artery disease. JF - Alcoholism, clinical and experimental research AU - Huang, C M AU - Elin, R J AU - Ruddel, M AU - Schmitz, J AU - Linnoila, M AD - Clinical Pathology Department, Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 895 EP - 898 VL - 16 IS - 5 SN - 0145-6008, 0145-6008 KW - Apolipoprotein A-I KW - 0 KW - Apolipoproteins B KW - Cholesterol, HDL KW - Cholesterol, LDL KW - Lipids KW - Lipoprotein(a) KW - Cholesterol KW - 97C5T2UQ7J KW - Index Medicus KW - Cholesterol, LDL -- blood KW - Cholesterol -- blood KW - Substance Abuse Treatment Centers KW - Cholesterol, HDL -- blood KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Liver Function Tests KW - Male KW - Female KW - Lipids -- blood KW - Alcoholism -- rehabilitation KW - Lipoprotein(a) -- blood KW - Alcohol Withdrawal Delirium -- blood KW - Apolipoprotein A-I -- metabolism KW - Apolipoproteins B -- metabolism KW - Alcoholism -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73336430?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%2C+clinical+and+experimental+research&rft.atitle=The+effect+of+alcohol+withdrawal+on+serum+concentrations+of+Lp%28a%29%2C+apolipoproteins+A-1+and+B%2C+and+lipids.&rft.au=Huang%2C+C+M%3BElin%2C+R+J%3BRuddel%2C+M%3BSchmitz%2C+J%3BLinnoila%2C+M&rft.aulast=Huang&rft.aufirst=C&rft.date=1992-10-01&rft.volume=16&rft.issue=5&rft.spage=895&rft.isbn=&rft.btitle=&rft.title=Alcoholism%2C+clinical+and+experimental+research&rft.issn=01456008&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-08 N1 - Date created - 1992-12-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Alcohol Clin Exp Res. 1993 Aug;17(4):926 [8214436] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Timed treatment of the arthritic diseases: a review and hypothesis. AN - 73336284; 1439846 AB - Evidence has been accumulating regarding the importance of biological rhythms in the diagnosis and treatment of a variety of diseases and disorders. Increasingly, the arthritides have shown statistically quantifiable rhythmic parameters. Included in the latter group are joint pain and joint size. In addition, a number of drugs used to treat rheumatic diseases have varying therapeutic and toxic effects based on the time of day of administration. Among these drug classes are nonsteroidal antiinflammatory drugs, glucocorticoids, and a number of cytostatic agents. In the last group of agents, experience in treating malignant disease suggests that time-specified treatment may reduce the toxic effects of low-dose cytostatic treatment of rheumatoid arthritis (RA) and related diseases. This article reviews that evidence and suggests a rationale for the timed treatment of RA with methotrexate. JF - Seminars in arthritis and rheumatism AU - Vener, K J AU - Reddy, A AD - National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 83 EP - 97 VL - 22 IS - 2 SN - 0049-0172, 0049-0172 KW - Anti-Inflammatory Agents KW - 0 KW - Anti-Inflammatory Agents, Non-Steroidal KW - Index Medicus KW - Animals KW - Anti-Inflammatory Agents, Non-Steroidal -- therapeutic use KW - Humans KW - Anti-Inflammatory Agents -- therapeutic use KW - Periodicity KW - Time Factors KW - Arthritis -- therapy KW - Arthritis -- physiopathology KW - Models, Theoretical UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73336284?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+arthritis+and+rheumatism&rft.atitle=Timed+treatment+of+the+arthritic+diseases%3A+a+review+and+hypothesis.&rft.au=Vener%2C+K+J%3BReddy%2C+A&rft.aulast=Vener&rft.aufirst=K&rft.date=1992-10-01&rft.volume=22&rft.issue=2&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=Seminars+in+arthritis+and+rheumatism&rft.issn=00490172&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-08 N1 - Date created - 1992-12-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Toxicity and carcinogenicity studies of quercetin, a natural component of foods. AN - 73333144; 1459373 AB - Quercetin is a naturally occurring chemical found in our daily diet in fruits and vegetables. Toxicity and carcinogenicity studies of quercetin were conducted in male and female F344/N rats, under conditions which allowed comparison to results of approximately 400 previously tested chemicals. The chemical was administered in the feed for 2-years at concentrations of 0, 1000, 10,000, or 40,000 ppm, and the estimated dose delivered was approximately 40-1900 mg/kg/day. There were no treatment-related effects on survival and no treatment-related clinical signs of toxicity. The high-dose groups had reduced body weight gain in comparison to controls during the last half of the study. At interim evaluations at 6 and 15 months, treatment-related toxic lesions were not observed, but at 2 years toxic and neoplastic lesions were seen in the kidney of male rats, including increased severity of chronic nephropathy, hyperplasia, and neoplasia of the renal tubular epithelium. Under the conditions of these 2-year studies quercetin showed carcinogenic activity in the kidney of the male rat, causing primarily benign tumors of the renal tubular epithelium. Quercetin did not cause tumors at other sites. Quercetin is a genotoxic chemical, but the neoplastic response observed in the kidney may be due in part to a combination of nongenotoxic and genotoxic events. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Dunnick, J K AU - Hailey, J R AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 423 EP - 431 VL - 19 IS - 3 SN - 0272-0590, 0272-0590 KW - Carcinogens KW - 0 KW - Quercetin KW - 9IKM0I5T1E KW - Index Medicus KW - Eating -- drug effects KW - Animals KW - Liver -- pathology KW - Kidney -- pathology KW - Food Analysis KW - Neoplasms, Experimental -- pathology KW - Rats KW - Rats, Inbred F344 KW - Neoplasms, Experimental -- chemically induced KW - Body Weight -- drug effects KW - Female KW - Male KW - Organ Size -- drug effects KW - Quercetin -- toxicity KW - Carcinogens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73333144?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=Toxicity+and+carcinogenicity+studies+of+quercetin%2C+a+natural+component+of+foods.&rft.au=Dunnick%2C+J+K%3BHailey%2C+J+R&rft.aulast=Dunnick&rft.aufirst=J&rft.date=1992-10-01&rft.volume=19&rft.issue=3&rft.spage=423&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-13 N1 - Date created - 1993-01-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of acidic fibroblast growth factor in regenerating liver and during hepatic differentiation. AN - 73332987; 1279268 AB - Acidic fibroblast growth factor belongs to a family of growth factors that show a high affinity for heparin sulfate proteoglycans. In vitro, it participates in various cellular functions including proliferation, differentiation, angiogenesis, and cell migration, but in vivo, the physiologic role of this growth factor is still not clearly defined. The level of expression and also cellular distribution of transcripts for acidic fibroblast growth factor (aFGF) were studied in adult rat liver after partial hepatectomy and during hepatic differentiation in fetal, neonatal, and adult livers by Northern analysis and in situ hybridization techniques. After partial hepatectomy a significant increase in the transcripts for aFGF was observed at 24 hours, whereas at 4 and 12 hours after the operation, the level of transcripts were similar to those of sham-operated animals. In the postnatal liver a high level of aFGF expression was present when the most evident transition from 2 to 3 cell thick hepatic cords to normal hepatic structure is taking place (Ogawa K, Medine A, Farber E. Br J Cancer 1979;40: 782-90). In contrast during the prenatal period, when the liver is still a hemopoietic organ and only a small number of sinusoids are present, low level of aFGF transcripts could be found. Animals treated with 2-acetylaminofluorene and partial hepatectomy (Evarts RP, Nagy P, Marsden E, Thorgeirsson SS. Carcinogenesis 1987;8:1737-40) displayed a marked increase in hepatic aFGF transcripts at the peak of proliferation of primitive liver epithelial cells (oval cells) and perisinusoidal stellate cells (Ito cells) in addition to hepatocytes. In situ hybridization combined with immunocytochemistry using oval and Ito cell specific antibodies revealed the presence of transcripts both in oval cells and Ito cells. Basophilic areas composed of small hepatocytes had a 3-fold increase in the level of transcripts as compared with the surrounding hepatocytes. These experiments demonstrate that the expression of aFGF is highest during the late stages of hepatic morphogenesis in newborn animals as well as during hepatic differentiation in adult liver. JF - Laboratory investigation; a journal of technical methods and pathology AU - Marsden, E R AU - Hu, Z AU - Fujio, K AU - Nakatsukasa, H AU - Thorgeirsson, S S AU - Evarts, R P AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 427 EP - 433 VL - 67 IS - 4 SN - 0023-6837, 0023-6837 KW - Reticulin KW - 0 KW - Fibroblast Growth Factor 1 KW - 104781-85-3 KW - Index Medicus KW - Rats KW - Histocytochemistry -- methods KW - Animals KW - Rats, Inbred F344 KW - Blotting, Northern KW - Cell Differentiation KW - Nucleic Acid Hybridization KW - Reticulin -- metabolism KW - Staining and Labeling KW - Male KW - Liver -- cytology KW - Fibroblast Growth Factor 1 -- metabolism KW - Liver -- metabolism KW - Liver Regeneration UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73332987?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Laboratory+investigation%3B+a+journal+of+technical+methods+and+pathology&rft.atitle=Expression+of+acidic+fibroblast+growth+factor+in+regenerating+liver+and+during+hepatic+differentiation.&rft.au=Marsden%2C+E+R%3BHu%2C+Z%3BFujio%2C+K%3BNakatsukasa%2C+H%3BThorgeirsson%2C+S+S%3BEvarts%2C+R+P&rft.aulast=Marsden&rft.aufirst=E&rft.date=1992-10-01&rft.volume=67&rft.issue=4&rft.spage=427&rft.isbn=&rft.btitle=&rft.title=Laboratory+investigation%3B+a+journal+of+technical+methods+and+pathology&rft.issn=00236837&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-07 N1 - Date created - 1992-12-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Lab Invest. 1992 Oct;67(4):413-5 [1434525] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - An alternative hypothesis on the role of chemically induced protein droplet (alpha 2u-globulin) nephropathy in renal carcinogenesis. AN - 73325871; 1279759 AB - Based on associations between the accumulation of protein droplets containing alpha 2u-globulin in proximal tubular epithelial cells and increased incidences of renal tubular neoplasms in male rats, it has been suggested that the carcinogenicity of chemicals that cause alpha 2u-globulin nephropathy is unique to animals that synthesize this protein. Chemicals that caused alpha 2u-globulin nephropathy and renal carcinogenicity in male rats have not been shown to produce renal tumors in animals that lack the capability for hepatic alpha 2u-globulin synthesis, including female rats, male NBR rats, or mice of either sex. Because humans do not synthesize alpha 2u-globulin it has been suggested that chemicals which cause renal toxicity associated with alpha 2u-globulin accumulation do not pose an increased cancer risk to humans. In this review on the association between alpha 2u-globulin nephropathy and renal carcinogenesis, it is apparent that (a) there are data inconsistent with the hypothesis linking these occurrences, (b) alternative mechanisms of renal toxicity and carcinogenicity are plausible, (c) data on quantitative dose-response correspondences between the various stages of alpha 2u-globulin nephropathy and renal carcinogenicity are limited, and (d) a greater understanding of the molecular changes occurring during renal carcinogenesis is needed before assuming that the current hypothesis is correct. Future research aimed at resolving issues raised in this paper should help determine whether or not the association between alpha 2u-globulin nephropathy and renal carcinogenesis represents a cause-and-effect relationship. JF - Regulatory toxicology and pharmacology : RTP AU - Melnick, R L AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 111 EP - 125 VL - 16 IS - 2 SN - 0273-2300, 0273-2300 KW - Alpha-Globulins KW - 0 KW - Hydrocarbons KW - alpha 2u globulin KW - Index Medicus KW - Rats KW - Hyalin -- metabolism KW - Animals KW - Humans KW - Male KW - Hyalin -- drug effects KW - Female KW - Kidney Diseases -- metabolism KW - Kidney Neoplasms -- chemically induced KW - Kidney Diseases -- complications KW - Kidney Neoplasms -- etiology KW - Hydrocarbons -- toxicity KW - Alpha-Globulins -- metabolism KW - Kidney Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73325871?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Regulatory+toxicology+and+pharmacology+%3A+RTP&rft.atitle=An+alternative+hypothesis+on+the+role+of+chemically+induced+protein+droplet+%28alpha+2u-globulin%29+nephropathy+in+renal+carcinogenesis.&rft.au=Melnick%2C+R+L&rft.aulast=Melnick&rft.aufirst=R&rft.date=1992-10-01&rft.volume=16&rft.issue=2&rft.spage=111&rft.isbn=&rft.btitle=&rft.title=Regulatory+toxicology+and+pharmacology+%3A+RTP&rft.issn=02732300&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-23 N1 - Date created - 1992-12-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Regul Toxicol Pharmacol. 1992 Oct;16(2):109-10 [1438993] Regul Toxicol Pharmacol. 1993 Oct;18(2):357-64 [7506436] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Quinolinic acid and kynurenine pathway metabolism in inflammatory and non-inflammatory neurological disease. AN - 73313371; 1422788 AB - Neurological dysfunction, seizures and brain atrophy occur in a broad spectrum of acute and chronic neurological diseases. In certain instances, over-stimulation of N-methyl-D-aspartate receptors has been implicated. Quinolinic acid (QUIN) is an endogenous N-methyl-D-aspartate receptor agonist synthesized from L-tryptophan via the kynurenine pathway and thereby has the potential of mediating N-methyl-D-aspartate neuronal damage and dysfunction. Conversely, the related metabolite, kynurenic acid, is an antagonist of N-methyl-D-aspartate receptors and could modulate the neurotoxic effects of QUIN as well as disrupt excitatory amino acid neurotransmission. In the present study, markedly increased concentrations of QUIN were found in both lumbar cerebrospinal fluid (CSF) and post-mortem brain tissue of patients with inflammatory diseases (bacterial, viral, fungal and parasitic infections, meningitis, autoimmune diseases and septicaemia) independent of breakdown of the blood-brain barrier. The concentrations of kynurenic acid were also increased, but generally to a lesser degree than the increases in QUIN. In contrast, no increases in CSF QUIN were found in chronic neurodegenerative disorders, depression or myoclonic seizure disorders, while CSF kynurenic acid concentrations were significantly lower in Huntington's disease and Alzheimer's disease. In inflammatory disease patients, proportional increases in CSF L-kynurenine and reduced L-tryptophan accompanied the increases in CSF QUIN and kynurenic acid. These responses are consistent with induction of indoleamine-2,3-dioxygenase, the first enzyme of the kynurenine pathway which converts L-tryptophan to kynurenic acid and QUIN. Indeed, increases in both indoleamine-2,3-dioxygenase activity and QUIN concentrations were observed in the cerebral cortex of macaques infected with retrovirus, particularly those with local inflammatory lesions. Correlations between CSF QUIN, kynurenic acid and L-kynurenine with markers of immune stimulation (neopterin, white blood cell counts and IgG levels) indicate a relationship between accelerated kynurenine pathway metabolism and the degree of intracerebral immune stimulation. We conclude that inflammatory diseases are associated with accumulation of QUIN, kynurenic acid and L-kynurenine within the central nervous system, but that the available data do not support a role for QUIN in the aetiology of Huntington's disease or Alzheimer's disease. In conjunction with our previous reports that CSF QUIN concentrations are correlated to objective measures of neuropsychological deficits in HIV-1-infected patients, we hypothesize that QUIN and kynurenic acid are mediators of neuronal dysfunction and nerve cell death in inflammatory diseases. Therefore, strategies to attenuate the neurological effects of kynurenine pathway metabolites or attenuate the rate of their synthesis offer new approaches to therapy. JF - Brain : a journal of neurology AU - Heyes, M P AU - Saito, K AU - Crowley, J S AU - Davis, L E AU - Demitrack, M A AU - Der, M AU - Dilling, L A AU - Elia, J AU - Kruesi, M J AU - Lackner, A AD - Section on Analytical Biochemistry, NIMH, NIH, Bethesda, MD 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1249 EP - 1273 VL - 115 ( Pt 5) SN - 0006-8950, 0006-8950 KW - Kynurenine KW - 343-65-7 KW - Quinolinic Acid KW - F6F0HK1URN KW - Kynurenic Acid KW - H030S2S85J KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Humans KW - Macaca KW - Kynurenic Acid -- metabolism KW - Aged KW - Simian Acquired Immunodeficiency Syndrome -- complications KW - Brain Diseases -- metabolism KW - Kynurenic Acid -- cerebrospinal fluid KW - HIV Infections -- metabolism KW - Middle Aged KW - Encephalitis -- metabolism KW - HIV Infections -- cerebrospinal fluid KW - Female KW - Male KW - Neuritis -- veterinary KW - Kynurenine -- cerebrospinal fluid KW - Quinolinic Acid -- cerebrospinal fluid KW - Quinolinic Acid -- metabolism KW - Nervous System Diseases -- metabolism KW - Neuritis -- metabolism KW - Neuritis -- etiology KW - Kynurenine -- metabolism KW - Neuritis -- cerebrospinal fluid KW - Nervous System Diseases -- cerebrospinal fluid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73313371?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+%3A+a+journal+of+neurology&rft.atitle=Quinolinic+acid+and+kynurenine+pathway+metabolism+in+inflammatory+and+non-inflammatory+neurological+disease.&rft.au=Heyes%2C+M+P%3BSaito%2C+K%3BCrowley%2C+J+S%3BDavis%2C+L+E%3BDemitrack%2C+M+A%3BDer%2C+M%3BDilling%2C+L+A%3BElia%2C+J%3BKruesi%2C+M+J%3BLackner%2C+A&rft.aulast=Heyes&rft.aufirst=M&rft.date=1992-10-01&rft.volume=115+%28+Pt+5%29&rft.issue=&rft.spage=1249&rft.isbn=&rft.btitle=&rft.title=Brain+%3A+a+journal+of+neurology&rft.issn=00068950&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-10 N1 - Date created - 1992-12-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vivo evidence of hydroxyl radical formation after acute copper and ascorbic acid intake: electron spin resonance spin-trapping investigation. AN - 73313189; 1331758 AB - Copper has been suggested to facilitate oxidative tissue injury through a free radical-mediated pathway analogous to the Fenton reaction. By applying the ESR spin-trapping technique, evidence for hydroxyl radical formation in vivo was obtained in rats treated simultaneously with copper and ascorbic acid. A secondary radical spin-trapping technique was used in which the hydroxyl radical formed the methyl radical upon reaction with dimethylsulfoxide. The methyl radical was then detected by ESR spectroscopy as its adduct with the spin trap phenyl-N-t-butylnitrone (PBN). Because copper excreted into the bile from treated animals is expected to be maintained in the Cu(I) state (by ascorbic acid or glutathione), a chelating agent that would redox-stabilize it in the Cu(I) state was used to prevent ex vivo redox chemistry. Bile samples were collected directly into solutions of bathocuproinedisulfonic acid, a Cu(I)-stabilizing agent, and 2,2'-dipyridyl, a Fe(II)-stabilizing agent. If these precautions were not taken, radical adducts were generated ex vivo and could be mistaken for radical adducts generated in vivo and excreted into the bile. Besides the PBN/.CH3 adduct, three other radical adducts were produced in vivo and excreted in bile. JF - Molecular pharmacology AU - Kadiiska, M B AU - Hanna, P M AU - Hernandez, L AU - Mason, R P AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 723 EP - 729 VL - 42 IS - 4 SN - 0026-895X, 0026-895X KW - Free Radicals KW - 0 KW - Hydroxides KW - Copper KW - 789U1901C5 KW - Iron KW - E1UOL152H7 KW - Ascorbic Acid KW - PQ6CK8PD0R KW - Index Medicus KW - Rats KW - Bile -- chemistry KW - Animals KW - Rats, Sprague-Dawley KW - Electron Spin Resonance Spectroscopy KW - Bile -- metabolism KW - Time Factors KW - Male KW - Iron -- metabolism KW - Hydroxides -- chemistry KW - Ascorbic Acid -- chemistry KW - Copper -- toxicity KW - Copper -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73313189?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=In+vivo+evidence+of+hydroxyl+radical+formation+after+acute+copper+and+ascorbic+acid+intake%3A+electron+spin+resonance+spin-trapping+investigation.&rft.au=Kadiiska%2C+M+B%3BHanna%2C+P+M%3BHernandez%2C+L%3BMason%2C+R+P&rft.aulast=Kadiiska&rft.aufirst=M&rft.date=1992-10-01&rft.volume=42&rft.issue=4&rft.spage=723&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=0026895X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-01 N1 - Date created - 1992-12-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Major depression: its recognition and treatment. Part 1: First-generation antidepressants. AN - 73296865; 1442526 JF - American pharmacy AU - Grothe, D R AU - Cohen, L J AD - National Institute of Mental Health, National Institutes of Health, Bethesda, Md. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 33 EP - 40 VL - NS32 IS - 10 SN - 0160-3450, 0160-3450 KW - Antidepressive Agents KW - 0 KW - Index Medicus KW - Humans KW - Antidepressive Agents -- blood KW - Depressive Disorder -- physiopathology KW - Depressive Disorder -- drug therapy KW - Antidepressive Agents -- therapeutic use KW - Antidepressive Agents -- adverse effects KW - Depressive Disorder -- classification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73296865?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+pharmacy&rft.atitle=Major+depression%3A+its+recognition+and+treatment.+Part+1%3A+First-generation+antidepressants.&rft.au=Grothe%2C+D+R%3BCohen%2C+L+J&rft.aulast=Grothe&rft.aufirst=D&rft.date=1992-10-01&rft.volume=NS32&rft.issue=10&rft.spage=33&rft.isbn=&rft.btitle=&rft.title=American+pharmacy&rft.issn=01603450&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-18 N1 - Date created - 1992-12-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effect of sodium selenite on cell proliferation and transformation of primary rat tracheal epithelial cells. AN - 73289324; 1330341 AB - The effects of sodium selenite (Na2SeO3) on cell proliferation and the development of preneoplastic transformed variants were studied in primary cultures of rat tracheal epithelial cells. Results revealed a biphasic effect of Na2SeO3 on cell proliferation: at concentrations between 6 x 10(-8) and 6 x 10(-6) M, it stimulated and at concentrations of approximately 2 x 10(-5) and above it inhibited cell proliferation (presumably due to toxicity). Nontoxic concentrations of Na2SeO3 (6 x 10(-8) -6 x 10(-7) M) significantly reduced the spontaneous transformation frequency. Transformation induced by the tobacco-specific nitrosamine 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) was effectively inhibited by nontoxic as well as toxic concentrations of Na2SeO3. Treatment of cultures with Na2SeO3 after cessation of NNK exposure, i.e. during the selection period, also significantly reduced the transformation frequency. These experiments show that the inhibition of transformation by Na2SeO3 is not the result of an antiproliferative effect. They further indicate that the inhibitory effect occurs even when the chemical treatment occurs during the 'postinitiation' phase. Thus the inhibition of transformation by Na2SeO3 cannot solely be explained by its effects on drug metabolism. JF - Carcinogenesis AU - Zhu, S AU - Gray, T E AU - Nettesheim, P AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1725 EP - 1729 VL - 13 IS - 10 SN - 0143-3334, 0143-3334 KW - Anticarcinogenic Agents KW - 0 KW - Carcinogens KW - Nitrosamines KW - 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone KW - 7S395EDO61 KW - Selenium KW - H6241UJ22B KW - Sodium Selenite KW - HIW548RQ3W KW - Index Medicus KW - Rats KW - Animals KW - Epithelial Cells KW - Cells, Cultured KW - Anticarcinogenic Agents -- pharmacology KW - Cell Division -- drug effects KW - Epithelium -- pathology KW - Epithelium -- drug effects KW - Trachea -- pathology KW - Selenium -- pharmacology KW - Cell Transformation, Neoplastic -- drug effects KW - Trachea -- cytology KW - Trachea -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73289324?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=The+effect+of+sodium+selenite+on+cell+proliferation+and+transformation+of+primary+rat+tracheal+epithelial+cells.&rft.au=Zhu%2C+S%3BGray%2C+T+E%3BNettesheim%2C+P&rft.aulast=Zhu&rft.aufirst=S&rft.date=1992-10-01&rft.volume=13&rft.issue=10&rft.spage=1725&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-27 N1 - Date created - 1992-11-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Plasmacytomagenesis in mice: model of neoplastic development dependent upon chromosomal translocations. AN - 73288294; 1423827 AB - Three model systems of plasmacytomagenesis that are associated with mutations that affect c-myc transcription were discussed. Plasmacytoma induction by chronic peritoneal irritation induced by non-metabolized paraffin oils or plastic objects is strongly influenced by the immune status of the host. BALB/cAn mice must be exposed to natural environmental antigens to develop a high incidence of plasmacytomas. This may be related to T-cell priming. BALB/cAn mice raised under strict SPF conditions are refractory to plasmacytoma induction by pristane. The genotype of the mouse plays an important role in the chronic peritoneal irritation model of plasmacytomagenesis in mice. Only a few of the standard inbred strains are susceptible, notably BALB/cAn and NZB/B1. The genetic basis of susceptibility and resistance has been studied in crosses and congenic strains involving the susceptible BALB/cAn and resistant DBA/2 strains. While several genes play a role in determining resistance at least one resistance gene located on the distal end of Chr 4 reduces the incidence by at least 50% as determined in the BALB/cAn.DBA/2 Fv-1n/n congenic strain. The action of susceptibility and resistance genes is not known; hypothetically these genes could play a role in plasmacytomagenesis by increasing the probabilities of illegitimate exchanges between genes or by influencing the formation of mutations in genes that regulate mitotic cycling. Plasmacytomas appear to develop in the chronic inflammatory tissues induced by these agents. Fundamental unanswered questions are whether these inflammatory tissues provide products such as oxidants in vivo that damage DNA and promote mutagenesis. In the mouse there is a resident self-renewing B cell population that is CD5+. These B cells, which are known to be precursors of normal lamina propria IgA-secreting plasma cells, are directly in contact with the chronic inflammatory process induced by pristane; they may be targets in plasmacytomagenesis. The plasmacytomas that develop by the peritoneal mode of induction all have chromosomal translocations that directly or indirectly activate c-myc. The predominant MACTR found in 90% of these tumors is T(12;15) in which a heavy-chain switch region sequence is joined to the 5' region of c-myc. The evidence strongly suggests that the translocation develops in a late mature B cell that is in the process of isotype switching. An unanswered question is whether the switching associated T(12;15) takes place in a B cell that is exposed to the inflammatory microenvironment.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Carcinogenesis AU - Potter, M AU - Wiener, F AD - DCBDC, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1681 EP - 1697 VL - 13 IS - 10 SN - 0143-3334, 0143-3334 KW - E&mgr;-bcl-2 KW - E&mgr;-v-abl KW - Ld-IL-6 KW - PVA-1 KW - c-myc KW - Index Medicus KW - Animals KW - Mice, Inbred C3H KW - Mice KW - Mice, Transgenic KW - Mice, Inbred BALB C KW - Models, Biological KW - Mice, Inbred DBA KW - Translocation, Genetic -- genetics KW - Plasmacytoma -- etiology KW - Plasmacytoma -- genetics KW - Chromosomes -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73288294?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Plasmacytomagenesis+in+mice%3A+model+of+neoplastic+development+dependent+upon+chromosomal+translocations.&rft.au=Potter%2C+M%3BWiener%2C+F&rft.aulast=Potter&rft.aufirst=M&rft.date=1992-10-01&rft.volume=13&rft.issue=10&rft.spage=1681&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-27 N1 - Date created - 1992-11-27 N1 - Date revised - 2017-01-13 N1 - Gene symbol - E&mgr;-bcl-2; E&mgr;-v-abl; Ld-IL-6; PVA-1; c-myc N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The prevalence of illicit drug use in six metropolitan areas in the United States: results from the 1991 National Household Survey on Drug Abuse. AN - 73272065; 1422110 AB - National levels and trends of illicit drug use in the general population are well documented. However, little is known about how this phenomenon is distributed among various subnational areas such as state, metropolitan area, and other local areas. The sample design from the National Household Survey on Drug Abuse (NHSDA) was recently expanded such that estimates from several large metropolitan areas could be produced with reasonable precision. The prevalence of illicit drug use is examined in six large metropolitan areas of the United States. These findings indicate that, in some cases, drug use varies considerably by metropolitan area. JF - British journal of addiction AU - Hughes, A L AD - National Institute on Drug Abuse, Division of Epidemiology and Prevention Research, Rockville, Maryland 20857. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1481 EP - 1485 VL - 87 IS - 10 SN - 0952-0481, 0952-0481 KW - Street Drugs KW - 0 KW - Index Medicus KW - Cross-Sectional Studies KW - Humans KW - Incidence KW - United States -- epidemiology KW - Population Surveillance KW - Urban Population -- statistics & numerical data KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73272065?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+addiction&rft.atitle=The+prevalence+of+illicit+drug+use+in+six+metropolitan+areas+in+the+United+States%3A+results+from+the+1991+National+Household+Survey+on+Drug+Abuse.&rft.au=Hughes%2C+A+L&rft.aulast=Hughes&rft.aufirst=A&rft.date=1992-10-01&rft.volume=87&rft.issue=10&rft.spage=1481&rft.isbn=&rft.btitle=&rft.title=British+journal+of+addiction&rft.issn=09520481&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-04 N1 - Date created - 1992-12-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intravenous administration of recombinant human macrophage colony-stimulating factor to patients with metastatic cancer: a phase I study. AN - 73258423; 1403042 AB - Recombinant human macrophage colony-stimulating factor (M-CSF) has been shown to stimulate specifically macrophage lineage differentiation in vitro and to induce cells capable of antitumor activity alone or in combination with an antibody. The administration of M-CSF to mice has demonstrated antitumor therapeutic effects in vivo. Therefore, a phase I trial of M-CSF administration to patients with metastatic cancer was undertaken. M-CSF was given by intermittent intravenous bolus infusion every 8 hours for 7 days; the treatment cycle was repeated once after a week of rest. Cohorts of three patients underwent dose escalation from 10 to 100,000 micrograms/m2/d; 23 patients received 27 courses of M-CSF administration. All patients had metastatic solid tumors refractory to conventional therapy, including renal cell carcinoma (RCC) (nine), melanoma (seven), and colorectal carcinoma (seven). Treatment-related toxicity was minimal; five patients developed transient signs of ocular or periorbital inflammation, with iridocyclitis as the most severe manifestation. At the highest doses, platelet counts decreased with therapy (but remained > 100,000/mm3) and the absolute monocyte count increased during the course of therapy. Only at 30,000 and 100,000 micrograms/m2/d was treatment limited because of toxicity (iritis and malaise). Pharmacokinetic studies demonstrated up to a 1,000-fold increase in circulating serum M-CSF after bolus infusion; half-life varied from 1 to 6 hours. Complete regression of mediastinal adenopathy and multiple pulmonary metastases were observed in one patient with RCC. Recombinant M-CSF can be administered safely to patients with metastatic cancer at doses that demonstrate biologic activity. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Sanda, M G AU - Yang, J C AU - Topalian, S L AU - Groves, E S AU - Childs, A AU - Belfort, R AU - de Smet, M D AU - Schwartzentruber, D J AU - White, D E AU - Lotze, M T AD - Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1643 EP - 1649 VL - 10 IS - 10 SN - 0732-183X, 0732-183X KW - Recombinant Proteins KW - 0 KW - Macrophage Colony-Stimulating Factor KW - 81627-83-0 KW - Index Medicus KW - Infusions, Intravenous KW - Humans KW - Adult KW - Treatment Outcome KW - Recombinant Proteins -- adverse effects KW - Neoplasm Metastasis KW - Aged KW - Middle Aged KW - Recombinant Proteins -- administration & dosage KW - Male KW - Female KW - Neoplasms -- drug therapy KW - Macrophage Colony-Stimulating Factor -- administration & dosage KW - Macrophage Colony-Stimulating Factor -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73258423?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Intravenous+administration+of+recombinant+human+macrophage+colony-stimulating+factor+to+patients+with+metastatic+cancer%3A+a+phase+I+study.&rft.au=Sanda%2C+M+G%3BYang%2C+J+C%3BTopalian%2C+S+L%3BGroves%2C+E+S%3BChilds%2C+A%3BBelfort%2C+R%3Bde+Smet%2C+M+D%3BSchwartzentruber%2C+D+J%3BWhite%2C+D+E%3BLotze%2C+M+T&rft.aulast=Sanda&rft.aufirst=M&rft.date=1992-10-01&rft.volume=10&rft.issue=10&rft.spage=1643&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=0732183X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-30 N1 - Date created - 1992-10-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Noncompetitive inhibition of N-methyl-D-aspartate by conantokin-G: evidence for an allosteric interaction at polyamine sites. AN - 73257409; 1328523 AB - Conantokins T and G are polypeptide toxins present in snails of the genus Conus. These substances were recently reported to act as N-methyl-D-aspartate (NMDA) antagonists. In the present study, we examined the possible mechanisms producing this antagonism. Conantokin-G inhibited spermine- and spermidine-stimulated [3H]MK-801 binding to extensively washed rat forebrain membranes in a noncompetitive manner with IC50 values of approximately 507 and approximately 946 nM, respectively. In contrast, glutamate-enhanced [3H]MK-801 binding was unaffected by conantokin-G concentrations of less than or equal to 20 microM. At concentrations greater than or equal to 5 microM, conantokin-G effected a modest, noncompetitive inhibition of glycine-stimulated [3H]MK-801 binding and also produced a small enhancement of basal [3H]MK-801 binding. Conantokin-G reduced (IC50 approximately 1.08 microM) the NMDA-stimulated accumulation of cyclic GMP in cerebellar granule cell cultures to basal values, but did not affect kainate-mediated increases in cyclic GMP. These findings indicate that conantokin-G acts as a noncompetitive NMDA antagonist through an allosteric inhibition of polyamine responses. The neurochemical profile of this polypeptide is distinct from previously described noncompetitive NMDA antagonists. JF - Journal of neurochemistry AU - Skolnick, P AU - Boje, K AU - Miller, R AU - Pennington, M AU - Maccecchini, M L AD - Laboratory of Neuroscience, NIDDK, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1516 EP - 1521 VL - 59 IS - 4 SN - 0022-3042, 0022-3042 KW - Conotoxins KW - 0 KW - Mollusk Venoms KW - Peptides, Cyclic KW - Polyamines KW - N-Methylaspartate KW - 6384-92-5 KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - conotoxin GV KW - 93438-65-4 KW - Cyclic GMP KW - H2D2X058MU KW - Index Medicus KW - Osmolar Concentration KW - Animals KW - Dizocilpine Maleate -- metabolism KW - Prosencephalon -- metabolism KW - Dizocilpine Maleate -- antagonists & inhibitors KW - Granulocytes -- metabolism KW - Binding Sites KW - Cerebellum -- metabolism KW - Rats KW - Rats, Sprague-Dawley KW - Cerebellum -- cytology KW - Cyclic GMP -- metabolism KW - Male KW - Polyamines -- pharmacology KW - Mollusk Venoms -- pharmacology KW - N-Methylaspartate -- antagonists & inhibitors KW - Polyamines -- metabolism KW - Peptides, Cyclic -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73257409?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=Noncompetitive+inhibition+of+N-methyl-D-aspartate+by+conantokin-G%3A+evidence+for+an+allosteric+interaction+at+polyamine+sites.&rft.au=Skolnick%2C+P%3BBoje%2C+K%3BMiller%2C+R%3BPennington%2C+M%3BMaccecchini%2C+M+L&rft.aulast=Skolnick&rft.aufirst=P&rft.date=1992-10-01&rft.volume=59&rft.issue=4&rft.spage=1516&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-26 N1 - Date created - 1992-10-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Vimentin metaplasia in renal cortical tubules of preneoplastic, neoplastic, aging, and regenerative lesions of rats and humans. AN - 73252098; 1415487 AB - Vimentin expression was studied immunohistochemically in renal cortical tubules of untreated male rats of various ages, rats exposed to toxins (barbital sodium, folic acid) and carcinogens (streptozotocin, N-bis(2-hydroxypropyl)nitrosamine, barbital sodium, and in humans of various ages with or without renal epithelial tumors. Fetal, neonatal, and young adult rats did not express vimentin in renal cortical tubules. Regenerative renal tubular lesions from rats with aging nephropathy and from rats with toxic nephropathy both expressed vimentin. Mitogenic lesions induced by folic acid at 24 hours, however, were not immunoreactive for vimentin. Carcinogen-induced preneoplastic renal cortical tubular lesions in rats were most often focally immunoreactive whereas strong vimentin expression was found in almost all induced renal tumors. In kidneys of three children (younger than 2 years of age), vimentin was not found in renal cortical tubular cells except in rare individual cells in one case. Vimentin was abundant in basophilic regenerative tubules in kidneys of aged individuals, however. Most (7/10) human renal carcinomas and latent preneoplastic or neoplastic renal tubular lesions found incidentally at autopsy (2/4) showed vimentin expression. The authors suggest that the switching to vimentin expression in phenotypically normal renal cortical tubular cells in rats and humans, which do not usually express the intermediate filament protein vimentin, should be considered vimentin metaplasia. Vimentin expression is dissociated from increased cell proliferation in hyperplastic and neoplastic lesions, however. Instead the degree of dedifferentiation of the tubule cells and changes in phenotype were associated with vimentin expression. JF - The American journal of pathology AU - Ward, J M AU - Stevens, J L AU - Konishi, N AU - Kurata, Y AU - Uno, H AU - Diwan, B A AU - Ohmori, T AD - Tumor Pathology and Pathogenesis Section, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 955 EP - 964 VL - 141 IS - 4 SN - 0002-9440, 0002-9440 KW - Vimentin KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Animals, Newborn KW - Animals KW - Age Factors KW - Humans KW - Regeneration KW - Aged KW - Fetus -- metabolism KW - Male KW - Kidney Neoplasms -- metabolism KW - Vimentin -- metabolism KW - Kidney Tubules -- metabolism KW - Precancerous Conditions -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73252098?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+pathology&rft.atitle=Vimentin+metaplasia+in+renal+cortical+tubules+of+preneoplastic%2C+neoplastic%2C+aging%2C+and+regenerative+lesions+of+rats+and+humans.&rft.au=Ward%2C+J+M%3BStevens%2C+J+L%3BKonishi%2C+N%3BKurata%2C+Y%3BUno%2C+H%3BDiwan%2C+B+A%3BOhmori%2C+T&rft.aulast=Ward&rft.aufirst=J&rft.date=1992-10-01&rft.volume=141&rft.issue=4&rft.spage=955&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+pathology&rft.issn=00029440&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-03 N1 - Date created - 1992-11-03 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Environ Health Perspect. 1991 Jun;93:233-46 [1773795] Acta Pathol Jpn. 1982 Jul;32(4):585-93 [7113698] Mutat Res. 1991 Jun;248(2):239-60 [2046683] IARC Sci Publ. 1990;(99):301-44 [2093652] Exp Pathol. 1990;40(4):301-12 [2098275] Carcinogenesis. 1990 Dec;11(12):2149-56 [2148284] Dev Biol. 1985 Apr;108(2):481-90 [2416612] Lab Invest. 1987 Jun;56(6):642-53 [2439772] Am J Pathol. 1987 Oct;129(1):1-8 [2444108] Biochem Biophys Res Commun. 1988 Dec 30;157(3):1316-22 [2462870] Acta Pathol Jpn. 1989 Nov;39(11):731-6 [2618660] FASEB J. 1989 Aug;3(10):2141-50 [2666230] Fundam Appl Toxicol. 1989 Aug;13(2):332-40 [2792600] Br J Cancer. 1978 Jul;38(1):1-23 [356869] J Histochem Cytochem. 1991 Jun;39(6):741-8 [1709656] Histochem J. 1991 Jan;23(1):13-21 [1938467] Prog Exp Tumor Res. 1991;33:1-20 [2028021] Histopathology. 1991 Apr;18(4):315-22 [2071090] J Cancer Res Clin Oncol. 1990;116(4):372-8 [2143998] Toxicol Lett. 1990 Sep;53(1-2):121-6 [2219151] Am J Clin Pathol. 1987 Sep;88(3):286-96 [2443000] Cancer Res. 1988 Apr 15;48(8):1996-2004 [2450643] Jpn J Cancer Res. 1989 Aug;80(8):771-7 [2511186] Histochemistry. 1989;90(6):489-96 [2715055] Virchows Arch B Cell Pathol Incl Mol Pathol. 1986;51(5):385-404 [2876545] Crit Rev Toxicol. 1988;19(2):147-83 [3069333] Histochemistry. 1988;89(1):81-90 [3366668] Lab Invest. 1968 Jul;19(1):92-6 [5671357] Am J Pathol. 1984 Feb;114(2):309-21 [6320650] Eur J Cell Biol. 1984 May;34(1):137-43 [6428888] Lab Invest. 1992 Apr;66(4):474-84 [1374823] Lab Invest. 1991 Jul;65(1):74-86 [1712875] Vet Pathol. 1989 Jan;26(1):6-10 [2913704] Crit Rev Toxicol. 1987;17(4):279-343 [3308322] J Cell Sci Suppl. 1987;8:293-312 [3332664] J Urol. 1971 Oct;106(4):503-6 [4330359] Lab Invest. 1983 Sep;49(3):317-26 [6193332] Lab Invest. 1984 May;50(5):552-9 [6201675] Histochemistry. 1983;77(3):365-94 [6345481] Cancer Res. 1991 Apr 1;51(7):1922-9 [2004377] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of nitroxide radioprotectors. AN - 73251821; 1410280 AB - The nitroxide Tempol, a stable free radical, has recently been shown to protect mammalian cells against several forms of oxidative stress including radiation-induced cytotoxicity. To extend this observation, six additional water-soluble nitroxides with different structural features were evaluated for potential radioprotective properties using Chinese hamster V79 cells and clonogenic assays. Nitroxides (10 mM) were added 10 min prior to radiation exposure and full radiation dose-response curves were determined. In addition to Tempol, five of the six nitroxides afforded in vitro radioprotection. The best protectors were found to be the positively charged nitroxides, Tempamine and 3-aminomethyl-PROXYL, with protection factors of 2.3 and 2.4, respectively, compared with Tempol, which had a protection factor of 1.3. 3-Carboxy-PROXYL, a negatively charged nitroxide, provided minimal protection. DNA binding characteristics as studied by nonequilibrium dialysis of DNA with each of the nitroxides demonstrated that Tempamine and 3-amino-methyl-PROXYL bound more strongly to DNA than did Tempol. Since DNA is assumed to be the target of radiation-induced cytotoxicity, differences in protection may be explained by variabilities in affinity of the protector for the target. This study establishes nitroxides as a general class of new nonthiol radioprotectors and suggests other parameters that may be exploited to find even better nitroxide-induced radioprotection. JF - Radiation research AU - Hahn, S M AU - Wilson, L AU - Krishna, C M AU - Liebmann, J AU - DeGraff, W AU - Gamson, J AU - Samuni, A AU - Venzon, D AU - Mitchell, J B AD - Radiobiology Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 87 EP - 93 VL - 132 IS - 1 SN - 0033-7587, 0033-7587 KW - Cyclic N-Oxides KW - 0 KW - Protein Synthesis Inhibitors KW - Pyrrolidines KW - Radiation-Protective Agents KW - Spin Labels KW - tempamine KW - 14691-88-4 KW - 2,2,5,5-tetramethyl-1-pyrrolidinyloxy-3-carboxylic acid KW - 2154-68-9 KW - 3-cyano-2,2,5,5-tetramethyl-1-pyrrolidinyl-N-oxyl KW - 2154-70-3 KW - Triacetoneamine-N-Oxyl KW - 2896-70-0 KW - 3-carbamoyl-2,2,5,5-tetramethyl-1-pyrrolidinyl-N-oxyl KW - 4399-80-8 KW - 3-aminomethyl-2,2,5,5-tetramethyl-1-pyrrolidinyl-N-oxyl KW - 54606-49-4 KW - tempol KW - U78ZX2F65X KW - Index Medicus KW - Space life sciences KW - Animals KW - Protein Synthesis Inhibitors -- pharmacology KW - Cell Survival -- drug effects KW - Dose-Response Relationship, Radiation KW - Cell Survival -- radiation effects KW - Cell Line KW - Cricetinae KW - Cyclic N-Oxides -- pharmacology KW - Triacetoneamine-N-Oxyl -- pharmacology KW - Pyrrolidines -- pharmacology KW - Radiation-Protective Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73251821?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Radiation+research&rft.atitle=Identification+of+nitroxide+radioprotectors.&rft.au=Hahn%2C+S+M%3BWilson%2C+L%3BKrishna%2C+C+M%3BLiebmann%2C+J%3BDeGraff%2C+W%3BGamson%2C+J%3BSamuni%2C+A%3BVenzon%2C+D%3BMitchell%2C+J+B&rft.aulast=Hahn&rft.aufirst=S&rft.date=1992-10-01&rft.volume=132&rft.issue=1&rft.spage=87&rft.isbn=&rft.btitle=&rft.title=Radiation+research&rft.issn=00337587&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-20 N1 - Date created - 1992-11-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Who will relapse? Symptoms of nicotine dependence predict long-term relapse after smoking cessation. AN - 73247482; 1401396 AB - Results of a prospective examination (N = 618) of factors associated with smoking relapse are reported. At 1-year follow-up, a modified version of the Fagerstrom Tolerance Questionnaire (Dependence Index; DI) and a measure of craving entered the logistic model (odds ratio of 2.7 [p less than .001]). At Year 2, only the DI entered the model (odds ratio of 2.2 [p less than .001]). The ability of signal detection analysis (SDA) to produce clinically useful decision rules was also examined. At Year 1, SDA produced 1 subgroup with a 25% nonrelapse rate and another with a 9% nonrelapse rate (odds ratio of 3.4 [p less than .001]). At Year 2, SDA produced 1 subgroup with a nonrelapse rate of 19% and another with a nonrelapse rate of 7% (odds ratio of 3.0 [p less than .001]). The use of signal detection methods may help clinicians to identify those at greater or lesser risk of relapse. JF - Journal of consulting and clinical psychology AU - Killen, J D AU - Fortmann, S P AU - Kraemer, H C AU - Varady, A AU - Newman, B AD - National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 797 EP - 801 VL - 60 IS - 5 SN - 0022-006X, 0022-006X KW - Nicotine KW - 6M3C89ZY6R KW - Index Medicus KW - Combined Modality Therapy KW - Behavior Therapy KW - Risk Factors KW - Humans KW - Adult KW - Recurrence KW - Male KW - Female KW - Smoking Cessation -- psychology KW - Substance Withdrawal Syndrome -- prevention & control KW - Nicotine -- adverse effects KW - Smoking -- adverse effects KW - Nicotine -- administration & dosage KW - Substance Withdrawal Syndrome -- psychology KW - Smoking -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73247482?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+consulting+and+clinical+psychology&rft.atitle=Who+will+relapse%3F+Symptoms+of+nicotine+dependence+predict+long-term+relapse+after+smoking+cessation.&rft.au=Killen%2C+J+D%3BFortmann%2C+S+P%3BKraemer%2C+H+C%3BVarady%2C+A%3BNewman%2C+B&rft.aulast=Killen&rft.aufirst=J&rft.date=1992-10-01&rft.volume=60&rft.issue=5&rft.spage=797&rft.isbn=&rft.btitle=&rft.title=Journal+of+consulting+and+clinical+psychology&rft.issn=0022006X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-12 N1 - Date created - 1992-11-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Conservation of mouse alpha A-crystallin promoter activity in chicken lens epithelial cells. AN - 73241701; 1404419 AB - Previous transfection experiments have shown that 162 base pairs (bp) of the 5' flanking sequence of the chicken alpha A-crystallin gene are required for promoter activity in primary chicken lens epithelial cells (PLE), while only 111 bp of the 5' flanking sequence are needed for activity of the mouse alpha A-crystallin promoter in transfected chicken PLE cells or in a SV40 T-antigen-transformed transfected mouse lens epithelial cell line (alpha TN4-1). The effect of site-directed mutations covering positions -111 to -34 of the mouse alpha A-crystallin promoter fused to the bacterial chloramphenicol acetyltransferase (CAT) gene was compared in transfected chicken PLE cells and mouse alpha TN4-1 cells; selected mutations were also examined in a nontransformed rabbit lens epithelial cell line (N/N1003A). In general, the same mutations reduced promoter activity in the transfected lens cells from all three species, although differences were noted. The mutations severely affected regions -111/-106 and -69/-40 regions in all the transfected cells examined; by contrast, mutations at positions -105/-99 and -87/-70 had a somewhat greater effect in the chicken PLE than the mouse alpha TN4-1 cells, while mutations of the -93/-88 sequence reduced expression in the alpha TN4-1 but not the PLE cells. A partial cDNA with sequence similarity to alpha A-CRYPB1 of the mouse has been isolated from a chicken lens library; mouse alpha A-CRYBP1 is a putative transcription factor which binds to the -66/-55 sequence of the mouse alpha A-crystallin promoter.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Journal of molecular evolution AU - Donovan, D M AU - Sax, C M AU - Klement, J F AU - Li, X AU - Chepelinsky, A B AU - Piatigorsky, J AD - Laboratory of Molecular and Developmental Biology, NEI, NIH, Bethesda, MD 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 337 EP - 345 VL - 35 IS - 4 SN - 0022-2844, 0022-2844 KW - Crystallins KW - 0 KW - Recombinant Fusion Proteins KW - Index Medicus KW - Animals KW - Plasmids -- genetics KW - Chick Embryo KW - Amino Acid Sequence KW - Mice KW - Cloning, Molecular KW - Mutagenesis, Site-Directed KW - Polymerase Chain Reaction KW - Base Sequence KW - Transfection KW - Blotting, Southern KW - Cells, Cultured KW - Molecular Sequence Data KW - Lens, Crystalline -- metabolism KW - Lens, Crystalline -- cytology KW - Recombinant Fusion Proteins -- genetics KW - Crystallins -- chemistry KW - Promoter Regions, Genetic -- genetics KW - Crystallins -- genetics KW - Recombinant Fusion Proteins -- chemistry KW - Gene Expression Regulation -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73241701?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+molecular+evolution&rft.atitle=Conservation+of+mouse+alpha+A-crystallin+promoter+activity+in+chicken+lens+epithelial+cells.&rft.au=Donovan%2C+D+M%3BSax%2C+C+M%3BKlement%2C+J+F%3BLi%2C+X%3BChepelinsky%2C+A+B%3BPiatigorsky%2C+J&rft.aulast=Donovan&rft.aufirst=D&rft.date=1992-10-01&rft.volume=35&rft.issue=4&rft.spage=337&rft.isbn=&rft.btitle=&rft.title=Journal+of+molecular+evolution&rft.issn=00222844&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-26 N1 - Date created - 1992-10-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pelvic radioiodine uptake in a rectal wall teratoma after thyroidectomy for papillary carcinoma. AN - 73232268; 1403156 AB - A 30-yr-old woman with previously resected papillary thyroid carcinoma was found to have a pelvic lesion which concentrated radioiodine. By performing simultaneous 131I whole-body and 99mTc-methylene diphosphonate bone scans, we found the lesion to be in soft tissue between the sacrum and bladder. Radioiodine therapy was postponed so that the lesion, a benign teratoma of the rectal wall, could be surgically removed. Prior to laparotomy, the patient received a second tracer dose of 131I so that the lesion could be located at surgery with a hand-held gamma detector. A postoperative whole-body 131I scan confirmed that the lesion had been removed, thus reducing the absorbed radiation that would have been received by the ovaries during radioiodine therapy. Although the lesion contained both thyroid and gastric epithelium, accumulated 131I was limited to the area with thyroid follicles. JF - Journal of nuclear medicine : official publication, Society of Nuclear Medicine AU - Lakshmanan, M AU - Reynolds, J C AU - Del Vecchio, S AU - Merino, M J AU - Norton, J A AU - Robbins, J AD - Clinical Endocrinology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1848 EP - 1850 VL - 33 IS - 10 SN - 0161-5505, 0161-5505 KW - Iodine Radioisotopes KW - 0 KW - Technetium Tc 99m Medronate KW - X89XV46R07 KW - Index Medicus KW - Thyroidectomy KW - Intraoperative Care KW - Humans KW - Adult KW - Bone and Bones -- diagnostic imaging KW - Female KW - Radionuclide Imaging KW - Rectal Neoplasms -- diagnostic imaging KW - Neoplasms, Multiple Primary -- diagnostic imaging KW - Carcinoma, Papillary -- surgery KW - Dermoid Cyst -- diagnostic imaging KW - Thyroid Neoplasms -- surgery KW - Sigmoid Neoplasms -- diagnostic imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73232268?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+nuclear+medicine+%3A+official+publication%2C+Society+of+Nuclear+Medicine&rft.atitle=Pelvic+radioiodine+uptake+in+a+rectal+wall+teratoma+after+thyroidectomy+for+papillary+carcinoma.&rft.au=Lakshmanan%2C+M%3BReynolds%2C+J+C%3BDel+Vecchio%2C+S%3BMerino%2C+M+J%3BNorton%2C+J+A%3BRobbins%2C+J&rft.aulast=Lakshmanan&rft.aufirst=M&rft.date=1992-10-01&rft.volume=33&rft.issue=10&rft.spage=1848&rft.isbn=&rft.btitle=&rft.title=Journal+of+nuclear+medicine+%3A+official+publication%2C+Society+of+Nuclear+Medicine&rft.issn=01615505&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-19 N1 - Date created - 1992-11-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular and genetic analysis of liver oncogenesis in transforming growth factor alpha transgenic mice. AN - 73230037; 1394122 AB - Overexpression of a transforming growth factor alpha (TGF-alpha) transgene induced the development of liver tumors in 69 of 93 (74%) adult male mice. To identify factors associated with oncogenesis, liver tumors from transgenic animals were characterized at the molecular level. TGF-alpha RNA transcripts were elevated in 17 of 25 (68%) liver tumors, relative to adjacent nontumorous tissue. Expression of the endogenous c-myc and insulin-like growth factor II genes was enhanced in 7 of 19 (37%) and 12 of 16 (75%) tumors, respectively. In contrast, epidermal growth factor receptor RNA levels were unchanged or reduced in all liver tumors, and mutations were not detected in either the Ha-ras or Ki-ras genes. The occurrence of liver tumors in castrated TGF-alpha transgenic mice was reduced about 7-fold, while in ovariectomized transgenic animals the incidence was increased about 6-fold. The progeny of a cross between CD1-derived TGF-alpha transgenic (MT42) and C57BL/6 mice exhibited no reduction in tumor burden (83%); however, the incidence of tumor formation in MT42 x FVB/N offspring was substantially lower (19%). We conclude that in these transgenic mice TGF-alpha promotes tumor formation and appears to play a major role in tumor progression. Moreover, other factors that may collaborate in TGF-alpha-induced hepatocarcinogenesis include c-myc, insulin-like growth factor II, sex hormones, and the genetic background upon which the transgene operates. JF - Cancer research AU - Takagi, H AU - Sharp, R AU - Hammermeister, C AU - Goodrow, T AU - Bradley, M O AU - Fausto, N AU - Merlino, G AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/10/01/ PY - 1992 DA - 1992 Oct 01 SP - 5171 EP - 5177 VL - 52 IS - 19 SN - 0008-5472, 0008-5472 KW - Ha-ras KW - IGF-II KW - Ki-ras KW - TGF-&agr; KW - c-myc KW - DNA, Neoplasm KW - 0 KW - Gonadal Steroid Hormones KW - Growth Substances KW - RNA, Neoplasm KW - Transforming Growth Factor alpha KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Disease Models, Animal KW - Mice KW - RNA, Neoplasm -- genetics KW - Mice, Transgenic KW - Growth Substances -- physiology KW - Phenotype KW - Base Sequence KW - Gene Expression -- genetics KW - DNA -- genetics KW - Molecular Sequence Data KW - Mice, Inbred C57BL KW - DNA, Neoplasm -- genetics KW - Gonadal Steroid Hormones -- physiology KW - Female KW - Male KW - Liver Neoplasms, Experimental -- genetics KW - Oncogenes -- genetics KW - Transforming Growth Factor alpha -- genetics KW - Liver Neoplasms, Experimental -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73230037?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Molecular+and+genetic+analysis+of+liver+oncogenesis+in+transforming+growth+factor+alpha+transgenic+mice.&rft.au=Takagi%2C+H%3BSharp%2C+R%3BHammermeister%2C+C%3BGoodrow%2C+T%3BBradley%2C+M+O%3BFausto%2C+N%3BMerlino%2C+G&rft.aulast=Takagi&rft.aufirst=H&rft.date=1992-10-01&rft.volume=52&rft.issue=19&rft.spage=5171&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-29 N1 - Date created - 1992-10-29 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Ha-ras; IGF-II; Ki-ras; TGF-&agr;; c-myc N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Stimulus deprivation increases pineal Gs alpha and G beta. AN - 73226351; 1402887 AB - Denervation and other forms of stimulus deprivation cause an increase in the magnitude of subsequent responses, a phenomenon commonly referred to as denervation supersensitivity. This has been well demonstrated with the cyclic AMP response to norepinephrine in the pineal gland. In the present report, we address the question of whether stimulus deprivation alters alpha and beta subunits of the GTP binding regulatory protein that stimulates adenylyl cyclase activity (Gs). Stimulus deprivation of the pineal gland was produced by denervation (superior cervical ganglionectomy), decentralization of the superior cervical ganglia, or by exposure of the animal to continuous lighting. All increased both the alpha and beta subunits of Gs (Gs alpha and G beta) by up to fourfold, as estimated using semiquantitative western blot technology. These effects were detectable after 1 day of stimulus deprivation and were sustained for 2 weeks. The stimulatory effects of constant light-induced stimulus deprivation were also apparent by measuring cholera toxin-dependent ADP-ribosylation of Gs alpha, which revealed a four-fold increase in the amount of labeled substrate. The results of in vivo studies were confirmed with in vitro studies, which demonstrated a spontaneous increase in both Gs alpha and G beta during 72 h of organ culture. The constant light-induced increases in both Gs alpha and G beta were prevented by continuous administration of isoproterenol (0.3 mg/kg/day), supporting the suggestion that adrenergic stimulation controls the levels of Gs alpha and G beta. These studies indicate that stimulus deprivation increases both Gs alpha and G beta.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Journal of neurochemistry AU - Babila, T AU - Klein, D C AD - Section on Neuroendocrinology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1356 EP - 1362 VL - 59 IS - 4 SN - 0022-3042, 0022-3042 KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Cholera Toxin KW - 9012-63-9 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Isoproterenol KW - L628TT009W KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Ganglionectomy KW - Cholera Toxin -- pharmacology KW - Adenosine Diphosphate Ribose -- metabolism KW - Organ Culture Techniques KW - Male KW - Isoproterenol -- pharmacology KW - Pineal Gland -- metabolism KW - GTP-Binding Proteins -- metabolism KW - Ganglia, Sympathetic -- physiology KW - GTP-Binding Proteins -- chemistry KW - Light UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73226351?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=Stimulus+deprivation+increases+pineal+Gs+alpha+and+G+beta.&rft.au=Babila%2C+T%3BKlein%2C+D+C&rft.aulast=Babila&rft.aufirst=T&rft.date=1992-10-01&rft.volume=59&rft.issue=4&rft.spage=1356&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-26 N1 - Date created - 1992-10-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inflammatory and toxic myopathies. AN - 73224375; 1327303 AB - The major advances in the immunopathogenesis and treatment of inflammatory myopathies, and the main criteria that distinguish polymyositis (PM) from dermatomyositis (DM) or inclusion-body myositis (IBM) are presented. The origin and implications of the amyloid and ubiquitin deposits found within the vacuolated fibers of patients with IBM are considered. The pathogenesis of human immunodeficiency virus (HIV) and human T-cell lymphotrophic virus (HTLV)-I-associated PM is presented, and the role of retroviruses in triggering PM, even in the absence of detectable viral genome within the muscle fibers, is discussed. In addition, three toxic myopathies with distinct morphologic, biochemical, or molecular characteristics, caused by zidovudine [azidothymidine (AZT) myopathy], the cholesterol-lowering-agent myopathy (CLAM), and the combination of blocking agents with corticosteroids are presented. JF - Current opinion in neurology and neurosurgery AU - Dalakas, M C AD - Neuromuscular Diseases Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 645 EP - 654 VL - 5 IS - 5 SN - 0951-7383, 0951-7383 KW - Adrenal Cortex Hormones KW - 0 KW - Hypolipidemic Agents KW - Zidovudine KW - 4B9XT59T7S KW - Pancuronium KW - J76UF062FS KW - Index Medicus KW - AIDS/HIV KW - Pancuronium -- adverse effects KW - Diagnosis, Differential KW - Zidovudine -- adverse effects KW - Humans KW - Biopsy KW - Muscles -- pathology KW - Hypolipidemic Agents -- adverse effects KW - Adrenal Cortex Hormones -- adverse effects KW - Dermatomyositis -- chemically induced KW - Dermatomyositis -- pathology KW - Polymyositis -- pathology KW - Polymyositis -- etiology KW - Polymyositis -- chemically induced KW - Inclusion Bodies -- ultrastructure KW - Dermatomyositis -- etiology KW - Myositis -- pathology KW - Myositis -- chemically induced KW - Myositis -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73224375?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+opinion+in+neurology+and+neurosurgery&rft.atitle=Inflammatory+and+toxic+myopathies.&rft.au=Dalakas%2C+M+C&rft.aulast=Dalakas&rft.aufirst=M&rft.date=1992-10-01&rft.volume=5&rft.issue=5&rft.spage=645&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+neurology+and+neurosurgery&rft.issn=09517383&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-20 N1 - Date created - 1992-11-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - N omega-amino-L-arginine, an inhibitor of nitric oxide synthase, raises vascular resistance but increases mortality rates in awake canines challenged with endotoxin. AN - 73224000; 1383377 AB - Inhibitors of nitric oxide synthase (NOS) have been reported to increase mean arterial pressure in animal models of sepsis and recently have been given to patients in septic shock. However, controlled studies to determine the effects of these agents on cardiovascular function and survival in awake animal models of sepsis have not been reported. To examine the therapeutic potential of NOS inhibition in septic shock, we challenged canines with endotoxin (2 or 4 mg/kg i.v.) and treated them with either normal saline or N omega-amino-L-arginine (10 or 1 mg/kg/h), the most specific inhibitor available for the isoform of NOS implicated in septic shock. Endotoxemic animals treated with N omega-amino-L-arginine (n = 11) had higher systemic and pulmonary vascular resistance indices (SVRI and PVRI, p less than or equal to 0.033) and decreased heart rates (p = 0.009), cardiac indices (CI, p = 0.01), oxygen delivery indices (p = 0.027), and oxygen consumption indices (p = 0.046) compared with controls (n = 6). Moreover, N omega-amino-L-arginine increased mortality rates after endotoxin challenge (10 of 11 vs. 1 of 6 controls, p = 0.005). Administration of L-arginine did not improve survival or alter the cardiopulmonary effects of N omega-amino-L-arginine, which suggests that inhibition of NOS may not have been competitive. In normal animals, N omega-amino-L-arginine alone (n = 3) increased SVRI (p = 0.0008) and mean arterial pressure (p = 0.016), and decreased CI (p = 0.01) compared with saline-treated controls (n = 3), but, at the high dose, also produced neuromuscular rigidity and seizure-like activity that was not apparent in the endotoxemic model. Thus, the mortality rate from endotoxemia increased either because of NOS inhibition per se or because of properties unique to N omega-amino-L-arginine, or both. JF - The Journal of experimental medicine AU - Cobb, J P AU - Natanson, C AU - Hoffman, W D AU - Lodato, R F AU - Banks, S AU - Koev, C A AU - Solomon, M A AU - Elin, R J AU - Hosseini, J M AU - Danner, R L AD - Department of Critical Care Medicine, Warren G. Magnusen Clinical Center, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10/01/ PY - 1992 DA - 1992 Oct 01 SP - 1175 EP - 1182 VL - 176 IS - 4 SN - 0022-1007, 0022-1007 KW - Endotoxins KW - 0 KW - N(G)-aminoarginine KW - 57444-72-1 KW - Arginine KW - 94ZLA3W45F KW - Nitric Oxide Synthase KW - EC 1.14.13.39 KW - Amino Acid Oxidoreductases KW - EC 1.4.- KW - Index Medicus KW - Animals KW - Oxygen Consumption -- drug effects KW - Heart Rate -- drug effects KW - Analysis of Variance KW - Pulmonary Circulation -- drug effects KW - Dogs KW - Heart -- drug effects KW - Time Factors KW - Amino Acid Oxidoreductases -- antagonists & inhibitors KW - Arginine -- toxicity KW - Vascular Resistance -- drug effects KW - Shock, Septic -- physiopathology KW - Shock, Septic -- blood KW - Endotoxins -- toxicity KW - Arginine -- analogs & derivatives KW - Arginine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73224000?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+experimental+medicine&rft.atitle=N+omega-amino-L-arginine%2C+an+inhibitor+of+nitric+oxide+synthase%2C+raises+vascular+resistance+but+increases+mortality+rates+in+awake+canines+challenged+with+endotoxin.&rft.au=Cobb%2C+J+P%3BNatanson%2C+C%3BHoffman%2C+W+D%3BLodato%2C+R+F%3BBanks%2C+S%3BKoev%2C+C+A%3BSolomon%2C+M+A%3BElin%2C+R+J%3BHosseini%2C+J+M%3BDanner%2C+R+L&rft.aulast=Cobb&rft.aufirst=J&rft.date=1992-10-01&rft.volume=176&rft.issue=4&rft.spage=1175&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+experimental+medicine&rft.issn=00221007&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-02 N1 - Date created - 1992-11-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: N Engl J Med. 1975 Nov 6;293(19):970-6 [1101063] Am J Physiol. 1966 Apr;210(4):817-20 [5906810] Lancet. 1991 Dec 21-28;338(8782-8783):1555-7 [1683974] Proc Natl Acad Sci U S A. 1990 Dec;87(24):10043-7 [1702214] Epilepsy Res. 1991 Mar;8(2):142-8 [1712286] Lancet. 1991 Dec 21-28;338(8782-8783):1557-8 [1720856] Br J Pharmacol. 1991 Apr;102(4):967-73 [1855125] Am J Physiol. 1991 Aug;261(2 Pt 2):R323-8 [1877690] Br J Pharmacol. 1991 May;103(1):1218-24 [1908734] Br J Pharmacol. 1990 Dec;101(4):815-20 [2085706] Nature. 1990 May 10;345(6271):161-3 [2110626] Ann Intern Med. 1990 Aug 1;113(3):227-42 [2197912] Chest. 1990 Dec;98(6):1480-7 [2245691] Proc Natl Acad Sci U S A. 1990 May;87(9):3629-32 [2333306] Biochem Biophys Res Commun. 1989 Apr 28;160(2):881-6 [2719705] Am J Physiol. 1988 Mar;254(3 Pt 2):H558-69 [3279822] Surgery. 1986 Feb;99(2):140-53 [3511560] Crit Care Med. 1985 Feb;13(2):85-90 [3967509] N Engl J Med. 1982 Nov 11;307(20):1225-30 [6752708] Lancet. 1992 Feb 15;339(8790):435 [1346701] Eur J Pharmacol. 1991 Aug 6;200(2-3):375-6 [1664333] Br J Pharmacol. 1991 May;103(1):1047-52 [1678981] J Natl Cancer Inst. 1990 May 2;82(9):726-8 [1691302] Biochem Biophys Res Commun. 1991 May 15;176(3):1136-41 [1710109] Epilepsy Res. 1991 Mar;8(2):134-41 [1712285] Biochem Biophys Res Commun. 1991 Aug 15;178(3):823-9 [1714727] Br J Pharmacol. 1991 Sep;104(1):21-4 [1723915] J Appl Physiol (1985). 1991 May;70(5):2155-63 [1864798] Biochem Biophys Res Commun. 1991 Aug 15;178(3):1135-40 [1872835] Crit Care Med. 1991 Sep;19(9):1146-51 [1884613] J Clin Invest. 1991 Jun;87(6):1964-8 [2040689] Biochem Biophys Res Commun. 1991 Jun 14;177(2):828-33 [2049105] J Natl Cancer Inst. 1990 May 2;82(9):772-6 [2109093] Biochem Biophys Res Commun. 1990 Apr 30;168(2):458-65 [2159292] Am J Physiol. 1990 Oct;259(4 Pt 2):H1038-43 [2221111] Biochem Biophys Res Commun. 1990 Nov 15;172(3):1132-8 [2244897] Biochem Biophys Res Commun. 1990 Mar 30;167(3):1037-43 [2322257] Biochem Biophys Res Commun. 1990 Jul 16;170(1):96-103 [2372300] J Exp Med. 1989 Mar 1;169(3):823-32 [2647895] Proc Natl Acad Sci U S A. 1988 Nov;85(22):8664-7 [3263652] Nature. 1987 Jun 11-17;327(6122):524-6 [3495737] Crit Care Med. 1987 Oct;15(10):923-9 [3652707] J Clin Invest. 1986 Jul;78(1):259-70 [3722379] J Pharmacol Exp Ther. 1991 Jun;257(3):1208-15 [1646327] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phase I study of continuous-infusion soluble CD4 as a single agent and in combination with oral dideoxyinosine therapy in children with symptomatic human immunodeficiency virus infection. AN - 73222934; 1357124 AB - To determine the safety and pharmacokinetics of recombinant soluble CD4 (sCD4) administered by continuous intravenous infusion to children with symptomatic human immunodeficiency virus type 1 infection, we conducted a phase I study at the National Cancer Institute. Three dose levels of sCD4 were evaluated: 100, 300, and 1000 micrograms/kg per day. After an initial 12 weeks of treatment with sCD4 alone, dideoxyinosine at a dose of 90 mg/m2 every 8 hours was added and subjects were observed for an additional 12 weeks. Combination therapy was continued in patients in whom it was well tolerated. In addition to toxicity and pharmacokinetic monitoring, surrogate markers of antiviral activity were evaluated. Eleven children were enrolled in the study. During the 12 weeks of treatment with sCD4 alone, and during subsequent sCD4 plus dideoxyinosine combination therapy, no significant toxic reaction attributable to sCD4 or dideoxyinosine was encountered. Low-level anti-CD4 antibodies developed in two patients. Steady-state sCD4 levels increased proportionately at higher doses. The CD4 cell counts and serum p24 antigen levels did not provide evidence of antiviral activity. We conclude that sCD4 was well tolerated at doses up to 1000 micrograms/kg per day when administered by continuous intravenous infusion; however, evidence of in vivo antiviral activity was not observed in this study. JF - The Journal of pediatrics AU - Husson, R N AU - Chung, Y AU - Mordenti, J AU - Butler, K M AU - Chen, S AU - Duliege, A M AU - Brouwers, P AU - Jarosinski, P AU - Mueller, B U AU - Ammann, A AD - Pediatric Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 627 EP - 633 VL - 121 IS - 4 SN - 0022-3476, 0022-3476 KW - Antigens, CD4 KW - 0 KW - Antigens, Viral KW - Recombinant Proteins KW - Didanosine KW - K3GDH6OH08 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Infusions, Intravenous KW - Humans KW - Recombinant Proteins -- pharmacokinetics KW - Child KW - CD4-Positive T-Lymphocytes KW - Leukocyte Count KW - Child, Preschool KW - Drug Therapy, Combination KW - Infant KW - Drug Evaluation KW - Treatment Outcome KW - Adolescent KW - Recombinant Proteins -- therapeutic use KW - Recombinant Proteins -- administration & dosage KW - Male KW - Antigens, Viral -- blood KW - Female KW - Didanosine -- therapeutic use KW - Acquired Immunodeficiency Syndrome -- immunology KW - Didanosine -- administration & dosage KW - Antigens, CD4 -- therapeutic use KW - Antigens, CD4 -- administration & dosage KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Didanosine -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73222934?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pediatrics&rft.atitle=Phase+I+study+of+continuous-infusion+soluble+CD4+as+a+single+agent+and+in+combination+with+oral+dideoxyinosine+therapy+in+children+with+symptomatic+human+immunodeficiency+virus+infection.&rft.au=Husson%2C+R+N%3BChung%2C+Y%3BMordenti%2C+J%3BButler%2C+K+M%3BChen%2C+S%3BDuliege%2C+A+M%3BBrouwers%2C+P%3BJarosinski%2C+P%3BMueller%2C+B+U%3BAmmann%2C+A&rft.aulast=Husson&rft.aufirst=R&rft.date=1992-10-01&rft.volume=121&rft.issue=4&rft.spage=627&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pediatrics&rft.issn=00223476&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-13 N1 - Date created - 1992-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dose-dependent smooth muscle cell proliferation induced by thermal injury with pulsed infrared lasers. AN - 73221222; 1394931 AB - Recently, laser-heated and radio frequency-heated balloon angioplasty techniques have been proposed as a means to treat or minimize dissection and elastic recoil but have been associated with a high rate of clinical restenosis. Similarly, pulsed laser angioplasty techniques proposed to minimize thermal injury while ablating obstructing atheroma have failed to reduce clinical restenosis. Because "hot balloon" and pulsed laser angioplasty create both mechanical and thermal injury, it has been difficult to discern the cause of the smooth muscle cell (SMC) proliferation resulting in restenosis and whether such magnitude of proliferation is predictable and dose related. This study was undertaken to explore these issues. Localized thermal lesions accompanying efficient ablation were created with a pulsed Tm:YAG laser in nine rabbit aortas, which consistently led to a focal proliferation of SMC that filled the ablated region by 4 weeks. Transcutaneous Ho:YAG pulsed laser irradiation at multiple independent sites of 24 central rabbit ear arteries without ablation led to brief approximately 30 degrees C thermal transients and thermal damage to the artery wall resulting in significant neointimal proliferation by 3 weeks and a mean cross-sectional narrowing of 59 +/- 17% at a dose of 390 mJ/mm2. Acute and chronic responses to varying total energy deposition were studied by histology after the rabbits were killed at 2 hours to 4 weeks. Arterial segments midway between laser injuries were unaffected and served as internal controls. Neointimal proliferation at 3 weeks after laser injury exhibited a clear dose dependence. Mean cross-sectional narrowing increased from 34 +/- 10% to 85 +/- 15% as laser fluence increased from 240 mJ/cm2 to 640 mJ/cm2 (r = 0.84). Similarly, cross-sectional narrowing caused by SMC neointimal proliferation increased from 20 +/- 10% to 77 +/- 17% for a fixed surface irradiation as the depth of the most superficial arterial media decreased from 600 microns to 330 microns (r = 0.94). Thermal injury to the arterial wall is a potent stimulus for SMC proliferation and may necessitate reduction in laser or thermal energy used for angioplasty. Moreover, a dose-response relation exists between the degree of thermal injury and SMC proliferative response. Hence, this technique could be used as a practical model of restenosis suitable for screening therapies for inhibition of SMC proliferation. JF - Circulation AU - Douek, P C AU - Correa, R AU - Neville, R AU - Unger, E F AU - Shou, M AU - Banai, S AU - Ferrans, V J AU - Epstein, S E AU - Leon, M B AU - Bonner, R F AD - National Center for Research Resources, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md. 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1249 EP - 1256 VL - 86 IS - 4 SN - 0009-7322, 0009-7322 KW - Abridged Index Medicus KW - Index Medicus KW - Aorta -- radiation effects KW - Animals KW - Ear -- blood supply KW - Arteries -- radiation effects KW - Aorta -- pathology KW - Rabbits KW - Dose-Response Relationship, Radiation KW - Arteries -- pathology KW - Cell Division -- radiation effects KW - Burns -- pathology KW - Infrared Rays KW - Muscle, Smooth, Vascular -- radiation effects KW - Muscle, Smooth, Vascular -- pathology KW - Laser Therapy -- methods KW - Laser Therapy -- adverse effects KW - Burns -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73221222?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Circulation&rft.atitle=Dose-dependent+smooth+muscle+cell+proliferation+induced+by+thermal+injury+with+pulsed+infrared+lasers.&rft.au=Douek%2C+P+C%3BCorrea%2C+R%3BNeville%2C+R%3BUnger%2C+E+F%3BShou%2C+M%3BBanai%2C+S%3BFerrans%2C+V+J%3BEpstein%2C+S+E%3BLeon%2C+M+B%3BBonner%2C+R+F&rft.aulast=Douek&rft.aufirst=P&rft.date=1992-10-01&rft.volume=86&rft.issue=4&rft.spage=1249&rft.isbn=&rft.btitle=&rft.title=Circulation&rft.issn=00097322&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-13 N1 - Date created - 1992-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pesticides and non-Hodgkin's lymphoma. AN - 73219755; 1394159 AB - The incidence of non-Hodgkin's lymphoma (NHL) has increased over 50% in the last 15 years. This paper reviews the possible role of pesticides in this increase. While small increases in risk of NHL among farmers have been observed in general occupational surveys, recent studies focusing on specific pesticides have observed much larger risks. Frequent use of phenoxyacetic acid herbicides, in particular, 2,4-dichlorophenoxyacetic acid, has been associated with 2- to 8-fold increases of NHL in studies conducted in Sweden, Kansas, Nebraska, Canada, and elsewhere. Canine malignant lymphoma has also been associated with dog owner use of 2,4-dichlorophenoxyacetic acid and commercial lawn pesticide treatments. There are much fewer data linking NHL to other types of pesticides, but triazine herbicides, organophosphate insecticides, fungicides, and fumigants have also been associated with increased risk of NHL. Pesticide exposures are not limited to agricultural populations but are widespread in the general population through use on lawns, golf courses, rights-of-way, and elsewhere. Since the use of pesticides, particularly phenoxy herbicides, has increased dramatically preceding and during the time period in which the incidence of NHL has increased, they could have contributed to the rising incidence of NHL. JF - Cancer research AU - Zahm, S H AU - Blair, A AD - Occupational Studies Section, National Cancer Institute, Rockville, Maryland 20892. Y1 - 1992/10/01/ PY - 1992 DA - 1992 Oct 01 SP - 5485s EP - 5488s VL - 52 IS - 19 Suppl SN - 0008-5472, 0008-5472 KW - Pesticides KW - 0 KW - Index Medicus KW - Humans KW - Lymphoma, Non-Hodgkin -- epidemiology KW - Agricultural Workers' Diseases -- epidemiology KW - Agricultural Workers' Diseases -- chemically induced KW - Lymphoma, Non-Hodgkin -- chemically induced KW - Pesticides -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73219755?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Pesticides+and+non-Hodgkin%27s+lymphoma.&rft.au=Zahm%2C+S+H%3BBlair%2C+A&rft.aulast=Zahm&rft.aufirst=S&rft.date=1992-10-01&rft.volume=52&rft.issue=19+Suppl&rft.spage=5485s&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-29 N1 - Date created - 1992-10-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Monovalent immunotoxin containing truncated form of Pseudomonas exotoxin as potent antitumor agent. AN - 73219586; 1394141 AB - Recombinant truncated forms of Pseudomonas exotoxin A that lack the cell binding domain of Pseudomonas exotoxin A were coupled to an F(ab') fragment of a monoclonal antibody HB21 directed against the human transferrin receptor. One of these was NlysPE40. The other, NlysPE38QQR, has two amino groups on residues near the NH2-terminus and has no amino groups near the COOH-terminus. The proteins were linked by a stable thioether bond that connected the sulfhydryl group present in the hinge region of the antibody fragment to an amino group on the toxin. The F(ab')-PE40 immunotoxin, containing NlysPE40, exhibited potent cytotoxic activity on human carcinoma cell lines with a concentration of immunotoxin at which isotope incorporation falls by 50% when compared to nontreated cells (ID50) of 5.3 pM (0.5 ng/ml) on both the epidermoid carcinoma A431 and on the colon carcinoma Colo205. Immunotoxins made with whole antibody were considerably less active, with an ID50 of 15.9 pM (3.1 ng/ml) on these cell lines. F(ab')-PE38QQR, the immunotoxin containing NlysPE38QQR, was found to be the most active agent with an ID50 of 1.05 pM (0.1 ng/ml) on A431 cells. The greater cytotoxicity of immunotoxins containing fragmented antibody was probably due to the higher binding affinity of F(ab') conjugates in comparison to whole antibody conjugates to the transferrin receptor. The increase in cytotoxic activity of the immunotoxin made with NlysPE38QQR than that with NlysPE40 may reflect selective coupling of the toxin through NH2-terminal amino groups. The monovalent and divalent immunotoxins had dose-dependent antitumor effects on human epidermoid carcinoma xenografts in nude mice. A431 tumors completely regressed in all animals at a total dose of 105 pmol (10 micrograms) of F(ab')-PE38QQR and of 154 pmol (30 micrograms) of IgG-PE38QQR. Furthermore, the F(ab') immunotoxin was less toxic to mice than the conjugate containing IgG (840 pmol or 80 micrograms of total dose causing measurable adverse effects versus 208 pmol or 40 micrograms, respectively). Thus, a truncated Pseudomonas exotoxin A molecule coupled to the F(ab') fragment of an antibody is more active and less toxic in mice than an immunotoxin made with a whole antibody. Therefore, the therapeutic index for the monovalent immunotoxin is about four times better than that for the divalent immunotoxin. JF - Cancer research AU - Debinski, W AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/10/01/ PY - 1992 DA - 1992 Oct 01 SP - 5379 EP - 5385 VL - 52 IS - 19 SN - 0008-5472, 0008-5472 KW - Antibodies, Monoclonal KW - 0 KW - Antineoplastic Agents KW - Bacterial Toxins KW - Exotoxins KW - Immunoglobulin Fragments KW - Immunotoxins KW - Peptide Fragments KW - Receptors, Transferrin KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Neoplasm Transplantation KW - Animals KW - Immunoglobulin Fragments -- administration & dosage KW - Antibodies, Monoclonal -- metabolism KW - Humans KW - Immunoglobulin Fragments -- metabolism KW - Mice, Nude KW - Mice KW - Neoplasms, Experimental -- drug therapy KW - Neoplasms, Experimental -- pathology KW - Female KW - Antibodies, Monoclonal -- administration & dosage KW - Receptors, Transferrin -- metabolism KW - Peptide Fragments -- metabolism KW - Exotoxins -- pharmacology KW - Peptide Fragments -- pharmacology KW - Antineoplastic Agents -- metabolism KW - Exotoxins -- metabolism KW - Immunotoxins -- metabolism KW - Immunotoxins -- administration & dosage KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73219586?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Monovalent+immunotoxin+containing+truncated+form+of+Pseudomonas+exotoxin+as+potent+antitumor+agent.&rft.au=Debinski%2C+W%3BPastan%2C+I&rft.aulast=Debinski&rft.aufirst=W&rft.date=1992-10-01&rft.volume=52&rft.issue=19&rft.spage=5379&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-29 N1 - Date created - 1992-10-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Myalgia and elevated creatine kinase activity associated with subcutaneous injections of diluent. AN - 73216396; 1403405 AB - A 16-year-old boy with short stature and mild primary hypothyroidism received subcutaneous injections of either recombinant human growth hormone or placebo in diluent that contained glycerol and m-cresol as a preservative. While he was receiving the study drug, myalgia developed and serum creatine kinase values were elevated. Both resolved when injections were stopped and recurred when injections of diluent alone were given. The myalgia and elevated creatine kinase activity were apparently caused by a component of the diluent. JF - The Journal of pediatrics AU - Bach, M A AU - Blum, D M AU - Rose, S R AU - Charnas, L R AD - Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 650 EP - 651 VL - 121 IS - 4 SN - 0022-3476, 0022-3476 KW - Cresols KW - 0 KW - Preservatives, Pharmaceutical KW - Growth Hormone KW - 9002-72-6 KW - Creatine Kinase KW - EC 2.7.3.2 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Growth Hormone -- administration & dosage KW - Injections, Subcutaneous KW - Adolescent KW - Male KW - Creatine Kinase -- blood KW - Muscular Diseases -- chemically induced KW - Pain -- chemically induced KW - Muscular Diseases -- enzymology KW - Cresols -- adverse effects KW - Preservatives, Pharmaceutical -- adverse effects KW - Pain -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73216396?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pediatrics&rft.atitle=Myalgia+and+elevated+creatine+kinase+activity+associated+with+subcutaneous+injections+of+diluent.&rft.au=Bach%2C+M+A%3BBlum%2C+D+M%3BRose%2C+S+R%3BCharnas%2C+L+R&rft.aulast=Bach&rft.aufirst=M&rft.date=1992-10-01&rft.volume=121&rft.issue=4&rft.spage=650&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pediatrics&rft.issn=00223476&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-13 N1 - Date created - 1992-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comments on occupational and environmental factors in the origin of non-Hodgkin's lymphoma. AN - 73212177; 1394163 AB - The review of the literature regarding non-Hodgkin's lymphoma and occupational and environmental factors presented at this workshop suggested associations with viruses, solvents, and hair dyes. A population-based case-control study among men from Iowa and Minnesota notes similar associations. Workers engaged in metal working, hair care, painting, and dry cleaning experienced nonsignificant excesses. Risks from specific exposures showed some variation by histological type. Both follicular and diffuse non-Hodgkin's lymphoma were associated with benzene. The diffuse type was linked to solvents other than benzene and formaldehyde, while the follicular was excessive among workers exposed to oils and greases. JF - Cancer research AU - Blair, A AU - Linos, A AU - Stewart, P A AU - Burmeister, L F AU - Gibson, R AU - Everett, G AU - Schuman, L AU - Cantor, K P AD - Environmental Epidemiology Branch, National Cancer Institute, Rockville, Maryland 20892. Y1 - 1992/10/01/ PY - 1992 DA - 1992 Oct 01 SP - 5501s EP - 5502s VL - 52 IS - 19 Suppl SN - 0008-5472, 0008-5472 KW - Index Medicus KW - Risk Factors KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Minnesota -- epidemiology KW - Male KW - Iowa -- epidemiology KW - Lymphoma, Non-Hodgkin -- epidemiology KW - Occupational Diseases -- etiology KW - Lymphoma, Non-Hodgkin -- etiology KW - Occupational Diseases -- epidemiology KW - Lymphoma, Non-Hodgkin -- chemically induced KW - Occupational Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73212177?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Comments+on+occupational+and+environmental+factors+in+the+origin+of+non-Hodgkin%27s+lymphoma.&rft.au=Blair%2C+A%3BLinos%2C+A%3BStewart%2C+P+A%3BBurmeister%2C+L+F%3BGibson%2C+R%3BEverett%2C+G%3BSchuman%2C+L%3BCantor%2C+K+P&rft.aulast=Blair&rft.aufirst=A&rft.date=1992-10-01&rft.volume=52&rft.issue=19+Suppl&rft.spage=5501s&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-29 N1 - Date created - 1992-10-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Radiation and non-Hodgkin's lymphoma. AN - 73206085; 1394160 AB - Lymphomas are rarely, if ever, found to be in excess following exposure to ionizing radiation. Hodgkin's disease has never been linked to radiation, and the evidence for non-Hodgkin's lymphoma (NHL) is very weak. Low doses of radiation from diagnostic X-ray procedures or from occupational exposures do not appear to cause NHL. Mortality studies of atomic bomb survivors in Japan and other epidemiological studies with quantitative estimates of radiation dose also fail to find dose-response relationships. NHL may arise infrequently following high-dose, possibly near lethal, radiation treatments. Immunosuppression associated with the disease being treated, such as Hodgkin's disease, may contribute to the development of NHL. If radiation does not cause NHL, at least not by its accepted mechanism of action of breaking chromosomes, creating rearrangements, gene deletions, and mutations, perhaps other environmental mutagens and clastogens should not be considered likely causes of NHL. JF - Cancer research AU - Boice, J D AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/10/01/ PY - 1992 DA - 1992 Oct 01 SP - 5489s EP - 5491s VL - 52 IS - 19 Suppl SN - 0008-5472, 0008-5472 KW - Index Medicus KW - Humans KW - Lymphoma, Non-Hodgkin -- epidemiology KW - Neoplasms, Radiation-Induced -- etiology KW - Neoplasms, Radiation-Induced -- epidemiology KW - Lymphoma, Non-Hodgkin -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73206085?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Radiation+and+non-Hodgkin%27s+lymphoma.&rft.au=Boice%2C+J+D&rft.aulast=Boice&rft.aufirst=J&rft.date=1992-10-01&rft.volume=52&rft.issue=19+Suppl&rft.spage=5489s&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-29 N1 - Date created - 1992-10-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - New sites of proviral integration associated with murine promonocytic leukemias and evidence for alternate modes of c-myb activation. AN - 73177064; 1527851 AB - Murine promonocytic leukemias involving insertional mutagenesis of the c-myb locus can be induced by replication-competent retroviruses. In previously studied promonocytic leukemic cells induced by Moloney murine leukemia virus (called MML), the provirus has been invariably integrated upstream of exons 3 or 4 and the leukemic cells expressed aberrant RNAs with fused virus-myb sequences. Furthermore, Myb expressed by these cells has been shown to be truncated by 47 or 71 amino acids. The present report examines the mechanisms of myb activation in leukemias induced by two other retroviruses, amphotropic virus 4070A and Friend strain FB29 (the leukemias are called AMPH-ML and FB-ML, respectively). This study revealed two additional c-myb proviral insertion sites in these promonocytic leukemias. One FB-ML had a proviral integration in exon 9, and expressed a C-terminally truncated Myb protein of 47 kDa similar to that previously demonstrated to be expressed in the myelomonocytic cell lines NFS60 and VFL-2. However, a sequence of reverse-transcribed and amplified RNA from this leukemia demonstrated that the truncation involved a loss of 248 amino acids compared with a loss of 240 amino acids in the myelomonocytic cell lines. Another leukemia had a provirus integrated in the 5' end of c-myb upstream of exon 2 (in the first intron) and produced a Myb protein that was indistinguishable on sodium dodecyl sulfate-polyacrylamide gel electrophoresis from normal Myb. This latter leukemia (FB-ML R1-4-10) expressed Myb with the smallest N-terminal truncation observed so far in promonocytic leukemias; translation begins at an ATG within c-myb exon 2, leading to loss of only 20 amino acids from the N terminus. Unlike the proteins produced in Moloney murine leukemia virus-induced promonocytic leukemias (MML) that have larger truncations, this protein has an intact DNA binding region and does not contain N-terminal amino acids encoded by gag. However, this protein is similar to all N-terminally truncated Mybs so far studied, in that the truncation resulted in deletion of a casein kinase II phosphorylation site which has been proposed to be involved in regulation of DNA binding. JF - Journal of virology AU - Mukhopadhyaya, R AU - Wolff, L AD - Laboratory of Genetics, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 6035 EP - 6044 VL - 66 IS - 10 SN - 0022-538X, 0022-538X KW - c-myb KW - gag KW - Proto-Oncogene Proteins KW - 0 KW - Proto-Oncogene Proteins c-myb KW - DNA KW - 9007-49-2 KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Index Medicus KW - Animals KW - Blotting, Northern KW - Transcription, Genetic KW - Amino Acid Sequence KW - Mice KW - Precipitin Tests KW - Plasmids KW - Mice, Inbred DBA KW - Polymerase Chain Reaction KW - Base Sequence KW - Oncogenes KW - Tumor Cells, Cultured KW - Blotting, Southern KW - Molecular Sequence Data KW - Genes, gag KW - Female KW - Protein-Tyrosine Kinases -- genetics KW - Proviruses -- physiology KW - Proto-Oncogene Proteins -- metabolism KW - Protein-Tyrosine Kinases -- metabolism KW - Virus Integration KW - Proto-Oncogene Proteins -- genetics KW - Leukemia, Experimental -- microbiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73177064?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=New+sites+of+proviral+integration+associated+with+murine+promonocytic+leukemias+and+evidence+for+alternate+modes+of+c-myb+activation.&rft.au=Mukhopadhyaya%2C+R%3BWolff%2C+L&rft.aulast=Mukhopadhyaya&rft.aufirst=R&rft.date=1992-10-01&rft.volume=66&rft.issue=10&rft.spage=6035&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-19 N1 - Date created - 1992-10-19 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-myb; gag N1 - SuppNotes - Cited By: Nucleic Acids Res. 1982 Jan 22;10(2):459-72 [7063411] J Immunol. 1978 Aug;121(2):641-7 [308074] Nucleic Acids Res. 1991 Dec 25;19(24):6950 [1762923] Nature. 1990 Apr 5;344(6266):517-22 [2157164] J Virol. 1990 Jan;64(1):155-60 [2403439] J Virol. 1987 Sep;61(9):2754-63 [2441077] J Virol. 1989 Apr;63(4):1630-40 [2538646] EMBO J. 1989 Jun;8(6):1767-75 [2670561] J Virol. 1988 Apr;62(4):1423-32 [2831403] J Virol. 1987 Jul;61(7):2339-43 [2884332] Virology. 1985 Feb;141(1):110-8 [2983493] Proc Natl Acad Sci U S A. 1986 Jul;83(14):5010-4 [3014527] Proc Natl Acad Sci U S A. 1986 Jul;83(13):4685-9 [3088565] Cell. 1988 Jan 29;52(2):185-95 [3277717] Virology. 1970 Dec;42(4):1136-9 [4099080] Nucleic Acids Res. 1984 Jan 25;12(2):857-72 [6694911] J Virol. 1992 Jan;66(1):512-23 [1309260] J Virol. 1991 Jul;65(7):3607-16 [1645785] EMBO J. 1991 Mar;10(3):655-64 [1825810] Genes Dev. 1990 Dec;4(12B):2235-41 [2279697] Nature. 1990 Feb 15;343(6259):662-5 [2406607] Anal Biochem. 1987 Apr;162(1):156-9 [2440339] J Mol Biol. 1989 Jan 20;205(2):363-72 [2538626] Proc Natl Acad Sci U S A. 1989 Mar;86(6):1836-40 [2538817] Oncogene Res. 1989;4(4):259-69 [2549488] J Virol. 1987 Dec;61(12):3721-5 [2824810] J Immunol. 1988 Jul 15;141(2):681-9 [2838552] Biotechniques. 1988 Feb;6(2):114-6 [2908499] Nucleic Acids Res. 1989 Mar 11;17(5):2141 [2928127] Proc Natl Acad Sci U S A. 1986 May;83(10):3204-8 [3010282] Nucleic Acids Res. 1986 Jul 11;14(13):5309-20 [3016644] Mol Cell Biol. 1986 Feb;6(2):380-92 [3023843] Proc Natl Acad Sci U S A. 1988 Aug;85(15):5698-702 [3165197] J Virol. 1985 Jun;54(3):864-8 [3999195] Nature. 1981 Oct 15-21;293(5833):543-8 [6169994] J Virol. 1981 Sep;39(3):777-91 [6270351] Erratum In: J Virol 1993 May;67(5):2960 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reduced fertility among women employed as dental assistants exposed to high levels of nitrous oxide. AN - 73163748; 1298226 AB - Fertility is reduced in female rats exposed to levels of nitrous oxide similar to those found in some dental offices. Epidemiologic studies have suggested an association between exposure to mixed anesthetic gases and impaired fertility. We investigated the effects of occupational exposure to nitrous oxide on the fertility of female dental assistants. Screening questionnaires were mailed to 7000 female dental assistants, ages 18 to 39, registered by the California Department of Consumer Affairs. Sixty-nine percent responded. Four hundred fifty-nine women were determined to be eligible, having become pregnant during the previous four years for reasons unrelated to the failure of birth control, and 91 percent of these women completed telephone interviews. Detailed information was collected on exposure to nitrous oxide and fertility (measured by the number of menstrual cycles without contraception that the women required to become pregnant). After controlling for covariates, we found that women exposed to high levels of nitrous oxide were significantly less fertile than women who were unexposed or exposed to lower levels of nitrous oxide. The effect was evident only in the 19 women with five or more hours of exposure per week. These women were only 41 percent (95 percent confidence interval, 23 to 74 percent; P less than 0.003) as likely as unexposed women to conceive during each menstrual cycle. Occupational exposure to high levels of nitrous oxide may adversely affect women's ability to become pregnant. JF - The New England journal of medicine AU - Rowland, A S AU - Baird, D D AU - Weinberg, C R AU - Shore, D L AU - Shy, C M AU - Wilcox, A J AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/10/01/ PY - 1992 DA - 1992 Oct 01 SP - 993 EP - 997 VL - 327 IS - 14 SN - 0028-4793, 0028-4793 KW - Nitrous Oxide KW - K50XQU1029 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Adult KW - Surveys and Questionnaires KW - Retrospective Studies KW - Adolescent KW - Female KW - Occupational Exposure KW - Nitrous Oxide -- adverse effects KW - Dental Assistants KW - Fertility -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73163748?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+New+England+journal+of+medicine&rft.atitle=Reduced+fertility+among+women+employed+as+dental+assistants+exposed+to+high+levels+of+nitrous+oxide.&rft.au=Rowland%2C+A+S%3BBaird%2C+D+D%3BWeinberg%2C+C+R%3BShore%2C+D+L%3BShy%2C+C+M%3BWilcox%2C+A+J&rft.aulast=Rowland&rft.aufirst=A&rft.date=1992-10-01&rft.volume=327&rft.issue=14&rft.spage=993&rft.isbn=&rft.btitle=&rft.title=The+New+England+journal+of+medicine&rft.issn=00284793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-06 N1 - Date created - 1992-10-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: N Engl J Med. 1993 Jan 28;328(4):284-5 [8418413] N Engl J Med. 1993 Jan 28;328(4):284 [8466571] N Engl J Med. 1992 Oct 1;327(14):1026-7 [1518538] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Adolescent Nonsexual and Sex-Related Problem Behaviors AN - 61289152; 93Z8385 AB - Data from a subsample (N = 1,197 males [Ms] & 1,834 females [Fs], 75% white & 25% black) of the 1980 National Longitudinal Survey of Youth are drawn on to compare the involvement in problem behaviors of those who were: (1) virgins, (2) sexually experienced but never pregnant, & (3) pregnant or parents. Logistic regression analyses reveal that, after controlling for the effects of sociodemographic status, age, school status, & frequency of attendance at religious services, sexually experienced, never pregnant adolescents are more likely than virgins to have been involved in four types of nonsexual problem behaviors. However, pregnant/parenting adolescents are no more likely to engage in such behaviors than are their experienced but never pregnant peers. For Ms, but not for Fs, early age at first intercourse is associated with increased involvement in problem behaviors. Implications for policy & interventions for adolescents at risk are discussed. 4 Tables, 1 Appendix, 82 References. Adapted from the source document. JF - Journal of Adolescent Research AU - Ketterlinus, Robert D AU - Lamb, Michael E AU - Nitz, Katherine AU - Elster, Arthur B AD - NIH/NICHD, 9190 Rockville Pike BSA Bldg #333 Bethesda MD 20892-9901 Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 431 EP - 456 VL - 7 IS - 4 SN - 0743-5584, 0743-5584 KW - problem behaviors, virgin/sexually experienced/pregnant/parenting adolescents KW - 1980 national survey data KW - black/white males/females KW - Sexual Behavior KW - Black White Differences KW - Sex Differences KW - Parenthood KW - Virginity KW - Sexual Reproduction KW - Adolescents KW - article KW - 1939: the family and socialization; adolescence & youth UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/61289152?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocabs&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Adolescent+Research&rft.atitle=Adolescent+Nonsexual+and+Sex-Related+Problem+Behaviors&rft.au=Ketterlinus%2C+Robert+D%3BLamb%2C+Michael+E%3BNitz%2C+Katherine%3BElster%2C+Arthur+B&rft.aulast=Ketterlinus&rft.aufirst=Robert&rft.date=1992-10-01&rft.volume=7&rft.issue=4&rft.spage=431&rft.isbn=&rft.btitle=&rft.title=Journal+of+Adolescent+Research&rft.issn=07435584&rft_id=info:doi/ LA - English DB - Sociological Abstracts N1 - Date revised - 2007-04-01 N1 - Last updated - 2016-09-28 N1 - CODEN - JADREZ N1 - SubjectsTermNotLitGenreText - Adolescents; Black White Differences; Sex Differences; Sexual Behavior; Virginity; Sexual Reproduction; Parenthood ER - TY - JOUR T1 - Analysis of the backbone dynamics of the ribonuclease H domain of the human immunodeficiency virus reverse transcriptase using 15N relaxation measurements. AN - 73210893; 1382587 AB - The backbone dynamics of the uniformly 15N-labeled ribonuclease H (RNase H) domain of human immunodeficiency virus (HIV-1) reverse transcriptase have been investigated using two-dimensional inverse-detected heteronuclear 15N-1HNMR spectroscopy. 15N T1, T2, and nuclear Overhauser enhancement (NOE) data were obtained for 107 out of a total of 134 backbone amide groups. The overall rotational correlation time (tau R) for the protein at 26 degrees C is 10.4 ns. The backbone N-H vectors for all the measurable residues exhibit very fast motions on a time scale of less than or equal to 20 ps. The 15N relaxation data for only 14 residues can be explained by this single internal motion alone. A further 39 residues display a second motion on a time scale ranging from 28.8 ps to 3.9 ns, while another 15 residues are characterized by an additional motion on the 170-ns to 2.25-ms time scale resulting in 15N T2 exchange line broadening. There are 39 residues that exhibit both the additional 15N T2 exchange line broadening and the slow (28.8 ps-3.9 ns) internal motion. Thus, the RNase H domain experiences extensive mobility throughout its structure as evidenced by the 93 residues which exhibit multiple modes of motion. Distinctly mobile regions of the protein are identified by large decreases in the overall order parameter (S2) and correspond to the C-terminal residues and the loop regions between beta-strands beta 1 and beta 2 and between alpha-helix alpha B and beta-strand beta 4.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Biochemistry AU - Powers, R AU - Clore, G M AU - Stahl, S J AU - Wingfield, P T AU - Gronenborn, A AD - Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09/29/ PY - 1992 DA - 1992 Sep 29 SP - 9150 EP - 9157 VL - 31 IS - 38 SN - 0006-2960, 0006-2960 KW - Nitrogen Isotopes KW - 0 KW - Recombinant Proteins KW - HIV Reverse Transcriptase KW - EC 2.7.7.49 KW - RNA-Directed DNA Polymerase KW - Ribonuclease H KW - EC 3.1.26.4 KW - Index Medicus KW - AIDS/HIV KW - Mutagenesis, Site-Directed KW - Magnetic Resonance Spectroscopy -- methods KW - Models, Molecular KW - Recombinant Proteins -- chemistry KW - Protein Conformation KW - Ribonuclease H -- chemistry KW - RNA-Directed DNA Polymerase -- chemistry KW - HIV-1 -- enzymology KW - RNA-Directed DNA Polymerase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73210893?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=Analysis+of+the+backbone+dynamics+of+the+ribonuclease+H+domain+of+the+human+immunodeficiency+virus+reverse+transcriptase+using+15N+relaxation+measurements.&rft.au=Powers%2C+R%3BClore%2C+G+M%3BStahl%2C+S+J%3BWingfield%2C+P+T%3BGronenborn%2C+A&rft.aulast=Powers&rft.aufirst=R&rft.date=1992-09-29&rft.volume=31&rft.issue=38&rft.spage=9150&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-13 N1 - Date created - 1992-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Controlled trial of pulse methylprednisolone versus two regimens of pulse cyclophosphamide in severe lupus nephritis. AN - 73196845; 1356175 AB - Pulse cyclophosphamide is more effective than prednisone alone in preventing renal failure in lupus nephritis. We undertook a randomised, controlled trial to find out whether pulse methylprednisolone could equal pulse cyclophosphamide in preserving renal function in patients with lupus nephritis, and whether there was a difference between long and short courses of pulse cyclophosphamide in preventing exacerbations. 65 patients (60 female, 5 male; median [range] age 29 [10-48] years) with severe lupus nephritis were assigned randomly to monthly pulse methylprednisolone for 6 months (25 patients), monthly pulse cyclophosphamide for 6 months (20), or monthly cyclophosphamide for 6 months followed by quarterly pulse cyclophosphamide for 2 additional years (20). Patients treated with pulse methylprednisolone had a higher probability of doubling serum creatinine than those treated with long-course cyclophosphamide (p less than 0.04). Risk of doubling creatinine was not significantly different between short and long course cyclophosphamide. However, patients treated with short-course cyclophosphamide had a higher probability of exacerbations than those treated with long-course cyclophosphamide (p less than 0.01). An extended course of pulse cyclophosphamide is more effective than 6 months of pulse methylprednisolone in preserving renal function in patients with severe lupus nephritis. Addition of a quarterly maintenance regimen to monthly pulse cyclophosphamide reduces the rate of exacerbations. JF - Lancet (London, England) AU - Boumpas, D T AU - Austin, H A AU - Vaughn, E M AU - Klippel, J H AU - Steinberg, A D AU - Yarboro, C H AU - Balow, J E AD - Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland 20892. Y1 - 1992/09/26/ PY - 1992 DA - 1992 Sep 26 SP - 741 EP - 745 VL - 340 IS - 8822 SN - 0140-6736, 0140-6736 KW - Cyclophosphamide KW - 8N3DW7272P KW - Creatinine KW - AYI8EX34EU KW - Methylprednisolone KW - X4W7ZR7023 KW - Abridged Index Medicus KW - Index Medicus KW - Drug Administration Schedule KW - Humans KW - Adult KW - Treatment Outcome KW - Middle Aged KW - Child KW - Adolescent KW - Creatinine -- blood KW - Recurrence KW - Male KW - Female KW - Survival Analysis KW - Cyclophosphamide -- administration & dosage KW - Methylprednisolone -- administration & dosage KW - Lupus Nephritis -- drug therapy KW - Lupus Nephritis -- blood KW - Methylprednisolone -- adverse effects KW - Cyclophosphamide -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73196845?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lancet+%28London%2C+England%29&rft.atitle=Controlled+trial+of+pulse+methylprednisolone+versus+two+regimens+of+pulse+cyclophosphamide+in+severe+lupus+nephritis.&rft.au=Boumpas%2C+D+T%3BAustin%2C+H+A%3BVaughn%2C+E+M%3BKlippel%2C+J+H%3BSteinberg%2C+A+D%3BYarboro%2C+C+H%3BBalow%2C+J+E&rft.aulast=Boumpas&rft.aufirst=D&rft.date=1992-09-26&rft.volume=340&rft.issue=8822&rft.spage=741&rft.isbn=&rft.btitle=&rft.title=Lancet+%28London%2C+England%29&rft.issn=01406736&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of conserved threonine and tyrosine residues in acetylcholine binding and muscarinic receptor activation. A study with m3 muscarinic receptor point mutants. AN - 73185356; 1527051 AB - Structure-function relationship studies of the m3 muscarinic acetylcholine receptor have recently identified a series of threonine and tyrosine residues (all located within the hydrophobic receptor core) that are critically involved in acetylcholine binding (Wess, J., Gdula, D., and Brann, M.R. (1991) EMBO J. 10, 3729-3734). To gain further insight into the functional roles of these amino acids, the agonist binding properties of six rat m3 muscarinic receptor point mutants, in which the critical threonine and tyrosine residues had been individually replaced by alanine and phenylalanine, respectively, were studied in greater detail following their transient expression in COS-7 cells. The binding profiles of a series of acetylcholine derivatives suggest that the altered threonine and tyrosine residues are primarily involved in the interaction of the acetylcholine ester moiety with the receptor protein. The two m3 receptor point mutants, Thr234----Ala and Tyr506----Phe, which showed the most pronounced decreases in acetylcholine binding affinities (approximately 40-60-fold as compared with the wild-type receptor), were stably expressed in CHO cells for further functional analysis. Both mutant receptors were found to be severely impaired in their ability to stimulate agonist-dependent phosphatidylinositol hydrolysis. Consistent with this observation, acetylcholine binding to the two mutant receptors was not significantly affected by addition of the GTP analog Gpp(NH)p (5'-guanylyl imidodiphosphate). Our data suggest that Thr234 and Tyr506 (located within transmembrane domains V and VI, respectively), which are conserved among all muscarinic receptors (m1-m5), may play an important role in agonist-induced muscarinic receptor activation. JF - The Journal of biological chemistry AU - Wess, J AU - Maggio, R AU - Palmer, J R AU - Vogel, Z AD - National Institute of Neurological Disorders and Stroke, Laboratory of Molecular Biology, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09/25/ PY - 1992 DA - 1992 Sep 25 SP - 19313 EP - 19319 VL - 267 IS - 27 SN - 0021-9258, 0021-9258 KW - Inositol Phosphates KW - 0 KW - Receptors, Muscarinic KW - Threonine KW - 2ZD004190S KW - Guanylyl Imidodiphosphate KW - 34273-04-6 KW - Tyrosine KW - 42HK56048U KW - Acetylcholine KW - N9YNS0M02X KW - Index Medicus KW - Animals KW - Threonine -- metabolism KW - Inositol Phosphates -- metabolism KW - Amino Acid Sequence KW - Structure-Activity Relationship KW - Mutagenesis, Site-Directed KW - Rats KW - Guanylyl Imidodiphosphate -- metabolism KW - In Vitro Techniques KW - Molecular Sequence Data KW - CHO Cells KW - Tyrosine -- metabolism KW - Signal Transduction KW - Cricetinae KW - Acetylcholine -- metabolism KW - Receptors, Muscarinic -- chemistry KW - Receptors, Muscarinic -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73185356?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Role+of+conserved+threonine+and+tyrosine+residues+in+acetylcholine+binding+and+muscarinic+receptor+activation.+A+study+with+m3+muscarinic+receptor+point+mutants.&rft.au=Wess%2C+J%3BMaggio%2C+R%3BPalmer%2C+J+R%3BVogel%2C+Z&rft.aulast=Wess&rft.aufirst=J&rft.date=1992-09-25&rft.volume=267&rft.issue=27&rft.spage=19313&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytotoxic ribonuclease chimeras. Targeted tumoricidal activity in vitro and in vivo. AN - 73176371; 1527074 AB - Monoclonal antibodies to the transferrin receptor or to the T cell antigen, CD5, were chemically linked to mammalian RNase A and found to specifically inhibit protein synthesis in antigen-positive cells. Antibody-mediated specificity of these cytotoxic ribonuclease chimeras (CRCs) was demonstrated in three ways. 1) Toxicity was due to the chemical linkage of RNase to antibody, as the individual components added separately or in combination did not inhibit protein synthesis; 2) the anti-transferrin receptor CRCs inhibited protein synthesis in those cells expressing the human transferrin receptor (K562, U251, Jurkat cells) but had no detectable toxicity to cells lacking the human transferrin receptor (Vero or NIH 3T3 cells); 3) free antibody to either the human transferrin receptor (454A12 or 5E-9) or to the T cell antigen, CD5 (T101), blocked the cytotoxicity of the respective CRC. Two CRC species, designated P1 and P2, that differed in size and stoichiometry of RNase A to antibody, were purified by size-exclusion high performance liquid chromatography. The higher molecular weight P1 conjugate had an IC50 of 20-30 nM, whereas the P2 conjugate had a higher IC50 of 300-500 nM. Bioactivity could be reversibly increased more than 10-fold by freezing. The cytotoxicity of the CRCs was examined in vivo in a solid tumor animal model. Intratumoral injections of an anti-transferrin receptor CRC into established U251 human glioblastoma tumors grown in the flanks of nude mice prevented tumor growth, whereas RNase A mixed with antibody was ineffective. CRCs, therefore, express cytotoxicity in vitro and in vivo. Mammalian nucleases coupled to antibodies may be utilized as cell type-selective cytotoxins and have potential as pharmacologic reagents. The systemic toxicity and immunogenicity observed with mammalian derived cytotoxins may be significantly less than that of the currently employed plant- and bacterial-derived immunotoxins. JF - The Journal of biological chemistry AU - Newton, D L AU - Ilercil, O AU - Laske, D W AU - Oldfield, E AU - Rybak, S M AU - Youle, R J AD - National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09/25/ PY - 1992 DA - 1992 Sep 25 SP - 19572 EP - 19578 VL - 267 IS - 27 SN - 0021-9258, 0021-9258 KW - Antibodies, Monoclonal KW - 0 KW - Antineoplastic Agents KW - Cross-Linking Reagents KW - Cytotoxins KW - Immunotoxins KW - Receptors, Transferrin KW - Ribonucleases KW - EC 3.1.- KW - Index Medicus KW - Neoplasm Transplantation KW - Protein Biosynthesis KW - Animals KW - Tumor Cells, Cultured KW - In Vitro Techniques KW - Receptors, Transferrin -- immunology KW - Mice, Nude KW - Mice KW - Immunotoxins -- chemistry KW - Ribonucleases -- toxicity KW - Cell Survival -- drug effects KW - Ribonucleases -- chemistry KW - Antibodies, Monoclonal -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73176371?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Cytotoxic+ribonuclease+chimeras.+Targeted+tumoricidal+activity+in+vitro+and+in+vivo.&rft.au=Newton%2C+D+L%3BIlercil%2C+O%3BLaske%2C+D+W%3BOldfield%2C+E%3BRybak%2C+S+M%3BYoule%2C+R+J&rft.aulast=Newton&rft.aufirst=D&rft.date=1992-09-25&rft.volume=267&rft.issue=27&rft.spage=19572&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytochrome P450-benzphetamine interactions in the endoplasmic reticulum: studies using a monoclonal antibody to P450b. AN - 73203422; 1390673 AB - A monoclonal antibody (MAb) to phenobarbital-induced rat cytochrome P450b was used to study the interaction of the substrate benzphetamine (Bz) with cytochromes P450 in liver microsomes. Binding of Bz to liver microsomes from phenobarbital-treated rats was monitored by the substrate-induced type I spectral change. The MAb maximally inhibited this spectral change by 49%, providing a probe to distinguish MAb-specific P450b from other Bz-binding P450s. Thermodynamic parameters of the interaction were determined in the absence and presence of MAb. The MAb did not influence the spin-state equilibrium of substrate-free P450b, but it increased the low spin content of substrate-bound P450b. The MAb also decreased the affinity of both high and low spin P450b for Bz. The temperature dependence of the Bz-binding interactions revealed a transition near 20 degrees C. Fluorescence polarization measurements of the membrane probe 1,6-diphenyl-1,3,5-hexatriene also revealed a transition at this temperature. The MAb comparably inhibited Bz binding to high spin P450b in the low and high temperature regions, whereas MAb inhibition of Bz binding to low spin P450b was greater in the low temperature region than in the high temperature region. These results indicate temperature-dependent changes in membrane structure that modulate both Bz binding to P450b and MAb-P450b-Bz interactions. These results also demonstrate the utility of MAbs for evaluating P450-substrate binding microequilibria of MAb-specific P450s in the presence of other P450s while in the natural membrane environment of the endoplasmic reticulum. JF - Biochemistry AU - Omata, Y AU - Friedman, F K AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09/22/ PY - 1992 DA - 1992 Sep 22 SP - 8862 EP - 8867 VL - 31 IS - 37 SN - 0006-2960, 0006-2960 KW - Antibodies, Monoclonal KW - 0 KW - Benzphetamine KW - 0M3S43XK27 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - benzphetamine N-demethylase KW - EC 1.14.14.1 KW - Oxidoreductases, N-Demethylating KW - EC 1.5.- KW - Index Medicus KW - Rats KW - Antigen-Antibody Reactions KW - Animals KW - Rats, Sprague-Dawley KW - Viscosity KW - Thermodynamics KW - Spectrum Analysis KW - Binding, Competitive KW - Temperature KW - Endoplasmic Reticulum -- enzymology KW - Microsomes, Liver -- enzymology KW - Oxidoreductases, N-Demethylating -- immunology KW - Cytochrome P-450 Enzyme System -- immunology KW - Cytochrome P-450 Enzyme System -- metabolism KW - Benzphetamine -- metabolism KW - Oxidoreductases, N-Demethylating -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73203422?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=Cytochrome+P450-benzphetamine+interactions+in+the+endoplasmic+reticulum%3A+studies+using+a+monoclonal+antibody+to+P450b.&rft.au=Omata%2C+Y%3BFriedman%2C+F+K&rft.aulast=Omata&rft.aufirst=Y&rft.date=1992-09-22&rft.volume=31&rft.issue=37&rft.spage=8862&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-26 N1 - Date created - 1992-10-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A transient transfection system for identifying biosynthesized proteins processed and presented to class I MHC restricted T lymphocytes. AN - 73252118; 1401939 AB - CD8+ cytotoxic T lymphocytes (CTL) constitute a major portion of immune responses to foreign and self antigens. CTL recognize class I major histocompatibility complex molecules complexed to peptides of 8-10 residues derived from cytosolic proteins. To understand CTL responses to these antigens and to manipulate CTL responses optimally, it is necessary to identify the specific peptides recognized by CTL. The methods currently used for this purpose have significant drawbacks. We describe a plasmid transfection method that results in significant lysis of histocompatible target cells. Influenza virus-specific CTLs specifically lysed target cells that were transfected with plasmids bearing cDNAs encoding full length gene products, fragments containing the region that encodes the CTL epitope, or even a ten residue peptide. This significantly lessens the time and effort required to define genes, and gene segments that contain CTL epitopes. JF - Journal of immunological methods AU - Eisenlohr, L C AU - Yewdell, J W AU - Bennink, J R AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1992/09/18/ PY - 1992 DA - 1992 Sep 18 SP - 131 EP - 138 VL - 154 IS - 1 SN - 0022-1759, 0022-1759 KW - Histocompatibility Antigens Class I KW - 0 KW - Index Medicus KW - Animals KW - Vaccinia virus KW - Mice KW - Antigen-Presenting Cells -- immunology KW - Plasmids KW - Orthomyxoviridae Infections -- immunology KW - Fluorescent Antibody Technique KW - Cell Line KW - Cytotoxicity Tests, Immunologic -- methods KW - Transfection KW - Histocompatibility Antigens Class I -- immunology KW - T-Lymphocytes, Cytotoxic -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73252118?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunological+methods&rft.atitle=A+transient+transfection+system+for+identifying+biosynthesized+proteins+processed+and+presented+to+class+I+MHC+restricted+T+lymphocytes.&rft.au=Eisenlohr%2C+L+C%3BYewdell%2C+J+W%3BBennink%2C+J+R&rft.aulast=Eisenlohr&rft.aufirst=L&rft.date=1992-09-18&rft.volume=154&rft.issue=1&rft.spage=131&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunological+methods&rft.issn=00221759&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-26 N1 - Date created - 1992-10-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Photosensitization by anticancer agents. 11. Mechanisms of photosensitization of human leukemic cells by diaminoanthraquinones: singlet oxygen and radical reactions. AN - 73314683; 1331388 AB - The synthesis of several aminoanthraquinone derivatives (AAQs), designed to suppress the dark toxicity and to promote more efficient cancer cell photosensitization for potential use in photodynamic therapy (PDT), is described. The following AAQs were synthesized: 1-NH2-4,5-(MeO)2-AQ (1), 1,5-(NH2)2-4,8-(MeO)2-AQ (2), 1,8-(NH2)2-4,5-(MeO)2-AQ (3), and 1,5-(NHPhMe)2-4,8-(MeO)2-AQ (8). The agents exhibit strong absorption in the region 480-620 nm. Possible mechanisms of photosensitization were studied by measuring 1O2 phosphorescence at 1270 nm, detecting superoxide radicals employing an electron paramagnetic resonance (EPR)-spin trapping technique, and measuring oxygen consumption during the photo-oxidation of a representative biological electron donor, NADH. Strong phosphorescence from 1O2 was observed upon illumination of 2 and 3 in C6H6 (quantum yield of 0.25 and 0.5 respectively), and in EtOH (quantum yield of 0.23 and 0.34). The 1-amino-AQ (1) was the weakest 1O2 sensitizer, with quantum yield of 0.13 in benzene. No phosphorescence was observed in EtOH. A superoxide radical was detected as a spin adduct of 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) in irradiated benzene solutions of 1, 2 or 3 and DMPO. AAQs 2 and 3 sensitized photo-oxidation of NADH in H2O/EtOH mixture with the intermediacy of singlet oxygen as judged by the effect of sodium azide on the photostimulated oxygen consumption. Evolution of O2 upon addition of catalase to the illuminated solution confirmed the ultimate formation of hydrogen peroxide. These findings suggested that the (di)amino-dimethoxyanthraquinones might exert photosensitization via both Type I and Type II mechanisms. The AAQs were tested for their ability to photosensitize K562 human chronic myeloid leukemic cells in culture. Viability was measured using the 3,4,5-diethylthiazol-2,5-diphenyl tetrazolium blue assay, and DNA and possible membrane damage were assessed. The results from illuminating cells with light > 475 nm show that for the 1,5-compounds, the presence of methoxy substituents at 4,8 positions reduces the dark toxicity from ID50 of 23 to 250 microM and for the 1,8-compounds correspondingly from ID50 of 53 to > 300 microM. In the 1,5-series this decrease of the dark toxicity is accompanied by an increase in light-induced dose modification from 8.85 to 14.4. Differences exist in the mechanisms of cytotoxicity between the prototype phenolic AAQs and their methoxy counterparts. It appears that the cytotoxic action of the latter causes cell damage by the formation of a high proportion of alkali labile sites in addition to frank strand breaks.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Journal of photochemistry and photobiology. B, Biology AU - Reszka, K J AU - Bilski, P AU - Chignell, C F AU - Hartley, J A AU - Khan, N AU - Souhami, R L AU - Mendonca, A J AU - Lown, J W AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/09/15/ PY - 1992 DA - 1992 Sep 15 SP - 317 EP - 335 VL - 15 IS - 4 SN - 1011-1344, 1011-1344 KW - Anthraquinones KW - 0 KW - Antineoplastic Agents KW - Free Radicals KW - Radiation-Sensitizing Agents KW - Cycloleucine KW - 0TQU7668EI KW - NAD KW - 0U46U6E8UK KW - Singlet Oxygen KW - 17778-80-2 KW - Oxygen KW - S88TT14065 KW - Index Medicus KW - Oxygen Consumption -- drug effects KW - Humans KW - Oxygen -- metabolism KW - Photochemotherapy KW - Free Radicals -- metabolism KW - Structure-Activity Relationship KW - NAD -- metabolism KW - Tumor Cells, Cultured KW - Electron Spin Resonance Spectroscopy KW - Kinetics KW - Leukemia, Myelogenous, Chronic, BCR-ABL Positive KW - Spectrophotometry KW - Cycloleucine -- metabolism KW - Radiation-Sensitizing Agents -- chemistry KW - Cell Survival -- drug effects KW - DNA Damage KW - Radiation-Sensitizing Agents -- pharmacology KW - Radiation-Sensitizing Agents -- chemical synthesis KW - Anthraquinones -- chemical synthesis KW - Anthraquinones -- pharmacology KW - Antineoplastic Agents -- chemical synthesis KW - Anthraquinones -- chemistry KW - Antineoplastic Agents -- chemistry KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73314683?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+photochemistry+and+photobiology.+B%2C+Biology&rft.atitle=Photosensitization+by+anticancer+agents.+11.+Mechanisms+of+photosensitization+of+human+leukemic+cells+by+diaminoanthraquinones%3A+singlet+oxygen+and+radical+reactions.&rft.au=Reszka%2C+K+J%3BBilski%2C+P%3BChignell%2C+C+F%3BHartley%2C+J+A%3BKhan%2C+N%3BSouhami%2C+R+L%3BMendonca%2C+A+J%3BLown%2C+J+W&rft.aulast=Reszka&rft.aufirst=K&rft.date=1992-09-15&rft.volume=15&rft.issue=4&rft.spage=317&rft.isbn=&rft.btitle=&rft.title=Journal+of+photochemistry+and+photobiology.+B%2C+Biology&rft.issn=10111344&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-02 N1 - Date created - 1992-12-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interleukin 10 inhibits macrophage microbicidal activity by blocking the endogenous production of tumor necrosis factor alpha required as a costimulatory factor for interferon gamma-induced activation. AN - 73183991; 1528880 AB - Interleukin 10 (IL-10) inhibits interferon gamma-induced macrophage activation for cytotoxicity against larvae of the human parasite Schistosoma mansoni by suppressing production of the toxic effector molecule nitric oxide (NO). In this study, the mechanism of IL-10 action was identified as inhibition of endogenous tumor necrosis factor alpha (TNF-alpha) production by interferon gamma-activated macrophages. TNF-alpha appears to serve as a cofactor for interferon gamma-mediated activation, since both schistosomulum killing and NO production were inhibited by anti-TNF-alpha antibody, whereas TNF-alpha alone was unable to stimulate these macrophage functions. IL-10 blocked TNF-alpha production by interferon gamma-treated macrophages at the levels of both protein and mRNA synthesis. Addition of exogenous TNF-alpha reversed IL-10-mediated suppression of macrophage cytotoxic activity as well as NO production. Likewise, addition of a macrophage-triggering agent (bacterial lipopolysaccharide or muramyl dipeptide), which induced the production of TNF-alpha, also reversed the suppressive effect of IL-10 on cytotoxic function. In contrast to IL-10, two other cytokines, IL-4 and transforming growth factor beta, which also inhibit macrophage activation for schistosomulum killing and NO production, did not substantially suppress endogenous TNF-alpha production. These results, therefore, describe a separate pathway by which macrophage microbicidal function is inhibited by the down-regulatory cytokine IL-10. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Oswald, I P AU - Wynn, T A AU - Sher, A AU - James, S L AD - Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20814. Y1 - 1992/09/15/ PY - 1992 DA - 1992 Sep 15 SP - 8676 EP - 8680 VL - 89 IS - 18 SN - 0027-8424, 0027-8424 KW - Cytokines KW - 0 KW - Lipopolysaccharides KW - Oligodeoxyribonucleotides KW - RNA, Messenger KW - Recombinant Proteins KW - Transforming Growth Factor beta KW - Tumor Necrosis Factor-alpha KW - Interleukin-10 KW - 130068-27-8 KW - Interleukin-4 KW - 207137-56-2 KW - Nitric Oxide KW - 31C4KY9ESH KW - Acetylmuramyl-Alanyl-Isoglutamine KW - 53678-77-6 KW - Interferon-gamma KW - 82115-62-6 KW - Index Medicus KW - Transforming Growth Factor beta -- pharmacology KW - Animals KW - Cytokines -- genetics KW - Lipopolysaccharides -- administration & dosage KW - Interleukin-4 -- pharmacology KW - Gene Expression KW - Nitric Oxide -- metabolism KW - RNA, Messenger -- genetics KW - Base Sequence KW - Acetylmuramyl-Alanyl-Isoglutamine -- pharmacology KW - Oligodeoxyribonucleotides -- chemistry KW - Schistosoma mansoni -- immunology KW - Immunity, Cellular -- drug effects KW - Molecular Sequence Data KW - Macrophages -- immunology KW - Interleukin-10 -- pharmacology KW - Interferon-gamma -- pharmacology KW - Tumor Necrosis Factor-alpha -- biosynthesis KW - Cytotoxicity, Immunologic -- drug effects KW - Macrophage Activation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73183991?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Interleukin+10+inhibits+macrophage+microbicidal+activity+by+blocking+the+endogenous+production+of+tumor+necrosis+factor+alpha+required+as+a+costimulatory+factor+for+interferon+gamma-induced+activation.&rft.au=Oswald%2C+I+P%3BWynn%2C+T+A%3BSher%2C+A%3BJames%2C+S+L&rft.aulast=Oswald&rft.aufirst=I&rft.date=1992-09-15&rft.volume=89&rft.issue=18&rft.spage=8676&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Methods Enzymol. 1986;132:649-58 [3102898] Immunol Rev. 1987 Jun;97:5-27 [2957307] Biochem Biophys Res Commun. 1988 Nov 30;157(1):87-94 [3196352] Eur J Immunol. 1988 Oct;18(10):1587-92 [3142779] Immunol Rev. 1992 Jun;127:183-204 [1354651] J Immunol. 1992 Mar 15;148(6):1792-6 [1541819] J Immunol. 1992 Jun 1;148(11):3578-82 [1588047] Int Immunol. 1992 May;4(5):563-9 [1627494] J Exp Med. 1991 Oct 1;174(4):915-24 [1655948] Int Immunol. 1990;2(9):821-32 [1703785] J Immunol. 1991 Oct 1;147(7):2391-7 [1717559] J Immunol. 1992 Jan 15;148(2):568-74 [1729374] J Exp Med. 1992 Jan 1;175(1):169-74 [1730915] J Exp Med. 1991 Dec 1;174(6):1549-55 [1744584] J Immunol. 1991 May 15;146(10):3444-51 [1827484] J Immunol. 1991 Dec 1;147(11):3815-22 [1940369] J Exp Med. 1991 Nov 1;174(5):1209-20 [1940799] J Immunol. 1990 Dec 15;145(12):4290-7 [2124240] Science. 1990 Jun 8;248(4960):1230-4 [2161559] J Exp Med. 1989 Dec 1;170(6):2081-95 [2531194] J Immunol. 1989 Dec 15;143(12):4208-12 [2592772] J Immunol. 1981 Jul;127(1):179-83 [7240741] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of erythroid differentiation and fetal hemoglobin production in human leukemic cells treated with phenylacetate. AN - 73183771; 1381630 AB - There is considerable interest in identifying nontoxic differentiation inducers for the treatment of various malignant and nonmalignant blood disorders, including inborn beta-chain hemoglobinopathies. Using the human leukemic K562 cell line as a model, we explored the efficacy of phenylacetate, an amino acid derivative with a low toxicity index when administered to humans. Treatment of K562 cultures with pharmacologically attainable concentrations of phenylacetate resulted in erythroid differentiation, evident by the reduced growth rate and increased hemoglobin production. The effect was time- and dose-dependent, further augmented by glutamine starvation (phenylacetate is known to deplete circulating glutamine in vivo), and reversible upon cessation of treatment. Molecular analysis showed that phenylacetate induced gamma globin gene expression with subsequent accumulation of the fetal form of hemoglobin (HbF). Interestingly, the addition of phenylacetate to antitumor agents of clinical interest, eg, hydroxyurea and 5-azacytidine, caused superinduction of HbF biosynthesis. The results suggest that phenylacetate, used alone or in combination with other drugs, might offer a safe and effective new approach to treatment of some hematopoietic neoplasms and severe hemoglobinopathies. JF - Blood AU - Samid, D AU - Yeh, A AU - Prasanna, P AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/09/15/ PY - 1992 DA - 1992 Sep 15 SP - 1576 EP - 1581 VL - 80 IS - 6 SN - 0006-4971, 0006-4971 KW - Phenylacetates KW - 0 KW - decitabine KW - 776B62CQ27 KW - Fetal Hemoglobin KW - 9034-63-3 KW - Azacitidine KW - M801H13NRU KW - Hydroxyurea KW - X6Q56QN5QC KW - Abridged Index Medicus KW - Index Medicus KW - Azacitidine -- pharmacology KW - Leukemia, Experimental KW - Humans KW - Azacitidine -- analogs & derivatives KW - Cell Division -- drug effects KW - Cell Differentiation KW - Hydroxyurea -- pharmacology KW - Phenylacetates -- pharmacology KW - Tumor Cells, Cultured -- metabolism KW - Tumor Cells, Cultured -- drug effects KW - Fetal Hemoglobin -- biosynthesis KW - Erythroid Precursor Cells -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73183771?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+arthritis+and+rheumatism&rft.atitle=Timed+treatment+of+the+arthritic+diseases%3A+a+review+and+hypothesis.&rft.au=Vener%2C+K+J%3BReddy%2C+A&rft.aulast=Vener&rft.aufirst=K&rft.date=1992-10-01&rft.volume=22&rft.issue=2&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=Seminars+in+arthritis+and+rheumatism&rft.issn=00490172&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-13 N1 - Date created - 1992-10-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reversal by nickel(II) of inhibitory effects of some scavengers of active oxygen species upon hydroxylation of 2'-deoxyguanosine in vitro. AN - 73201466; 1327552 AB - Effects of ethanol (EtOH), mannitol (Man), L-histidine (His) and glutathione (GSH) on the oxidation of 2'-deoxyguanosine (dG) to its 8-hydroxy derivative (8-OH-dG) with H2O2 plus L-ascorbic acid (Ascb) in the absence and presence of Ni(II) were investigated in order to unveil the nature of active oxygen species involved in that oxidation. In the absence of Ni(II), production of 8-OH-dG was inhibited by His much greater than GSH greater than or equal to GSSG (oxidized glutathione) much greater than EtOH, but not by Man. The latter tended to enhance the production of 8-OH-dG. In the presence of Ni(II), the inhibition by His, GSH and GSSG, but not EtOH, was prevented. The results indicate involvement of a 'crypto-hydroxyl' radical as the dG oxidizing species in both the absence and presence of Ni(II). Also, the results provide evidence that Ni(II) complexes with His, GSH and GSSG may lack antioxidant capacity. Moreover, the Ni(II) complex with His was found capable of enhancing 8-OH-dG production by the Ascb+H2O2 system to a greater extent than Ni(II) alone. Likewise, although to a lesser extent, the formation of 8-OH-dG was enhanced by the combination of Ni(II) and Man which do not form complexes at pH 7.4. Since His is a major Ni(II) carrier in animal tissues, the dG oxidation enhancing capacity of the Ni(II) complex with His may contribute to the toxic and carcinogenic effects of Ni(II). JF - Chemico-biological interactions AU - Kasprzak, K S AU - North, S L AU - Hernandez, L AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, MD 21702. Y1 - 1992/09/14/ PY - 1992 DA - 1992 Sep 14 SP - 11 EP - 19 VL - 84 IS - 1 SN - 0009-2797, 0009-2797 KW - Free Radical Scavengers KW - 0 KW - Hydroxides KW - Hydroxyl Radical KW - 3352-57-6 KW - Ethanol KW - 3K9958V90M KW - Mannitol KW - 3OWL53L36A KW - Histidine KW - 4QD397987E KW - Nickel KW - 7OV03QG267 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Deoxyguanosine KW - G9481N71RO KW - Glutathione KW - GAN16C9B8O KW - Ascorbic Acid KW - PQ6CK8PD0R KW - Oxygen KW - S88TT14065 KW - Index Medicus KW - Oxidation-Reduction KW - Ethanol -- pharmacology KW - Hydrogen Peroxide -- metabolism KW - Hydroxides -- metabolism KW - Ascorbic Acid -- metabolism KW - Mannitol -- pharmacology KW - Glutathione -- pharmacology KW - Hydroxylation KW - Histidine -- pharmacology KW - Deoxyguanosine -- metabolism KW - Nickel -- pharmacology KW - Oxygen -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73201466?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemico-biological+interactions&rft.atitle=Reversal+by+nickel%28II%29+of+inhibitory+effects+of+some+scavengers+of+active+oxygen+species+upon+hydroxylation+of+2%27-deoxyguanosine+in+vitro.&rft.au=Kasprzak%2C+K+S%3BNorth%2C+S+L%3BHernandez%2C+L&rft.aulast=Kasprzak&rft.aufirst=K&rft.date=1992-09-14&rft.volume=84&rft.issue=1&rft.spage=11&rft.isbn=&rft.btitle=&rft.title=Chemico-biological+interactions&rft.issn=00092797&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-26 N1 - Date created - 1992-10-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Solid phase synthesis of the proteinase of bovine leukemia virus. Comparison of its specificity to that of HIV-2 proteinase. AN - 73174200; 1325379 AB - The 126-residue proteinase (PR) of bovine leukemia virus (BLV) was synthesized by solid-phase peptide synthesis and its activity was shown using various oligopeptide substrates representing cleavage sites in BLV, human T-cell leukemia virus type 1 (HTLV-1), murine leukemia virus (MuLV) and human immunodeficiency virus type 1 (HIV-1). The specificity of the BLV PR was also compared to that of chemically synthesized human immunodeficiency virus type 2 (HIV-2) PR. Many of the peptides were cleaved at the expected site, however, 6 out of 15 were hydrolyzed only by one of the PRs. Furthermore, one BLV peptide was processed differently by the two enzymes. These results, together with the relative activities and the lack of inhibition of BLV PR by two HIV-1 PR inhibitors, suggest that the BLV PR specificity is substantially different from that of HIV PRs. JF - FEBS letters AU - Bláha, I AU - Tözsér, J AU - Kim, Y AU - Copeland, T D AU - Oroszlan, S AD - Laboratory of Molecular Virology and Carcinogenesis, NCI-Frederick Cancer Research and Development Center, MD 21702. Y1 - 1992/09/14/ PY - 1992 DA - 1992 Sep 14 SP - 389 EP - 393 VL - 309 IS - 3 SN - 0014-5793, 0014-5793 KW - Endopeptidases KW - EC 3.4.- KW - Aspartic Acid Endopeptidases KW - EC 3.4.23.- KW - HIV Protease KW - p16 protease, Human immunodeficiency virus 2 KW - Index Medicus KW - AIDS/HIV KW - Sequence Alignment KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Substrate Specificity KW - Chromatography, High Pressure Liquid KW - Endopeptidases -- chemical synthesis KW - Leukemia Virus, Bovine -- enzymology KW - Endopeptidases -- metabolism KW - Aspartic Acid Endopeptidases -- metabolism KW - Aspartic Acid Endopeptidases -- chemical synthesis KW - Aspartic Acid Endopeptidases -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73174200?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+letters&rft.atitle=Solid+phase+synthesis+of+the+proteinase+of+bovine+leukemia+virus.+Comparison+of+its+specificity+to+that+of+HIV-2+proteinase.&rft.au=Bl%C3%A1ha%2C+I%3BT%C3%B6zs%C3%A9r%2C+J%3BKim%2C+Y%3BCopeland%2C+T+D%3BOroszlan%2C+S&rft.aulast=Bl%C3%A1ha&rft.aufirst=I&rft.date=1992-09-14&rft.volume=309&rft.issue=3&rft.spage=389&rft.isbn=&rft.btitle=&rft.title=FEBS+letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-06 N1 - Date created - 1992-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effect of dilauroyl-L-3-phosphatidylcholine on the interaction between cytochrome P-450 1A1 and benzo[a]pyrene. AN - 73156705; 1516694 AB - Fluorescence quenching of benzo[a]pyrene (BP) by cytochrome P-450 1A1 was used to probe the effect of the lipid, dilauroyl-L-3-phosphatidylcholine, on this substrate-enzyme interaction. In the presence of lipid, a monoclonal antibody to this P-450 maximally inhibited BP binding at an antibody-to-P-450 ratio of 1:2, corresponding to an antibody crosslinked P-450 complex. The antibody did not inhibit BP binding in the absence of lipid. These results indicate that when P-450 is subjected to the orientational constraints imposed by antibody-mediated crosslinking, the lipid alters the conformation or quaternary structure of the P-450 oligomer in a manner which changes its affinity for BP. JF - FEBS letters AU - Omata, Y AU - Friedman, F K AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09/14/ PY - 1992 DA - 1992 Sep 14 SP - 249 EP - 252 VL - 309 IS - 3 SN - 0014-5793, 0014-5793 KW - Antibodies, Monoclonal KW - 0 KW - Phosphatidylcholines KW - 1,2-dilauroylphosphatidylcholine KW - 18285-71-7 KW - Benzo(a)pyrene KW - 3417WMA06D KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Rats KW - Animals KW - Antibodies, Monoclonal -- metabolism KW - Binding, Competitive KW - Cytochrome P-450 Enzyme System -- immunology KW - Cytochrome P-450 Enzyme System -- metabolism KW - Phosphatidylcholines -- pharmacology KW - Benzo(a)pyrene -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73156705?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+letters&rft.atitle=The+effect+of+dilauroyl-L-3-phosphatidylcholine+on+the+interaction+between+cytochrome+P-450+1A1+and+benzo%5Ba%5Dpyrene.&rft.au=Omata%2C+Y%3BFriedman%2C+F+K&rft.aulast=Omata&rft.aufirst=Y&rft.date=1992-09-14&rft.volume=309&rft.issue=3&rft.spage=249&rft.isbn=&rft.btitle=&rft.title=FEBS+letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-06 N1 - Date created - 1992-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Efficacy of atovaquone in treatment of toxoplasmosis in patients with AIDS. The NIAID-Clinical Center Intramural AIDS Program. AN - 73140488; 1355212 AB - Atovaquone (formerly 566C80) is a hydroxynaphthoquinone with potent activity against Toxoplasma in vitro and in laboratory animals. Eight patients with AIDS and presumed or biopsy confirmed toxoplasmosis who were intolerant of or had not responded to standard therapies were treated with oral atovaquone 750 mg four times a day. Seven patients showed radiographic improvement; the other remained radiographically stable. Six patients died 6-60 weeks after enrollment with no clinical (six) or necropsy (three) evidence of recurrent toxoplasmosis; two patients relapsed at 10 and 32 weeks. Toxicity was mild: only one patient required temporary discontinuation of drug due to a rash. Atovaquone is a well-tolerated drug that appears to be an effective alternative for patients with toxoplasmosis who are intolerant of standard therapies. JF - Lancet (London, England) AU - Kovacs, J A AD - Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09/12/ PY - 1992 DA - 1992 Sep 12 SP - 637 EP - 638 VL - 340 IS - 8820 SN - 0140-6736, 0140-6736 KW - Anti-Infective Agents KW - 0 KW - Naphthoquinones KW - Atovaquone KW - Y883P1Z2LT KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Magnetic Resonance Imaging KW - Administration, Oral KW - Humans KW - Adult KW - Enzyme-Linked Immunosorbent Assay KW - Middle Aged KW - Biopsy KW - Recurrence KW - Male KW - Naphthoquinones -- therapeutic use KW - Anti-Infective Agents -- therapeutic use KW - Acquired Immunodeficiency Syndrome -- complications KW - Naphthoquinones -- administration & dosage KW - Naphthoquinones -- pharmacology KW - Toxoplasmosis, Cerebral -- drug therapy KW - Anti-Infective Agents -- administration & dosage KW - Toxoplasmosis, Cerebral -- etiology KW - Anti-Infective Agents -- pharmacology KW - Toxoplasmosis, Cerebral -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73140488?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lancet+%28London%2C+England%29&rft.atitle=Efficacy+of+atovaquone+in+treatment+of+toxoplasmosis+in+patients+with+AIDS.+The+NIAID-Clinical+Center+Intramural+AIDS+Program.&rft.au=Kovacs%2C+J+A&rft.aulast=Kovacs&rft.aufirst=J&rft.date=1992-09-12&rft.volume=340&rft.issue=8820&rft.spage=637&rft.isbn=&rft.btitle=&rft.title=Lancet+%28London%2C+England%29&rft.issn=01406736&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-01 N1 - Date created - 1992-10-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Multitarget-ribozyme directed to cleave at up to nine highly conserved HIV-1 env RNA regions inhibits HIV-1 replication--potential effectiveness against most presently sequenced HIV-1 isolates. AN - 19713262; 8744700 AB - Several mono-, di-, tetra-, penta- and nonaribozymes were developed. These multitarget-ribozymes were targeted to cleave HIV-1 env RNA at up to nine different conserved sites. Each multitarget-ribozyme consisted of a chain of up to nine hammerhead motifs, each flanked by a different targeting sequence. The multitarget-ribozymes were functional in vitro and gave rise to multiple, specific partial and/or complete RNA digestion products. Per RNA copy, multitarget-ribozymes were more efficient than monoribozymes or ribozymes targeting a subset of the same sites. In contrast to monoribozymes, a 400nt nonaribozyme, targeted to cleave at nine different sites within a 1.3kb HIV-1 env RNA substrate, was active and showed the same specificity of cleavage when it was part of a large 3.3kb transcript. We conclude that multitarget-ribozymes retain the specificity of monoribozymes, but they are more efficient per ribozyme RNA copy and they remain active when they are part of a large transcript. A tetra-, penta- or nonaribozyme under control of the SV40 late promoter, the beta-actin gene promoter or the HIV-1 LTR, respectively, were cotransfected with the infectious HIV-1 DNA clone pNL4-3 into permissive HeLa T4 cells. Each cotransfection resulted in a specific inhibition of HIV-1 replication as determined by syncytia formation and p24 antigen release. In addition, coexpression of the nonaribozyme with an HIV-1 env RNA transcript resulted in the specific dramatic reduction of the env transcript. We conclude that the multitarget-ribozymes are also functional intracellularly. A nucleotide sequence comparison of the target sites indicates that the multitarget-ribozymes could potentially be effective against all thirty HIV-1 isolates presently sequenced. Their use may help to slow the selection of viral escape mutants and thereby prolong their effectiveness. We anticipate that multitarget-ribozymes will also be more effective in the successful targeting of less variable cellular RNAs. Images JF - Nucleic Acids Research AU - Chen, C J AU - Banerjea, A C AU - Harmison, G G AU - Haglund, K AU - Schubert, M AD - Laboratory of Viral and Molecular Pathogenesis, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09/11/ PY - 1992 DA - 1992 Sep 11 SP - 4581 EP - 4589 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 20 IS - 17 SN - 0305-1048, 0305-1048 KW - Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - p24 protein KW - Replication KW - Nucleotide sequence KW - Transcription KW - Digestion KW - Promoters KW - RNA KW - Human immunodeficiency virus 1 KW - Simian virus 40 KW - DNA KW - Syncytia KW - Actin KW - Ribozymes KW - V 22360:AIDS and HIV KW - W 30940:Products KW - N 14815:Nucleotide Sequence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19713262?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+Acids+Research&rft.atitle=Multitarget-ribozyme+directed+to+cleave+at+up+to+nine+highly+conserved+HIV-1+env+RNA+regions+inhibits+HIV-1+replication--potential+effectiveness+against+most+presently+sequenced+HIV-1+isolates.&rft.au=Chen%2C+C+J%3BBanerjea%2C+A+C%3BHarmison%2C+G+G%3BHaglund%2C+K%3BSchubert%2C+M&rft.aulast=Chen&rft.aufirst=C&rft.date=1992-09-11&rft.volume=20&rft.issue=17&rft.spage=4581&rft.isbn=&rft.btitle=&rft.title=Nucleic+Acids+Research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2008-12-01 N1 - Last updated - 2015-03-27 N1 - SubjectsTermNotLitGenreText - Digestion; p24 protein; Promoters; RNA; Replication; Nucleotide sequence; DNA; Syncytia; Transcription; Actin; Ribozymes; Human immunodeficiency virus 1; Simian virus 40 ER - TY - JOUR T1 - Sequence of a rat TIS11 cDNA, an immediate early gene induced by growth factors and phorbol esters. AN - 73156957; 1511903 AB - We report here the nucleotide sequence of a rat TIS11 cDNA, an immediate early gene, induced by nerve growth factor and epidermal growth factor, by 12-O-tetradecanoyl phorbol-13-acetate, and other stimuli in PC12 pheochromocytoma cells. The deduced protein consists of 320 amino acid residues with two tandem repeats of a putative Zn(2+)-finger motif. JF - Gene AU - Kaneda, N AU - Oshima, M AU - Chung, S Y AU - Guroff, G AD - Section on Growth Factors, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09/10/ PY - 1992 DA - 1992 Sep 10 SP - 289 EP - 291 VL - 118 IS - 2 SN - 0378-1119, 0378-1119 KW - DNA-Binding Proteins KW - 0 KW - Growth Substances KW - Immediate-Early Proteins KW - Proteins KW - RNA, Messenger KW - Tristetraprolin KW - Zfp36 protein, rat KW - DNA KW - 9007-49-2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Rats KW - Animals KW - Base Sequence KW - Tumor Cells, Cultured KW - DNA -- genetics KW - Molecular Sequence Data KW - Amino Acid Sequence KW - RNA, Messenger -- genetics KW - Proteins -- chemistry KW - Zinc Fingers -- genetics KW - Growth Substances -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Gene Expression Regulation -- drug effects KW - Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73156957?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene&rft.atitle=Sequence+of+a+rat+TIS11+cDNA%2C+an+immediate+early+gene+induced+by+growth+factors+and+phorbol+esters.&rft.au=Kaneda%2C+N%3BOshima%2C+M%3BChung%2C+S+Y%3BGuroff%2C+G&rft.aulast=Kaneda&rft.aufirst=N&rft.date=1992-09-10&rft.volume=118&rft.issue=2&rft.spage=289&rft.isbn=&rft.btitle=&rft.title=Gene&rft.issn=03781119&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-30 N1 - Date created - 1992-09-30 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - X63369; GENBANK; M74892; M79310; M74891; S43293; S43295; S43286; M90357; S43297; M79309 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The study of markers of biological effect in cancer prevention research trials. AN - 73185104; 1521908 AB - Biological markers may provide a valuable tool for the development of cancer prevention agents, for monitoring patient compliance to a selected intervention, or for further defining the carcinogenic process. This discussion focuses on markers of biological effect and the rationale for their use in cancer prevention trials. Recent studies with biological markers are investigating their incorporation into phase-I, -II, and -III chemoprevention clinical trial designs. Their use in clinical studies is expected to increase the number of agents that may be evaluated and to provide valuable information on the biological effectiveness of agents, doses, and schedules. Markers may also provide information to help in selecting high-risk groups for prevention research, and to indicate the pathways inhibited and the stage of carcinogenesis affected. Such information may prove of crucial importance in strengthening the rationale for long-term trials and other ancillary research. Biomarker research for colon carcinogenesis is discussed, including examples of a number of recent trials that may influence future progress in this area of prevention research. A crucial step in this process is marker validation as an aspect of major prospective observational and intervention studies where cancer incidence is the endpoint. We cannot be fully confident of markers as intermediate endpoints until the evidence from clinical trials is sufficiently strong to support major public health initiatives for prevention. JF - International journal of cancer AU - Greenwald, P AU - Witkin, K M AU - Malone, W F AU - Byar, D P AU - Freedman, L S AU - Stern, H R AD - Division of Cancer Prevention and Control, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09/09/ PY - 1992 DA - 1992 Sep 09 SP - 189 EP - 196 VL - 52 IS - 2 SN - 0020-7136, 0020-7136 KW - Antineoplastic Agents KW - 0 KW - Biomarkers, Tumor KW - Index Medicus KW - Sensitivity and Specificity KW - Drug Evaluation KW - Colonic Neoplasms -- genetics KW - Patient Compliance KW - Colon -- pathology KW - Cell Transformation, Neoplastic -- chemistry KW - Risk Factors KW - Humans KW - Prognosis KW - Clinical Trials as Topic KW - Intestinal Mucosa -- pathology KW - Research KW - Antineoplastic Agents -- therapeutic use KW - Precancerous Conditions -- chemistry KW - Biomarkers, Tumor -- analysis KW - Neoplasms -- prevention & control KW - Precancerous Conditions -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73185104?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=The+study+of+markers+of+biological+effect+in+cancer+prevention+research+trials.&rft.au=Greenwald%2C+P%3BWitkin%2C+K+M%3BMalone%2C+W+F%3BByar%2C+D+P%3BFreedman%2C+L+S%3BStern%2C+H+R&rft.aulast=Greenwald&rft.aufirst=P&rft.date=1992-09-09&rft.volume=52&rft.issue=2&rft.spage=189&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=00207136&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-13 N1 - Date created - 1992-10-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prescription drug diversion control and medical practice. AN - 73131286; 1507377 AB - Concern about the role of prescription drug diversion in drug abuse has led to demands for more stringent regulation and for better ways to detect prescription drug diversion. Advances in technology now allow point-of-sale computer systems to report prescriptions filled by pharmacies to state agencies rapidly and possibly more economically. However, the advantages of more comprehensive control systems must be balanced against their possible effects on medical practice and patient care. Our limited knowledge about prescription drug diversion and the impact of diversion control systems on medical practice is summarized. Needed research is outlined together with the components of a diversion control program that balances reducing drug diversion with minimizing adverse effects on medical practice and patient care. We stress the need for broadly defined practice parameters and peer review by medical experts thoroughly familiar with the complexities of medical practice. JF - JAMA AU - Cooper, J R AU - Czechowicz, D J AU - Petersen, R C AU - Molinari, S P AD - National Institute on Drug Abuse, Rockville, MD. Y1 - 1992/09/09/ PY - 1992 DA - 1992 Sep 09 SP - 1306 EP - 1310 VL - 268 IS - 10 SN - 0098-7484, 0098-7484 KW - Abridged Index Medicus KW - Index Medicus KW - United States KW - Humans KW - Health Services Research KW - Databases, Factual KW - Online Systems KW - Practice Management, Medical KW - Drug Utilization KW - Drug and Narcotic Control -- legislation & jurisprudence KW - Drug Prescriptions KW - Substance-Related Disorders -- prevention & control KW - Clinical Pharmacy Information Systems -- legislation & jurisprudence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73131286?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=JAMA&rft.atitle=Prescription+drug+diversion+control+and+medical+practice.&rft.au=Cooper%2C+J+R%3BCzechowicz%2C+D+J%3BPetersen%2C+R+C%3BMolinari%2C+S+P&rft.aulast=Cooper&rft.aufirst=J&rft.date=1992-09-09&rft.volume=268&rft.issue=10&rft.spage=1306&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-22 N1 - Date created - 1992-09-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Functional expression of renal organic anion transport in Xenopus laevis oocytes. AN - 73387559; 1281263 AB - Secretion of organic anions by the kidney plays a critical role in the elimination of toxic agents from the body. Recent findings in isolated membranes and intact tissue have demonstrated the participation of multiple transport proteins in this process. As a first step toward molecular characterization of these proteins through expression cloning, the studies reported below demonstrate functional expression of both fumarate- and lithium-sensitive glutarate and probenecid-sensitive p-aminohippurate transport in Xenopus oocytes injected with rat kidney poly(A)+ RNA. Maximal increase in substrate uptake over buffer-injected controls was reached by 5 days after mRNA injection. Expression of size-fractionated mRNA indicated that the active species with respect to both transport activities were in the range of 1.8 to 3.5 kb. JF - Molecular and cellular biochemistry AU - Wolff, N A AU - Philpot, R M AU - Miller, D S AU - Pritchard, J B AD - Laboratory of Cellular and Molecular Pharmacology, NIH/National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/09/08/ PY - 1992 DA - 1992 Sep 08 SP - 35 EP - 41 VL - 114 IS - 1-2 SN - 0300-8177, 0300-8177 KW - Anions KW - 0 KW - Glutarates KW - Ion Channels KW - RNA, Messenger KW - p-Aminohippuric Acid KW - Y79XT83BJ9 KW - Index Medicus KW - Rats KW - Xenopus laevis KW - Animals KW - Glutarates -- metabolism KW - Biological Transport KW - p-Aminohippuric Acid -- metabolism KW - Microinjections KW - RNA, Messenger -- genetics KW - Oocytes -- metabolism KW - Kidney -- physiology KW - Anions -- metabolism KW - Ion Channels -- genetics KW - Ion Channels -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73387559?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+cellular+biochemistry&rft.atitle=Functional+expression+of+renal+organic+anion+transport+in+Xenopus+laevis+oocytes.&rft.au=Wolff%2C+N+A%3BPhilpot%2C+R+M%3BMiller%2C+D+S%3BPritchard%2C+J+B&rft.aulast=Wolff&rft.aufirst=N&rft.date=1992-09-08&rft.volume=114&rft.issue=1-2&rft.spage=35&rft.isbn=&rft.btitle=&rft.title=Molecular+and+cellular+biochemistry&rft.issn=03008177&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-08 N1 - Date created - 1993-01-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A leucine----proline mutation in the H1 subdomain of keratin 1 causes epidermolytic hyperkeratosis. AN - 73152605; 1381288 AB - Epidermolytic hyperkeratosis is an autosomal dominant disorder affecting the structural integrity of the suprabasal layers of human epidermis. We have recently documented in one family linkage of the disease phenotype to the cluster of type II keratins. We have now identified a leucine----proline amino acid substitution in the conserved H1 subdomain of keratin 1 that is present only in affected family members. Using a quantitative assay and electron microscopy with synthetic peptides, we show that, whereas the wild-type H1 peptide rapidly disassembles preformed keratin filaments in vitro, the mutant peptide does this far less efficiently. Therefore the mutation in keratin 1 is likely to cause defective keratin filaments and hence a defective cytoskeleton in the epidermal cells in vivo. JF - Cell AU - Chipev, C C AU - Korge, B P AU - Markova, N AU - Bale, S J AU - DiGiovanna, J J AU - Compton, J G AU - Steinert, P M AD - Skin Biology Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09/04/ PY - 1992 DA - 1992 Sep 04 SP - 821 EP - 828 VL - 70 IS - 5 SN - 0092-8674, 0092-8674 KW - Keratins KW - 68238-35-7 KW - Proline KW - 9DLQ4CIU6V KW - Leucine KW - GMW67QNF9C KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Intermediate Filaments -- chemistry KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Keratins -- genetics KW - Ichthyosiform Erythroderma, Congenital -- pathology KW - Ichthyosiform Erythroderma, Congenital -- etiology KW - Ichthyosiform Erythroderma, Congenital -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73152605?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell&rft.atitle=A+leucine----proline+mutation+in+the+H1+subdomain+of+keratin+1+causes+epidermolytic+hyperkeratosis.&rft.au=Chipev%2C+C+C%3BKorge%2C+B+P%3BMarkova%2C+N%3BBale%2C+S+J%3BDiGiovanna%2C+J+J%3BCompton%2C+J+G%3BSteinert%2C+P+M&rft.aulast=Chipev&rft.aufirst=C&rft.date=1992-09-04&rft.volume=70&rft.issue=5&rft.spage=821&rft.isbn=&rft.btitle=&rft.title=Cell&rft.issn=00928674&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-07 N1 - Date created - 1992-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Predicting responses of nonlinear neurons in monkey striate cortex to complex patterns. AN - 85233499; pmid-1527596 AB - The overwhelming majority of neurons in primate visual cortex are nonlinear. For those cells, the techniques of linear system analysis, used with some success to model retinal ganglion cells and striate simple cells, are of limited applicability. As a start toward understanding the properties of nonlinear visual neurons, we have recorded responses of striate complex cells to hundreds of images, including both simple stimuli (bars and sinusoids) as well as complex stimuli (random textures and 3-D shaded surfaces). The latter set tended to give the strongest response. We created a neural network model for each neuron using an iterative optimization algorithm. The recorded responses to some stimulus patterns (the training set) were used to create the model, while responses to other patterns were reserved for testing the networks. The networks predicted recorded responses to training set patterns with a median correlation of 0.95. They were able to predict responses to test stimuli not in the training set with a correlation of 0.78 overall, and a correlation of 0.65 for complex stimuli considered alone. Thus, they were able to capture much of the input/output transfer function of the neurons, even for complex patterns. Examining connection strengths within each network, different parts of the network appeared to handle information at different spatial scales. To gain further insights, the network models were inverted to construct "optimal" stimuli for each cell, and their receptive fields were mapped with high-resolution spots. The receptive field properties of complex cells could not be reduced to any simpler mathematical formulation than the network models themselves. JF - The Journal of Neuroscience AU - Lehky, S R AU - Sejnowski, T J AU - Desimone, R AD - Laboratory of Neuropsychology, National Institute of Mental Health, Bethesda, Maryland 20892. PY - 1992 SP - 3568 EP - 3581 VL - 12 IS - 9 SN - 0270-6474, 0270-6474 KW - Visual Cortex KW - Photic Stimulation KW - Neural Networks (Computer) KW - Neurons KW - Animal KW - Support, Non-U.S. Gov't KW - Forecasting KW - Macaca mulatta KW - Female KW - Nerve Net KW - Visual Perception UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85233499?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+Neuroscience&rft.atitle=Predicting+responses+of+nonlinear+neurons+in+monkey+striate+cortex+to+complex+patterns.&rft.au=Lehky%2C+S+R%3BSejnowski%2C+T+J%3BDesimone%2C+R&rft.aulast=Lehky&rft.aufirst=S&rft.date=1992-09-01&rft.volume=12&rft.issue=9&rft.spage=3568&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Neuroscience&rft.issn=02706474&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Dissociations among memory measures in memory-impaired subjects: evidence for a processing account of memory. AN - 85216382; pmid-1453972 AB - Deficits in conceptual transfer on both implicit and explicit memory tests were obtained for memory-impaired temporal lobe epileptic (TLE) subjects in three studies. In Experiment 1, in which a generate-read paradigm was employed, memory-impaired TLEs failed to show normal generation effects on conceptually driven tests of semantic cued recall and general knowledge questions, although their data-driven memory as measured by word-fragment completion and graphemic cued recall tasks was normal. In Experiment 2, memory-impaired patients having left temporal lobe seizure foci were tested on these four tasks and compared with nonimpaired TLEs having right temporal foci. The left TLEs showed deficits on conceptually driven tasks and normal memory for data-driven tests. These findings were extended in Experiment 3, in which left TLE patients failed to show any benefit from blocked study, as compared with random study, on category production and semantic cued-recall tests, although right TLEs and normal controls showed blocking effects on both tasks. These findings may be accommodated by a processing framework of memory in which memory-impaired patients are characterized as having deficits in conceptual, but not in data-driven, processing capabilities. JF - Memory and Cognition AU - Blaxton, T A AD - National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892. PY - 1992 SP - 549 EP - 562 VL - 20 IS - 5 SN - 0090-502X, 0090-502X KW - Wechsler Scales KW - Human KW - Adult KW - Word Association Tests KW - Neuropsychological Tests KW - Research Design KW - Female KW - Male KW - Memory Disorders UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85216382?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Memory+and+Cognition&rft.atitle=Dissociations+among+memory+measures+in+memory-impaired+subjects%3A+evidence+for+a+processing+account+of+memory.&rft.au=Blaxton%2C+T+A&rft.aulast=Blaxton&rft.aufirst=T&rft.date=1992-09-01&rft.volume=20&rft.issue=5&rft.spage=549&rft.isbn=&rft.btitle=&rft.title=Memory+and+Cognition&rft.issn=0090502X&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Cyclic cortical reorganization during early childhood. AN - 85209883; pmid-1389121 AB - EEG coherence was computed from 8 left and 8 right intrahemispheric electrode pairs from 253 children ranging in mean age from 6 months to 7 years. The first derivative of mean coherence was computed in order to study growth spurts or rapid changes in mean coherence over the early childhood period. Growth spurts in EEG coherence were approximately 6 months to 1 year in duration and involved a cyclical process composed of a sequential lengthening of intracortical connections in the left hemisphere and a sequential contraction of intracortical connections in the right hemisphere. Each growth spurt cycle had a period of approximately 2 to 4 years and involved both a rostral-caudal expansion and contraction as well as a lateral-to-medial rotation. Data support the view that the functions of the left and right hemisphere are established early in human development through complementary developmental sequences and that these sequences appear to recapitulate differences in adult hemispheric function. JF - Brain and Cognition AU - Thatcher, R W AD - Clinical Neuroscience Program, National Institutes of Health, National Institutes of Neurological Disorders and Stroke, Bethesda, MD 20892. PY - 1992 SP - 24 EP - 50 VL - 20 IS - 1 SN - 0278-2626, 0278-2626 KW - Synapses KW - Age Factors KW - Sex Factors KW - Human KW - Electroencephalography KW - Infant, Newborn KW - Child KW - Child, Preschool KW - Cerebral Cortex KW - Frontal Lobe KW - Infant KW - Neural Pathways KW - Child Development KW - Models, Neurological KW - Laterality KW - Male KW - Female UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85209883?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+and+Cognition&rft.atitle=Cyclic+cortical+reorganization+during+early+childhood.&rft.au=Thatcher%2C+R+W&rft.aulast=Thatcher&rft.aufirst=R&rft.date=1992-09-01&rft.volume=20&rft.issue=1&rft.spage=24&rft.isbn=&rft.btitle=&rft.title=Brain+and+Cognition&rft.issn=02782626&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Clinical, pathologic, and biochemical features of a cholesterol lipidosis accompanied by hyperlipidemia and xanthomas. AN - 85161384; pmid-1513468 AB - We describe the unique clinical and histopathologic features of a child with biochemical and immunocytochemical features of Niemann-Pick disease type C (NPC). Clinically, she was found to have multiple xanthomas of the upper aerodigestive tract with dysphagia and expressive language delay, splenomegaly, bony infarcts, and type IIb hyperlipidemia. Neurologic examination was otherwise normal. Microscopy revealed foam cells in her bone marrow, liver, tongue, tonsils, glottis, and in normal-appearing peritonsillar mucosa. Lipid analysis of a liver biopsy specimen showed a small increase in phospholipids, a twofold increase in sphingomyelin, a fivefold increase in cholesterol, and a marked (25-fold) increase in bis(monoacylglycerol) phosphate. Lysosomal acid hydrolase activities in cultured skin fibroblasts were nondiagnostic. Biochemical and immunocytochemical studies of cultured fibroblasts demonstrated lysosomal accumulation of unesterified LDL-derived cholesterol as well as delayed induction of homeostatic responses to endogenous cholesterol consistent with a diagnosis of NPC. Based upon these observations, we speculate that this patient could have a new phenotypic expression of NPC or represents a new cholesterol lipidosis biochemically resembling NPC. The chance occurrence of two separate lipid disorders seems less likely. JF - Neurology AU - Filling-Katz, M R AU - Miller, S P AU - Merrick, H F AU - Travis, W D AU - Gregg, R E AU - Tsokos, M AU - Comly, M AU - Kaneski, C R AU - Mackie, S AU - Lebovics, R S AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892. PY - 1992 SP - 1768 EP - 1774 VL - 42 IS - 9 SN - 0028-3878, 0028-3878 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85161384?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurology&rft.atitle=Clinical%2C+pathologic%2C+and+biochemical+features+of+a+cholesterol+lipidosis+accompanied+by+hyperlipidemia+and+xanthomas.&rft.au=Filling-Katz%2C+M+R%3BMiller%2C+S+P%3BMerrick%2C+H+F%3BTravis%2C+W+D%3BGregg%2C+R+E%3BTsokos%2C+M%3BComly%2C+M%3BKaneski%2C+C+R%3BMackie%2C+S%3BLebovics%2C+R+S&rft.aulast=Filling-Katz&rft.aufirst=M&rft.date=1992-09-01&rft.volume=42&rft.issue=9&rft.spage=1768&rft.isbn=&rft.btitle=&rft.title=Neurology&rft.issn=00283878&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Selective amplification and partial sequencing of cDNAs encoding G protein alpha subunits from cochlear tissues. AN - 85156007; pmid-1429253 AB - An approach utilizing the polymerase chain reaction (PCR) was devised to clone members of a family of cDNAs encoding the alpha subunit of G proteins in the cochlea. RNA was extracted from the whole cochlea of the mouse and from the organ of Corti or the lateral wall of the cochlea microdissected from the guinea pig cochlea. The RNA was reverse-transcribed to cDNA which was selectively amplified by PCR using degenerate primers corresponding to two conserved regions of the G protein coding sequence. PCR products were cloned into a plasmid for sequencing. The following seven cDNA clones of particular interest were obtained: three clones putatively coding for part of the alpha-subunit of a stimulatory G protein (Gs), one clone putatively coding for part of the alpha-subunit of an inhibitory G protein (Gi) and three clones putatively coding for part of the alpha-subunit of a transducin (Gi)-like protein. Possible functions in the cochlea of putative G proteins with alpha-subunits partly encoded by these cDNA clones are briefly discussed and future studies are suggested. JF - Hearing Research AU - Tachibana, M AU - Wilcox, E AU - Yokotani, N AU - Schneider, M AU - Fex, J AD - Laboratory of Molecular Biology, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 82 EP - 88 VL - 62 IS - 1 SN - 0378-5955, 0378-5955 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85156007?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hearing+Research&rft.atitle=Selective+amplification+and+partial+sequencing+of+cDNAs+encoding+G+protein+alpha+subunits+from+cochlear+tissues.&rft.au=Tachibana%2C+M%3BWilcox%2C+E%3BYokotani%2C+N%3BSchneider%2C+M%3BFex%2C+J&rft.aulast=Tachibana&rft.aufirst=M&rft.date=1992-09-01&rft.volume=62&rft.issue=1&rft.spage=82&rft.isbn=&rft.btitle=&rft.title=Hearing+Research&rft.issn=03785955&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Construction of a cDNA library from microdissected guinea pig organ of Corti. AN - 85155700; pmid-1358871 AB - Poly (A) RNA was isolated from microdissected guinea pig organ of Corti and converted into cDNA with RNase H- murine leukemia virus reverse transcriptase. After size fractionation, the cDNA was directionally ligated into the vector pSPORT 1 and the plasmids were transformed into DH10B E. coli via electroporation. The library was found to have 3.35 x 10(6) independent colonies with ten percent of the colonies lacking an insert. After checking 33 randomly selected colonies for inserts, the average insert size was 1218 base pairs, ranging from 3300 base pairs to 400 base pairs. The library was screened with a beta-actin oligonucleotide probe and 1.4% of the colonies contained an insert hybridizing to the probe. JF - Hearing Research AU - Wilcox, E R AU - Fex, J AD - Laboratory of Molecular Biology, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland 20892. PY - 1992 SP - 124 EP - 126 VL - 62 IS - 1 SN - 0378-5955, 0378-5955 KW - Oligonucleotide Probes KW - RNA, Messenger KW - Animals KW - Poly A KW - Base Sequence KW - Guinea Pigs KW - Actins KW - DNA KW - Molecular Sequence Data KW - Organ of Corti KW - Plasmids KW - Gene Library UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85155700?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hearing+Research&rft.atitle=Construction+of+a+cDNA+library+from+microdissected+guinea+pig+organ+of+Corti.&rft.au=Wilcox%2C+E+R%3BFex%2C+J&rft.aulast=Wilcox&rft.aufirst=E&rft.date=1992-09-01&rft.volume=62&rft.issue=1&rft.spage=124&rft.isbn=&rft.btitle=&rft.title=Hearing+Research&rft.issn=03785955&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - CONF T1 - The role of biological markers in epidemiological research: future directions. AN - 73583747; 1363834 JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology AU - Iwamoto, K AU - Obrams, G I AU - Schottenfeld, D Y1 - 1992 PY - 1992 DA - 1992 SP - 519 EP - 522 VL - 1 IS - 6 KW - Biomarkers KW - 0 KW - Carcinogens KW - Hormones KW - Index Medicus KW - Smoking KW - Hormones -- analysis KW - Disease Susceptibility KW - Humans KW - Forecasting KW - Carcinogens -- analysis KW - Diet KW - Neoplasms -- chemistry KW - Biomarkers -- analysis KW - Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73583747?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.atitle=The+role+of+biological+markers+in+epidemiological+research%3A+future+directions.&rft.au=Iwamoto%2C+K%3BObrams%2C+G+I%3BSchottenfeld%2C+D&rft.aulast=Iwamoto&rft.aufirst=K&rft.date=1992-09-01&rft.volume=1&rft.issue=6&rft.spage=519&rft.isbn=&rft.btitle=&rft.title=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.issn=10559965&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-17 N1 - Date created - 1993-06-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Allelic frequency of a p53 polymorphism in human lung cancer. AN - 73522303; 1302561 AB - p53 is a tumor suppressor gene that is mutated in diverse tumor types. Here we report the frequencies of common polymorphic variants at codon 72 of the p53 gene in germline DNA of lung cancer cases and controls as determined by a polymerase chain reaction strategy. The observed allelic distribution was found to be significantly different between African-Americans and Caucasians in this U.S. population. The frequency of polymorphic variants was similar in lung cancer cases and controls after adjustment for race. However, among lung cancer patients the proline variant at codon 72 was in excess in adenocarcinoma patients by comparison with other histologies. JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology AU - Weston, A AU - Perrin, L S AU - Forrester, K AU - Hoover, R N AU - Trump, B F AU - Harris, C C AU - Caporaso, N E AD - Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda 20892. PY - 1992 SP - 481 EP - 483 VL - 1 IS - 6 SN - 1055-9965, 1055-9965 KW - Codon KW - 0 KW - DNA, Neoplasm KW - Arginine KW - 94ZLA3W45F KW - Proline KW - 9DLQ4CIU6V KW - Index Medicus KW - Codon -- genetics KW - Homozygote KW - Humans KW - Adenocarcinoma -- genetics KW - European Continental Ancestry Group -- genetics KW - Lung Diseases, Obstructive -- genetics KW - Proline -- genetics KW - Exons -- genetics KW - Genotype KW - African Continental Ancestry Group -- genetics KW - Arginine -- genetics KW - Heterozygote KW - Case-Control Studies KW - DNA, Neoplasm -- genetics KW - Middle Aged KW - Carcinoma -- genetics KW - Alleles KW - Gene Frequency KW - Polymorphism, Genetic KW - Genes, p53 -- genetics KW - Lung Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73522303?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.atitle=Allelic+frequency+of+a+p53+polymorphism+in+human+lung+cancer.&rft.au=Weston%2C+A%3BPerrin%2C+L+S%3BForrester%2C+K%3BHoover%2C+R+N%3BTrump%2C+B+F%3BHarris%2C+C+C%3BCaporaso%2C+N+E&rft.aulast=Weston&rft.aufirst=A&rft.date=1992-09-01&rft.volume=1&rft.issue=6&rft.spage=481&rft.isbn=&rft.btitle=&rft.title=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.issn=10559965&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-17 N1 - Date created - 1993-06-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effects of a non-competitive NMDA receptor antagonist, MK-801, on behavioral hyperalgesia and dorsal horn neuronal activity in rats with unilateral inflammation. AN - 73384771; 1454389 AB - The involvement of NMDA receptors in rats with peripheral inflammation and hyperalgesia was evaluated by administration of the non-competitive NMDA receptor antagonist, MK-801. Inflammation and hyperalgesia was induced by intradermal injection of complete Freund's adjuvant (CFA) or carrageenan into the left hind paw. The latency of paw withdrawal from a thermal stimulus was used as a measure of hyperalgesia in awake rats. MK-801 (1.6 mg/kg, i.p., or 31.5 micrograms, intrathecal) significantly attenuated thermal hyperalgesia and reduced its duration in comparison to saline-injected rats (P less than 0.05). The receptive field size of nociceptive-specific and wide-dynamic-range neurons in the superficial and deep spinal dorsal horn recorded 24 h after injection of CFA was significantly reduced to 73 +/- 6% (P less than 0.05, n = 8) and 74 +/- 4% (P less than 0.05, n = 8) of control values, respectively, by a cumulative dose of 3 mg/kg of MK-801 (i.v.). MK-801 (2 mg/kg) prevented the expansion of the receptive fields of dorsal horn neurons recorded 5 +/- 0.4 h (n = 5) after intradermal injection of CFA as compared to saline-injected rats (P less than 0.05). MK-801 had no significant effect on receptive field size of dorsal horn neurons in rats without CFA-induced inflammation but blocked a transient expansion of the receptive fields induced by 1 Hz, C-fiber intensity electrical stimulation of the sciatic nerve. The background activity and noxious heat-evoked response of dorsal horn neurons in rats with CFA-induced inflammation were primarily inhibited and noxious pinch-evoked activity was both facilitated and inhibited by the administration of MK-801. These results support the hypothesis that NMDA receptors are involved in the dorsal horn neuronal plasticity and behavioral hyperalgesia that follows peripheral tissue inflammation. JF - Pain AU - Ren, K AU - Hylden, J L AU - Williams, G M AU - Ruda, M A AU - Dubner, R AD - Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 331 EP - 344 VL - 50 IS - 3 SN - 0304-3959, 0304-3959 KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - Freund's Adjuvant KW - 9007-81-2 KW - Index Medicus KW - Rats KW - Animals KW - Neurons -- drug effects KW - Neurons -- physiology KW - Pain KW - Physical Stimulation KW - Electric Stimulation KW - Male KW - Behavior, Animal -- drug effects KW - Hyperalgesia -- physiopathology KW - Spinal Cord -- drug effects KW - Myelitis -- chemically induced KW - Spinal Cord -- pathology KW - Myelitis -- physiopathology KW - Myelitis -- pathology KW - Dizocilpine Maleate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73384771?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pain&rft.atitle=The+effects+of+a+non-competitive+NMDA+receptor+antagonist%2C+MK-801%2C+on+behavioral+hyperalgesia+and+dorsal+horn+neuronal+activity+in+rats+with+unilateral+inflammation.&rft.au=Ren%2C+K%3BHylden%2C+J+L%3BWilliams%2C+G+M%3BRuda%2C+M+A%3BDubner%2C+R&rft.aulast=Ren&rft.aufirst=K&rft.date=1992-09-01&rft.volume=50&rft.issue=3&rft.spage=331&rft.isbn=&rft.btitle=&rft.title=Pain&rft.issn=03043959&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-06 N1 - Date created - 1993-01-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential expression of carboxyl terminal derivatives of amyloid precursor protein among cell lines. AN - 73357065; 1453480 AB - Understanding the pathway for amyloid percursor protein (APP) catabolism has become an important line of investigation. APP is a ubiquitous membrane bound protein that is rapidly cleaved at the membrane, yielding a secreted protein identical to protease nexin II and an internalized 11.5 kDa 100 residue C terminal derivative (CTD). The levels of CTDs in a variety of cell lines have been examined and were found to differ. Cell types associated with the pathology of Alzheimer's disease (AD), such as olfactory neuroblasts (ON) and cortical vascular endothelial cells, have higher levels of CTDs than lymphoblasts and melanoma cells. The mechanism of CTD catabolism appears to involve the lysosome because blockade of lysosomal but not endosomal or mitochondrial function results in increased levels of CTDs. Under these conditions, production of larger, amyloidogenic CTDs is also seen. In cells possessing higher levels of CTDs we find that the mechanism for production of amyloidogenic CTDs may involve the internalization of intact full-length APP. Thus, inhibition of the lysosomal system appears capable of generating amyloidogenic peptides. The amount of amyloidogenic peptides appears to vary among cell lines. Such variation may shed light on why amyloid accumulates around specific cell types such as vascular endothelial cells, neurons, and glia. Finally, disfunction of the lysosomal system may play a role in the pathogenesis of Alzheimer's disease. JF - Journal of neuroscience research AU - Wolozin, B AU - Bacic, M AU - Merrill, M J AU - Lesch, K P AU - Chen, C AU - Lebovics, R S AU - Sunderland, T AD - Laboratory of Clinical Science, NIMH, Bethesda, MD 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 163 EP - 169 VL - 33 IS - 1 SN - 0360-4012, 0360-4012 KW - Amyloid beta-Protein Precursor KW - 0 KW - Antimetabolites KW - Chloroquine KW - 886U3H6UFF KW - Monensin KW - 906O0YJ6ZP KW - Index Medicus KW - Antimetabolites -- pharmacology KW - Immunoblotting KW - Humans KW - Chloroquine -- metabolism KW - Monensin -- pharmacology KW - Lysosomes -- metabolism KW - Lysosomes -- drug effects KW - Alzheimer Disease -- metabolism KW - Immunohistochemistry KW - Cell Line KW - Alzheimer Disease -- pathology KW - Neurons -- metabolism KW - Neurons -- drug effects KW - Amyloid beta-Protein Precursor -- biosynthesis KW - Neurons -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73357065?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neuroscience+research&rft.atitle=Differential+expression+of+carboxyl+terminal+derivatives+of+amyloid+precursor+protein+among+cell+lines.&rft.au=Wolozin%2C+B%3BBacic%2C+M%3BMerrill%2C+M+J%3BLesch%2C+K+P%3BChen%2C+C%3BLebovics%2C+R+S%3BSunderland%2C+T&rft.aulast=Wolozin&rft.aufirst=B&rft.date=1992-09-01&rft.volume=33&rft.issue=1&rft.spage=163&rft.isbn=&rft.btitle=&rft.title=Journal+of+neuroscience+research&rft.issn=03604012&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-06 N1 - Date created - 1993-01-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The use of stable isotopes to identify reactive metabolites and target macromolecules associated with toxicities of halogenated hydrocarbon compounds. AN - 73338804; 1441605 AB - 1. Halogenated compounds, such as the inhalation anaesthetics, halothane and enflurane, and the chemicals chloroform, carbon tetrachloride, and bromotrichloromethane can cause hepatotoxicity, nephrotoxicity, and inactivation of cytochromes P-450. Each of these toxicities is mediated by reactive metabolites. 2. Stable isotopes of hydrogen, carbon, chlorine and oxygen have been used in conjunction with mass spectrometry and n.m.r. spectrometry to identify the structures of these metabolites, to elucidate the mechanisms of their formation, and to characterize the structures of their macromolecular adducts. 3. In a number of cases, oxidative pathways of metabolism to toxic metabolites have been defined by kinetic deuterium isotope effects. 4. Recently, we have found that the trichloromethyl radical metabolite of bromotrichloromethane can activate myoglobin by causing the covalent cross-linking of haem to protein. The structure of a haem-myoglobin adduct has been defined by the use of stable isotope studies. JF - Xenobiotica; the fate of foreign compounds in biological systems AU - Osawa, Y AU - Highet, R J AU - Pohl, L R AD - Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 1147 EP - 1156 VL - 22 IS - 9-10 SN - 0049-8254, 0049-8254 KW - Carbon Isotopes KW - 0 KW - Hydrocarbons, Halogenated KW - Isotopes KW - Macromolecular Substances KW - Oxygen Isotopes KW - Chlorine KW - 4R7X1O2820 KW - Deuterium KW - AR09D82C7G KW - Index Medicus KW - Oxidation-Reduction KW - Animals KW - Kinetics KW - Hydrocarbons, Halogenated -- toxicity KW - Hydrocarbons, Halogenated -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73338804?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Xenobiotica%3B+the+fate+of+foreign+compounds+in+biological+systems&rft.atitle=The+use+of+stable+isotopes+to+identify+reactive+metabolites+and+target+macromolecules+associated+with+toxicities+of+halogenated+hydrocarbon+compounds.&rft.au=Osawa%2C+Y%3BHighet%2C+R+J%3BPohl%2C+L+R&rft.aulast=Osawa&rft.aufirst=Y&rft.date=1992-09-01&rft.volume=22&rft.issue=9-10&rft.spage=1147&rft.isbn=&rft.btitle=&rft.title=Xenobiotica%3B+the+fate+of+foreign+compounds+in+biological+systems&rft.issn=00498254&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-23 N1 - Date created - 1992-12-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Massive intrahepatic hemorrhage following routine liver biopsy in a patient with rheumatoid arthritis treated with methotrexate. AN - 73328953; 1433018 AB - Massive intrahepatic hemorrhage occurred in a patient with rheumatoid arthritis (RA) after a routine liver biopsy done to assess possible methotrexate (MTX) hepatotoxicity. Major complications of liver biopsy occur about once in every 600 biopsies, and mortality from liver biopsy has been reported. Life threatening hepatic toxicity occurs rarely during low dose MTX administration, and it is unclear whether routine liver biopsies identify patients at high risk for these complications. Until the relative risks of liver biopsy and serious MTX liver toxicity are better defined, the use of routine liver biopsies should be recommended only after careful consideration of potential procedural complications in patients with RA treated with MTX. JF - The Journal of rheumatology AU - Cash, J M AU - Swain, M AU - Di Bisceglie, A M AU - Wilder, R L AU - Crofford, L J AD - Arthritis and Rheumatism Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 1466 EP - 1468 VL - 19 IS - 9 SN - 0315-162X, 0315-162X KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Liver -- pathology KW - Dose-Response Relationship, Drug KW - Humans KW - Chemical and Drug Induced Liver Injury KW - Adult KW - Female KW - Arthritis, Rheumatoid -- drug therapy KW - Methotrexate -- adverse effects KW - Liver Diseases -- pathology KW - Methotrexate -- therapeutic use KW - Liver Diseases -- etiology KW - Biopsy -- adverse effects KW - Hemorrhage -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73328953?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+rheumatology&rft.atitle=Massive+intrahepatic+hemorrhage+following+routine+liver+biopsy+in+a+patient+with+rheumatoid+arthritis+treated+with+methotrexate.&rft.au=Cash%2C+J+M%3BSwain%2C+M%3BDi+Bisceglie%2C+A+M%3BWilder%2C+R+L%3BCrofford%2C+L+J&rft.aulast=Cash&rft.aufirst=J&rft.date=1992-09-01&rft.volume=19&rft.issue=9&rft.spage=1466&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+rheumatology&rft.issn=0315162X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-23 N1 - Date created - 1992-12-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of individual benzo[c]phenanthrene dihydrodiol epoxide-DNA adducts by the 32P-postlabeling assay. AN - 73328254; 1446010 AB - Purine deoxyribonucleoside 3'-phosphates were reacted separately with the four configurational isomers of benzo[c]phenanthrene 3,4-dihydrodiol 1,2-epoxide. Products resulting from the cis and trans opening of the epoxide ring by the exocyclic amino groups of deoxyadenosine and deoxyguanosine 3'-phosphates were separated by high-pressure liquid chromatography and identified by comparison of the observed circular dichroism spectra with the known spectra for the corresponding nucleoside adducts. The 16 structurally identified benzo[c]phenanthrene-purine deoxyribonucleoside 3'-phosphate adducts were then separately postlabeled according to the Randerath method, and the positions of the individual bisphosphates were mapped by thin-layer chromatography. Chromatographic conditions were developed that allowed separation of the four adducts for 3 of the 4 dihydrodiol epoxide isomers. JF - Chemical research in toxicology AU - Canella, K A AU - Peltonen, K AU - Yagi, H AU - Jerina, D M AU - Dipple, A AD - Chemistry of Carcinogenesis Laboratory, NCI-Frederick Cancer Research and Development Center, Maryland 21702. PY - 1992 SP - 685 EP - 690 VL - 5 IS - 5 SN - 0893-228X, 0893-228X KW - Epoxy Compounds KW - 0 KW - Mutagens KW - Phenanthrenes KW - benzo(c)phenanthrene 3,4-dihydrodiol KW - 73093-19-3 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Stereoisomerism KW - Circular Dichroism KW - Chromatography, Thin Layer KW - Chromatography, High Pressure Liquid KW - Epoxy Compounds -- chemistry KW - DNA -- chemistry KW - Phenanthrenes -- chemistry KW - Mutagens -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73328254?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=Identification+of+individual+benzo%5Bc%5Dphenanthrene+dihydrodiol+epoxide-DNA+adducts+by+the+32P-postlabeling+assay.&rft.au=Canella%2C+K+A%3BPeltonen%2C+K%3BYagi%2C+H%3BJerina%2C+D+M%3BDipple%2C+A&rft.aulast=Canella&rft.aufirst=K&rft.date=1992-09-01&rft.volume=5&rft.issue=5&rft.spage=685&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-29 N1 - Date created - 1992-12-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A method for increasing the yield of properly folded recombinant fusion proteins: single-chain immunotoxins from renaturation of bacterial inclusion bodies. AN - 73314306; 1332541 AB - Many proteins produced in Escherichia coli accumulate in inclusion bodies. We have systematically evaluated the parameters that affect the refolding and renaturation of enzymatically active molecules from bacterial inclusion bodies containing a recombinant single-chain immunotoxin, B3(Fv)-PE38KDEL. This recombinant molecule is composed of the variable domains of monoclonal antibody B3 (B3(Fv)) fused to a truncated mutant form of Pseudomonas exotoxin A (PE38KDEL). This immunotoxin kills carcinoma cells in vitro, causes tumor regression in animal tumor models, and is being developed as an anti-cancer therapeutic agent (Brinkmann et al., 1991, Proc. Natl. Acad. Sci. USA 88, 8616-8620). Like many other recombinant proteins, B3(Fv)-PE38KDEL is produced in E. coli in inclusion bodies and must be denatured and refolded to become active. This requires correct folding, formation of native disulfide bonds, and the association of different domains. All these steps are strongly dependent on the renaturation conditions used. Optimum conditions of refolding were obtained by the addition of reduced and oxidized thiol reagents to promote disulfide bond formation and the addition of a labilizing agent such as L-arginine. Furthermore, the necessity to reactivate proteins at low protein concentrations due to its tendency to aggregate at high concentrations was overcome by a step-by-step addition of denatured and reduced protein into the refolding solution. This approach should be useful for the production of active forms of other recombinant proteins. JF - Analytical biochemistry AU - Buchner, J AU - Pastan, I AU - Brinkmann, U AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 263 EP - 270 VL - 205 IS - 2 SN - 0003-2697, 0003-2697 KW - Antibodies, Monoclonal KW - 0 KW - Bacterial Toxins KW - Exotoxins KW - Immunoglobulin Variable Region KW - Immunotoxins KW - Recombinant Fusion Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Escherichia coli -- metabolism KW - Temperature KW - Protein Denaturation KW - Neoplasms -- immunology KW - Immunotoxins -- chemistry KW - Pseudomonas aeruginosa -- metabolism KW - Recombinant Fusion Proteins -- isolation & purification KW - Bacterial Toxins -- chemistry KW - Immunotoxins -- isolation & purification KW - Exotoxins -- chemistry KW - Inclusion Bodies -- chemistry KW - Recombinant Fusion Proteins -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73314306?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytical+biochemistry&rft.atitle=A+method+for+increasing+the+yield+of+properly+folded+recombinant+fusion+proteins%3A+single-chain+immunotoxins+from+renaturation+of+bacterial+inclusion+bodies.&rft.au=Buchner%2C+J%3BPastan%2C+I%3BBrinkmann%2C+U&rft.aulast=Buchner&rft.aufirst=J&rft.date=1992-09-01&rft.volume=205&rft.issue=2&rft.spage=263&rft.isbn=&rft.btitle=&rft.title=Analytical+biochemistry&rft.issn=00032697&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-01 N1 - Date created - 1992-12-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Toxicity and carcinogenicity of hydroquinone in F344/N rats and B6C3F1 mice. AN - 73308757; 1365401 AB - Toxicology and carcinogenesis studies were conducted by administering hydroquinone (more than 99% pure) by gavage to groups of F344/N rats and B6C3F1 mice of each sex for 14 days, 13 wk or 2 yr. 14-day studies were conducted by administering hydroquinone in corn oil to rats at doses ranging from 63 to 1000 mg/kg body weight and to mice at doses ranging from 31 to 500 mg/kg, 5 days/wk. In the 13-wk studies, doses for rats and mice ranged from 25 to 400 mg/kg. At those doses showing some indication of toxicity in the 14-day and 13-wk studies, the central nervous system, forestomach and liver were identified as target organs in both species and renal toxicity was observed in rats. Based on these results, 2-yr studies were conducted by administering 0, 25 or 50 mg hydroquinone/kg in deionized water by gavage to groups of 65 rats of each sex, 5 days/wk. Groups of 65 mice of each sex were given 0, 50 or 100 mg/kg on the same schedule. 10 rats and 10 mice from each group were killed and evaluated after 15 months. Mean body weights of high-dose male rats and high-dose mice were approx. 5-14% lower than those of controls during the second half of the study. No differences in survival were observed between dosed and control groups of rats or mice. Nearly all male rats and most female rats in all vehicle control and exposed groups had nephropathy, which was judged to be more severe in high-dose male rats. Hyperplasia of the renal pelvic transitional epithelium and renal cortical cysts were increased in male rats. Tubular cell hyperplasia of the kidney was seen in two high-dose male rats, and renal tubular adenomas were seen in 4/55 low-dose and 8/55 high-dose male rats; none was seen in vehicle controls or in female rats. Mononuclear cell leukaemia in female rats occurred with increased incidences in the dosed groups (vehicle control, 9/55; low dose, 15/55; high dose, 22/55). Compound-related lesions observed in the liver of high-dose male mice included anisokaryosis, syncytial alteration and basophilic foci. The incidences of hepatocellular neoplasms, primarily adenomas, were increased in dosed female mice (3/55; 16/55; 13/55). Follicular cell hyperplasia of the thyroid gland was increased in dosed mice.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association AU - Kari, F W AU - Bucher, J AU - Eustis, S L AU - Haseman, J K AU - Huff, J E AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 737 EP - 747 VL - 30 IS - 9 SN - 0278-6915, 0278-6915 KW - Hydroquinones KW - 0 KW - Corn Oil KW - 8001-30-7 KW - hydroquinone KW - XV74C1N1AE KW - Index Medicus KW - Seizures -- chemically induced KW - Administration, Oral KW - Thyroid Neoplasms -- chemically induced KW - Animals KW - Kidney -- pathology KW - Sex Factors KW - Dose-Response Relationship, Drug KW - Kidney -- drug effects KW - Mice KW - Tremor -- chemically induced KW - Stomach -- drug effects KW - Epithelium -- drug effects KW - Rats KW - Stomach -- pathology KW - Rats, Inbred F344 KW - Hyperplasia KW - Liver -- drug effects KW - Epithelium -- pathology KW - Female KW - Male KW - Leukemia, Myeloid -- chemically induced KW - Kidney Neoplasms -- chemically induced KW - Liver Neoplasms, Experimental -- chemically induced KW - Hydroquinones -- administration & dosage KW - Hydroquinones -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73308757?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Food+and+chemical+toxicology+%3A+an+international+journal+published+for+the+British+Industrial+Biological+Research+Association&rft.atitle=Toxicity+and+carcinogenicity+of+hydroquinone+in+F344%2FN+rats+and+B6C3F1+mice.&rft.au=Kari%2C+F+W%3BBucher%2C+J%3BEustis%2C+S+L%3BHaseman%2C+J+K%3BHuff%2C+J+E&rft.aulast=Kari&rft.aufirst=F&rft.date=1992-09-01&rft.volume=30&rft.issue=9&rft.spage=737&rft.isbn=&rft.btitle=&rft.title=Food+and+chemical+toxicology+%3A+an+international+journal+published+for+the+British+Industrial+Biological+Research+Association&rft.issn=02786915&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-01 N1 - Date created - 1992-12-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Food Chem Toxicol. 1994 Sep;32(9):863-7 [7927084] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Risk for affective disorder and alcohol and other drug abuse in the relatives of affectively ill adoptees. AN - 73304104; 1430667 AB - We investigated the risk for substance abuse in the biological relatives of adoptees with affective illness, controlling for potential confounds, and additionally assessed risk by probands' and relatives' gender. Our sample consisted of 67 index adoptees with affective illness, matched control adoptees, and their biological and adoptive relatives. Both affective illness and substance abuse were more common in the biological relatives of affectively ill adoptees than in controls' relatives. Affective illness was more common than substance abuse among female index biological relatives, with the opposite pattern observed among male relatives. JF - Journal of affective disorders AU - Ingraham, L J AU - Wender, P H AD - Laboratory of Psychology and Psychopathology, NIMH, Bethesda, MD 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 45 EP - 51 VL - 26 IS - 1 SN - 0165-0327, 0165-0327 KW - Index Medicus KW - Risk Factors KW - Models, Genetic KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Female KW - Depressive Disorder -- psychology KW - Child of Impaired Parents -- psychology KW - Bipolar Disorder -- genetics KW - Adoption -- psychology KW - Depressive Disorder -- genetics KW - Bipolar Disorder -- psychology KW - Substance-Related Disorders -- psychology KW - Alcoholism -- genetics KW - Alcoholism -- psychology KW - Substance-Related Disorders -- genetics KW - Social Environment UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73304104?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+affective+disorders&rft.atitle=Risk+for+affective+disorder+and+alcohol+and+other+drug+abuse+in+the+relatives+of+affectively+ill+adoptees.&rft.au=Ingraham%2C+L+J%3BWender%2C+P+H&rft.aulast=Ingraham&rft.aufirst=L&rft.date=1992-09-01&rft.volume=26&rft.issue=1&rft.spage=45&rft.isbn=&rft.btitle=&rft.title=Journal+of+affective+disorders&rft.issn=01650327&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-03 N1 - Date created - 1992-12-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selective stimulation of Ca2+ flux in cells by maitotoxin. AN - 73275947; 1330638 AB - Maitotoxin elicits a dose-dependent stimulation of 45Ca2+ influx in glioma C6, pheochromocytoma PC12, insulinoma HIT and human blood cells, while having no effect in liposomes. In HIT cells maitotoxin also elicited influx of 86Rb+ greater than 22Na+ greater than 54Mn2+, but the stimulation was far less than for 45Ca2+. Stimulation of 45Ca2+ influx was blocked by Ni2+, Co2+, Cd2+ and Mn2+, and markedly reduced by Ba2+. Divalent cations, in particular Ca2+, Ba2+, Mn2+ and Cd2+, enhanced influx of the monovalent cations 22Na+ and 86Rb+. JF - European journal of pharmacology AU - Murata, M AU - Gusovsky, F AU - Yasumoto, T AU - Daly, J W AD - Laboratory of Bioorganic Chemistry, NIDDK, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09/01/ PY - 1992 DA - 1992 Sep 01 SP - 43 EP - 49 VL - 227 IS - 1 SN - 0014-2999, 0014-2999 KW - Calcium Channels KW - 0 KW - Calcium Radioisotopes KW - Cations KW - Liposomes KW - Marine Toxins KW - Oxocins KW - Radioisotopes KW - Rubidium Radioisotopes KW - Sodium Radioisotopes KW - Manganese KW - 42Z2K6ZL8P KW - Chlorine KW - 4R7X1O2820 KW - maitotoxin KW - 9P59GES78D KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Manganese -- metabolism KW - Dose-Response Relationship, Drug KW - Liposomes -- metabolism KW - Chlorine -- metabolism KW - Rats KW - Tumor Cells, Cultured KW - Calcium Channels -- drug effects KW - Cricetinae KW - Marine Toxins -- pharmacology KW - Calcium -- metabolism KW - Calcium -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73275947?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+pharmacology&rft.atitle=Selective+stimulation+of+Ca2%2B+flux+in+cells+by+maitotoxin.&rft.au=Murata%2C+M%3BGusovsky%2C+F%3BYasumoto%2C+T%3BDaly%2C+J+W&rft.aulast=Murata&rft.aufirst=M&rft.date=1992-09-01&rft.volume=227&rft.issue=1&rft.spage=43&rft.isbn=&rft.btitle=&rft.title=European+journal+of+pharmacology&rft.issn=00142999&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-04 N1 - Date created - 1992-12-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of dose, strain, and dosing vehicle on methacrylonitrile disposition in rats and identification of a novel-exhaled metabolite. AN - 73271090; 1358567 AB - Methacrylonitrile (MAN), an aliphatic nitrile used in the production of plastics and elastomers, is structurally related to the known animal carcinogen, acrylonitrile. Although MAN has potential to cause significant toxicity, minimal information is available on its toxicity or fate. Current studies were designed to investigate the biological fate of [2-14C]MAN in male F344 rats. Following gavage administration of 115, 11.5, or 1.15 mg MAN/kg in water, male F344 rats were placed in glass metabolism cages and urine, expired air, and feces were collected. Rats were sacrificed at various times, and the concentration of MAN-derived radioactivity in tissues was determined. MAN was rapidly absorbed from the gastrointestinal tract and distributed to all major tissues. After gavage administration of 1.15-115 mg/kg, [2-14C]MAN is primarily eliminated in the expired air. Sixty to 70% of the low and medium doses were exhaled as 14CO2 in 72 hr compared with 25% of the highest dose. Whereas 40% of the high dose was expired as organic volatiles in 72 hr, only 9-12% of the low and medium doses were exhaled as such. It is therefore apparent that saturation of MAN metabolism occurs at the high dose. HPLC analysis of expired organic volatiles from MAN-treated rats showed that it contained two components that were identified as unchanged MAN and acetone. The MAN:acetone ratio was directly proportional to dose and decreased as a function of time. Urinary excretion accounted for 20-30% of all MAN doses within 72 hr after dosing. Investigating the effect of dosing vehicle on MAN disposition in rats revealed that administration of 115 mg MAN/kg in oil resulted in the death of rats within 24 hr after treatment. Furthermore, monitoring the fate of MAN in these rats before death showed that a significantly higher percentage of the dose was eliminated in urine and expired air. Analysis of this expired air also revealed that significantly more acetone and less unchanged MAN were exhaled by these animals. It is apparent that administration of MAN to F344 rats in oil resulted in slower absorption, decreased elimination of unchanged MAN, and increased metabolism to acetone and/or decreased degradation of acetone to CO2. The combination of these effects of an oil vehicle may have contributed to the death of rats by MAN. Comparison of the metabolism and disposition of MAN in F344 and Sprague-Dawley rats showed minor differences between the two strains.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Drug metabolism and disposition: the biological fate of chemicals AU - Ghanayem, B I AU - Sanchez, I M AU - Burka, L T AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1992 SP - 643 EP - 652 VL - 20 IS - 5 SN - 0090-9556, 0090-9556 KW - Methacrylates KW - 0 KW - Nitriles KW - Pharmaceutical Vehicles KW - methacrylonitrile KW - 04S4K38612 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Rats, Inbred F344 KW - Dose-Response Relationship, Drug KW - Tissue Distribution KW - Species Specificity KW - Male KW - Nitriles -- pharmacokinetics KW - Methacrylates -- pharmacokinetics KW - Nitriles -- administration & dosage KW - Methacrylates -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73271090?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+metabolism+and+disposition%3A+the+biological+fate+of+chemicals&rft.atitle=Effects+of+dose%2C+strain%2C+and+dosing+vehicle+on+methacrylonitrile+disposition+in+rats+and+identification+of+a+novel-exhaled+metabolite.&rft.au=Ghanayem%2C+B+I%3BSanchez%2C+I+M%3BBurka%2C+L+T&rft.aulast=Ghanayem&rft.aufirst=B&rft.date=1992-09-01&rft.volume=20&rft.issue=5&rft.spage=643&rft.isbn=&rft.btitle=&rft.title=Drug+metabolism+and+disposition%3A+the+biological+fate+of+chemicals&rft.issn=00909556&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-23 N1 - Date created - 1992-12-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vivo binding of [125I]RTI-55 to dopamine transporters: pharmacology and regional distribution with autoradiography. AN - 73256901; 1411962 AB - Previous studies have demonstrated that para-substituted WIN 35,065-2 analogs of cocaine show high binding affinity for dopamine uptake sites both in vitro and in vivo, and inhibit DA uptake in vitro. These analogs also produce potent cocaine-like behavioral effects in various procedures. The purpose of the present studies was to evaluate the iodinated WIN 35,065-2 analog [125I]RTI-55 as an in vivo ligand for the DA transporter. Following intravenous injection in mice, [125I]RTI-55 showed highest accumulation in areas with high densities of dopamine uptake sites. Light microscopic autoradiography was used to examine binding with higher resolution. Displacement studies demonstrated that [125I]RTI-55 binding in dopamine containing regions, striatum and olfactory tubercles, was saturable and inhibited by other cocaine analogs. GBR 12909 and WIN 35,428 significantly inhibited [125I]RTI-55 binding in striatum, while paroxetine significantly inhibited hypothalamic binding but had little effect in striatum. The latter finding suggests that [125I]RTI-55 also binds to the serotonin transporter. Haloperidol had no effect on [125I]RTI-55 binding in any brain region measured. In addition, treatment of animals with the dopamine neurotoxin MPTP caused significant reductions in striatal [125I]RTI-55 binding. The results of these studies indicate that [125I]RTI-55 binds primarily to the dopamine transporter in the mouse striatum in vivo. JF - Synapse (New York, N.Y.) AU - Cline, E J AU - Scheffel, U AU - Boja, J W AU - Mitchell, W M AU - Carroll, F I AU - Abraham, P AU - Lewin, A H AU - Kuhar, M J AD - Neuroscience Branch, Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland 21224. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 37 EP - 46 VL - 12 IS - 1 SN - 0887-4476, 0887-4476 KW - Carrier Proteins KW - 0 KW - Dopamine Plasma Membrane Transport Proteins KW - Iodine Radioisotopes KW - Membrane Glycoproteins KW - Membrane Transport Proteins KW - Nerve Tissue Proteins KW - 2beta-carbomethoxy-3beta-(4-iodophenyl)tropane KW - 4H1Z7121WS KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Kinetics KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- pharmacology KW - Organ Specificity KW - Mice KW - Autoradiography KW - Male KW - Cocaine -- analogs & derivatives KW - Carrier Proteins -- metabolism KW - Brain -- drug effects KW - Nerve Tissue Proteins -- metabolism KW - Brain -- metabolism KW - Cocaine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73256901?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Synapse+%28New+York%2C+N.Y.%29&rft.atitle=In+vivo+binding+of+%5B125I%5DRTI-55+to+dopamine+transporters%3A+pharmacology+and+regional+distribution+with+autoradiography.&rft.au=Cline%2C+E+J%3BScheffel%2C+U%3BBoja%2C+J+W%3BMitchell%2C+W+M%3BCarroll%2C+F+I%3BAbraham%2C+P%3BLewin%2C+A+H%3BKuhar%2C+M+J&rft.aulast=Cline&rft.aufirst=E&rft.date=1992-09-01&rft.volume=12&rft.issue=1&rft.spage=37&rft.isbn=&rft.btitle=&rft.title=Synapse+%28New+York%2C+N.Y.%29&rft.issn=08874476&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-12 N1 - Date created - 1992-11-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cirrhosis mortality and occupation. AN - 73246640; 1405639 AB - Cirrhosis, the ninth leading cause of death in the United States, has been associated with abusive alcohol consumption patterns. Since the workplace serves as a major exposure variable for alcohol consumption over a significant portion of the lifecourse, and since heavy drinking has been shown to differ by type of occupation, this study examines the relationship between type of occupation and cirrhosis mortality. The California Occupational Mortality Study data set (1979 to 1981) provided the information on primary occupation and liver cirrhosis mortality. Crude and sex-specific mortality rates were calculated based on information from a 20% sample of the 1980 California census (included in the data set). Ninety-five percent confidence intervals were calculated around all rates to determine if any were significantly different from rates for the entire state. The findings uphold the view that an association exists between occupation and cirrhosis mortality. The highest mortality rates were found among persons with blue-collar type jobs (e.g., construction laborers and machinists) or jobs where alcohol was easily available (e.g., bartenders and waitresses). Future research needs to specify the factors associated with occupation that may promote the chronic heavy drinking that leads to cirrhosis. JF - Journal of studies on alcohol AU - Harford, T C AU - Brooks, S D AD - Division of Biometry and Epidemiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 463 EP - 468 VL - 53 IS - 5 SN - 0096-882X, 0096-882X KW - Index Medicus KW - United States KW - California KW - Occupational Health KW - Sex Factors KW - Humans KW - Adult KW - Middle Aged KW - Occupations -- classification KW - Alcoholism -- complications KW - Male KW - Female KW - Occupational Exposure KW - Liver Cirrhosis -- etiology KW - Liver Cirrhosis -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73246640?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+studies+on+alcohol&rft.atitle=Cirrhosis+mortality+and+occupation.&rft.au=Harford%2C+T+C%3BBrooks%2C+S+D&rft.aulast=Harford&rft.aufirst=T&rft.date=1992-09-01&rft.volume=53&rft.issue=5&rft.spage=463&rft.isbn=&rft.btitle=&rft.title=Journal+of+studies+on+alcohol&rft.issn=0096882X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-04 N1 - Date created - 1992-11-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of ibuprofen and pentoxifylline on the cardiovascular response of normal humans to endotoxin. AN - 73239755; 1400057 AB - Endotoxin is a major mediator of the life-threatening cardiovascular dysfunction that characterizes Gram-negative sepsis. In animal models of endotoxemia, pretreatment with ibuprofen or pentoxifylline attenuates some of these cardiovascular changes. To evaluate the effects of these agents on the human cardiovascular response to endotoxemia, hemodynamic variables were measured serially in 24 normal subjects who were given intravenous endotoxin. The subjects were randomized to receive oral ibuprofen (n = 9), pentoxifylline (n = 10), or no medication before endotoxin administration (n = 5). The subjects were volume loaded 3-5 h after endotoxin administration, and hemodynamic measurements were reassessed. Core temperature after endotoxin alone or endotoxin-pentoxifylline approached a maximum at 3 h (greater than or equal to 38.6 degrees C), while the endotoxin-ibuprofen group remained afebrile. At 3 and 5 h, all three groups had significant increases in heart rate, cardiac index, oxygen delivery, and oxygen consumption, while systemic vascular resistance index decreased significantly from baseline. The oxygen extraction ratio remained unchanged. After volume loading, the left ventricular ejection fraction and left ventricular end-diastolic and end-systolic volume indexes did not differ among the groups. The hyperdynamic cardiovascular response to endotoxin in humans occurs in the absence of fever and is not significantly ameliorated by oral cyclooxygenase or phosphodiesterase inhibition. JF - Journal of applied physiology (Bethesda, Md. : 1985) AU - Martich, G D AU - Parker, M M AU - Cunnion, R E AU - Suffredini, A F AD - Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 925 EP - 931 VL - 73 IS - 3 SN - 8750-7587, 8750-7587 KW - Endotoxins KW - 0 KW - Tumor Necrosis Factor-alpha KW - Pentoxifylline KW - SD6QCT3TSU KW - Ibuprofen KW - WK2XYI10QM KW - Index Medicus KW - Ventricular Function, Left -- drug effects KW - Hemodynamics -- drug effects KW - Hemodynamics -- physiology KW - Oxygen Consumption -- drug effects KW - Humans KW - Shock, Septic -- etiology KW - Ventricular Function, Left -- physiology KW - Cardiovascular Physiological Phenomena KW - Adult KW - Shock, Septic -- physiopathology KW - Tumor Necrosis Factor-alpha -- metabolism KW - Female KW - Male KW - Shock, Septic -- prevention & control KW - Pentoxifylline -- pharmacology KW - Cardiovascular System -- drug effects KW - Ibuprofen -- pharmacology KW - Endotoxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73239755?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Sequence+specificity+of+aflatoxin+B1-induced+mutations+in+a+plasmid+replicated+in+xeroderma+pigmentosum+and+DNA+repair+proficient+human+cells.&rft.au=Levy%2C+D+D%3BGroopman%2C+J+D%3BLim%2C+S+E%3BSeidman%2C+M+M%3BKraemer%2C+K+H&rft.aulast=Levy&rft.aufirst=D&rft.date=1992-10-15&rft.volume=52&rft.issue=20&rft.spage=5668&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-23 N1 - Date created - 1992-11-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The incidence of illicit drug use in the United States, 1962-1989. AN - 73221566; 1392556 AB - Epidemiological descriptions of drug abuse in the US in the last three decades have generally not included data on the patterns and trends in the incidence of illicit drug use (i.e. new users). In this paper, estimates of illicit drug use incidence are presented, based on retrospective data from the National Household Survey on Drug Abuse. Incidence of marijuana use began increasing in the 1960s and reached a peak in 1973, after which a continuing decline was seen. Cocaine use incidence began to increase in the late 1960s and reached a peak in 1982, then declined. JF - British journal of addiction AU - Gfroerer, J AU - Brodsky, M AD - National Institute on Drug Abuse, Division of Epidemiology and Prevention Research, Rockville, Maryland 20857. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 1345 EP - 1351 VL - 87 IS - 9 SN - 0952-0481, 0952-0481 KW - Street Drugs KW - 0 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - United States KW - Cross-Sectional Studies KW - Heroin Dependence -- epidemiology KW - Humans KW - Adult KW - Retrospective Studies KW - Incidence KW - Marijuana Abuse -- epidemiology KW - Adolescent KW - Male KW - Female KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73221566?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+addiction&rft.atitle=The+incidence+of+illicit+drug+use+in+the+United+States%2C+1962-1989.&rft.au=Gfroerer%2C+J%3BBrodsky%2C+M&rft.aulast=Gfroerer&rft.aufirst=J&rft.date=1992-09-01&rft.volume=87&rft.issue=9&rft.spage=1345&rft.isbn=&rft.btitle=&rft.title=British+journal+of+addiction&rft.issn=09520481&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-04 N1 - Date created - 1992-11-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prenatal diethylstilbestrol exposure and performance on college entrance examinations. AN - 73218353; 1398561 AB - The fetal rodent brain is permanently altered by exposure to sex hormones. Long-term effects of prenatal sex hormones on the human brain are far less clear. In order to explore such effects, we studied a measure of cognitive function among young adults who had been exposed in utero to a powerful synthetic estrogen. In a randomized clinical trial conducted at the University of Chicago in 1950-1952, 1646 pregnant women were randomly assigned to receive either high doses of diethylstilbestrol or placebo. Women in this study gave birth to 1653 liveborn infants, of whom 1603 (820 sons and 783 daughters) survived to their fifteenth birthday. College entrance examination scores were obtained for 42% of these offspring. No differences in test performance were seen among exposed daughters. Among sons, test scores were marginally higher among the exposed, probably due to chance. JF - Hormones and behavior AU - Wilcox, A J AU - Maxey, J AU - Herbst, A L AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 433 EP - 439 VL - 26 IS - 3 SN - 0018-506X, 0018-506X KW - Diethylstilbestrol KW - 731DCA35BT KW - Index Medicus KW - Double-Blind Method KW - Cognition -- drug effects KW - Humans KW - Adult KW - Male KW - Female KW - Pregnancy KW - Aptitude KW - Intelligence -- drug effects KW - Brain -- drug effects KW - Diethylstilbestrol -- pharmacology KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73218353?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hormones+and+behavior&rft.atitle=Prenatal+diethylstilbestrol+exposure+and+performance+on+college+entrance+examinations.&rft.au=Wilcox%2C+A+J%3BMaxey%2C+J%3BHerbst%2C+A+L&rft.aulast=Wilcox&rft.aufirst=A&rft.date=1992-09-01&rft.volume=26&rft.issue=3&rft.spage=433&rft.isbn=&rft.btitle=&rft.title=Hormones+and+behavior&rft.issn=0018506X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-04 N1 - Date created - 1992-11-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - SV40 small t deletion mutants preferentially transform mononuclear phagocytes and B lymphocytes in vivo. AN - 73208951; 1529547 AB - Hamsters injected intracardiacally with wild-type SV40 developed diverse tumors, with no one type predominating. However, hamsters injected with small t deletion mutants of SV40 uniformly developed true histiocytic or B-cell lymphomas, both of which arise from rapidly dividing cell populations, with very few tumors of other types. Our results are consistent with in vitro studies which suggest a requirement for the small t function in SV40 transformation of nondividing cells. JF - Virology AU - Cicala, C AU - Pompetti, F AU - Nguyen, P AU - Dixon, K AU - Levine, A S AU - Carbone, M AD - Section on Viruses and Cellular Biology, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 475 EP - 479 VL - 190 IS - 1 SN - 0042-6822, 0042-6822 KW - Antigens, Polyomavirus Transforming KW - 0 KW - Index Medicus KW - Animals KW - Lymphoma, B-Cell -- microbiology KW - Lymphoma, Large B-Cell, Diffuse -- pathology KW - Osteosarcoma -- pathology KW - Lymphoma, B-Cell -- pathology KW - Lymphoma, Large B-Cell, Diffuse -- microbiology KW - Mesothelioma -- pathology KW - Mesocricetus KW - Lymphoma -- pathology KW - Mutagenesis KW - Cricetinae KW - B-Lymphocytes -- microbiology KW - Phagocytes -- microbiology KW - Antigens, Polyomavirus Transforming -- genetics KW - Cell Transformation, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73208951?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Virology&rft.atitle=SV40+small+t+deletion+mutants+preferentially+transform+mononuclear+phagocytes+and+B+lymphocytes+in+vivo.&rft.au=Cicala%2C+C%3BPompetti%2C+F%3BNguyen%2C+P%3BDixon%2C+K%3BLevine%2C+A+S%3BCarbone%2C+M&rft.aulast=Cicala&rft.aufirst=C&rft.date=1992-09-01&rft.volume=190&rft.issue=1&rft.spage=475&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=00426822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-16 N1 - Date created - 1992-10-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Progressive atypia in spontaneous and N-nitrosodiethylamine-induced hepatocellular adenomas of C3H/HeNCr mice. AN - 73206609; 1394837 AB - The progression of hepatocellular adenomas to carcinomas has been less well documented in mice than in rats. We studied progression of spontaneous and chemically induced hepatocellular adenomas in male C3H/HeNCr mice by image analysis. Spontaneous lesions in 15, 18 and 21 month old untreated male C3H/HeNCr mice and experimentally induced lesions were examined. Experimental group 1 received a single i.p. injection of N-nitrosodiethylamine (DEN) (5 mg/kg body wt) at 15 days of age. Groups 2 and 3 were injected a second time with DEN at 15 or 20 weeks of age (75 mg/kg body wt), with interim sacrifices at 11, 16 and 34 weeks after the second DEN injection. Atypia in adenomas were classified into four grades according to cell size, tinctorial changes, cellular pleomorphism and trabecular pattern. At earlier stages of the neoplastic process (11 or 16 weeks after the second DEN dose), most adenomas were well-differentiated lesions with no atypia or focal grade 1 or 2 atypia. At later stages (34 weeks after the second DEN dose), a large proportion of hepatocellular tumors were classified as adenoma with grade 3 atypia or carcinoma. The proportion of carcinomas in mice treated with a second dose of DEN at 20 weeks of age was significantly higher than in mice treated with a single dose of DEN or in mice given a second dose of DEN at 15 weeks. A positive correlation was found between increase in the size of lesions and increased atypia in both spontaneous and DEN-induced lesions and with age for spontaneous tumors. These results support the hypothesis that mouse hepatocellular adenomas are truly neoplastic lesions in different stages of progression toward malignancy. JF - Carcinogenesis AU - Jang, J J AU - Weghorst, C M AU - Henneman, J R AU - Devor, D E AU - Ward, J M AD - Tumor Pathology and Pathogenesis Section, National Cancer Institute, Frederick, MD 21702-1201. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 1541 EP - 1547 VL - 13 IS - 9 SN - 0143-3334, 0143-3334 KW - Diethylnitrosamine KW - 3IQ78TTX1A KW - Index Medicus KW - Body Weight KW - Animals KW - Liver -- pathology KW - Aging KW - Mice, Inbred C3H KW - Mice KW - Organ Size KW - Male KW - Female KW - Diethylnitrosamine -- toxicity KW - Liver Neoplasms, Experimental -- pathology KW - Liver Neoplasms, Experimental -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73206609?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Progressive+atypia+in+spontaneous+and+N-nitrosodiethylamine-induced+hepatocellular+adenomas+of+C3H%2FHeNCr+mice.&rft.au=Jang%2C+J+J%3BWeghorst%2C+C+M%3BHenneman%2C+J+R%3BDevor%2C+D+E%3BWard%2C+J+M&rft.aulast=Jang&rft.aufirst=J&rft.date=1992-09-01&rft.volume=13&rft.issue=9&rft.spage=1541&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-29 N1 - Date created - 1992-10-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human cytochromes P450: problems and prospects. AN - 73200886; 1529480 AB - Cytochromes P450 are a superfamily of haem-containing monooxygenases. In mammals, two general classes of P450s exist: six families involved in steroid and bile acid biosynthetic pathways of metabolism; four families containing numerous individual P450s, mainly responsible for metabolism of foreign compounds. Many of the latter P450s, particularly those in the CYP2 family, exhibit a large degree of inter- and intra-species variability in regulation and catalytic activities. From a practical standpoint, these variabilities suggest the need for careful characterization of P450 catalytic activities and determination of P450 expression levels in humans. Human P450-based in vitro systems are being developed to evaluate drug and carcinogen metabolism. JF - Trends in pharmacological sciences AU - Gonzalez, F J AD - National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 346 EP - 352 VL - 13 IS - 9 SN - 0165-6147, 0165-6147 KW - Bile Acids and Salts KW - 0 KW - Carcinogens KW - Steroids KW - Xenobiotics KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Biotransformation KW - Humans KW - Bile Acids and Salts -- metabolism KW - Steroids -- metabolism KW - Catalysis KW - Xenobiotics -- metabolism KW - Carcinogens -- pharmacokinetics KW - Cytochrome P-450 Enzyme System -- chemistry KW - Cytochrome P-450 Enzyme System -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73200886?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Trends+in+pharmacological+sciences&rft.atitle=Human+cytochromes+P450%3A+problems+and+prospects.&rft.au=Gonzalez%2C+F+J&rft.aulast=Gonzalez&rft.aufirst=F&rft.date=1992-09-01&rft.volume=13&rft.issue=9&rft.spage=346&rft.isbn=&rft.btitle=&rft.title=Trends+in+pharmacological+sciences&rft.issn=01656147&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Thymocyte injury after in vitro chemical exposure: potential mechanisms for thymic atrophy. AN - 73197012; 1527729 AB - In addition to hepatic injury, thymic atrophy is a common observation in rodent subchronic toxicity studies. We have examined representative chemicals which produce thymic atrophy in rodents for their ability to cause direct thymocyte injury because the mechanism(s) responsible for these effects have not been determined. Although a number of the compounds examined failed to have any observable direct effect on thymocytes, others either inhibited lymphocyte proliferation or initiated cell death. In the latter group, thymocyte death was always preceded by increases in intracellular Ca++ and involved, to varying degrees, necrotic and apoptotic events. Apoptosis, as evidenced by cellular DNA cleavage into multiples of 180-200-base pair oligonucleotides and partial cell protection by cycloheximide treatment, was most evident after treatment with acetaldehyde or dibutyltin dichloride. A number of compounds that produce thymic atrophy also inhibited T lymphocyte proliferation without evidence of cell death. Considering that many of the compounds tested failed to produce any evidence of direct thymocyte injury (i.e., necrosis, apoptosis or inhibition of cell proliferation), indirect mechanisms may also be involved in thymic atrophy and may target prothymocytes in the bone marrow, after normal homing patterns or injure the thymic epithelium. Thus, it appears that a variety of mechanisms may be responsible for chemical-induced thymic atrophy and/or injury. JF - The Journal of pharmacology and experimental therapeutics AU - Comment, C E AU - Blaylock, B L AU - Germolec, D R AU - Pollock, P L AU - Kouchi, Y AU - Brown, H W AU - Rosenthal, G J AU - Luster, M I AD - Systems Toxicity Branch, National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 1267 EP - 1273 VL - 262 IS - 3 SN - 0022-3565, 0022-3565 KW - Index Medicus KW - Rats KW - Atrophy -- chemically induced KW - Animals KW - Rats, Inbred F344 KW - Cell Survival -- drug effects KW - Liver -- drug effects KW - Cells, Cultured KW - Cell Division -- drug effects KW - Mice KW - Female KW - Thymus Gland -- ultrastructure KW - Drug-Related Side Effects and Adverse Reactions KW - Thymus Gland -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73197012?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.atitle=Thymocyte+injury+after+in+vitro+chemical+exposure%3A+potential+mechanisms+for+thymic+atrophy.&rft.au=Comment%2C+C+E%3BBlaylock%2C+B+L%3BGermolec%2C+D+R%3BPollock%2C+P+L%3BKouchi%2C+Y%3BBrown%2C+H+W%3BRosenthal%2C+G+J%3BLuster%2C+M+I&rft.aulast=Comment&rft.aufirst=C&rft.date=1992-09-01&rft.volume=262&rft.issue=3&rft.spage=1267&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=00223565&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 5-Fluorouracil (5-FU) and leucovorin in platinum-refractory advanced stage ovarian carcinoma. AN - 73195989; 1526510 AB - Twenty-nine patients with recurrent advanced stage ovarian cancer were treated with 5-fluorouracil (5-FU) and leucovorin by intravenous bolus on 5 consecutive days, repeated every 3 weeks. Twenty-one of these patients had experienced disease progression while receiving a cisplatin- or carboplatin-based regimen. There were 2 clinical complete responders and 1 partial responder to therapy (10% response rate; 95% confidence interval, 2 to 27%) and 11 individuals who experienced stable disease for periods ranging from 5 to 27 months. Of 204 cycles of therapy administered, 9 cycles were associated with hospitalization. These occurred in the more heavily pretreated members of the cohort. 5-FU and leucovorin appear to have activity in platinum-refractory ovarian cancer and form a well-tolerated regimen in most patients. JF - Gynecologic oncology AU - Reed, E AU - Jacob, J AU - Ozols, R F AU - Young, R C AU - Allegra, C AD - National Institute of Health, National Cancer Institute, Medicine Branch, Rockville, Maryland 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 326 EP - 329 VL - 46 IS - 3 SN - 0090-8258, 0090-8258 KW - Platinum KW - 49DFR088MY KW - Carboplatin KW - BG3F62OND5 KW - Leucovorin KW - Q573I9DVLP KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - Fluorouracil -- administration & dosage KW - Drug Administration Schedule KW - Neoplasm Staging KW - Leucovorin -- administration & dosage KW - Humans KW - Platinum -- therapeutic use KW - Adult KW - Drug Resistance KW - Aged KW - Middle Aged KW - Carboplatin -- therapeutic use KW - Female KW - Remission Induction KW - Ovarian Neoplasms -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Ovarian Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73195989?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gynecologic+oncology&rft.atitle=5-Fluorouracil+%285-FU%29+and+leucovorin+in+platinum-refractory+advanced+stage+ovarian+carcinoma.&rft.au=Reed%2C+E%3BJacob%2C+J%3BOzols%2C+R+F%3BYoung%2C+R+C%3BAllegra%2C+C&rft.aulast=Reed&rft.aufirst=E&rft.date=1992-09-01&rft.volume=46&rft.issue=3&rft.spage=326&rft.isbn=&rft.btitle=&rft.title=Gynecologic+oncology&rft.issn=00908258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-20 N1 - Date created - 1992-10-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Functional subsensitivity of 5-hydroxytryptamine1C or alpha 2 adrenergic heteroreceptors mediating clonidine-induced growth hormone release in the Fawn-Hooded rat strain relative to the Wistar rat strain. AN - 73187202; 1356149 AB - Administration of various doses of clonidine increased plasma growth hormone levels. Pretreatment with the alpha 2 adrenergic antagonists, yohimbine and 1-(2-pyrimidyl)piperazine, completely blocked clonidine's effect on growth hormone levels. Pretreatment with the 5-hydroxytryptamine3 (5-HT3) receptor antagonist, MDL-72222, the 5-HT1A/5-HT2 antagonist, spiperone, and the mixed beta adrenergic/5-HT1B antagonists, l-propranolol and CGP361A, did not attenuate clonidine-induced increases in growth hormone levels. In contrast, pretreatment with the non-selective 5-HT1/2 antagonist, metergoline, and the 5-HT1C/5-HT2-selective antagonist, mesulergine, reduced clonidine-induced increases in growth hormone levels 81 to 87% without affecting clonidine-induced decreases in locomotor activity. Two other 5-HT1C/5-HT2 antagonists, ritanserin and mianserin, also attenuated (47%) clonidine-induced increases in growth hormone levels. Pretreatment with the noradrenergic neurotoxin, DSP4, did not block clonidine's effect on growth hormone levels. Clonidine administration decreased locomotor activity in both the Fawn-Hooded and the Wistar rat strains to the same extent. On the other hand, clonidine administration failed to increase growth hormone levels in the Fawn-Hooded rat strain. These findings suggest that clonidine stimulates growth hormone secretion by activation of alpha 2 adrenergic heteroreceptors present on 5-HT nerve terminals which, in turn, enhance 5-HT activity via stimulation of postsynaptic 5-HT1C receptors to promote growth hormone releasing factor. Furthermore, either 5-HT1C receptors or alpha 2 adrenergic heteroreceptors or both are functionally sub-sensitive in the Fawn-Hooded rat strain relative to the Wistar rat strain. JF - The Journal of pharmacology and experimental therapeutics AU - Aulakh, C S AU - Hill, J L AU - Lesch, K P AU - Murphy, D L AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 1038 EP - 1043 VL - 262 IS - 3 SN - 0022-3565, 0022-3565 KW - Adrenergic alpha-Antagonists KW - 0 KW - Receptors, Serotonin KW - Serotonin Antagonists KW - Growth Hormone KW - 9002-72-6 KW - Clonidine KW - MN3L5RMN02 KW - Index Medicus KW - Receptors, Serotonin -- drug effects KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Drug Interactions KW - Dose-Response Relationship, Drug KW - Motor Activity -- drug effects KW - Species Specificity KW - Male KW - Adrenergic alpha-Antagonists -- pharmacology KW - Serotonin Antagonists -- pharmacology KW - Growth Hormone -- blood KW - Clonidine -- pharmacology KW - Growth Hormone -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73187202?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.atitle=Functional+subsensitivity+of+5-hydroxytryptamine1C+or+alpha+2+adrenergic+heteroreceptors+mediating+clonidine-induced+growth+hormone+release+in+the+Fawn-Hooded+rat+strain+relative+to+the+Wistar+rat+strain.&rft.au=Aulakh%2C+C+S%3BHill%2C+J+L%3BLesch%2C+K+P%3BMurphy%2C+D+L&rft.aulast=Aulakh&rft.aufirst=C&rft.date=1992-09-01&rft.volume=262&rft.issue=3&rft.spage=1038&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=00223565&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pathophysiological and pharmacological mechanisms of acute cocaine toxicity in conscious rats. AN - 73184124; 1527734 AB - In conscious rats, continuous i.v. infusion of cocaine (2 mg/kg/min) produced a marked increase in blood pressure, an initial moderate increase followed by a decrease in heart rate, tonic-clonic convulsions and, finally, a lethal episode of status epilepticus. No change in rectal temperature was observed. Infusion of cocaine methiodide (2 mg/kg/min), a quaternary derivative of cocaine, also produced a lethal episode of status epilepticus, but it was 6 times less potent than cocaine on a molar basis. In pentobarbital-anesthetized, spontaneously breathing rats, cocaine produced death by respiratory failure. Artificial ventilation of pentobarbital-anesthetized rats elevated the lethal dose of cocaine by 15-fold and these animals died of marked hypotension. In conscious rats, pretreatment with dl-, d- or l-propranolol or the alpha 2-selective adrenoceptor antagonist yohimbine enhanced the convulsive and lethal effects of cocaine. In contrast, the alpha 2-selective adrenoceptor agonist clonidine or the alpha 1-selective adrenoceptor antagonist prazosin attenuated these effects. Yohimbine antagonized the protective effect of clonidine. The nonselective alpha adrenoceptor antagonist phentolamine, the autonomic ganglionic blocker chlorisondamine and various calcium channel blockers had no effect on the convulsive or lethal doses of cocaine. The pressor response to cocaine was attenuated by calcium channel blockers, clonidine, phentolamine and dl- or l-propranolol, but not by d-propranolol. The pressor response to cocaine was abolished by chlorisondamine, reversed to a depressor response by prazosin and enhanced by yohimbine. The initial tachycardiac response to cocaine was reversed to bradycardia by dl- and l-propranolol, prazosin, yohimbine or high doses of the calcium channel blockers, but was unaffected by phentolamine, d-propranolol, clonidine or chlorisondamine. These results indicate that in spontaneously breathing animals, acute i.v. infusions of lethal doses of cocaine produce death primarily by central effects, namely by status epilepticus in conscious rats and by respiratory arrest in pentobarbital-anesthetized rats. In artificially ventilated, pentobarbital-anesthetized rats, however, cocaine produces death by effects on the cardiovascular system. In conscious rats, endogenous alpha 1 adrenoceptors exert a deleterious influence on cocaine-induced convulsive and lethal effects, whereas alpha 2 adrenoceptors provide protective influence. Propranolol appears to enhance cocaine-induced acute lethality through a mechanism independent of beta adrenoceptors. Calcium channel blockers appear ineffective in antagonizing cocaine's lethality. JF - The Journal of pharmacology and experimental therapeutics AU - Tella, S R AU - Korupolu, G R AU - Schindler, C W AU - Goldberg, S R AD - Behavioral Pharmacology and Genetics Section, National Institute on Drug Abuse Addiction Research Center, Baltimore, Maryland. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 936 EP - 946 VL - 262 IS - 3 SN - 0022-3565, 0022-3565 KW - Calcium Channel Blockers KW - 0 KW - Cocaine KW - I5Y540LHVR KW - Chlorisondamine KW - JD3M24F66I KW - Index Medicus KW - Seizures -- chemically induced KW - Respiratory Insufficiency -- chemically induced KW - Rats, Inbred Strains KW - Rats KW - Chlorisondamine -- pharmacology KW - Animals KW - Drug Interactions KW - Infusions, Intravenous KW - Body Temperature -- drug effects KW - Seizures -- physiopathology KW - Body Weight -- drug effects KW - Respiratory Insufficiency -- physiopathology KW - Male KW - Hemodynamics -- drug effects KW - Calcium Channel Blockers -- pharmacology KW - Cocaine -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73184124?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.atitle=Pathophysiological+and+pharmacological+mechanisms+of+acute+cocaine+toxicity+in+conscious+rats.&rft.au=Tella%2C+S+R%3BKorupolu%2C+G+R%3BSchindler%2C+C+W%3BGoldberg%2C+S+R&rft.aulast=Tella&rft.aufirst=S&rft.date=1992-09-01&rft.volume=262&rft.issue=3&rft.spage=936&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=00223565&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Autoantibodies against the amino-terminal cadherin-like binding domain of pemphigus vulgaris antigen are pathogenic. AN - 73182104; 1522242 AB - Complementary DNA cloning of the 130-kD pemphigus vulgaris (PV) autoantigen (PVA) has indicated that it is a member of the cadherin family of Ca(2+)-dependent cell adhesion molecules. By homology with typical cadherins, PVA has five extracellular domains (EC1 through EC5). To localize immunogenic domains and to determine whether antibodies against them might be pathogenic, we produced beta-galactosidase fusion proteins with cDNA encoding different portions of the extracellular domains of PVA (EC1-2, EC3-5, and each individual domain). Immunoblot analysis of these fusion proteins with 23 PV patients' sera demonstrated that major immunogenic regions of PVA are located on the EC1, EC2, and EC4 domains. IgG was affinity-purified from PV sera on fusion proteins representing the amino (EC1-2) and carboxy (EC3-5) terminus of the extracellular PVA, and injected into neonatal mice. PV IgG affinity-purified on the EC1-2 fusion protein caused suprabasilar acantholysis, the typical histological finding of PV, but IgG affinity-purified on the EC3-5 fusion protein or beta-galactosidase alone did not. These results indicate that at least one pathogenic epitope, which is sufficient to cause suprabasilar acantholysis in neonatal mice, is located on the amino-terminal region of PVA, an area thought to be important in cadherin homophilic adhesion. JF - The Journal of clinical investigation AU - Amagai, M AU - Karpati, S AU - Prussick, R AU - Klaus-Kovtun, V AU - Stanley, J R AD - Dermatology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 919 EP - 926 VL - 90 IS - 3 SN - 0021-9738, 0021-9738 KW - Autoantibodies KW - 0 KW - Autoantigens KW - Cadherins KW - Immunoglobulin G KW - Peptide Fragments KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Immunoglobulin G -- isolation & purification KW - Molecular Sequence Data KW - Mice KW - Amino Acid Sequence KW - Mice, Inbred BALB C KW - Cell Adhesion KW - Autoantigens -- immunology KW - Pemphigus -- immunology KW - Cadherins -- immunology KW - Autoantibodies -- toxicity KW - Peptide Fragments -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73182104?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+clinical+investigation&rft.atitle=Autoantibodies+against+the+amino-terminal+cadherin-like+binding+domain+of+pemphigus+vulgaris+antigen+are+pathogenic.&rft.au=Amagai%2C+M%3BKarpati%2C+S%3BPrussick%2C+R%3BKlaus-Kovtun%2C+V%3BStanley%2C+J+R&rft.aulast=Amagai&rft.aufirst=M&rft.date=1992-09-01&rft.volume=90&rft.issue=3&rft.spage=919&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+clinical+investigation&rft.issn=00219738&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-13 N1 - Date created - 1992-10-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Cell Biol. 1988 Mar;106(3):873-81 [2831236] Cell. 1991 Nov 29;67(5):869-77 [1720352] EMBO J. 1987 Dec 1;6(12):3647-53 [3501370] J Invest Dermatol. 1985 Jan;84(1):41-6 [3965577] Curr Opin Cell Biol. 1991 Oct;3(5):854-61 [1931086] J Cell Biol. 1991 Apr;113(2):381-91 [2010468] Proc Natl Acad Sci U S A. 1991 May 15;88(10):4476-80 [2034686] J Invest Dermatol. 1990 Mar;94(3):327-31 [2307852] Dev Biol. 1990 May;139(1):227-9 [2328837] J Neurochem. 1990 Sep;55(3):805-12 [2384753] J Clin Invest. 1989 May;83(5):1443-8 [2651476] J Cell Biol. 1989 Oct;109(4 Pt 1):1787-94 [2793940] J Clin Invest. 1988 Mar;81(3):807-12 [3343340] EMBO J. 1987 Dec 1;6(12):3655-61 [3428270] Nature. 1987 Sep 24-30;329(6137):341-3 [3498123] J Immunol. 1986 Feb 15;136(4):1227-30 [3511144] J Cell Biol. 1986 Mar;102(3):1109-17 [3512579] J Clin Invest. 1984 Aug;74(2):313-20 [6378972] J Exp Med. 1983 Jan 1;157(1):259-72 [6681540] N Engl J Med. 1982 May 20;306(20):1189-96 [7040962] Arch Dermatol Res. 1977 Oct 27;260(1):1-6 [337911] Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4 [388439] Proc Natl Acad Sci U S A. 1991 Jun 1;88(11):4796-800 [1711210] J Cell Sci. 1991 Aug;99 ( Pt 4):809-21 [1770008] Science. 1991 Mar 22;251(5000):1451-5 [2006419] Annu Rev Biochem. 1990;59:237-52 [2197976] Cell. 1990 Apr 6;61(1):147-55 [2317870] J Exp Med. 1987 Jun 1;165(6):1719-24 [2438368] Science. 1989 Aug 11;245(4918):631-5 [2762814] J Exp Med. 1984 Nov 1;160(5):1509-18 [6491602] J Invest Dermatol. 1981 Aug;77(2):240-3 [7024426] Int J Dermatol. 1979 May;18(4):271-81 [378879] Biochem Biophys Res Commun. 1990 Dec 31;173(3):1224-30 [1702628] Eur J Cell Biol. 1990 Oct;53(1):1-12 [1706270] Proc Natl Acad Sci U S A. 1987 May;84(9):2808-12 [3472238] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A parkinsonian syndrome induced in the goldfish by the neurotoxin MPTP. AN - 73181231; 1521741 AB - Parkinson's disease has been modeled in humans, lower primates, and to a lesser extent in some other vertebrates by administration of the potent neurotoxin MPTP (1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine). The MPTP model has thus drawn considerable attention as a system to search for anti-Parkinson's disease drugs, although the cost and scarcity of primates has limited extensive applications. We now report that a parkinsonian syndrome can be elicited in the common goldfish (Carassius auratus) by a single dose of MPTP. The syndrome is characterized by profound bradykinesia (slow movement), the full extent of which is reached 3 days after MPTP administration. The reduction in movement is paralleled by loss of dopamine and norepinephrine from the forebrain and midbrain and in other brain regions as well. The toxic oxidative product of MPTP, MPP+, is also accumulated predominantly in forebrain and midbrain, and pretreatment with the monoamine oxidase blocker tranylcypromine substantially reduces accumulation of the toxic metabolite. A barely perceptible coarseness in balance adjustment also occurs in treated animals. The MPTP-treated goldfish recover normal movement and normal brain monoamine levels within 10-13 days after administration of the drug. We interpret these and other data to indicate that MPTP can induce a Parkinson's disease-like syndrome in the goldfish that is similar in many aspects to the syndrome induced by MPTP in humans and other primates. This remarkable parallel may permit the goldfish to supplement expensive and scarce primates for the purpose of searching and screening neuroprotective drugs with specific relevance to Parkinson's disease. JF - FASEB journal : official publication of the Federation of American Societies for Experimental Biology AU - Pollard, H B AU - Dhariwal, K AU - Adeyemo, O M AU - Markey, C J AU - Caohuy, H AU - Levine, M AU - Markey, S AU - Youdim, M B AD - Laboratory of Cell Biology and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 3108 EP - 3116 VL - 6 IS - 12 SN - 0892-6638, 0892-6638 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Monoamine Oxidase KW - EC 1.4.3.4 KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Brain -- enzymology KW - Animals KW - Norepinephrine -- metabolism KW - Brain -- pathology KW - Brain -- drug effects KW - Goldfish KW - Dopamine -- metabolism KW - Disease Models, Animal KW - Locomotion -- drug effects KW - Monoamine Oxidase -- metabolism KW - Parkinson Disease, Secondary -- metabolism KW - Parkinson Disease, Secondary -- chemically induced KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73181231?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FASEB+journal+%3A+official+publication+of+the+Federation+of+American+Societies+for+Experimental+Biology&rft.atitle=A+parkinsonian+syndrome+induced+in+the+goldfish+by+the+neurotoxin+MPTP.&rft.au=Pollard%2C+H+B%3BDhariwal%2C+K%3BAdeyemo%2C+O+M%3BMarkey%2C+C+J%3BCaohuy%2C+H%3BLevine%2C+M%3BMarkey%2C+S%3BYoudim%2C+M+B&rft.aulast=Pollard&rft.aufirst=H&rft.date=1992-09-01&rft.volume=6&rft.issue=12&rft.spage=3108&rft.isbn=&rft.btitle=&rft.title=FASEB+journal+%3A+official+publication+of+the+Federation+of+American+Societies+for+Experimental+Biology&rft.issn=08926638&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-15 N1 - Date created - 1992-10-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Brain vascular endothelial cells express JC virus large tumor antigen in immunocompetent and cyclophosphamide-treated hamsters. AN - 73179319; 1325648 AB - When injected intracerebrally into newborn hamsters, the human polyomavirus JC virus (JCV) establishes a nonproductive infection resulting in brain tumor formation. Using immunostaining methods to detect the JCV regulatory protein, large tumor antigen (T antigen), we have now demonstrated JCV infection of brain vascular endothelial cells (EC) in infected hamsters. JCV T antigen was detected in lectin-labeled EC as well as in von Willebrand factor-expressing EC in both cyclophosphamide-treated and nonimmunosuppressed hamster brains 16, 21, and 31 days after birth. Cyclophosphamide-treated hamsters exhibited a greater number of JCV-infected EC, whereas T-antigen expression in nonvascular cells was not affected. The influence of cyclophosphamide was most pronounced in the cerebellum where increased numbers of JCV-infected EC were located predominantly at the internal granular layer-white matter junction, also a prominent location for T-antigen-expressing neoplastic foci. The hamster model demonstrates in vivo infection of EC by a human polyomavirus and directs interest toward the role of these cells in human JCV infection. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Ressetar, H G AU - Webster, H D AU - Stoner, G L AD - Laboratory of Experimental Neuropathology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09/01/ PY - 1992 DA - 1992 Sep 01 SP - 8170 EP - 8174 VL - 89 IS - 17 SN - 0027-8424, 0027-8424 KW - Antigens, Polyomavirus Transforming KW - 0 KW - von Willebrand Factor KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - Animals KW - von Willebrand Factor -- metabolism KW - Cerebellum -- microbiology KW - Mesocricetus KW - Immunoenzyme Techniques KW - Cricetinae KW - Blood-Brain Barrier KW - JC Virus -- immunology KW - Tumor Virus Infections -- immunology KW - Antigens, Polyomavirus Transforming -- metabolism KW - Endothelium, Vascular -- microbiology KW - Endothelium, Vascular -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73179319?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Brain+vascular+endothelial+cells+express+JC+virus+large+tumor+antigen+in+immunocompetent+and+cyclophosphamide-treated+hamsters.&rft.au=Ressetar%2C+H+G%3BWebster%2C+H+D%3BStoner%2C+G+L&rft.aulast=Ressetar&rft.aufirst=H&rft.date=1992-09-01&rft.volume=89&rft.issue=17&rft.spage=8170&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-07 N1 - Date created - 1992-10-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Infect Immun. 1981 Jul;33(1):319-21 [7196387] Infect Immun. 1981 Jul;33(1):297-303 [7263066] J Gen Virol. 1979 Jan;42(1):49-57 [215712] Infect Immun. 1979 Nov;26(2):705-13 [397932] Lab Invest. 1990 Mar;62(3):287-96 [1690314] Lab Invest. 1986 Sep;55(3):328-36 [3018360] Coll Relat Res. 1986 Oct;6(4):333-49 [3028708] J Immunol. 1986 Jul 1;137(1):245-54 [3086451] Ann Intern Med. 1987 Jul;107(1):78-87 [3296901] Histochem J. 1987 Apr;19(4):225-34 [3597137] Biochemistry. 1985 Sep 24;24(20):5480-6 [4074709] Am J Pathol. 1972 Jul;68(1):15-22 [4342991] J Infect Dis. 1973 Apr;127(4):467-70 [4571704] Br J Exp Pathol. 1970 Aug;51(4):434-9 [4991966] J Exp Med. 1972 Aug 1;136(2):261-76 [5043412] J Comp Neurol. 1970 Jan;138(1):31-47 [5412719] J Cell Biol. 1967 Jul;34(1):207-17 [6033532] EMBO J. 1984 Jul;3(7):1485-91 [6204863] J Comput Assist Tomogr. 1980 Jun;4(3):285-90 [6246149] Blood. 1980 Jun;55(6):1056-9 [6769518] Transplant Proc. 1981 Mar;13(1 Pt 1):262-6 [7022837] Cancer Res. 1977 Mar;37(3):718-20 [189911] Science. 1978 Sep 29;201(4362):1246-9 [211583] Microvasc Res. 1977 Jul;14(1):53-65 [895546] J Neuroimmunol. 1988 Sep;19(3):223-36 [2842376] Acta Pathol Jpn. 1986 Jun;36(6):815-25 [3020865] Acta Neuropathol. 1988;77(2):175-81 [3227814] J Immunol. 1986 Aug 15;137(4):1270-4 [3525675] J Exp Med. 1971 Feb 1;133(2):275-88 [4332371] Science. 1973 Aug 17;181(4100):674-6 [4353360] J Clin Invest. 1973 Nov;52(11):2757-64 [4583980] Brain Res. 1969 Oct;15(2):532-6 [5344385] Nature. 1968 Oct 26;220(5165):399-401 [5684888] J Clin Microbiol. 1980 Feb;11(2):178-83 [6244330] Clin Exp Immunol. 1983 Aug;53(2):289-96 [6309442] Am J Surg Pathol. 1980 Jun;4(3):273-6 [6772042] Cell. 1976 Dec;9(4 PT 2):685-93 [189941] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Radiation therapy of acromegaly. AN - 73171083; 1521519 AB - Conventional megavoltage irradiation of GH-secreting tumors has predictable effects on tumor mass, GH, and pituitary function. 1. Further growth of the tumor is prevented in more than 99% of patients, with only a fraction of a percent of patients requiring subsequent surgery for tumor mass effects. 2. GH falls predictably with time. By 2 years GH falls by about 50% from the baseline level, and by 5 years by about 75% from the baseline level. The initial GH elevation and the size and erosive features of the sella turcica do not affect the percent decrease in GH from the baseline elevation. 3. With prolonged follow-up, further decrease in GH is seen at 10 and 15 years, with the fraction of surviving patients achieving GH levels less than 5 ng/mL approaching 90% after 15 years in our experience. Gender, previous surgery, and hyperprolactinemia do not seem to affect the response to treatment. Patients with initial GH greater than 100 ng/mL are significantly less likely to achieve GH values less than 5 ng/mL during long-term follow-up. 4. Hypopituitarism is a predictable outcome of treatment, is delayed, and may be more likely in patients who have had surgery prior to irradiation. There is no evidence that this complication is more common in patients with acromegaly than in patients with other pituitary adenomas receiving similar treatment. 5. Vision loss due to megavoltage irradiation--using modern techniques and limiting the total dose to 4680 rad given in 25 fractions over 35 days, with individual fractions not exceeding 180 rad--is extremely rare. The reported cases have occurred almost entirely in patients who have received larger doses or higher fractional doses. The theory that patients with acromegaly are prone to radiation-induced injury to the CNS and optic nerves and chiasm because of small vessel disease is not supported by a review of the reported cases. 6. Brain necrosis and secondary neoplasms induced by irradiation are extremely rare. 7. Although anecdotal evidence raises the question of changes in intellectual function following irradiation, this has not been studied in adults receiving pituitary irradiation. JF - Endocrinology and metabolism clinics of North America AU - Eastman, R C AU - Gorden, P AU - Glatstein, E AU - Roth, J AD - Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 693 EP - 712 VL - 21 IS - 3 SN - 0889-8529, 0889-8529 KW - Growth Hormone KW - 9002-72-6 KW - Index Medicus KW - Adenoma -- radiotherapy KW - Pituitary Neoplasms -- pathology KW - Humans KW - Pituitary Neoplasms -- radiotherapy KW - Adenoma -- pathology KW - Radiation Injuries KW - Growth Hormone -- secretion KW - Acromegaly -- pathology KW - Acromegaly -- radiotherapy KW - Acromegaly -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73171083?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrinology+and+metabolism+clinics+of+North+America&rft.atitle=Radiation+therapy+of+acromegaly.&rft.au=Eastman%2C+R+C%3BGorden%2C+P%3BGlatstein%2C+E%3BRoth%2C+J&rft.aulast=Eastman&rft.aufirst=R&rft.date=1992-09-01&rft.volume=21&rft.issue=3&rft.spage=693&rft.isbn=&rft.btitle=&rft.title=Endocrinology+and+metabolism+clinics+of+North+America&rft.issn=08898529&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-13 N1 - Date created - 1992-10-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genetic vulnerability to drug abuse. The D2 dopamine receptor Taq I B1 restriction fragment length polymorphism appears more frequently in polysubstance abusers. AN - 73170326; 1355337 AB - Alcoholics are more likely than nonalcoholics to display the Taq I A1 restriction fragment length polymorphism of the D2 dopamine receptor gene, according to four of six studies that examined alcoholics and controls. The current study examines whether the association observed in alcoholism might extend to other addictive substances by examining D2 dopamine receptor Taq I A and B restriction fragment length polymorphisms in polysubstance users and controls free of significant substance use. We hypothesized a stronger association for the B1 restriction fragment length polymorphism since it lies closer to dopamine receptor protein coding and 5' regulatory regions. Heavy polysubstance users and subjects with DSM-III-R psychoactive substance use diagnoses displayed significantly higher Taq I B1 frequencies than control subjects; Taq I A1 results for these comparisons were less robust. These results are consistent with a role for a D2 dopamine receptor gene variant marked by these restriction fragment length polymorphisms in enhanced substance abuse vulnerability. JF - Archives of general psychiatry AU - Smith, S S AU - O'Hara, B F AU - Persico, A M AU - Gorelick, D A AU - Newlin, D B AU - Vlahov, D AU - Solomon, L AU - Pickens, R AU - Uhl, G R AD - Addiction Research Center, National Institute on Drug Abuse, Bethesda, Md. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 723 EP - 727 VL - 49 IS - 9 SN - 0003-990X, 0003-990X KW - Genetic Markers KW - 0 KW - Receptors, Dopamine KW - Abridged Index Medicus KW - Index Medicus KW - Alleles KW - Humans KW - Alcoholism -- genetics KW - Male KW - Female KW - Polymorphism, Restriction Fragment Length KW - Receptors, Dopamine -- genetics KW - Substance-Related Disorders -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73170326?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+general+psychiatry&rft.atitle=Genetic+vulnerability+to+drug+abuse.+The+D2+dopamine+receptor+Taq+I+B1+restriction+fragment+length+polymorphism+appears+more+frequently+in+polysubstance+abusers.&rft.au=Smith%2C+S+S%3BO%27Hara%2C+B+F%3BPersico%2C+A+M%3BGorelick%2C+D+A%3BNewlin%2C+D+B%3BVlahov%2C+D%3BSolomon%2C+L%3BPickens%2C+R%3BUhl%2C+G+R&rft.aulast=Smith&rft.aufirst=S&rft.date=1992-09-01&rft.volume=49&rft.issue=9&rft.spage=723&rft.isbn=&rft.btitle=&rft.title=Archives+of+general+psychiatry&rft.issn=0003990X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-28 N1 - Date created - 1992-09-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transforming growth factor-alpha in human hepatocellular carcinoma and coexpression with hepatitis B surface antigen in adjacent liver. AN - 73167964; 1325266 AB - Hepatitis B virus (HBV) infection is closely associated with the development of hepatocellular carcinoma (HCC) in many patients, but the mechanisms by which HBV contributes to HCC are not known. Transforming growth factor-alpha (TGF-alpha), a regulator of growth and regeneration in rat liver that can be found in high levels in some human cancers, theoretically could play such an intermediate role in the development of HCC. The expression of TGF-alpha and its relation to the HBV antigens were evaluated in human HCC and adjacent nontumorous livers from 33 patients from the United States and China using immunoperoxidase staining of paraffin-embedded sections. TGF-alpha was detected in HCC from 27 of 33 (82%) patients; the frequencies were similar in patients from the United States and China. TGF-alpha was detected in HCC more frequently in patients whose adjacent nontumorous livers had detectable hepatitis B surface antigen (HBsAg) and/or hepatitis B core antigen (HBcAg) than in those whose adjacent livers lacked HBsAg and HBcAg. Detection of TGF-alpha was not affected by tumor size, histologic type, or grade. TGF-alpha was detected in adjacent nontumorous livers from 31 of 33 patients (94%). Coexpression at a high intensity of TGF-alpha and HBsAg in the same hepatocytes could be demonstrated by specific staining of consecutively cut sections for 17 of 33 patients (52%). TGF-alpha is expressed at a high level in 82% of human HCC. Localization of HBsAg within the same hepatocytes as TGF-alpha suggests a possible interaction between HBV and TGF-alpha during hepatocarcinogenesis in humans. Stimulation of TGF-alpha expression could be part of a chain of events by which HBV contributes to the development of HCC in some patients. JF - Cancer AU - Hsia, C C AU - Axiotis, C A AU - Di Bisceglie, A M AU - Tabor, E AD - Biological Carcinogenesis Program, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09/01/ PY - 1992 DA - 1992 Sep 01 SP - 1049 EP - 1056 VL - 70 IS - 5 SN - 0008-543X, 0008-543X KW - Hepatitis B Surface Antigens KW - 0 KW - Transforming Growth Factor alpha KW - Abridged Index Medicus KW - Index Medicus KW - Sensitivity and Specificity KW - Hepatitis B virus KW - Humans KW - Aged KW - Cell Differentiation KW - Hepatitis B -- complications KW - China -- epidemiology KW - Adult KW - Middle Aged KW - United States -- epidemiology KW - Immunohistochemistry KW - Female KW - Male KW - Liver Neoplasms -- pathology KW - Liver -- immunology KW - Hepatitis B Surface Antigens -- analysis KW - Transforming Growth Factor alpha -- physiology KW - Liver Neoplasms -- chemistry KW - Carcinoma, Hepatocellular -- pathology KW - Liver -- metabolism KW - Carcinoma, Hepatocellular -- chemistry KW - Transforming Growth Factor alpha -- analysis KW - Liver -- chemistry KW - Carcinoma, Hepatocellular -- immunology KW - Liver Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73167964?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Transforming+growth+factor-alpha+in+human+hepatocellular+carcinoma+and+coexpression+with+hepatitis+B+surface+antigen+in+adjacent+liver.&rft.au=Hsia%2C+C+C%3BAxiotis%2C+C+A%3BDi+Bisceglie%2C+A+M%3BTabor%2C+E&rft.aulast=Hsia&rft.aufirst=C&rft.date=1992-09-01&rft.volume=70&rft.issue=5&rft.spage=1049&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-07 N1 - Date created - 1992-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interferon gamma induces the expression of human immunodeficiency virus in persistently infected promonocytic cells (U1) and redirects the production of virions to intracytoplasmic vacuoles in phorbol myristate acetate-differentiated U1 cells. AN - 73163476; 1512539 AB - Interferon gamma (IFN-gamma), a lymphokine that exerts multiple immunoregulatory effects, has been found to be elevated in the plasma, cerebrospinal fluid, and lymph nodes of human immunodeficiency virus (HIV)-infected individuals and has shown variable effects on HIV replication in acutely infected cells. In the present study, we have demonstrated that IFN-gamma is a potent modulator of HIV expression in persistently infected U1 promonocytic cells in which virus production is characterized by a constitutive state of relative latency. Direct stimulation of U1 cells with IFN-gamma (10-1,000 U/ml) activated HIV expression, as measured by reverse transcriptase (RT) activity in the culture supernatant and increased levels of cell-associated viral protein and mRNAs. These effects on virus expression were not accounted for by the induction of endogenous TNF-alpha secretion, as previously described in U1 cells stimulated with phorbol myristate acetate (PMA). At the ultrastructural level, the stimulatory activity of IFN-gamma was correlated with HIV particle production in intracytoplasmic vacuoles along with the differentiation of U1 into macrophage-like cells. Furthermore, costimulation of U1 cells with IFN-gamma and PMA significantly increased the accumulation of vacuole-associated HIV concomitant with decreasing membrane-associated particles and RT activity production, as compared with cells stimulated with PMA alone. No evidence of spontaneous secretion of intracellular vacuole-associated virus was obtained by kinetic analysis of the RT activity released in the supernatants throughout the culture period unless cells were deliberately disrupted. These findings suggest that vacuole-associated virions likely represent a relatively stable intracellular reservoir of HIV, as previously described in primary macrophages infected in vitro or in infected macrophages in the brains of patients with acquired immune deficiency syndrome. The reduced levels of RT activity observed in the culture supernatants of U1 cells stimulated with PMA in the presence of IFN-gamma were not indicative of a suppressive effect of IFN-gamma on PMA-induced expression of HIV proteins and mRNAs, either directly or mediated by the release of IFN-alpha/beta. This study suggests that IFN-gamma may play an important role as an inducer of HIV expression in infected mononuclear phagocytes. JF - The Journal of experimental medicine AU - Biswas, P AU - Poli, G AU - Kinter, A L AU - Justement, J S AU - Stanley, S K AU - Maury, W J AU - Bressler, P AU - Orenstein, J M AU - Fauci, A S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09/01/ PY - 1992 DA - 1992 Sep 01 SP - 739 EP - 750 VL - 176 IS - 3 SN - 0022-1007, 0022-1007 KW - Interferon-gamma KW - 82115-62-6 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - AIDS/HIV KW - Kinetics KW - Humans KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Differentiation KW - Microscopy, Electron KW - Virion -- growth & development KW - Up-Regulation KW - Virus Activation KW - Cell Line KW - HIV -- growth & development KW - Monocytes -- cytology KW - Monocytes -- drug effects KW - Monocytes -- microbiology KW - Interferon-gamma -- physiology KW - Vacuoles -- microbiology KW - HIV -- ultrastructure KW - Monocytes -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73163476?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+experimental+medicine&rft.atitle=Interferon+gamma+induces+the+expression+of+human+immunodeficiency+virus+in+persistently+infected+promonocytic+cells+%28U1%29+and+redirects+the+production+of+virions+to+intracytoplasmic+vacuoles+in+phorbol+myristate+acetate-differentiated+U1+cells.&rft.au=Biswas%2C+P%3BPoli%2C+G%3BKinter%2C+A+L%3BJustement%2C+J+S%3BStanley%2C+S+K%3BMaury%2C+W+J%3BBressler%2C+P%3BOrenstein%2C+J+M%3BFauci%2C+A+S&rft.aulast=Biswas&rft.aufirst=P&rft.date=1992-09-01&rft.volume=176&rft.issue=3&rft.spage=739&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+experimental+medicine&rft.issn=00221007&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-30 N1 - Date created - 1992-09-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1988 Sep 23;241(4873):1673-5 [3047875] J Immunol. 1988 Jan 1;140(1):120-4 [3121735] J Virol. 1988 Aug;62(8):2578-86 [3260631] J Immunol. 1985 Mar;134(3):1503-7 [3918102] N Engl J Med. 1985 Dec 12;313(24):1504-10 [3934537] J Leukoc Biol. 1991 Jun;49(6):566-78 [1673992] FASEB J. 1991 Jul;5(10):2382-90 [1676689] Leuk Res. 1990;14(11-12):1027-33 [1704084] Exp Cell Res. 1991 Mar;193(1):20-6 [1825297] Neurology. 1991 Jan;41(1):69-74 [1898675] Leuk Res. 1991;15(5):327-39 [1904515] J Immunol. 1991 Nov 1;147(9):2922-7 [1918999] J Immunol. 1990 Jun 15;144(12):4628-32 [1972163] FASEB J. 1991 Jul;5(10):2391-7 [2065887] J Clin Invest. 1990 Jul;86(1):148-59 [2114424] J Interferon Res. 1990 Dec;10(6):599-603 [2128302] Semin Oncol. 1990 Dec;17(6 Suppl 9):38-46 [2148026] Immunol Today. 1990 Jun;11(6):217-23 [2191685] Proc Natl Acad Sci U S A. 1990 Jan;87(2):782-5 [2300561] Clin Exp Immunol. 1985 Oct;62(1):128-35 [2415279] J Interferon Res. 1986 Apr;6(2):143-52 [2425014] Annu Rev Biochem. 1987;56:727-77 [2441659] Science. 1988 Nov 11;242(4880):919-22 [2460922] Science. 1989 May 5;244(4904):575-7 [2470148] Proc Natl Acad Sci U S A. 1989 Jan;86(2):675-9 [2492110] Science. 1989 Jul 21;245(4915):305-8 [2665081] Blood. 1986 Jul;68(1):281-4 [3013342] Science. 1986 Jul 11;233(4760):215-9 [3014648] Onkologie. 1986 Jun;9(3):163-6 [3018647] AIDS Res Hum Retroviruses. 1987 Summer;3(2):125-33 [3113463] AIDS Res Hum Retroviruses. 1988 Aug;4(4):287-94 [3144996] J Exp Med. 1988 Apr 1;167(4):1428-41 [3258626] Hum Pathol. 1988 Mar;19(3):350-61 [3346011] N Engl J Med. 1984 Apr 5;310(14):883-9 [6422299] AIDS Res Hum Retroviruses. 1992 Feb;8(2):199-207 [1371692] Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9838-42 [1682922] J Virol. 1991 Jul;65(7):3968-71 [1710293] J Leukoc Biol. 1991 Mar;49(3):294-301 [1847718] Clin Exp Immunol. 1991 Jul;85(1):143-50 [1906383] J Infect Dis. 1991 Dec;164(6):1051-7 [1955708] Pharmacol Ther. 1990;45(1):137-51 [2105509] Biochem Pharmacol. 1990 Oct 1;40(7):1433-9 [2121146] J Exp Pathol. 1990;5(3):127-32 [2128842] J Exp Med. 1990 Jul 1;172(1):151-8 [2193094] Cell. 1990 Jun 29;61(7):1271-6 [2364429] Proc Natl Acad Sci U S A. 1986 Nov;83(22):8734-8 [2430298] J Immunol. 1988 Feb 15;140(4):1117-22 [2449497] J Exp Med. 1989 Mar 1;169(3):1137-51 [2466937] N Engl J Med. 1985 Jul 11;313(2):79-84 [2582258] Proc Natl Acad Sci U S A. 1989 Aug;86(15):5974-8 [2762307] Science. 1986 Sep 5;233(4768):1089-93 [3016903] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inter-relationships between quinolinic acid, neuroactive kynurenines, neopterin and beta 2-microglobulin in cerebrospinal fluid and serum of HIV-1-infected patients. AN - 73159494; 1387655 AB - Quinolinic acid (QUIN) is an neurotoxic N-methyl-D-aspartate receptor agonist and an L-tryptophan metabolite of the kynurenine pathway. Increased concentrations of QUIN occur in both cerebrospinal fluid (CSF) and blood of patients infected with human immunodeficiency virus (HIV)-1, particularly those with neurologic disturbances. In the present study of HIV-1 infected patients in Walter Reed stages 4, 5 and 6, reductions in L-tryptophan accompanied proportional increases in L-kynurenine and QUIN in both serum and CSF. Further, close inter-correlations exist between QUIN kynurenic acid and L-kynurenine with both beta 2-microglobulin and neopterin in CSF and serum. These correlations support the hypotheses that the kynurenine pathway is activated in association with inflammation and induction of indoleamine-2,3-dioxygenase. There were no relationships between CSF QUIN, L-kynurenine or kynurenic acid with the ratio of serum:CSF albumin concentrations, which indicates that the increases in CSF QUIN, L-kynurenine or kynurenic acid were not dependent on a breakdown of the blood-brain barrier. Kynurenic acid is also a kynurenine pathway metabolite that can attenuate the excitotoxic effects of QUIN when present in higher molar concentrations. While CSF kynurenic acid levels were increased in HIV-1-infected patients, the magnitude of the increases were smaller than those of QUIN and the molar concentrations of kynurenic acid were consistently lower than QUIN by at least one order of magnitude. We conclude that immune activation increases the levels of neuroactive kynurenines within the central nervous system of HIV-1-infected patients secondary to activation of indoleamine-2,3-dioxygenase. JF - Journal of neuroimmunology AU - Heyes, M P AU - Brew, B J AU - Saito, K AU - Quearry, B J AU - Price, R W AU - Lee, K AU - Bhalla, R B AU - Der, M AU - Markey, S P AD - Section on Analytical Biochemistry, NIMH, NIH, Bethesda, MD 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 71 EP - 80 VL - 40 IS - 1 SN - 0165-5728, 0165-5728 KW - Neurotoxins KW - 0 KW - Quinolinic Acids KW - beta 2-Microglobulin KW - Biopterin KW - 22150-76-1 KW - Serotonin KW - 333DO1RDJY KW - Kynurenine KW - 343-65-7 KW - Neopterin KW - 670-65-5 KW - Quinolinic Acid KW - F6F0HK1URN KW - Index Medicus KW - AIDS/HIV KW - AIDS Dementia Complex -- metabolism KW - Serotonin -- cerebrospinal fluid KW - Humans KW - Serotonin -- blood KW - Nervous System Physiological Phenomena KW - AIDS Dementia Complex -- psychology KW - Blood-Brain Barrier KW - Quinolinic Acids -- blood KW - beta 2-Microglobulin -- metabolism KW - Biopterin -- cerebrospinal fluid KW - HIV-1 KW - Biopterin -- analogs & derivatives KW - Kynurenine -- blood KW - Kynurenine -- cerebrospinal fluid KW - Kynurenine -- physiology KW - Acquired Immunodeficiency Syndrome -- blood KW - Biopterin -- blood KW - beta 2-Microglobulin -- cerebrospinal fluid KW - Quinolinic Acids -- cerebrospinal fluid KW - Acquired Immunodeficiency Syndrome -- cerebrospinal fluid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73159494?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neuroimmunology&rft.atitle=Inter-relationships+between+quinolinic+acid%2C+neuroactive+kynurenines%2C+neopterin+and+beta+2-microglobulin+in+cerebrospinal+fluid+and+serum+of+HIV-1-infected+patients.&rft.au=Heyes%2C+M+P%3BBrew%2C+B+J%3BSaito%2C+K%3BQuearry%2C+B+J%3BPrice%2C+R+W%3BLee%2C+K%3BBhalla%2C+R+B%3BDer%2C+M%3BMarkey%2C+S+P&rft.aulast=Heyes&rft.aufirst=M&rft.date=1992-09-01&rft.volume=40&rft.issue=1&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=Journal+of+neuroimmunology&rft.issn=01655728&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-08 N1 - Date created - 1992-10-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - GGT to GTT transversions in codon 12 of the K-ras oncogene in rat renal sarcomas induced with nickel subsulfide or nickel subsulfide/iron are consistent with oxidative damage to DNA. AN - 73159492; 1511440 AB - Nickel is a toxic, mutagenic, and carcinogenic metal of significant occupational and environmental concern. Although several cellular targets of nickel have been identified, considerable evidence suggests that it can act indirectly upon DNA by inducing the formation of oxidized purines or pyrimidines that constitute promutagenic lesions. In this study, we examined nickel subsulfide (Ni3S2)- or Ni3S2/iron-induced renal sarcomas in F344 rats for the presence of transforming mutations in the K-ras oncogene. Selective oligonucleotide hybridization analysis of K-ras gene sequences amplified by polymerase chain reaction revealed that 1 of 12 primary tumors induced with Ni3S2 and 7 of 9 primary tumors induced with Ni3S2/iron contained exclusively GGT to GTT activating mutations in codon 12. These mutations are consistent with the known ability of nickel, in the presence of an oxidizing agent, to catalyze formation of 8-hydroxydeoxyguanosine, which in turn promotes misincorporation of dATP opposite the oxidized guanine residue. The presence of GGT to GTT transversions was confirmed by direct sequencing of the polymerase chain reaction products. Sequencing also revealed that there were no transforming mutations in codons 13 or 59-61. Additionally, a direct correlation between shortened tumor latency and the presence of activating ras mutations was noted. These results show that, in rat kidney, Ni3S2 can induce transforming mutations that are consistent with the ability of nickel to produce oxidative lesions and that iron, which exacerbates the extent of cellular oxidative damage, can enhance the frequency of these transforming mutations. JF - Cancer research AU - Higinbotham, K G AU - Rice, J M AU - Diwan, B A AU - Kasprzak, K S AU - Reed, C D AU - Perantoni, A O AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, Maryland 21702-1201. Y1 - 1992/09/01/ PY - 1992 DA - 1992 Sep 01 SP - 4747 EP - 4751 VL - 52 IS - 17 SN - 0008-5472, 0008-5472 KW - Codon KW - 0 KW - Oligodeoxyribonucleotides KW - nickel subsulfide KW - 12035-72-2 KW - Nickel KW - 7OV03QG267 KW - DNA KW - 9007-49-2 KW - Iron KW - E1UOL152H7 KW - Proto-Oncogene Proteins p21(ras) KW - EC 3.6.5.2 KW - Index Medicus KW - Rats KW - Oxidation-Reduction KW - Animals KW - Rats, Inbred F344 KW - Base Sequence KW - Oligodeoxyribonucleotides -- chemistry KW - Molecular Sequence Data KW - DNA -- chemistry KW - Kidney Neoplasms -- genetics KW - Genes, ras KW - Sarcoma, Experimental -- chemically induced KW - Kidney Neoplasms -- chemically induced KW - DNA Damage KW - Iron -- chemistry KW - Nickel -- toxicity KW - Sarcoma, Experimental -- genetics KW - Iron -- toxicity KW - Nickel -- chemistry KW - Proto-Oncogene Proteins p21(ras) -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73159492?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=GGT+to+GTT+transversions+in+codon+12+of+the+K-ras+oncogene+in+rat+renal+sarcomas+induced+with+nickel+subsulfide+or+nickel+subsulfide%2Firon+are+consistent+with+oxidative+damage+to+DNA.&rft.au=Higinbotham%2C+K+G%3BRice%2C+J+M%3BDiwan%2C+B+A%3BKasprzak%2C+K+S%3BReed%2C+C+D%3BPerantoni%2C+A+O&rft.aulast=Higinbotham&rft.aufirst=K&rft.date=1992-09-01&rft.volume=52&rft.issue=17&rft.spage=4747&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-29 N1 - Date created - 1992-09-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 95-kilodalton B-Raf serine/threonine kinase: identification of the protein and its major autophosphorylation site. AN - 73157874; 1508179 AB - B-Raf, a member of the Raf family of serine/threonine kinases, is expressed primarily in the brain and in the nervous system. In this study, the biochemical properties of the B-Raf protein were investigated in nerve growth factor (NGF)-responsive cell lines and in brain tissues. B-Raf was identified by using phosphopeptide mapping analysis and cDNA analysis as a 95-kDa protein which is primarily localized in the cytosol. NGF rapidly stimulated both serine and threonine phosphorylation in vivo and autophosphorylation activity in vitro of the B-Raf protein. In PC12 cells, B-Raf autokinase activity was induced by both differentiation factors and mitogens, with maximal activity observed after 5 min of factor addition. B-Raf kinase activity was also observed following NGF treatment of SH-SY5Y neuroblastoma cells and in adult mouse brain and hippocampus. Induction of B-Raf kinase activity in NGF-treated PC12 cells required expression of kinase-active trk receptors. Exogenous substrates or a peptide containing the autophosphorylation site became phosphorylated when added to immune complex kinase assays and reduced the in vitro autophosphorylation activity of B-Raf, suggesting that in vitro autophosphorylation sites and exogenous substrates compete for active sites of the B-Raf kinase. Finally, the major in vitro autophosphorylation site of B-Raf was identified as threonine 372 in the conserved region 2 domain. A threonine residue is present at similar positions in all three mammalian Raf family members and may represent a regulatory site for these proteins. JF - Molecular and cellular biology AU - Stephens, R M AU - Sithanandam, G AU - Copeland, T D AU - Kaplan, D R AU - Rapp, U R AU - Morrison, D K AD - Molecular Mechanisms of Carcinogenesis Laboratory, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 3733 EP - 3742 VL - 12 IS - 9 SN - 0270-7306, 0270-7306 KW - Nerve Growth Factors KW - 0 KW - Proto-Oncogene Proteins KW - Protein Kinases KW - EC 2.7.- KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Proto-Oncogene Proteins c-raf KW - EC 2.7.11.1 KW - Index Medicus KW - Brain -- enzymology KW - Animals KW - Blotting, Western KW - Phosphorylation KW - Peptide Mapping KW - Enzyme Activation KW - Molecular Sequence Data KW - Nerve Growth Factors -- physiology KW - Mice KW - Amino Acid Sequence KW - Protein-Tyrosine Kinases -- metabolism KW - PC12 Cells KW - Protein Kinases -- metabolism KW - Proto-Oncogene Proteins -- chemistry KW - Proto-Oncogene Proteins -- metabolism KW - Protein Kinases -- genetics KW - Proto-Oncogene Proteins -- genetics KW - Protein Kinases -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73157874?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+cellular+biology&rft.atitle=95-kilodalton+B-Raf+serine%2Fthreonine+kinase%3A+identification+of+the+protein+and+its+major+autophosphorylation+site.&rft.au=Stephens%2C+R+M%3BSithanandam%2C+G%3BCopeland%2C+T+D%3BKaplan%2C+D+R%3BRapp%2C+U+R%3BMorrison%2C+D+K&rft.aulast=Stephens&rft.aufirst=R&rft.date=1992-09-01&rft.volume=12&rft.issue=9&rft.spage=3733&rft.isbn=&rft.btitle=&rft.title=Molecular+and+cellular+biology&rft.issn=02707306&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-23 N1 - Date created - 1992-09-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell. 1991 May 17;65(4):663-75 [2032290] Cold Spring Harb Symp Quant Biol. 1985;50:253-62 [3938363] Mol Cell Biol. 1990 Jun;10(6):2503-12 [2188091] Methods Enzymol. 1990;182:194-203 [2314237] Science. 1986 Apr 25;232(4749):485-7 [2421409] Proc Natl Acad Sci U S A. 1989 Dec;86(24):10128-32 [2602361] Mol Cell Biol. 1989 Feb;9(2):639-47 [2710120] Nucleic Acids Res. 1988 Dec 9;16(23):11057-74 [2905047] J Cell Biol. 1986 Mar;102(3):830-43 [3005338] Nucleic Acids Res. 1987 Jan 26;15(2):595-609 [3029685] Mol Cell Biol. 1988 Jun;8(6):2651-4 [3043188] Proc Natl Acad Sci U S A. 1988 Jul;85(13):4691-5 [3133658] EMBO J. 1988 Oct;7(10):3053-60 [3181128] Science. 1987 Nov 6;238(4828):797-9 [3672127] J Neurosci. 1986 Aug;6(8):2155-62 [3746405] J Neurosci Res. 1982;8(2-3):375-91 [6296415] Proc Natl Acad Sci U S A. 1976 Jul;73(7):2424-8 [1065897] Cell. 1991 Sep 6;66(5):961-6 [1653650] J Biol Chem. 1991 Jan 25;266(3):1359-62 [1703147] Nature. 1991 Mar 14;350(6314):158-60 [1706478] J Biol Chem. 1991 Oct 25;266(30):19908-16 [1718957] Cell. 1991 Apr 5;65(1):189-97 [1849459] Nature. 1991 Apr 25;350(6320):678-83 [1850821] Brain Res. 1991 May 3;547(2):309-14 [1884206] Methods Enzymol. 1991;201:110-49 [1943760] Mol Cell Biol. 1991 Feb;11(2):913-9 [1990291] Nature. 1991 Jan 31;349(6308):426-8 [1992343] Exp Brain Res. 1991;84(2):403-10 [2065747] Eur J Biochem. 1990 Nov 13;193(3):661-9 [2174361] Mol Cell Biol. 1990 Jul;10(7):3828-33 [2192265] Oncogene. 1990 Dec;5(12):1775-80 [2284096] J Biol Chem. 1990 Sep 15;265(26):15471-80 [2394735] Cell. 1989 Aug 25;58(4):649-57 [2475255] Cell. 1989 Sep 22;58(6):1121-33 [2550144] J Gen Virol. 1977 Jul;36(1):59-74 [886304] Oncogene. 1990 Mar;5(3):345-51 [1690378] Eur J Biochem. 1989 Jul 15;183(1):227-33 [2666134] J Biol Chem. 1989 May 25;264(15):8646-52 [2785993] Virology. 1985 Oct 15;146(1):78-89 [2994296] Proc Natl Acad Sci U S A. 1991 Jul 1;88(13):5650-4 [1712104] J Biol Chem. 1991 Dec 15;266(35):23753-60 [1748651] Science. 1991 Apr 26;252(5005):554-8 [1850549] Genes Dev. 1991 Sep;5(9):1553-67 [1884998] Methods Enzymol. 1991;201:149-52 [1943761] Nucleic Acids Res. 1986 Jan 24;14(2):1009-15 [3003687] Cell. 1986 Nov 21;47(4):545-54 [3022937] EMBO J. 1986 Dec 20;5(13):3441-7 [3030727] Proc Natl Acad Sci U S A. 1987 Apr;84(7):1819-23 [3031652] Cell. 1988 Apr 8;53(1):37-43 [3127059] J Biol Chem. 1988 Nov 5;263(31):15853-6 [3141398] Nucleic Acids Res. 1987 Oct 26;15(20):8125-48 [3313277] Proc Natl Acad Sci U S A. 1986 Apr;83(8):2353-7 [3458200] Science. 1987 Dec 18;238(4834):1726-8 [3686012] Nature. 1985 Feb 14-20;313(6003):545-51 [3918274] Cancer Cells. 1990 Dec;2(12):377-82 [2150916] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cross-talk between excitatory and inhibitory amino acids in the regulation of luteinizing hormone-releasing hormone secretion. AN - 73151890; 1354606 AB - Inhibitory (IAA) and excitatory amino acid (EAA) neurotransmitters appear to play an important role in regulating reproductive functions. L-Glutamic acid (GLU), the major representative of the EAA system, stimulates LHRH release from arcuate nucleus-median eminence (AN-ME) fragments in vitro. Several studies have provided evidence for considering gamma-aminobutyric acid (GABA), a major IAA neurotransmitter, as another regulator of LHRH secretion. Recent reports have indicated that a cross-talk between GABA and GLU participates in the regulation of synaptic transmission in the brain. In concert with this notion, we present evidence indicating that this cross-talk between GABA and GLU appears to be also involved in neuroendocrinological paradigms. In this respect, bicuculline, a GABA-A receptor antagonist, blocked GLU-evoked LHRH secretion from AN-ME fragments in vitro without affecting basal LHRH release. In addition, activation of GABA-A receptors by muscimol (MUS) stimulated basal LHRH secretion. Interestingly, when MUS and GLU were added together to the incubation medium, an additive, stimulatory effect was observed. These observations clearly indicate that a GABAergic mechanism participates, via GABA-A receptors, in GLU-induced LHRH secretion from terminals of the ME. Furthermore, GABA-B receptors appear to negatively modulate the effects of GLU. Activation of GABA-B receptors by baclofen (BAC) blocked GLU-induced LHRH secretion, while phaclofen, a GABA-B receptor antagonist, reversed this effect. In summary, our data provide evidence for a cross-talk between EAA and IAA systems in the regulation of LHRH release, and, therefore, in the control of gonadal function. JF - Endocrinology AU - Donoso, A O AU - López, F J AU - Negro-Vilar, A AD - Reproductive Neuroendocrinology Section, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 1559 EP - 1561 VL - 131 IS - 3 SN - 0013-7227, 0013-7227 KW - Excitatory Amino Acid Antagonists KW - 0 KW - GABA-A Receptor Antagonists KW - Glutamates KW - Receptors, GABA-A KW - phaclofen KW - 108351-35-5 KW - Muscimol KW - 2763-96-4 KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 KW - Glutamic Acid KW - 3KX376GY7L KW - gamma-Aminobutyric Acid KW - 56-12-2 KW - Baclofen KW - H789N3FKE8 KW - Bicuculline KW - Y37615DVKC KW - Abridged Index Medicus KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Drug Interactions KW - Receptors, GABA-A -- physiology KW - In Vitro Techniques KW - Baclofen -- analogs & derivatives KW - Male KW - Baclofen -- pharmacology KW - Bicuculline -- pharmacology KW - Median Eminence -- secretion KW - Glutamates -- pharmacology KW - Arcuate Nucleus of Hypothalamus -- drug effects KW - gamma-Aminobutyric Acid -- pharmacology KW - Arcuate Nucleus of Hypothalamus -- secretion KW - Gonadotropin-Releasing Hormone -- secretion KW - Muscimol -- pharmacology KW - Median Eminence -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73151890?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrinology&rft.atitle=Cross-talk+between+excitatory+and+inhibitory+amino+acids+in+the+regulation+of+luteinizing+hormone-releasing+hormone+secretion.&rft.au=Donoso%2C+A+O%3BL%C3%B3pez%2C+F+J%3BNegro-Vilar%2C+A&rft.aulast=Donoso&rft.aufirst=A&rft.date=1992-09-01&rft.volume=131&rft.issue=3&rft.spage=1559&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-22 N1 - Date created - 1992-09-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of ICRF-187 on the pulmonary damage induced by hyperoxia in the rat. AN - 73148320; 1519241 AB - Histological and ultrastructural studies were made of the lungs of rats that were exposed to 100% oxygen for 60 h and were treated with either normal saline or with ICRF-187, a bis-diketopiperazine derivative of EDTA that has the capacity to chelate iron. This metal is thought to be needed to catalyze the formation of toxic oxygen free radicals. ICRF-187 (20 mg/kg) was given intraperitoneally at approximately 12 h intervals (5 doses) during the 60 h exposure. Seven of the ten saline-treated rats exposed to oxygen died prior to the end of the study whereas only one of the 10 rats in the ICRF-187-treated group died. This difference in mortality is found to be statistically significant (P less than 0.05). All saline-treated rats showed light and electron microscopic evidence of pulmonary damage. ICRF-187 attenuated the morphologic alterations observed by light microscopy (intra-alveolar edema, inflammatory exudates and bronchiolar epithelial cell swelling and hyperplasia; P less than 0.05). In addition, electron microscopic evaluation revealed that capillary thrombi, endothelial cell alterations and alveolar epithelial cell damage also were less severe in ICRF-187-treated rats. It is concluded that ICRF-187 may provide a new and useful approach for the prevention of hyperoxia-induced pulmonary damage. JF - Toxicology AU - Fukuda, Y AU - Herman, E H AU - Ferrans, V J AD - Pathology Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 185 EP - 202 VL - 74 IS - 2-3 SN - 0300-483X, 0300-483X KW - Free Radicals KW - 0 KW - Razoxane KW - 5AR83PR647 KW - Iron KW - E1UOL152H7 KW - Oxygen KW - S88TT14065 KW - Index Medicus KW - Space life sciences KW - Rats, Inbred Strains KW - Rats KW - Injections, Intraperitoneal KW - Animals KW - Chelation Therapy KW - Microscopy, Electron KW - Male KW - Razoxane -- pharmacology KW - Razoxane -- administration & dosage KW - Oxygen -- toxicity KW - Lung -- drug effects KW - Lung -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73148320?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology&rft.atitle=Effect+of+ICRF-187+on+the+pulmonary+damage+induced+by+hyperoxia+in+the+rat.&rft.au=Fukuda%2C+Y%3BHerman%2C+E+H%3BFerrans%2C+V+J&rft.aulast=Fukuda&rft.aufirst=Y&rft.date=1992-09-01&rft.volume=74&rft.issue=2-3&rft.spage=185&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-08 N1 - Date created - 1992-10-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vitro and in vivo suppression of interleukin-2-activated killer cell activity by chimeric proteins between interleukin-2 and Pseudomonas exotoxin. AN - 73148168; 1511480 AB - The biological effects of IL-2 are mediated through high (complex of alpha and beta chain) or intermediate (beta chain) affinity IL-2 receptors. Previously, chimeric proteins composed of IL-2 and Pseudomonas exotoxin (IL-2-PE) were shown to be specifically cytotoxic to cells bearing IL-2 receptors. It has also been shown that IL-2-PE chimeric proteins can abrogate T cell-mediated immune response in vitro. In the current study, we have investigated the effects of IL-2-PE on LAK activity both in vivo and in vitro. We administered either IL-2-PE40 (comprised of IL-2 and 40-kDa portion of PE) or IL-2-PE66 (comprised of IL-2 and 66-kDa molecule of PE) to normal C57BL/6 mice for 3 or 8 days and LAK activity was assessed in various organs of mice. We found that IL-2-PE40 generated LAK activity in various compartments of mice and the level of activity was slightly lower than that observed with an equivalent amount of recombinant (r) IL-2 alone. However, IL-2-PE66 failed to generate LAK activity which would have been induced due to an equivalent concentration of rIL-2. IL-2-PE66 also did not induce LAK activity from the splenocytes during in vitro culture while IL-2-PE40 generated good LAK activity. An equivalent amount of IL-2 also generated potent LAK activity. The suppression of LAK activity by IL-2-PE66 was also evident in cells preactivated with IL-2; however, this inhibition was partial. The suppressive activity of IL-2-PE66 was shown to be mediated through IL-2 receptor interactions as excess amounts of rIL-2 were able to abrogate its effect. Both IL-2 toxins were equivalently cytotoxic to IL-2 receptor-bearing HUT 102 cells and both were able to compete from high and intermediate affinity IL-2 receptors. Taken together, our data indicate that IL-2-PE66 is highly cytotoxic to LAK cells while IL-2-PE40 is less cytotoxic. Thus, data from our study and from other published reports indicate that IL-2-PE66 is more potent immunosuppressive agent than IL-2-PE40. JF - Cellular immunology AU - Puri, R K AU - FitzGerald, D AU - Leland, P AU - Kozak, R W AU - Pastan, I AD - Laboratory of Cellular Immunology, Food and Drug Administration, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 324 EP - 334 VL - 143 IS - 2 SN - 0008-8749, 0008-8749 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Interleukin-2 KW - Receptors, Interleukin-2 KW - Recombinant Fusion Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Recombinant Fusion Proteins -- metabolism KW - Lymphocyte Activation -- drug effects KW - Animals KW - Receptors, Interleukin-2 -- metabolism KW - In Vitro Techniques KW - Mice, Inbred C57BL KW - Immunity, Cellular -- drug effects KW - Mice KW - Recombinant Fusion Proteins -- toxicity KW - Female KW - Interleukin-2 -- antagonists & inhibitors KW - Interleukin-2 -- metabolism KW - Killer Cells, Lymphokine-Activated -- immunology KW - Killer Cells, Lymphokine-Activated -- drug effects KW - Exotoxins -- toxicity KW - Exotoxins -- chemistry KW - Cytotoxicity, Immunologic -- drug effects KW - Interleukin-2 -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73148168?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cellular+immunology&rft.atitle=In+vitro+and+in+vivo+suppression+of+interleukin-2-activated+killer+cell+activity+by+chimeric+proteins+between+interleukin-2+and+Pseudomonas+exotoxin.&rft.au=Puri%2C+R+K%3BFitzGerald%2C+D%3BLeland%2C+P%3BKozak%2C+R+W%3BPastan%2C+I&rft.aulast=Puri&rft.aufirst=R&rft.date=1992-09-01&rft.volume=143&rft.issue=2&rft.spage=324&rft.isbn=&rft.btitle=&rft.title=Cellular+immunology&rft.issn=00088749&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-01 N1 - Date created - 1992-10-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evidence for IFN-gamma as a mediator of the lethality of endotoxin and tumor necrosis factor-alpha. AN - 73130231; 1506688 AB - Current evidence indicates that endogenously produced peptide cytokines, most notably TNF-alpha and IL-1, mediate the lethality of experimental endotoxemia. Because circulating serum levels of IFN-gamma can be detected soon after TNF-alpha and IL-1 in response to endotoxin, we investigated the role of IFN-gamma in endotoxin and TNF-alpha lethality. Specific neutralizing antibodies to murine TNF-alpha (anti-TNF-alpha Ab) or murine IFN gamma (anti-IFN-gamma Ab) produced in our laboratory protected mice against the lethality of Escherichia coli endotoxin (LPS) administered 6 h later. Serum IFN-gamma levels 2 h after i.v. LPS were lower in mice treated with anti-TNF-alpha Ab compared to mice that received nonimmune IgG (median less than 2.5 vs 3.0 U/ml, P2 less than 0.05). In contrast, serum TNF-alpha levels 1 h after i.v. LPS peaked more than fourfold higher in mice treated with anti-IFN-gamma Ab compared to controls (median greater than 6400 vs 1405 pg/ml, p2 less than 0.05). Doses of TNF-alpha (300 micrograms/kg) and IFN-gamma (50,000 U) which were well tolerated when given individually were synergistically lethal in combination (0% lethality vs 100% lethality, P2 less than 0.001), and were associated with higher serum levels of IL-6 than with either cytokine alone. Anti-IFN-gamma Ab provided complete protection against exogenous human rTNF-alpha at the LD100 dose (1400 micrograms/kg, p2 less than 0.001), and in fact prevented lethality at doses four- to fivefold greater than the LD100 human rTNF-alpha (up to 6000 micrograms/kg). We conclude that IFN-gamma is synergistic with TNF-alpha, is essential for the lethality of LPS and TNF-alpha, and may have modulating effects on the negative control of serum levels of TNF-alpha after LPS in mice. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Doherty, G M AU - Lange, J R AU - Langstein, H N AU - Alexander, H R AU - Buresh, C M AU - Norton, J A AD - Surgical Metabolism Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09/01/ PY - 1992 DA - 1992 Sep 01 SP - 1666 EP - 1670 VL - 149 IS - 5 SN - 0022-1767, 0022-1767 KW - Antibodies KW - 0 KW - Endotoxins KW - Interleukin-6 KW - Lipopolysaccharides KW - Tumor Necrosis Factor-alpha KW - Interferon-gamma KW - 82115-62-6 KW - Abridged Index Medicus KW - Index Medicus KW - Interleukin-6 -- blood KW - Antibodies -- immunology KW - Animals KW - Mice, Inbred C3H KW - Rabbits KW - Mice KW - Female KW - Tumor Necrosis Factor-alpha -- toxicity KW - Tumor Necrosis Factor-alpha -- analysis KW - Lipopolysaccharides -- toxicity KW - Interferon-gamma -- physiology KW - Interferon-gamma -- blood KW - Endotoxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73130231?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Angiogenin+is+a+cytotoxic%2C+tRNA-specific+ribonuclease+in+the+RNase+A+superfamily.&rft.au=Saxena%2C+S+K%3BRybak%2C+S+M%3BDavey%2C+R+T%3BYoule%2C+R+J%3BAckerman%2C+E+J&rft.aulast=Saxena&rft.aufirst=S&rft.date=1992-10-25&rft.volume=267&rft.issue=30&rft.spage=21982&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-22 N1 - Date created - 1992-09-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - CONF T1 - Multistage carcinogenesis: the Twenty-Second International Symposium of the Princess Takamatsu Cancer Research Fund. AN - 73128225; 1511448 JF - Cancer research AU - Harris, C C AU - Hirohashi, S AU - Ito, N AU - Pitot, H C AU - Sugimura, T AU - Terada, M AU - Yokota, J Y1 - 1992/09/01/ PY - 1992 DA - 1992 Sep 01 SP - 4837 EP - 4840 VL - 52 IS - 17 KW - DNA, Neoplasm KW - 0 KW - Index Medicus KW - Neoplasm Invasiveness KW - Animals KW - Humans KW - Neoplasm Metastasis KW - DNA, Neoplasm -- genetics KW - Cell Differentiation KW - Cell Division KW - Neoplasms -- pathology KW - Neoplasms -- genetics KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73128225?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=Cancer+research&rft.atitle=Multistage+carcinogenesis%3A+the+Twenty-Second+International+Symposium+of+the+Princess+Takamatsu+Cancer+Research+Fund.&rft.au=Harris%2C+C+C%3BHirohashi%2C+S%3BIto%2C+N%3BPitot%2C+H+C%3BSugimura%2C+T%3BTerada%2C+M%3BYokota%2C+J&rft.aulast=Harris&rft.aufirst=C&rft.date=1992-09-01&rft.volume=52&rft.issue=17&rft.spage=4837&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-29 N1 - Date created - 1992-09-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential isoprenylation of carboxy-terminal mutants of an inhibitory G-protein alpha-subunit: neither farnesylation nor geranylgeranylation is sufficient for membrane attachment. AN - 73124507; 1510988 AB - To determine the effect of protein isoprenylation with farnesyl vs geranylgeranyl groups on membrane association in vivo, COS cells were transfected with cDNAs encoding the wild-type G-protein alpha i1 (WT) subunit, the soluble nonmyristoylated G-protein alpha i1 glycine to alanine mutant (GA), a double mutant in which the carboxy-terminal residues CGLF of GA were mutated to CVLS (GA-CVLS), and a double mutant in which the carboxy terminus of GA was mutated to CALL (GA-CALL). As opposed to the WT and GA proteins, the GA-CVLS and GA-CALL proteins were not pertussis toxin substrates nor were they recognized by antibodies that recognize the nonmutated alpha i1 carboxy terminus. Only the GA-CVLS and GA-CALL proteins incorporated [3H]mevalonate in the form of a farnesyl and a geranylgeranyl moiety, respectively. Subcellular localization, as assessed by immunoblotting and immunoprecipitation, revealed that the WT protein localizes almost exclusively to the membrane fraction, whereas the GA, GA-CVLS, and GA-CALL proteins localize predominantly to the soluble fraction. The soluble GA-CVLS and GA-CALL proteins were not carboxyl methylated, but the small amount localized to the membrane was partially carboxyl methylated. These results indicate that neither farnesylation nor geranylgeranylation is sufficient alone to lead to membrane association. JF - Biochemistry AU - Butrynski, J E AU - Jones, T L AU - Backlund, P S AU - Spiegel, A M AD - Molecular Pathophysiology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1992/09/01/ PY - 1992 DA - 1992 Sep 01 SP - 8030 EP - 8035 VL - 31 IS - 34 SN - 0006-2960, 0006-2960 KW - Macromolecular Substances KW - 0 KW - Polyisoprenyl Phosphates KW - Sesquiterpenes KW - geranylgeranyl pyrophosphate KW - 6699-20-3 KW - farnesyl pyrophosphate KW - 79W6B01D07 KW - DNA KW - 9007-49-2 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Mevalonic Acid KW - S5UOB36OCZ KW - Index Medicus KW - Animals KW - Protein Processing, Post-Translational KW - Amino Acid Sequence KW - Chromatography, High Pressure Liquid KW - Rats KW - Mutagenesis, Site-Directed KW - Transfection KW - DNA -- genetics KW - Mevalonic Acid -- metabolism KW - Molecular Sequence Data KW - DNA -- chemistry KW - Immunosorbent Techniques KW - Methylation KW - Cell Line KW - Polyisoprenyl Phosphates -- metabolism KW - GTP-Binding Proteins -- metabolism KW - GTP-Binding Proteins -- chemistry KW - Cell Membrane -- metabolism KW - GTP-Binding Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73124507?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=Differential+isoprenylation+of+carboxy-terminal+mutants+of+an+inhibitory+G-protein+alpha-subunit%3A+neither+farnesylation+nor+geranylgeranylation+is+sufficient+for+membrane+attachment.&rft.au=Butrynski%2C+J+E%3BJones%2C+T+L%3BBacklund%2C+P+S%3BSpiegel%2C+A+M&rft.aulast=Butrynski&rft.aufirst=J&rft.date=1992-09-01&rft.volume=31&rft.issue=34&rft.spage=8030&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-30 N1 - Date created - 1992-09-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Predictors of smoking cessation and relapse in older adults. AN - 73124350; 1503170 AB - We examined longitudinal changes in smoking behavior among older adults in three community cohorts of the Established Populations for Epidemiologic Studies of the Elderly. Smoking prevalence declined from 15% at baseline to 9% during 6 years of follow-up. Annual smoking cessation and relapse rates were 10% and less than 1%, respectively. Interval diagnosis of myocardial infarction, stroke, or cancer increased subsequent smoking cessation but not relapse. Although smoking cessation around diagnosis is increased, primary prevention could yield greater benefits. JF - American journal of public health AU - Salive, M E AU - Cornoni-Huntley, J AU - LaCroix, A Z AU - Ostfeld, A M AU - Wallace, R B AU - Hennekens, C H AD - Epidemiology, Demography and Biometry Program, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 1268 EP - 1271 VL - 82 IS - 9 SN - 0090-0036, 0090-0036 KW - Abridged Index Medicus KW - Index Medicus KW - Aged, 80 and over KW - Risk Factors KW - Humans KW - Aged KW - United States -- epidemiology KW - Recurrence KW - Male KW - Female KW - Prevalence KW - Tobacco Use Disorder -- epidemiology KW - Smoking Cessation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73124350?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+public+health&rft.atitle=Predictors+of+smoking+cessation+and+relapse+in+older+adults.&rft.au=Salive%2C+M+E%3BCornoni-Huntley%2C+J%3BLaCroix%2C+A+Z%3BOstfeld%2C+A+M%3BWallace%2C+R+B%3BHennekens%2C+C+H&rft.aulast=Salive&rft.aufirst=M&rft.date=1992-09-01&rft.volume=82&rft.issue=9&rft.spage=1268&rft.isbn=&rft.btitle=&rft.title=American+journal+of+public+health&rft.issn=00900036&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-17 N1 - Date created - 1992-09-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Psychoactive Drugs. 1989 Jul-Sep;21(3):293-8 [2809895] Am J Public Health. 1983 Apr;73(4):446-50 [6829829] N Engl J Med. 1988 Nov 24;319(21):1365-9 [3185646] JAMA. 1984 Nov 23-30;252(20):2831-4 [6492363] Am J Public Health. 1977 Oct;67(10):921-30 [911003] N Engl J Med. 1991 Jun 6;324(23):1619-25 [2030718] Am Fam Physician. 1990 Oct;42(4):1017-26 [2220510] Am Fam Physician. 1990 Oct;42(4):959-60, 962, 965 [2220522] Prev Med. 1990 Sep;19(5):552-61 [2235922] J Clin Epidemiol. 1990;43(12):1399-405 [2254778] JAMA. 1990 May 23-30;263(20):2760-5 [2271019] Am J Prev Med. 1990 Mar-Apr;6(2):61-70 [2363951] Prev Med. 1990 May;19(3):335-45 [2377595] J Natl Cancer Inst. 1990 Sep 5;82(17):1402-6 [2388290] Am J Public Health. 1989 Feb;79(2):144-51 [2913831] Am J Public Health. 1987 Oct;77(10):1301-5 [3631364] J Natl Cancer Inst. 1983 Sep;71(3):473-9 [6577223] Erratum In: Am J Public Health 1992 Nov;82(11):1489 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ras controls coupling of growth factor receptors and protein kinase C in the membrane to Raf-1 and B-Raf protein serine kinases in the cytosol. AN - 73122215; 1386920 AB - A dominant negative mutant of Ras, M17 Ras, was used to study the role of Ras in receptor coupling of Raf-1 and B-Raf protein serine/threonine kinases (PSKs). We found that mutant Ras blocks serum- and 12-O-tetradecanoyl phorbol 13-acetate-induced activation of Raf-1 kinase in NIH3T3 cells and Raf-1 as well as B-Raf PSK stimulation by nerve growth factor (NGF) in PC12 pheochromocytoma cells. Mitogen stimulation of Raf kinase was measured by determination of Raf hyperphosphorylation and activity towards exogenous substrates and both of these events were inhibited in cells expressing M17 Ras. In contrast, tyrosine phosphorylation of a direct substrate of activated tyrosine kinase receptors, phospholipase C-gamma 1 (PLC-gamma 1), was unaffected. These data indicate that tyrosine phosphorylation of PLC-gamma 1 is not sufficient for growth induction in NIH3T3 cells and that Ras mediates signal transfer from activated membrane receptors to Raf kinases in the cytosol. As activated Raf induced differentiation in PC12 cells expressing M17 Ras we conclude that Raf kinase activation may be sufficient to account for this aspect of NGF function. JF - Oncogene AU - Troppmair, J AU - Bruder, J T AU - App, H AU - Cai, H AU - Liptak, L AU - Szeberényi, J AU - Cooper, G M AU - Rapp, U R AD - Viral Pathology Section, National Cancer Institute, Frederick, Maryland 21702-1201. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 1867 EP - 1873 VL - 7 IS - 9 SN - 0950-9232, 0950-9232 KW - Nerve Growth Factors KW - 0 KW - Proto-Oncogene Proteins KW - Dexamethasone KW - 7S5I7G3JQL KW - Protein Kinases KW - EC 2.7.- KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Receptor, Epidermal Growth Factor KW - Receptor, Macrophage Colony-Stimulating Factor KW - Protein-Serine-Threonine Kinases KW - EC 2.7.11.1 KW - Proto-Oncogene Proteins c-raf KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Cytosol -- metabolism KW - Nerve Growth Factors -- pharmacology KW - Dexamethasone -- pharmacology KW - Receptor, Macrophage Colony-Stimulating Factor -- physiology KW - Receptor, Epidermal Growth Factor -- physiology KW - Amino Acid Sequence KW - Mice KW - Protein-Tyrosine Kinases -- metabolism KW - Phosphorylation KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Blood Physiological Phenomena KW - Genes, ras KW - Protein Kinases -- physiology KW - Protein Kinase C -- physiology KW - Proto-Oncogene Proteins -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73122215?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=Ras+controls+coupling+of+growth+factor+receptors+and+protein+kinase+C+in+the+membrane+to+Raf-1+and+B-Raf+protein+serine+kinases+in+the+cytosol.&rft.au=Troppmair%2C+J%3BBruder%2C+J+T%3BApp%2C+H%3BCai%2C+H%3BLiptak%2C+L%3BSzeber%C3%A9nyi%2C+J%3BCooper%2C+G+M%3BRapp%2C+U+R&rft.aulast=Troppmair&rft.aufirst=J&rft.date=1992-09-01&rft.volume=7&rft.issue=9&rft.spage=1867&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=09509232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-15 N1 - Date created - 1992-09-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Purification of immature cores of mouse mammary tumor virus and immunolocalization of protein domains. AN - 73121252; 1380097 AB - The immature capsids of the mouse mammary tumor virus (MMTV), known as intracytoplasmic A particles, have been isolated from murine L1210 leukemia cells. The diameter of the isolated particles was 80 nm as determined by negative staining. Two polypeptides of 77 and 110 kDa were found to be their major polypeptide components, in agreement with the expected sizes of the Gag and Gag-Pro precursor polypeptides of the mature MMTV proteins. Both polypeptides were recognized by antibodies directed toward the matrix (p10) and capsid (p27) proteins of MMTV. Immunogold labeling of p10 on isolated A particles, visualized by negative staining, showed that this protein is located at the surface of the immature capsids, whereas p27 can be detected only in broken or disrupted particles, suggesting that it has an internal location. These observations were confirmed by immunolabeling of both proteins on thin sections of A particle-producing cells. In addition, the viral protease had a more internal position than p27. Since the sequential order of the viral proteins in the Gag precursor is p10-pp21-p27-p14 and that in Gag-Pro is p10-pp21-p27-p30-protease, our results demonstrate the radial organization of the polypeptide precursors forming the intracytoplasmic A particles. JF - Journal of virology AU - Menéndez-Arias, L AU - Risco, C AU - Pinto da Silva, P AU - Oroszlan, S AD - Laboratory of Molecular Virology and Carcinogenesis, NCI-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 5615 EP - 5620 VL - 66 IS - 9 SN - 0022-538X, 0022-538X KW - Antigens, Viral KW - 0 KW - Epitopes KW - Viral Core Proteins KW - Dexamethasone KW - 7S5I7G3JQL KW - Index Medicus KW - Animals KW - Tumor Cells, Cultured KW - Virus Replication -- drug effects KW - Dexamethasone -- pharmacology KW - Antigens, Viral -- immunology KW - Molecular Sequence Data KW - Mice KW - Amino Acid Sequence KW - Immunohistochemistry KW - Leukemia L1210 KW - Capsid -- isolation & purification KW - Viral Core Proteins -- immunology KW - Capsid -- ultrastructure KW - Viral Core Proteins -- ultrastructure KW - Mammary Tumor Virus, Mouse -- immunology KW - Viral Core Proteins -- isolation & purification KW - Mammary Tumor Virus, Mouse -- ultrastructure KW - Capsid -- immunology KW - Mammary Tumor Virus, Mouse -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73121252?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Purification+of+immature+cores+of+mouse+mammary+tumor+virus+and+immunolocalization+of+protein+domains.&rft.au=Men%C3%A9ndez-Arias%2C+L%3BRisco%2C+C%3BPinto+da+Silva%2C+P%3BOroszlan%2C+S&rft.aulast=Men%C3%A9ndez-Arias&rft.aufirst=L&rft.date=1992-09-01&rft.volume=66&rft.issue=9&rft.spage=5615&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-16 N1 - Date created - 1992-09-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Virology. 1977 Feb;76(2):835-50 [65829] Virology. 1977 Aug;81(1):91-106 [196403] Proc Natl Acad Sci U S A. 1978 Mar;75(3):1404-8 [206897] Anal Biochem. 1976 May 7;72:248-54 [942051] J Virol. 1990 Oct;64(10):5076-92 [1697912] Cell. 1990 Oct 5;63(1):77-86 [2170021] Proc Natl Acad Sci U S A. 1987 Oct;84(20):7041-5 [2823251] Proc Natl Acad Sci U S A. 1987 Jun;84(12):4298-302 [3035577] Virology. 1972 Jul;49(1):61-78 [4114180] J Virol. 1973 Apr;11(4):575-84 [4349496] Proc Natl Acad Sci U S A. 1981 Jun;78(6):3403-7 [6167985] J Virol. 1983 May;46(2):355-61 [6302307] Virology. 1977 Mar;77(1):135-48 [65834] J Gen Virol. 1978 Oct;41(1):193-200 [81268] Virology. 1978 Mar;85(1):157-67 [205999] Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4 [388439] Proc Natl Acad Sci U S A. 1977 Aug;74(8):3446-50 [410020] J Biol Chem. 1992 Jun 5;267(16):11392-8 [1375941] EMBO J. 1991 Mar;10(3):535-46 [1705884] J Virol. 1989 Jun;63(6):2543-9 [2542570] Infect Immun. 1989 Sep;57(9):2878-85 [2668192] J Virol. 1987 Feb;61(2):480-90 [3027377] Virology. 1987 Jan;156(1):171-6 [3643678] Cancer Res. 1986 Nov;46(11):5851-7 [3756926] Appl Microbiol. 1974 Dec;28(6):1040-6 [4141598] Science. 1974 Apr 12;184(4133):158-60 [4361099] Virology. 1981 Feb;109(1):201-4 [6258309] Virology. 1981 Dec;115(2):262-71 [6274085] Science. 1978 Jan 13;199(4325):183-6 [202022] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The precore gene of the woodchuck hepatitis virus genome is not essential for viral replication in the natural host. AN - 73115351; 1501300 AB - A number of naturally occurring hepatitis B virus mutants that cannot synthesize the virus precore protein have been identified. Such mutants have been associated with more severe forms of hepatitis, including fulminant hepatitis. The most common mutation observed is a substitution of G to A in the distal precore gene that converts a codon specifying Trp (TGG) to a termination codon (TAG). Using oligonucleotide-directed mutagenesis, we have produced the same point mutation in the precore gene of an infectious clone of woodchuck hepatitis virus (WHV). Transfection of mutant WHV DNA into the livers of adult woodchucks resulted in replication of the mutant in three of three susceptible animals. Levels of virus replication and transient elevations in liver enzymes in serum were similar to those of adult animals infected with wild-type WHV. Virions, found to possess mutant precore genes by polymerase chain reaction amplification and DNA sequencing, were recovered from the serum of one of the animals and inoculated subcutaneously into neonatal woodchucks. They produced infection in all five animals studied. The level of virus replication in neonatal animals infected with this mutant virus was comparable to that found in neonatal woodchucks infected with wild-type WHV, but none of five woodchucks infected with the precore mutant virus as neonates became chronic virus carriers. It was concluded that the precore gene of the WHV genome is not essential for virus replication in the natural host but may be important for chronic infection. JF - Journal of virology AU - Chen, H S AU - Kew, M C AU - Hornbuckle, W E AU - Tennant, B C AU - Cote, P J AU - Gerin, J L AU - Purcell, R H AU - Miller, R H AD - Hepatitis Viruses Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 5682 EP - 5684 VL - 66 IS - 9 SN - 0022-538X, 0022-538X KW - Protein Precursors KW - 0 KW - Viral Core Proteins KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - Base Sequence KW - Protein Precursors -- metabolism KW - Protein Precursors -- genetics KW - Molecular Sequence Data KW - Carrier State KW - Animals, Newborn -- microbiology KW - Liver -- microbiology KW - Virus Replication KW - Marmota -- microbiology KW - Hepatitis, Animal -- metabolism KW - Hepatitis, Animal -- microbiology KW - Viral Core Proteins -- genetics KW - Hepadnaviridae -- physiology KW - Hepadnaviridae -- genetics KW - Viral Core Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73115351?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=The+precore+gene+of+the+woodchuck+hepatitis+virus+genome+is+not+essential+for+viral+replication+in+the+natural+host.&rft.au=Chen%2C+H+S%3BKew%2C+M+C%3BHornbuckle%2C+W+E%3BTennant%2C+B+C%3BCote%2C+P+J%3BGerin%2C+J+L%3BPurcell%2C+R+H%3BMiller%2C+R+H&rft.aulast=Chen&rft.aufirst=H&rft.date=1992-09-01&rft.volume=66&rft.issue=9&rft.spage=5682&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-16 N1 - Date created - 1992-09-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Virology. 1991 Apr;181(2):733-7 [2014646] Proc Natl Acad Sci U S A. 1990 Dec;87(23):9329-32 [2251274] Cancer Detect Prev. 1989;14(2):227-9 [2695243] Lab Anim Sci. 1985 Aug;35(4):376-81 [2864472] Proc Natl Acad Sci U S A. 1989 Mar;86(6):1846-9 [2928306] Proc Natl Acad Sci U S A. 1986 Mar;83(6):1578-82 [3006057] Proc Natl Acad Sci U S A. 1987 Feb;84(3):866-70 [3468514] J Hepatol. 1991;13 Suppl 4:S68-73 [1668333] Proc Natl Acad Sci U S A. 1991 May 15;88(10):4186-90 [2034663] J Virol. 1990 Mar;64(3):1298-303 [2304145] Hepatology. 1989 Feb;9(2):322-7 [2643549] J Clin Microbiol. 1989 Sep;27(9):1930-3 [2778059] Nucleic Acids Res. 1989 Feb 11;17(3):1266 [2922271] J Infect Dis. 1985 Jun;151(6):1081-92 [2987366] Nucleic Acids Res. 1986 Dec 22;14(24):9679-98 [3027659] J Virol. 1987 Oct;61(10):3322-5 [3041052] J Virol. 1987 Dec;61(12):3701-9 [3682059] N Engl J Med. 1991 Jun 13;324(24):1699-704 [2034246] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Quisqualic acid-induced neurotoxicity is protected by NMDA and non-NMDA receptor antagonists. AN - 73291299; 1359473 AB - Quisqualic acid-mediated excitotoxicity has been attributed essentially to the activation of non-N-methyl-D-aspartate (non-NMDA) receptors. In the present study we demonstrate the possible involvement of both NMDA and non-NMDA receptors in quisqualic acid-induced toxicity in mouse brain slices, in vitro. Incubation of mouse brain sagittal slices with various concentrations of quisqualic acid resulted in significant increase in the leakage of lactate dehydrogenase and potassium from the slices into the medium. Prior incubation of mouse brain slices with NMDA (MK-801 or AP7) or non-NMDA receptor antagonists (GDEE or quinoxalinediones) protected against quisqualic acid-mediated toxicity. Slices prepared from animals pretreated in vivo with MK-801 (5 mg/kg b.wt.) were also resistant to the toxic effects of quisqualic acid, indicating the possible involvement of NMDA receptors in quisqualic acid toxicity. JF - Neuroscience letters AU - Pai, K S AU - Ravindranath, V AD - Department of Neurochemistry, National Institute of Mental Health and Neuroscience, Bangalore, India. Y1 - 1992/08/31/ PY - 1992 DA - 1992 Aug 31 SP - 177 EP - 180 VL - 143 IS - 1-2 SN - 0304-3940, 0304-3940 KW - Amino Acids KW - 0 KW - Excitatory Amino Acid Antagonists KW - Glutamates KW - Quinoxalines KW - Receptors, AMPA KW - Receptors, Glutamate KW - Receptors, Kainic Acid KW - Receptors, N-Methyl-D-Aspartate KW - 2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline KW - 118876-58-7 KW - Glutamic Acid KW - 3KX376GY7L KW - FG 9041 KW - 62T278S1MX KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - 6-Cyano-7-nitroquinoxaline-2,3-dione KW - 6OTE87SCCW KW - 2-Amino-5-phosphonovalerate KW - 76726-92-6 KW - Quisqualic Acid KW - 8OC22C1B99 KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - 2-amino-7-phosphonoheptanoic acid KW - P34K80CUSM KW - Potassium KW - RWP5GA015D KW - Index Medicus KW - Animals KW - Brain -- drug effects KW - L-Lactate Dehydrogenase -- analysis KW - Receptors, Glutamate -- physiology KW - Mice KW - Dizocilpine Maleate -- pharmacology KW - Ion Channel Gating -- drug effects KW - Glutamates -- pharmacology KW - Amino Acids -- pharmacology KW - Potassium -- analysis KW - Quinoxalines -- pharmacology KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - 2-Amino-5-phosphonovalerate -- analogs & derivatives KW - Receptors, N-Methyl-D-Aspartate -- antagonists & inhibitors KW - Quisqualic Acid -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73291299?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+letters&rft.atitle=Quisqualic+acid-induced+neurotoxicity+is+protected+by+NMDA+and+non-NMDA+receptor+antagonists.&rft.au=Pai%2C+K+S%3BRavindranath%2C+V&rft.aulast=Pai&rft.aufirst=K&rft.date=1992-08-31&rft.volume=143&rft.issue=1-2&rft.spage=177&rft.isbn=&rft.btitle=&rft.title=Neuroscience+letters&rft.issn=03043940&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-23 N1 - Date created - 1992-12-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Okadaic acid is a potent inducer of AP-1, NF-kappa B, and tumor necrosis factor-alpha in human B lymphocytes. AN - 73181754; 1520341 AB - Treatment of human B lymphocytes with an optimal concentration of okadaic acid, an inhibitor of phosphatases 1 and 2A, resulted in the induction of the transcription factor, AP-1 and a marked increase in NF-kappa B levels. In contrast, no effect on the levels of the octamer binding proteins, Oct-1 or Oct-2, were found. Since both AP-1 and NF-kappa B have been reported to be important in the induction of the tumor necrosis factor-alpha (TNF-alpha) gene we examined the effects of okadaic acid on TNF-alpha mRNA levels. Treatment with okadaic acid resulted in a striking increase in TNF-alpha mRNA transcripts within 1 h of stimulation and large amounts of TNF-alpha were released into the culture media. Although okadaic acid provides a potent inductive signal for AP-1 and NF-kappa B it did not induce either B cell proliferation or immunoglobulin secretion. JF - Biochemical and biophysical research communications AU - Rieckmann, P AU - Thévenin, C AU - Kehrl, J H AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08/31/ PY - 1992 DA - 1992 Aug 31 SP - 51 EP - 57 VL - 187 IS - 1 SN - 0006-291X, 0006-291X KW - c-fos KW - c-jun KW - Ethers, Cyclic KW - 0 KW - Immunoglobulins KW - NF-kappa B KW - Proto-Oncogene Proteins c-jun KW - RNA, Messenger KW - Tumor Necrosis Factor-alpha KW - Okadaic Acid KW - 1W21G5Q4N2 KW - Cycloheximide KW - 98600C0908 KW - Index Medicus KW - RNA, Messenger -- metabolism KW - Cells, Cultured KW - Immunoglobulins -- metabolism KW - Humans KW - Cycloheximide -- pharmacology KW - Genes, fos -- genetics KW - Genes, jun -- genetics KW - Cell Division KW - B-Lymphocytes -- drug effects KW - NF-kappa B -- biosynthesis KW - Tumor Necrosis Factor-alpha -- biosynthesis KW - Proto-Oncogene Proteins c-jun -- biosynthesis KW - Ethers, Cyclic -- pharmacology KW - B-Lymphocytes -- metabolism KW - Tumor Necrosis Factor-alpha -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73181754?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+biophysical+research+communications&rft.atitle=Okadaic+acid+is+a+potent+inducer+of+AP-1%2C+NF-kappa+B%2C+and+tumor+necrosis+factor-alpha+in+human+B+lymphocytes.&rft.au=Rieckmann%2C+P%3BTh%C3%A9venin%2C+C%3BKehrl%2C+J+H&rft.aulast=Rieckmann&rft.aufirst=P&rft.date=1992-08-31&rft.volume=187&rft.issue=1&rft.spage=51&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+biophysical+research+communications&rft.issn=0006291X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-07 N1 - Date created - 1992-10-07 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-fos; c-jun N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The met proto-oncogene receptor and lumen formation. AN - 73164819; 1387731 AB - The met proto-oncogene product (Met) and its ligand, hepatocyte growth factor/scatter factor (HGF/SF), have been implicated in cell mitogenic response, cell motility, and the promotion of the ordered spatial arrangement of tissue. By means of confocal laser-scanning microscopy, it was shown that Met is expressed in cells bordering lumen-like structures that resemble ducts in the human mammary cell line T47D. In human breast tissue biopsies, Met staining was intense in normal cells bordering mammary ducts but was reduced in adjacent tumor tissue. Met staining in lumen-forming organs colocalizes with staining of antibody to phosphotyrosine, which suggests that the Met receptor and its substrates may be activated in lumen structures or ducts. HGF/SF treatment of human epithelial carcinoma cell lines resulted in the formation of lumen-like structures in vitro. Reduced expression of Met could be related to the extent of tumor cell differentiation. JF - Science (New York, N.Y.) AU - Tsarfaty, I AU - Resau, J H AU - Rulong, S AU - Keydar, I AU - Faletto, D L AU - Vande Woude, G F AD - ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702. Y1 - 1992/08/28/ PY - 1992 DA - 1992 Aug 28 SP - 1258 EP - 1261 VL - 257 IS - 5074 SN - 0036-8075, 0036-8075 KW - Growth Substances KW - 0 KW - Proto-Oncogene Proteins KW - Hepatocyte Growth Factor KW - 67256-21-7 KW - Proto-Oncogene Proteins c-met KW - EC 2.7.10.1 KW - Index Medicus KW - Adenocarcinoma -- metabolism KW - Animals KW - Dose-Response Relationship, Drug KW - Humans KW - Digestive System -- metabolism KW - Breast Neoplasms -- metabolism KW - Cell Differentiation -- genetics KW - Mice KW - Mice, Inbred BALB C KW - Colonic Neoplasms -- chemically induced KW - Chromosomes, Human, Pair 7 KW - Adenocarcinoma -- pathology KW - Microscopy, Fluorescence KW - Breast Neoplasms -- pathology KW - Colonic Neoplasms -- metabolism KW - Microscopy, Immunoelectron KW - Colonic Neoplasms -- pathology KW - Growth Substances -- pharmacology KW - Growth Substances -- physiology KW - Proto-Oncogene Proteins -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73164819?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft.atitle=The+met+proto-oncogene+receptor+and+lumen+formation.&rft.au=Tsarfaty%2C+I%3BResau%2C+J+H%3BRulong%2C+S%3BKeydar%2C+I%3BFaletto%2C+D+L%3BVande+Woude%2C+G+F&rft.aulast=Tsarfaty&rft.aufirst=I&rft.date=1992-08-28&rft.volume=257&rft.issue=5074&rft.spage=1258&rft.isbn=&rft.btitle=&rft.title=Science+%28New+York%2C+N.Y.%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-06 N1 - Date created - 1992-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The intrathecal administration of excitatory amino acid receptor antagonists selectively attenuated carrageenan-induced behavioral hyperalgesia in rats. AN - 73307682; 1358641 AB - A single unilateral injection of carrageenan (4.5-6.0 mg in 0.15-0.20 ml saline) into the rat hindpaw induced behavioral hyperalgesia as evidenced by a significant reduction in hindpaw withdrawal latency to a noxious thermal stimulus. The involvement of N-methyl-D-aspartate (NMDA) receptors in this model of hyperalgesia was examined by intrathecal administration of the selective excitatory amino acid (EAA) receptor antagonists: (+/-)-2-amino-5-phosphonopentanoic acid (AP-5), (+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), ketamine hydrochloride (ketamine), 7-chlorokynurenic acid (7-Cl kynurenic acid), and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). The effects of dizocilpine maleate (MK-801) were studied under the same conditions and published previously (Ren et al., 1992) and the data are presented for comparison. While the withdrawal latencies of the non-injected paws and of the paws of naive rats were not significantly affected by application of the EAA receptor antagonists at doses tested, the paw withdrawal latencies of the carrageenan-injected paws were elevated dose dependently. The rank order of potency of these agents to reduce hyperalgesia was: MK-801 greater than or equal to AP-5 greater than or equal to CPP = 7-Cl kynurenic acid = ketamine much greater than CNQX greater than 0. In contrast, intrathecal injection of the opioid receptor agonists, [D-Ala2,MePhe4,Gly-ol5]enkephalin (DAMGO, mu-selective) and [D-Pen2,D-Pen5] enkephalin (DPDPE, delta-selective), produced antinociception in both injected and non-injected paws. DAMGO was much more potent, while DPDPE was less potent, than MK-801.(ABSTRACT TRUNCATED AT 250 WORDS) JF - European journal of pharmacology AU - Ren, K AU - Williams, G M AU - Hylden, J L AU - Ruda, M A AU - Dubner, R AD - Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08/25/ PY - 1992 DA - 1992 Aug 25 SP - 235 EP - 243 VL - 219 IS - 2 SN - 0014-2999, 0014-2999 KW - Analgesics KW - 0 KW - Enkephalins KW - Piperazines KW - Quinoxalines KW - Receptors, N-Methyl-D-Aspartate KW - Enkephalin, Ala(2)-MePhe(4)-Gly(5)- KW - 100929-53-1 KW - Ketamine KW - 690G0D6V8H KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - 6-Cyano-7-nitroquinoxaline-2,3-dione KW - 6OTE87SCCW KW - 2-amino-5-phosphopentanoic acid KW - 76326-31-3 KW - Enkephalin, D-Penicillamine (2,5)- KW - 88373-73-3 KW - Carrageenan KW - 9000-07-1 KW - 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid KW - 98Y1I8ZD4M KW - Kynurenic Acid KW - H030S2S85J KW - Valine KW - HG18B9YRS7 KW - 7-chlorokynurenic acid KW - S7936QON2K KW - Index Medicus KW - Animals KW - Analysis of Variance KW - Inflammation -- physiopathology KW - Analgesics -- pharmacology KW - Valine -- pharmacology KW - Piperazines -- pharmacology KW - Kynurenic Acid -- pharmacology KW - Ketamine -- pharmacology KW - Dizocilpine Maleate -- pharmacology KW - Rats KW - Behavior, Animal -- drug effects KW - Rats, Sprague-Dawley KW - Carrageenan -- toxicity KW - Enkephalins -- pharmacology KW - Injections, Spinal KW - Valine -- analogs & derivatives KW - Kynurenic Acid -- analogs & derivatives KW - Quinoxalines -- pharmacology KW - Male KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Receptors, N-Methyl-D-Aspartate -- antagonists & inhibitors KW - Hyperalgesia -- chemically induced KW - Hyperalgesia -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73307682?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+pharmacology&rft.atitle=The+intrathecal+administration+of+excitatory+amino+acid+receptor+antagonists+selectively+attenuated+carrageenan-induced+behavioral+hyperalgesia+in+rats.&rft.au=Ren%2C+K%3BWilliams%2C+G+M%3BHylden%2C+J+L%3BRuda%2C+M+A%3BDubner%2C+R&rft.aulast=Ren&rft.aufirst=K&rft.date=1992-08-25&rft.volume=219&rft.issue=2&rft.spage=235&rft.isbn=&rft.btitle=&rft.title=European+journal+of+pharmacology&rft.issn=00142999&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-07 N1 - Date created - 1992-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pertussis toxin-catalyzed ADP-ribosylation of G(o) alpha with mutations at the carboxyl terminus. AN - 73166043; 1510959 AB - The guanine nucleotide-binding protein G(o alpha) has been implicated in the regulation of Ca2+ channels in neural tissues. Covalent modification of G(o alpha) by pertussis toxin-catalyzed ADP-ribosylation of a cysteine (position 351) four amino acids from the carboxyl terminus decouples G(o alpha) from receptor. To define the structural requirements for ADP-ribosylation, preparations of recombinant G(o alpha) with mutations within the five amino acids at the carboxyl terminus were evaluated for their ability to serve as pertussis toxin substrates. As expected, the mutant in which cysteine 351 was replaced by glycine (C351G) was not a toxin substrate. Other inactive mutants were G352D and L353 delta/Y354 delta. Mutations that had no significant effect on toxin-catalyzed ADP-ribosylation included G350D, G350R, Y354 delta, and L353V/Y354 delta. Less active mutants were L353G/Y354 delta, L353A/Y354 delta, and L353G. ADP-ribosylation of the active mutants, like that of wild-type G(o alpha), was enhanced by the beta gamma subunits of bovine transducin. It appears that three of the four terminal amino acids critically influence pertussis toxin-catalyzed ADP-ribosylation of G(o alpha). JF - Biochemistry AU - Avigan, J AU - Murtagh, J J AU - Stevens, L A AU - Angus, C W AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08/25/ PY - 1992 DA - 1992 Aug 25 SP - 7736 EP - 7740 VL - 31 IS - 33 SN - 0006-2960, 0006-2960 KW - Macromolecular Substances KW - 0 KW - Oligodeoxyribonucleotides KW - Recombinant Proteins KW - Virulence Factors, Bordetella KW - NAD KW - 0U46U6E8UK KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Pertussis Toxin KW - EC 2.4.2.31 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Transducin KW - EC 3.6.5.1 KW - Index Medicus KW - Retina -- metabolism KW - Animals KW - Escherichia coli -- genetics KW - Cloning, Molecular KW - Recombinant Proteins -- isolation & purification KW - Base Sequence KW - Cattle KW - Recombinant Proteins -- metabolism KW - Genetic Vectors KW - Restriction Mapping KW - Polymerase Chain Reaction -- methods KW - Molecular Sequence Data KW - Transducin -- isolation & purification KW - Substrate Specificity KW - Transducin -- metabolism KW - Mutagenesis, Site-Directed KW - Virulence Factors, Bordetella -- pharmacology KW - NAD -- metabolism KW - Virulence Factors, Bordetella -- metabolism KW - GTP-Binding Proteins -- metabolism KW - GTP-Binding Proteins -- isolation & purification KW - Adenosine Diphosphate Ribose -- metabolism KW - GTP-Binding Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73166043?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=Pertussis+toxin-catalyzed+ADP-ribosylation+of+G%28o%29+alpha+with+mutations+at+the+carboxyl+terminus.&rft.au=Avigan%2C+J%3BMurtagh%2C+J+J%3BStevens%2C+L+A%3BAngus%2C+C+W%3BMoss%2C+J%3BVaughan%2C+M&rft.aulast=Avigan&rft.aufirst=J&rft.date=1992-08-25&rft.volume=31&rft.issue=33&rft.spage=7736&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-29 N1 - Date created - 1992-09-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Five PDGF B amino acid substitutions convert PDGF A to a PDGF B-like transforming molecule. AN - 73155190; 1380958 AB - We used site-directed mutagenesis to determine the minimum number of PDGF B residues needed to convert PDGF A to a potently transforming PDGF B-like molecule. Substitution of two PDGF B subdomains, 106-115 and 135-144, were found to be critical. These substitutions were sufficient to broaden the ability of PDGF A to activate beta as well as alpha platelet-derived growth factor (PDGF) receptors and increase its transforming efficiency to that of PDGF B. Within subdomain I, either PDGF B residues Arg-109 and Asn-115 or Arg-109, Leu-110, and Arg-113, in combination with subdomain II PDGF B residues Asn-136, Arg-137, and Arg-142 were identified as being essential. Those mutants with transforming ability comparable with PDGF B showed significantly lower efficiencies of beta receptor triggering. Thus, our studies identify a small number of PDGF B amino acids indispensable for beta PDGF receptor interaction and suggest that a low level of beta PDGF receptor activation is sufficient to dramatically increase PDGF transforming efficiency in NIH 3T3 cells. JF - The Journal of biological chemistry AU - LaRochelle, W J AU - Pierce, J H AU - May-Siroff, M AU - Giese, N AU - Aaronson, S A AD - Laboratory of Cellular and Molecular Biology, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08/25/ PY - 1992 DA - 1992 Aug 25 SP - 17074 EP - 17077 VL - 267 IS - 24 SN - 0021-9258, 0021-9258 KW - Macromolecular Substances KW - 0 KW - Platelet-Derived Growth Factor KW - Receptors, Cell Surface KW - Recombinant Proteins KW - Phosphotyrosine KW - 21820-51-9 KW - Tyrosine KW - 42HK56048U KW - Receptors, Platelet-Derived Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Recombinant Proteins -- pharmacology KW - Humans KW - Amino Acid Sequence KW - Mice KW - Tyrosine -- analysis KW - Mutagenesis, Site-Directed KW - Receptors, Cell Surface -- metabolism KW - Transfection KW - Recombinant Proteins -- metabolism KW - Molecular Sequence Data KW - Tyrosine -- analogs & derivatives KW - DNA Replication KW - Receptors, Cell Surface -- drug effects KW - Platelet-Derived Growth Factor -- pharmacology KW - Platelet-Derived Growth Factor -- genetics KW - Platelet-Derived Growth Factor -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73155190?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Five+PDGF+B+amino+acid+substitutions+convert+PDGF+A+to+a+PDGF+B-like+transforming+molecule.&rft.au=LaRochelle%2C+W+J%3BPierce%2C+J+H%3BMay-Siroff%2C+M%3BGiese%2C+N%3BAaronson%2C+S+A&rft.aulast=LaRochelle&rft.aufirst=W&rft.date=1992-08-25&rft.volume=267&rft.issue=24&rft.spage=17074&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-25 N1 - Date created - 1992-09-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular species analysis of a product of phospholipase D activation. Phosphatidylethanol is formed from phosphatidylcholine in phorbol ester- and bradykinin-stimulated PC12 cells. AN - 73135136; 1512226 AB - Tumor-promoting phorbol esters or calcium-mobilizing receptor ligands stimulate phosphatidylcholine breakdown and in many cells this is accompanied by phospholipase D (PLD) activation. We tested whether or not a direct relationship exists between these two phenomena. Pheochromocytoma (PC12) cells were stimulated with the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate or with the calcium-mobilizing receptor ligand bradykinin in media containing 1% ethanol. The fatty acid composition of the molecular species of phosphatidylethanol (PEt), a product of PLD activation, formed in stimulated cells was compared with the molecular species of endogenous phospholipids isolated from unstimulated PC12 cells. PEt was isolated and analyzed by fast atom bombardment-mass spectrometry (FAB-MS) in the negative ion mode. Fatty acid composition and headgroup structure of the major PEt molecular ions were confirmed by linked scan analysis. Phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, and phosphatidylinositol were isolated from unstimulated cells and converted into phosphatidic acids using PLD. Mass spectra of the respective phosphatidic acids were obtained by fast atom bombardment-mass spectrometry as described above. The molecular species of PEt formed in 12-O-tetradecanoylphorbol-13-acetate- and bradykinin-stimulated PC12 cell were identical to those of phosphatidylcholine isolated from untreated cells. JF - The Journal of biological chemistry AU - Holbrook, P G AU - Pannell, L K AU - Murata, Y AU - Daly, J W AD - Laboratory of Bioorganic Chemistry, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08/25/ PY - 1992 DA - 1992 Aug 25 SP - 16834 EP - 16840 VL - 267 IS - 24 SN - 0021-9258, 0021-9258 KW - Glycerophospholipids KW - 0 KW - Oleic Acids KW - Phosphatidic Acids KW - Phosphatidylcholines KW - Phospholipids KW - phosphatidylethanol KW - Oleic Acid KW - 2UMI9U37CP KW - Phospholipase D KW - EC 3.1.4.4 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Bradykinin KW - S8TIM42R2W KW - Index Medicus KW - Mass Spectrometry KW - Animals KW - Phospholipids -- isolation & purification KW - Oleic Acids -- metabolism KW - Kinetics KW - Phospholipids -- metabolism KW - PC12 Cells KW - Phospholipase D -- metabolism KW - Phosphatidic Acids -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Phosphatidylcholines -- metabolism KW - Bradykinin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73135136?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+addiction&rft.atitle=Dying+to+be+equal%3A+women%2C+alcohol%2C+and+cardiovascular+disease.&rft.au=Hanna%2C+E%3BDufour%2C+M+C%3BElliott%2C+S%3BStinson%2C+F%3BHarford%2C+T+C&rft.aulast=Hanna&rft.aufirst=E&rft.date=1992-11-01&rft.volume=87&rft.issue=11&rft.spage=1593&rft.isbn=&rft.btitle=&rft.title=British+journal+of+addiction&rft.issn=09520481&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-25 N1 - Date created - 1992-09-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Electrophysiological properties of early postnatal rat septal neurons in short-term culture. AN - 73243942; 1327409 AB - Electrophysiological properties of septal neurons dissociated from PN1-PN7 rats were examined between 1 and 5 days in vitro (DIV) with whole-cell patch-clamp recording. The neurons had RMPs in the range -40 to -80 mV, resistances 0.5-1.5 G omega, and 50-90 mV action potentials. By 2-3 DIV, most neurons were spontaneously active, with some cells exhibiting rhythmic firing patterns. Depolarizations from -80 mV holding potential elicited TTX-sensitive inward Na+ currents, and transient and sustained outward K+ currents. Pharmacological dissection of the outward currents in PN6/7 neurons suggest the presence of multiple types of K+ currents (IA, IC, IK). L-type Ca2+ currents were observed in all PN6/7 neurons examined but were not always detectable in PN1/2 neurons. All PN1/2 and PN6/7 neurons were sensitive to glutamate and GABA but did not respond to ACh or NE applications. Responses to GABA were excitatory i.e., characteristic of immature neurons. Comparison of the results obtained in this study with the properties of adult neurons characterized in vivo or in brain slice preparations in vitro, suggest that septal neurons from PN1-PN7 rats are still in the process of differentiation of their mature electrical and chemosensitive membrane properties. JF - Brain research AU - Suszkiw, J B AU - Schaffner, A E AU - Barker, J L AD - Laboratory of Neurophysiology, NINDS, NIH, Bethesda, MD 20892. Y1 - 1992/08/21/ PY - 1992 DA - 1992 Aug 21 SP - 246 EP - 254 VL - 588 IS - 2 SN - 0006-8993, 0006-8993 KW - Potassium Channels KW - 0 KW - Sodium Channels KW - Tetrodotoxin KW - 4368-28-9 KW - gamma-Aminobutyric Acid KW - 56-12-2 KW - Guanosine Triphosphate KW - 86-01-1 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Cells, Cultured KW - gamma-Aminobutyric Acid -- physiology KW - Membrane Potentials -- drug effects KW - Electrophysiology KW - Tetrodotoxin -- pharmacology KW - Potassium Channels -- drug effects KW - Sodium Channels -- drug effects KW - Immunohistochemistry KW - Guanosine Triphosphate -- pharmacology KW - Adenosine Triphosphate -- pharmacology KW - Brain -- cytology KW - Neurons -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73243942?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Electrophysiological+properties+of+early+postnatal+rat+septal+neurons+in+short-term+culture.&rft.au=Suszkiw%2C+J+B%3BSchaffner%2C+A+E%3BBarker%2C+J+L&rft.aulast=Suszkiw&rft.aufirst=J&rft.date=1992-08-21&rft.volume=588&rft.issue=2&rft.spage=246&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-13 N1 - Date created - 1992-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The origin of plagues: old and new. AN - 73154288; 1509258 AB - Viruses and bacteria emerge in new and old forms to cause disease epidemics. Some microorganisms recur when changing life-styles (including increased international travel) offer new opportunities; others arise from new genetic variations. These various epidemics connect the future with the past, offering lessons for guarding the health of generations to come--lessons learned from diseases such as tuberculosis, toxic shock syndrome, Lyme disease, streptococcal infection, influenza, and acquired immunodeficiency syndrome (AIDS). The public must be vigilant to the possibility of new epidemics, learn more about the biology and epidemiology of microbes, and strengthen systems of surveillance and detection. JF - Science (New York, N.Y.) AU - Krause, R M AD - Fogarty International Center for Advanced Study in the Health Sciences, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08/21/ PY - 1992 DA - 1992 Aug 21 SP - 1073 EP - 1078 VL - 257 IS - 5073 SN - 0036-8075, 0036-8075 KW - Index Medicus KW - AIDS/HIV KW - Genes, Bacterial KW - Acquired Immunodeficiency Syndrome -- epidemiology KW - Bacterial Infections -- microbiology KW - Bacterial Infections -- epidemiology KW - Humans KW - Molecular Sequence Data KW - Genes, Viral KW - Virus Diseases -- microbiology KW - Virus Diseases -- epidemiology KW - Disease Outbreaks UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73154288?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft.atitle=The+origin+of+plagues%3A+old+and+new.&rft.au=Krause%2C+R+M&rft.aulast=Krause&rft.aufirst=R&rft.date=1992-08-21&rft.volume=257&rft.issue=5073&rft.spage=1073&rft.isbn=&rft.btitle=&rft.title=Science+%28New+York%2C+N.Y.%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-23 N1 - Date created - 1992-09-23 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M95929; GENBANK N1 - SuppNotes - Comment In: Science. 1992 Aug 21;257(5073):1021 [1509248] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cigarette smoking and other risk factors for progression of precancerous stomach lesions. AN - 73086594; 1640486 AB - Stomach cancer is generally thought to evolve through a series of gastric mucosal changes, but the determinants of the precancerous lesions are not well understood. Our purpose was to assess risk factors for intestinal metaplasia and gastric dysplasia arising from chronic atrophic gastritis in a general population at high risk for stomach cancer. A population-based gastroscopic screening of more than 3000 residents was conducted in a county in China with one of the world's highest rates of stomach cancer. Information on the lifestyle and other characteristics of the participants was obtained by interview, and responses were compared between those in whom the most advanced gastric lesion was dysplasia or intestinal metaplasia versus those with chronic atrophic gastritis. Cigarette smoking was found to nearly double the risk of transition to dysplasia and to be a mild risk factor for intestinal metaplasia. Smoking accounted almost entirely for the 55% higher prevalence of dysplasia among men than among women. Risk of transition to dysplasia had a weak association with several dietary factors and was increased among those participants with a family history of stomach cancer and with blood type A. The findings provide strong evidence for a role of tobacco consumption and offer clues to other environmental and genetic factors involved in the process of gastric carcinogenesis. JF - Journal of the National Cancer Institute AU - Kneller, R W AU - You, W C AU - Chang, Y S AU - Liu, W D AU - Zhang, L AU - Zhao, L AU - Xu, G W AU - Fraumeni, J F AU - Blot, W J AD - Division of Cancer Etiology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08/19/ PY - 1992 DA - 1992 Aug 19 SP - 1261 EP - 1266 VL - 84 IS - 16 SN - 0027-8874, 0027-8874 KW - Index Medicus KW - Life Style KW - Intestines -- pathology KW - Logistic Models KW - Risk Factors KW - Metaplasia -- complications KW - Humans KW - Gastritis, Atrophic -- complications KW - Adult KW - Middle Aged KW - Male KW - Female KW - Prevalence KW - Precancerous Conditions -- etiology KW - Smoking -- adverse effects KW - Stomach Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73086594?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Cigarette+smoking+and+other+risk+factors+for+progression+of+precancerous+stomach+lesions.&rft.au=Kneller%2C+R+W%3BYou%2C+W+C%3BChang%2C+Y+S%3BLiu%2C+W+D%3BZhang%2C+L%3BZhao%2C+L%3BXu%2C+G+W%3BFraumeni%2C+J+F%3BBlot%2C+W+J&rft.aulast=Kneller&rft.aufirst=R&rft.date=1992-08-19&rft.volume=84&rft.issue=16&rft.spage=1261&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-01 N1 - Date created - 1992-09-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phosphorylation stimulates the transcriptional activity of the human beta 1 thyroid hormone nuclear receptor. AN - 73122312; 1502193 AB - The role of phosphorylation on the gene activation activity of the human beta 1 thyroid hormone nuclear receptor (h-TR beta 1) was examined. h-TR beta 1 was found to be a phosphoprotein when expressed in COS-1 cells, with serine, threonine, and tyrosine (85:10:5) as the phosphorylation sites. Okadaic acid (a potent inhibitor of phosphatases 1 and 2A) at 0.1, 0.25, and 0.5 microM increased the phosphorylation of h-TR beta 1 by 3-, 7-, and 11-fold, respectively. The increase in phosphorylation was accompanied by a concomitant increase in phosphorylation was accompanied by a concomitant increase in receptor-mediated transcription in transient transfection assays. h-TR beta 1 purified from Escherichia coli was phosphorylated in vitro by the endogenous kinase from cellular extracts. Serine, threonine, and tyrosine were phosphorylated in a similar ratio to that found in COS-1 cells. The in vitro phosphorylation was stimulated by okadaic acid. Phosphorylation did not affect the binding of h-TR beta 1 to 3,3',5-triiodo-L-thyronine. However, phosphorylation of h-TR beta 1 resulted in an increase of its binding to DNA and conferred on it the ability to bind to nuclear accessory proteins. The results indicate that phosphorylation plays an important role in the transcriptional activity of h-TR beta 1. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Lin, K H AU - Ashizawa, K AU - Cheng, S Y AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08/15/ PY - 1992 DA - 1992 Aug 15 SP - 7737 EP - 7741 VL - 89 IS - 16 SN - 0027-8424, 0027-8424 KW - DNA-Binding Proteins KW - 0 KW - Ethers, Cyclic KW - Phosphates KW - Receptors, Thyroid Hormone KW - Okadaic Acid KW - 1W21G5Q4N2 KW - Vanadates KW - 3WHH0066W5 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Methionine KW - AE28F7PNPL KW - Protein Kinase C KW - EC 2.7.11.13 KW - Index Medicus KW - Animals KW - HeLa Cells KW - Vanadates -- pharmacology KW - Humans KW - Methionine -- metabolism KW - Ethers, Cyclic -- pharmacology KW - Phosphates -- metabolism KW - Protein Kinase C -- antagonists & inhibitors KW - Phosphorylation KW - Transfection KW - Genetic Vectors KW - Kinetics KW - Adenosine Triphosphate -- metabolism KW - Cell Line KW - Cell Nucleus -- metabolism KW - Receptors, Thyroid Hormone -- metabolism KW - Receptors, Thyroid Hormone -- genetics KW - Transcription, Genetic KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73122312?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Phosphorylation+stimulates+the+transcriptional+activity+of+the+human+beta+1+thyroid+hormone+nuclear+receptor.&rft.au=Heineman%2C+E+F%3BOlsen%2C+J+H%3BPottern%2C+L+M%3BGomez%2C+M%3BRaffn%2C+E%3BBlair%2C+A&rft.aulast=Heineman&rft.aufirst=E&rft.date=1992-11-01&rft.volume=3&rft.issue=6&rft.spage=555&rft.isbn=&rft.btitle=&rft.title=Cancer+causes+%26+control+%3A+CCC&rft.issn=09575243&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-15 N1 - Date created - 1992-09-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: EMBO J. 1988 Aug;7(8):2425-33 [2903825] Nature. 1986 Dec 18-31;324(6098):641-6 [2879243] Cell. 1988 Jul 29;54(3):313-23 [3396073] Cell. 1981 Jun;24(3):741-52 [6166387] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Cell. 1991 Jun 28;65(7):1267-79 [1648451] Mol Endocrinol. 1991 Sep;5(9):1215-28 [1663212] Mol Endocrinol. 1991 Jan;5(1):94-9 [1850112] Mol Endocrinol. 1991 Apr;5(4):485-92 [1922081] Endocrinology. 1991 May;128(5):2601-9 [1708338] FASEB J. 1991 Jun;5(9):2243-9 [1860615] J Biol Chem. 1990 Apr 5;265(10):5403-8 [2108136] Cell. 1990 Oct 5;63(1):155-65 [2170018] Cell. 1990 Feb 9;60(3):375-86 [2302733] EMBO J. 1986 Nov;5(11):2867-72 [2431901] Oncogene. 1989 Oct;4(10):1247-54 [2552374] J Virol. 1988 Apr;62(4):1258-65 [2831386] Proc Natl Acad Sci U S A. 1988 Jul;85(14):5031-5 [2899322] Cell. 1988 Sep 9;54(6):855-64 [3044613] Endocrinology. 1987 Jun;120(6):2591-6 [3569145] Methods Enzymol. 1983;99:387-402 [6196603] Cell. 1991 Jun 28;65(7):1255-66 [1648450] J Biol Chem. 1990 Feb 15;265(5):2500-4 [1968058] Nature. 1990 Apr 12;344(6267):678-82 [2157987] J Biol Chem. 1990 Mar 25;265(9):5161-5 [2180960] Cell. 1990 Jun 29;61(7):1161-4 [2194664] J Biol Chem. 1990 Sep 25;265(27):16548-55 [2398063] Genes Dev. 1989 May;3(5):620-7 [2545525] Biochem Biophys Res Commun. 1989 Oct 16;164(1):238-44 [2553014] Mol Endocrinol. 1989 Dec;3(12):1996-2004 [2628734] Gene. 1986;45(1):107-11 [3023200] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of the cystic fibrosis transmembrane conductance regulator gene can be regulated by protein kinase C. AN - 73118297; 1379589 AB - Epithelial cells utilize at least two types of apical Cl- channels, the cAMP-activated cystic fibrosis transmembrane conductance regulator (CFTR) and the Ca2+/calmodulin-dependent Cl- channel. While phorbal ester (PMA) activates only CFTR-dependent Cl- secretion and the Ca2+ ionophore A23187 only the Ca2+/calmodulin-dependent Cl- secretion, PMA and A23187 share the ability to down-regulate expression of the CFTR gene at the transcriptional level. Since both PMA and A23187 can activate protein kinases, we hypothesized that protein kinase pathways may be involved in the regulation of CFTR gene expression. Exposure of HT-29 human colon carcinoma cells to the protein kinase C activator SC9 down-regulated CFTR mRNA levels in a dose-dependent fashion, similar to that seen with PMA. The reduction in CFTR transcript levels by SC9 and PMA was blocked by H7, an inhibitor of protein kinases. In a similar fashion, the down-regulation of CFTR transcript levels by A23187 was blocked by H7 as well as staurosporine, another protein kinase inhibitor. Interestingly, both H7 and staurosporine themselves increased CFTR mRNA levels. Quantification of CFTR gene transcription rate showed a reduction by SC9 (similar to that with PMA and A23187) that was prevented by H7 and that H7 by itself increased CFTR transcription. Together, these observations suggest that protein kinase pathways, likely including protein kinase C, are involved in the regulation of CFTR gene expression, with activation or inhibition of protein kinase activity down-regulating or up-regulating CFTR gene expression, respectively. JF - The Journal of biological chemistry AU - Bargon, J AU - Trapnell, B C AU - Yoshimura, K AU - Dalemans, W AU - Pavirani, A AU - Lecocq, J P AU - Crystal, R G AD - Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08/15/ PY - 1992 DA - 1992 Aug 15 SP - 16056 EP - 16060 VL - 267 IS - 23 SN - 0021-9258, 0021-9258 KW - CFTR protein, human KW - 0 KW - Isoquinolines KW - Membrane Proteins KW - Piperazines KW - RNA, Messenger KW - Sulfonamides KW - N-(6-phenylhexyl)-5-chloro-1-naphthalenesulfonamide KW - 102649-78-5 KW - Cystic Fibrosis Transmembrane Conductance Regulator KW - 126880-72-6 KW - Calcimycin KW - 37H9VM9WZL KW - 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine KW - 84477-87-2 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Isoquinolines -- pharmacology KW - Sulfonamides -- pharmacology KW - Enzyme Activation KW - Kinetics KW - Humans KW - Calcimycin -- pharmacology KW - Piperazines -- pharmacology KW - Colonic Neoplasms KW - Cell Line KW - Protein Kinase C -- metabolism KW - Gene Expression Regulation, Neoplastic KW - Protein Kinase C -- antagonists & inhibitors KW - Transcription, Genetic -- drug effects KW - RNA, Messenger -- metabolism KW - Cystic Fibrosis -- genetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Membrane Proteins -- genetics KW - RNA, Messenger -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73118297?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Expression+of+the+cystic+fibrosis+transmembrane+conductance+regulator+gene+can+be+regulated+by+protein+kinase+C.&rft.au=Bargon%2C+J%3BTrapnell%2C+B+C%3BYoshimura%2C+K%3BDalemans%2C+W%3BPavirani%2C+A%3BLecocq%2C+J+P%3BCrystal%2C+R+G&rft.aulast=Bargon&rft.aufirst=J&rft.date=1992-08-15&rft.volume=267&rft.issue=23&rft.spage=16056&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-10 N1 - Date created - 1992-09-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dopamine transporter site-directed mutations differentially alter substrate transport and cocaine binding. AN - 73116806; 1502198 AB - Polar amino acids lying within three hydrophobic regions of the dopamine transporter (DAT) are analogous to those important for ligand recognition by catecholamine receptors. Possible functional significance of these amino acids was examined by expressing DAT cDNAs mutated in these polar residues. Replacement of aspartate at position 79 with alanine, glycine, or glutamate dramatically reduced uptake of [3H]dopamine and the tritium-labeled Parkinsonism-inducing neurotoxin 1-methyl-4-phenylpyridinium (MPP+) and reduced the mutants' affinity for the tritium-labeled cocaine analog (-)-2 beta-carbomethoxy-3 beta-(4-fluorophenyl)tropane (CFT) without affecting Bmax. Replacement of the serine residues at positions 356 and 359 in the seventh hydrophobic region by alanine or glycine caused reductions in [3H]dopamine and [3H]MPP+ uptake, whereas [3H]CFT binding was less affected. Substitution of two serines in the eighth hydrophobic region yielded wild-type values for [3H]dopamine and [3H]MPP+ uptake and [3H]CFT binding. These results demonstrate that aspartate and serine residues lying within the first and seventh hydrophobic putative transmembrane regions are crucial for DAT function and provide identification of residues differentially important for cocaine binding and for dopamine uptake. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Kitayama, S AU - Shimada, S AU - Xu, H AU - Markham, L AU - Donovan, D M AU - Uhl, G R AD - Laboratory of Molecular Neurobiology, Addiction Research Center/National Institute on Drug Abuse, Baltimore, MD. Y1 - 1992/08/15/ PY - 1992 DA - 1992 Aug 15 SP - 7782 EP - 7785 VL - 89 IS - 16 SN - 0027-8424, 0027-8424 KW - Carrier Proteins KW - 0 KW - Dopamine Plasma Membrane Transport Proteins KW - Membrane Glycoproteins KW - Membrane Transport Proteins KW - Nerve Tissue Proteins KW - DNA KW - 9007-49-2 KW - Cocaine KW - I5Y540LHVR KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Animals KW - Models, Structural KW - Transfection KW - Kinetics KW - DNA -- genetics KW - Binding, Competitive KW - Molecular Sequence Data KW - Biological Transport KW - Amino Acid Sequence KW - 1-Methyl-4-phenylpyridinium -- metabolism KW - Cell Membrane -- metabolism KW - Cell Line KW - Protein Conformation KW - Mutagenesis, Site-Directed KW - Carrier Proteins -- metabolism KW - Carrier Proteins -- genetics KW - Dopamine -- metabolism KW - Cocaine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73116806?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Dopamine+transporter+site-directed+mutations+differentially+alter+substrate+transport+and+cocaine+binding.&rft.au=Kitayama%2C+S%3BShimada%2C+S%3BXu%2C+H%3BMarkham%2C+L%3BDonovan%2C+D+M%3BUhl%2C+G+R&rft.aulast=Kitayama&rft.aufirst=S&rft.date=1992-08-15&rft.volume=89&rft.issue=16&rft.spage=7782&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-15 N1 - Date created - 1992-09-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1992 Jan 5;267(1):649-52 [1370453] J Mol Biol. 1984 May 5;175(1):75-81 [6427470] Curr Opin Neurobiol. 1991 Jun;1(1):84-90 [1688010] Mol Pharmacol. 1991 Jun;39(6):733-9 [1828858] Brain Res Mol Brain Res. 1991 Feb;9(3):271-6 [1851530] Nature. 1991 Nov 7;354(6348):66-70 [1944572] Science. 1991 Oct 25;254(5031):576-8 [1948034] Science. 1991 Oct 25;254(5031):578-9 [1948035] Science. 1991 Oct 25;254(5031):579-80 [1948036] Science. 1990 Sep 14;249(4974):1303-6 [1975955] J Med Chem. 1991 Mar;34(3):883-6 [2002468] Nature. 1991 Mar 28;350(6316):350-4 [2008212] Prog Neurobiol. 1990;34(5):387-400 [2192393] Life Sci. 1990;46(9):635-45 [2308472] FASEB J. 1989 May;3(7):1825-32 [2541037] Science. 1987 Sep 4;237(4819):1219-23 [2820058] Neurology. 1986 Feb;36(2):250-8 [3080696] Methods Enzymol. 1987;154:367-82 [3323813] Biochem Pharmacol. 1986 Apr 1;35(7):1123-9 [3964292] Br J Pharmacol. 1971 Apr;41(4):571-91 [4397129] Mol Pharmacol. 1991 Aug;40(2):168-79 [1678850] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Monoclonal antibody MRK16 reverses the multidrug resistance of multidrug-resistant transgenic mice. AN - 73080394; 1353705 AB - Using multidrug-resistant (MDR)-transgenic mice, whose bone marrow cells express the human MDR1 gene at a level approximately equal to that found in many human cancers, we determined the efficacy of human-specific anti-P-glycoprotein monoclonal antibody MRK16 in overcoming multidrug resistance in an intact animal. MRK16 alone (2 mg) did not significantly affect the WBC counts of the MDR-transgenic mice, but MRK16, as well as the F(ab')2 fragments of MRK16, led to a dose-dependent circumvention of bone marrow resistance against daunomycin, doxorubicin, vincristine, vinblastine, etoposide, and taxol. This sensitizing effect could not be enhanced by combining MRK16 with low molecular weight chemosensitizing agents such as verapamil, quinine, quinidine, or cyclosporin A. We also investigated the concept of specifically targeting and killing multidrug-resistant cells by using MRK16 coupled to Pseudomonas exotoxin (PE). MRK16-PE resulted in a dose-dependent killing of bone marrow cells in MDR-transgenic mice, whereas no bone marrow toxicity was observed in normal control mice. Administration of excess MRK16 prior to injection of MRK16-PE successfully blocked the effect of MRK16-PE. MOPC-PE, a non-MDR-related control monoclonal antibody conjugate, did not target and kill multidrug-resistant bone marrow cells in MDR-transgenic mice. Thus, these immunological approaches to reversing multidrug resistance appear to be both specific and effective. JF - Cancer research AU - Mickisch, G H AU - Pai, L H AU - Gottesman, M M AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08/15/ PY - 1992 DA - 1992 Aug 15 SP - 4427 EP - 4432 VL - 52 IS - 16 SN - 0008-5472, 0008-5472 KW - MDR1 KW - Alkaloids KW - 0 KW - Antibodies, Monoclonal KW - Immunotoxins KW - Vincristine KW - 5J49Q6B70F KW - Vinblastine KW - 5V9KLZ54CY KW - Etoposide KW - 6PLQ3CP4P3 KW - Doxorubicin KW - 80168379AG KW - Paclitaxel KW - P88XT4IS4D KW - Daunorubicin KW - ZS7284E0ZP KW - Index Medicus KW - Etoposide -- pharmacology KW - Vinblastine -- pharmacology KW - Animals KW - Drug Screening Assays, Antitumor KW - Vincristine -- pharmacology KW - Mice KW - Mice, Transgenic KW - Leukocyte Count KW - Daunorubicin -- pharmacology KW - Doxorubicin -- pharmacology KW - Alkaloids -- pharmacology KW - Pseudomonas aeruginosa KW - Drug Resistance -- genetics KW - Immunotoxins -- therapeutic use KW - Antibodies, Monoclonal -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73080394?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Monoclonal+antibody+MRK16+reverses+the+multidrug+resistance+of+multidrug-resistant+transgenic+mice.&rft.au=Mickisch%2C+G+H%3BPai%2C+L+H%3BGottesman%2C+M+M%3BPastan%2C+I&rft.aulast=Mickisch&rft.aufirst=G&rft.date=1992-08-15&rft.volume=52&rft.issue=16&rft.spage=4427&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-10 N1 - Date created - 1992-09-10 N1 - Date revised - 2017-01-13 N1 - Gene symbol - MDR1 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A proteolytically sensitive region common to several rat liver cytochromes P450: effect of cleavage on substrate binding. AN - 73096720; 1643049 AB - Limited proteolysis of rat liver microsomes was used to probe the topography and structure of cytochrome P450 bound to the endoplasmic reticulum. Three cytochromes P450 from two families were examined. Monoclonal antibodies to cytochrome P450 forms 1A1, 2B1, and 2E1 were used to immunopurify these proteolyzed cytochromes P450 from microsomes from rats treated with 3-methylcholanthrene, phenobarbital, and acetone, respectively. Electrophoretic and immunoblot analysis of tryptic fragments revealed a highly sensitive cleavage site in all three cytochromes P450. N-Terminal sequencing was performed on the fragments after transfer onto poly(vinylidene difluoride) membranes and showed that this preferential cleavage site is at amino acid position 298 of P450 1A1, position 277 of P450 2B1, and position 278 of P450 2E1. Multiple sequence alignment revealed that these positions are at the amino terminal of a highly conserved region of these cytochromes P450. The important functional role implied by primary sequence conservation along with the proteolytic sensitivity at its amino terminal suggests that this region is a protein domain. Comparison with the known structure of the bacterial cytochrome P450cam predicts that this proteolytically sensitive site is within an interhelical turn region connected to the distal helix that partially encompasses the heme-containing active site. Substrate binding to the cleaved cytochromes P450 was examined in order to determine whether the newly added conformational freedom near the cleavage site functionally altered these cytochromes P450. Cleavage of P450 2B1 abolished benzphetamine binding, which indicates that the cleavage site contains an important structural determinant for binding this substrate. However, cleavage did not affect benzo[a]pyrene binding to P450 1A1. JF - Biochemistry AU - Tsokos, D C AU - Omata, Y AU - Robinson, R C AU - Krutzsch, H C AU - Gelboin, H V AU - Friedman, F K AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08/11/ PY - 1992 DA - 1992 Aug 11 SP - 7155 EP - 7159 VL - 31 IS - 31 SN - 0006-2960, 0006-2960 KW - Benzo(a)pyrene KW - 3417WMA06D KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Blotting, Western KW - Sequence Alignment KW - Electrophoresis, Polyacrylamide Gel KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Hydrolysis KW - Male KW - Benzo(a)pyrene -- metabolism KW - Microsomes, Liver -- enzymology KW - Cytochrome P-450 Enzyme System -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73096720?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=A+proteolytically+sensitive+region+common+to+several+rat+liver+cytochromes+P450%3A+effect+of+cleavage+on+substrate+binding.&rft.au=Tsokos%2C+D+C%3BOmata%2C+Y%3BRobinson%2C+R+C%3BKrutzsch%2C+H+C%3BGelboin%2C+H+V%3BFriedman%2C+F+K&rft.aulast=Tsokos&rft.aufirst=D&rft.date=1992-08-11&rft.volume=31&rft.issue=31&rft.spage=7155&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-10 N1 - Date created - 1992-09-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Microglial-produced nitric oxide and reactive nitrogen oxides mediate neuronal cell death. AN - 73190737; 1381982 AB - The role of inflammatory cytokines in the pathogenesis of neurological diseases is not well understood. The neurotoxic effects of cytokines could be mediated by immunostimulation of glial cells to produce toxic concentrations of nitric oxide (NO) and reactive nitrogen oxides. Cultured microglia and meningeal fibroblasts, but not Type 1 astrocytes, were induced by lipopolysaccharides and cytokines to synthesize NO and reactive nitrogen oxides from L-arginine. In co-cultures of immunostimulated microglia and cerebellar granule neurons, neurotoxicity was blocked by an inhibitor of NO synthase, NG-nitroarginine, and by oxyhemoglobin, which inactivates NO. Microglial-induced neurotoxicity was also partially attenuated by the N-methyl-D-aspartate (NMDA) receptor antagonists, MK-801 and 2-amino-5-phosphovalerate (APV). Superoxide dismutase, which stabilizes NO through inactivation of superoxide anion, augmented microglial-mediated neurotoxicity either alone or in combination with MK-801 or APV. Hence, immunostimulated microglia mediate neurotoxicity by NO, reactive nitrogen oxides, superoxide anion and NMDA-like substances. These findings suggest a novel role for microglial-produced NO and reactive nitrogen oxides as a neurotoxic agent in neurodegenerative disease states. JF - Brain research AU - Boje, K M AU - Arora, P K AD - Laboratory of Neuroscience, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08/07/ PY - 1992 DA - 1992 Aug 07 SP - 250 EP - 256 VL - 587 IS - 2 SN - 0006-8993, 0006-8993 KW - Cytokines KW - 0 KW - Nitrites KW - Nitrogen Oxides KW - Receptors, N-Methyl-D-Aspartate KW - Nitric Oxide KW - 31C4KY9ESH KW - Arginine KW - 94ZLA3W45F KW - Nitric Oxide Synthase KW - EC 1.14.13.39 KW - Amino Acid Oxidoreductases KW - EC 1.4.- KW - Index Medicus KW - Animals KW - Cell Death -- physiology KW - Amino Acid Oxidoreductases -- metabolism KW - Cytokines -- pharmacology KW - Nitrites -- metabolism KW - Immunization KW - Pregnancy KW - Cerebellum -- metabolism KW - Rats, Inbred Strains KW - Rats KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Cells, Cultured KW - Receptors, N-Methyl-D-Aspartate -- antagonists & inhibitors KW - Arginine -- physiology KW - Immunohistochemistry KW - Female KW - Neuroglia -- metabolism KW - Nitrogen Oxides -- metabolism KW - Nitric Oxide -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73190737?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Microglial-produced+nitric+oxide+and+reactive+nitrogen+oxides+mediate+neuronal+cell+death.&rft.au=Boje%2C+K+M%3BArora%2C+P+K&rft.aulast=Boje&rft.aufirst=K&rft.date=1992-08-07&rft.volume=587&rft.issue=2&rft.spage=250&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of myelin basic protein thyroid hormone response element and its function in the context of native and heterologous promoter. AN - 73097304; 1379237 AB - In this report we have characterized further the myelin basic protein (MBP) gene thyroid hormone response element (TRE) by functional and binding analysis. Mutation and deletion experiments revealed that this TRE, confined to the sequences -184 to -167 of the MBP promoter, is able to function as a classical regulatory element in the context of the native and a heterologous promoter. It is comprised of two regions, containing a motif that is highly conserved among other TREs: AGGACA, arranged as an inverted palindrome. Any mutation within the footprinted region impaired receptor binding and function. Moreover, the deletion of sequences outside of the receptor footprinted region (MBP-TRE-18) resulted in a higher triiodothyronine responsiveness and a concomitant increase in receptor-dependent, hormone-independent repression. Results of transfection assays showed that both receptors alpha and beta elicit indistinguishable triiodothyronine responses when the MBP-TRE functions as a regulator of a heterologous promoter activity. However, a preferential beta receptor transactivation was observed when the MBP-TRE was placed in the context of its native promoter. JF - The Journal of biological chemistry AU - Farsetti, A AU - Desvergne, B AU - Hallenbeck, P AU - Robbins, J AU - Nikodem, V M AD - Genetics and Biochemistry Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08/05/ PY - 1992 DA - 1992 Aug 05 SP - 15784 EP - 15788 VL - 267 IS - 22 SN - 0021-9258, 0021-9258 KW - Macromolecular Substances KW - 0 KW - Myelin Basic Protein KW - Oligodeoxyribonucleotides KW - Receptors, Thyroid Hormone KW - Recombinant Proteins KW - Triiodothyronine KW - 06LU7C9H1V KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Thymidine Kinase KW - EC 2.7.1.21 KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Thymidine Kinase -- metabolism KW - Mice KW - Plasmids KW - Chloramphenicol O-Acetyltransferase -- metabolism KW - Mutagenesis, Site-Directed KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Base Sequence KW - Transfection KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Binding, Competitive KW - Molecular Sequence Data KW - Thymidine Kinase -- genetics KW - Promoter Regions, Genetic KW - Triiodothyronine -- pharmacology KW - Myelin Basic Protein -- genetics KW - Receptors, Thyroid Hormone -- metabolism KW - Genes, Regulator UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73097304?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Characterization+of+myelin+basic+protein+thyroid+hormone+response+element+and+its+function+in+the+context+of+native+and+heterologous+promoter.&rft.au=Farsetti%2C+A%3BDesvergne%2C+B%3BHallenbeck%2C+P%3BRobbins%2C+J%3BNikodem%2C+V+M&rft.aulast=Farsetti&rft.aufirst=A&rft.date=1992-08-05&rft.volume=267&rft.issue=22&rft.spage=15784&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-28 N1 - Date created - 1992-08-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fusions of anthrax toxin lethal factor to the ADP-ribosylation domain of Pseudomonas exotoxin A are potent cytotoxins which are translocated to the cytosol of mammalian cells. AN - 73089346; 1639793 AB - The lethal factor (LF) and edema factor (EF) components of anthrax toxin are toxic to animal cells only if internalized by interaction with the protective antigen (PA) component. PA binds to a cell surface receptor and is proteolytically cleaved to expose a binding site for LF and EF. To study how LF and EF are internalized and trafficked within cells, LF was fused to the translocation and ADP-ribosylation domains (domains II and III, respectively) of Pseudomonas exotoxin A. LF fusion proteins containing Pseudomonas exotoxin A domains II and III were less toxic than those containing only domain III. Fusion proteins with a functional endoplasmic reticulum retention sequence, REDLK, at the carboxyl terminus of domain III were less toxic than those with a nonfunctional sequence, LDER. The most potent fusion protein, FP33, had an EC50 = 2 pM on Chinese hamster ovary cells, exceeding that of native Pseudomonas exotoxin A (EC50 = 420 pM). Toxicity of all the fusion proteins required the presence of PA and was blocked by monensin. These data suggest that LF and LF fusion proteins are efficiently translocated from acidified endosomes directly to the cytosol without trafficking through other organelles, as is required for Pseudomonas exotoxin A. This system provides a potential vehicle for importing diverse proteins into the cytosol of mammalian cells. JF - The Journal of biological chemistry AU - Arora, N AU - Klimpel, K R AU - Singh, Y AU - Leppla, S H AD - Laboratory of Microbial Ecology, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08/05/ PY - 1992 DA - 1992 Aug 05 SP - 15542 EP - 15548 VL - 267 IS - 22 SN - 0021-9258, 0021-9258 KW - Antigens, Bacterial KW - 0 KW - Bacterial Toxins KW - Exotoxins KW - Protein Synthesis Inhibitors KW - Recombinant Fusion Proteins KW - Virulence Factors KW - anthrax toxin KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Animals KW - Cytosol -- metabolism KW - Genes, Bacterial KW - Pseudomonas aeruginosa -- genetics KW - Dose-Response Relationship, Drug KW - Escherichia coli -- genetics KW - Mice KW - Plasmids KW - Adenosine Diphosphate Ribose -- metabolism KW - Binding Sites KW - Cloning, Molecular KW - Recombinant Fusion Proteins -- metabolism KW - Bacillus anthracis -- genetics KW - Kinetics KW - Restriction Mapping KW - Recombinant Fusion Proteins -- pharmacology KW - CHO Cells KW - Cricetinae KW - Macrophages -- cytology KW - Exotoxins -- genetics KW - Exotoxins -- pharmacology KW - Bacterial Toxins -- pharmacology KW - Macrophages -- drug effects KW - Bacterial Toxins -- genetics KW - Bacterial Toxins -- metabolism KW - Cell Survival -- drug effects KW - Protein Synthesis Inhibitors -- pharmacology KW - Exotoxins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73089346?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Fusions+of+anthrax+toxin+lethal+factor+to+the+ADP-ribosylation+domain+of+Pseudomonas+exotoxin+A+are+potent+cytotoxins+which+are+translocated+to+the+cytosol+of+mammalian+cells.&rft.au=Arora%2C+N%3BKlimpel%2C+K+R%3BSingh%2C+Y%3BLeppla%2C+S+H&rft.aulast=Arora&rft.aufirst=N&rft.date=1992-08-05&rft.volume=267&rft.issue=22&rft.spage=15542&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-28 N1 - Date created - 1992-08-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of focal transcranial magnetic stimulation on simple reaction time to acoustic, visual and somatosensory stimuli. AN - 85228695; pmid-1393501 AB - In a simple reaction time (RT) paradigm, magnetic stimulation of different intensities was delivered over different scalp positions and at variable delays before (negative) or after (positive) the go-signal. Magnetic stimulation shortened RT to different go-signals (auditory, visual and somatosensory stimuli) by approximately 30 ms when delivered over the motor cortex contralateral to the responding arm at intensities below motor threshold. This effect was maximal at a delay of approximately +10 ms. A similar effect was found with suprathreshold stimulation to the ipsilateral motor cortex. Magnetic stimulation over other scalp areas did not affect RT regardless of the delay. No differences were found between the effects on elbow flexion and thumb abduction. The shortening of RT was not associated with changes in the timing development of premovement excitability increase in the motor cortex. We conclude that magnetic stimulation shortens RT by inducing an earlier initiation of this excitability increase. JF - Brain AU - Pascual-Leone, A AU - Valls-Solé J AU - Wassermann, E M AU - Brasil-Neto, J AU - Cohen, L G AU - Hallett, M AD - Human Cortical Physiology Unit, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 1045 EP - 1059 VL - 115 ( Pt 4) SN - 0006-8950, 0006-8950 KW - Motor Cortex KW - Human KW - Adult KW - Electromyography KW - Support, Non-U.S. Gov't KW - Movement KW - Evoked Potentials, Somatosensory KW - Male KW - Female KW - Reaction Time KW - Photic Stimulation KW - Magnetics KW - Acoustic Stimulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85228695?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain&rft.atitle=Effects+of+focal+transcranial+magnetic+stimulation+on+simple+reaction+time+to+acoustic%2C+visual+and+somatosensory+stimuli.&rft.au=Pascual-Leone%2C+A%3BValls-Sol%C3%A9+J%3BWassermann%2C+E+M%3BBrasil-Neto%2C+J%3BCohen%2C+L+G%3BHallett%2C+M&rft.aulast=Pascual-Leone&rft.aufirst=A&rft.date=1992-08-01&rft.volume=115+%28+Pt+4%29&rft.issue=&rft.spage=1045&rft.isbn=&rft.btitle=&rft.title=Brain&rft.issn=00068950&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Rational immunotherapy with ribonuclease chimeras. An approach toward humanizing immunotoxins. AN - 75516262; 1285324 AB - Members of the pancreatic ribonuclease (RNase) family have diverse activities toward RNA that could cause them to function during host defense and physiological cell death pathways. This activity could be harnessed by coupling RNases to cell binding ligands for the purpose of engineering them into cell-type specific cytotoxins. Therefore, the cytotoxic potential of RNase was explored by linking bovine pancreatic ribonuclease A via a disulfide bond to human transferrin or antibodies to the transferrin receptor. The RNase hybrid proteins were cytotoxic to K562 human erythroleukemia cells in vitro with an IC50 around 10(-7) M, whereas > 10(-4) M of native RNase was required to inhibit protein synthesis. Cytotoxicity required both components of the conjugate since excess transferrin or ribonuclease inhibitors added to the medium protected the cells from the transferrin-RNase toxicity. Importantly, the RNase conjugates were found to have potent antitumor effects in vivo. Chimeric RNase fusion proteins were also developed. F(ab')2-like antibody-enzyme fusions were prepared by linking the gene for human RNase to a chimeric antitransferrin receptor heavy chain gene. The antibody enzyme fusion gene was introduced into a transfectoma that secreted the chimeric light chain of the same antibody, and cell lines were cloned that synthesized and secreted the antibody-enzyme fusion protein of the expected size at a concentration of 1-5 ng/mL. Culture supernatants from clones secreting the fusion protein caused inhibition of growth and protein synthesis toward K562 cells that express the human transferrin receptor but not toward a nonhuman derived cell line. Since human ribonucleases coupled to antibodies also exhibited receptor mediated toxicities, a new approach to selective cell killing is provided. This may allow the development of new therapeutics for cancer treatment that exhibit less systemic toxicity and, importantly, less immunogenicity than the currently employed ligand-toxin conjugates. JF - Cell biophysics AU - Rybak, S M AU - Hoogenboom, H R AU - Newton, D L AU - Raus, J C AU - Youle, R J AD - Surgical Neurology Branch, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, MD 20892. PY - 1992 SP - 121 EP - 138 VL - 21 IS - 1-3 SN - 0163-4992, 0163-4992 KW - Immunotoxins KW - 0 KW - DNA KW - 9007-49-2 KW - Ribonucleases KW - EC 3.1.- KW - Index Medicus KW - Base Sequence KW - Humans KW - DNA -- genetics KW - Molecular Sequence Data KW - DNA -- analysis KW - Amino Acid Sequence KW - Chimera KW - Immunotherapy KW - Ribonucleases -- therapeutic use KW - Immunotoxins -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75516262?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell+biophysics&rft.atitle=Rational+immunotherapy+with+ribonuclease+chimeras.+An+approach+toward+humanizing+immunotoxins.&rft.au=Rybak%2C+S+M%3BHoogenboom%2C+H+R%3BNewton%2C+D+L%3BRaus%2C+J+C%3BYoule%2C+R+J&rft.aulast=Rybak&rft.aufirst=S&rft.date=1992-08-01&rft.volume=21&rft.issue=1-3&rft.spage=121&rft.isbn=&rft.btitle=&rft.title=Cell+biophysics&rft.issn=01634992&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-03-31 N1 - Date created - 1994-03-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effective regional therapy of experimental cancer with paralesional administration of tumour necrosis factor-alpha + interferon-gamma. AN - 75510141; 1341263 AB - Systemically administered tumour necrosis factor (TNF) has anti-tumour effects in animal tumour models but its clinical application is limited by severe toxicity. Interferon-gamma(IFN-gamma) has been shown to augment the anti-tumour effect of TNF. We evaluated the effect of paralesional (p.I.) injections of TNF plus IFN-gamma in a murine tumour model and compared the toxicity and anti-tumour effect with that seen with systemic administration. C57BL6 mice with 10-day subcutaneous MCA sarcomas were treated with daily p.I. injections of recombinant huTNF +/- IFN-gamma for 5 days. Optimal mean survival and 30-day cure rate was seen with doses of 5 micrograms TNF-alpha + 5000 U IFN-gamma (P 5 micrograms TNF had initial complete necrosis of tumour with a variable degree of surrounding tissue necrosis, with rapid regrowth of tumour seen in some animals. Although treatment-related mortality was similar between i.v. and p.I. therapy, there was a higher percentage of animals cured with p.I. injections with overall cure rates in treated animals at 30 days of 17% vs. 72% (i.v. vs. p.I., P < 0.01) and 13% vs. 67% (P < 0.04) in a repeat study. 2+ clinical applications. JF - Surgical oncology AU - Thom, A K AU - Fraker, D L AU - Taubenberger, J K AU - Norton, J A AD - Surgical Metabolism Section, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 291 EP - 298 VL - 1 IS - 4 SN - 0960-7404, 0960-7404 KW - Recombinant Proteins KW - 0 KW - Tumor Necrosis Factor-alpha KW - Methylcholanthrene KW - 56-49-5 KW - Interferon-gamma KW - 82115-62-6 KW - Index Medicus KW - Neoplasm Transplantation KW - Drug Screening Assays, Antitumor KW - Animals KW - Injections, Intralesional KW - Random Allocation KW - Mice, Inbred C57BL KW - Mice KW - Drug Synergism KW - Female KW - Remission Induction KW - Tumor Necrosis Factor-alpha -- toxicity KW - Sarcoma, Experimental -- therapy KW - Tumor Necrosis Factor-alpha -- administration & dosage KW - Sarcoma, Experimental -- chemically induced KW - Interferon-gamma -- toxicity KW - Interferon-gamma -- administration & dosage KW - Sarcoma, Experimental -- pathology KW - Sarcoma, Experimental -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75510141?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Surgical+oncology&rft.atitle=Effective+regional+therapy+of+experimental+cancer+with+paralesional+administration+of+tumour+necrosis+factor-alpha+%2B+interferon-gamma.&rft.au=Thom%2C+A+K%3BFraker%2C+D+L%3BTaubenberger%2C+J+K%3BNorton%2C+J+A&rft.aulast=Thom&rft.aufirst=A&rft.date=1992-08-01&rft.volume=1&rft.issue=4&rft.spage=291&rft.isbn=&rft.btitle=&rft.title=Surgical+oncology&rft.issn=09607404&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-01-13 N1 - Date created - 1994-01-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phase I/II studies of the toxicity and immunogenicity of recombinant gp160 and p24 vaccines in HIV-infected individuals. AN - 73410622; 1466952 JF - AIDS research and human retroviruses AU - Zunich, K M AU - Lane, H C AU - Davey, R T AU - Falloon, J AU - Polis, M AU - Kovacs, J A AU - Masur, H AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 1335 VL - 8 IS - 8 SN - 0889-2229, 0889-2229 KW - AIDS Vaccines KW - 0 KW - Gene Products, env KW - HIV Core Protein p24 KW - HIV Envelope Protein gp160 KW - Protein Precursors KW - Recombinant Proteins KW - Vaccines, Synthetic KW - Index Medicus KW - AIDS/HIV KW - Recombinant Proteins -- toxicity KW - Humans KW - Recombinant Proteins -- immunology KW - Recombinant Proteins -- therapeutic use KW - Recombinant Proteins -- administration & dosage KW - Vaccines, Synthetic -- toxicity KW - AIDS Vaccines -- administration & dosage KW - AIDS Vaccines -- therapeutic use KW - AIDS Vaccines -- immunology KW - Vaccines, Synthetic -- therapeutic use KW - Gene Products, env -- therapeutic use KW - Gene Products, env -- toxicity KW - HIV Core Protein p24 -- toxicity KW - Protein Precursors -- toxicity KW - Protein Precursors -- immunology KW - HIV Infections -- immunology KW - HIV Infections -- therapy KW - Vaccines, Synthetic -- immunology KW - HIV Core Protein p24 -- therapeutic use KW - Immunotherapy, Active KW - Gene Products, env -- immunology KW - Protein Precursors -- therapeutic use KW - HIV Core Protein p24 -- immunology KW - AIDS Vaccines -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73410622?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+research+and+human+retroviruses&rft.atitle=Phase+I%2FII+studies+of+the+toxicity+and+immunogenicity+of+recombinant+gp160+and+p24+vaccines+in+HIV-infected+individuals.&rft.au=Zunich%2C+K+M%3BLane%2C+H+C%3BDavey%2C+R+T%3BFalloon%2C+J%3BPolis%2C+M%3BKovacs%2C+J+A%3BMasur%2C+H&rft.aulast=Zunich&rft.aufirst=K&rft.date=1992-08-01&rft.volume=8&rft.issue=8&rft.spage=1335&rft.isbn=&rft.btitle=&rft.title=AIDS+research+and+human+retroviruses&rft.issn=08892229&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-28 N1 - Date created - 1993-01-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Humoral immune responses to homologous envelope peptides in vaccinees and lab workers infected with HIV. AN - 73399852; 1466954 JF - AIDS research and human retroviruses AU - Pincus, S H AU - Messer, K AD - NIAID, Rocky Mountain Laboratories, Hamilton, MT 59840. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 1347 VL - 8 IS - 8 SN - 0889-2229, 0889-2229 KW - AIDS Vaccines KW - 0 KW - Gene Products, env KW - HIV Antibodies KW - HIV Antigens KW - Peptide Fragments KW - Index Medicus KW - AIDS/HIV KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Gene Products, env -- chemistry KW - HIV -- immunology KW - HIV Antibodies -- immunology KW - HIV Infections -- immunology KW - Gene Products, env -- immunology KW - HIV Antigens -- chemistry KW - Laboratory Infection -- immunology KW - HIV Antigens -- immunology KW - Vaccination KW - Peptide Fragments -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73399852?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+research+and+human+retroviruses&rft.atitle=Humoral+immune+responses+to+homologous+envelope+peptides+in+vaccinees+and+lab+workers+infected+with+HIV.&rft.au=Pincus%2C+S+H%3BMesser%2C+K&rft.aulast=Pincus&rft.aufirst=S&rft.date=1992-08-01&rft.volume=8&rft.issue=8&rft.spage=1347&rft.isbn=&rft.btitle=&rft.title=AIDS+research+and+human+retroviruses&rft.issn=08892229&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-28 N1 - Date created - 1993-01-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - HLA phenotype is a factor in determining rate of disease progression and outcome in HIV-1-infected individuals. AN - 73386616; 1361351 AB - HLA allele frequencies were examined for possible association(s) with the rate of disease progression and with the disease outcome (AIDS diagnosis) in a population of HIV-1-infected individuals. Certain alleles were associated with the relative rate of CD4+ T-cell decline. Association of particular alleles with several disease outcomes associated with infection was also observed. It is important to keep these two aspects (disease progression, AIDS diagnosis) separate when studying HLA in the HIV-1-infected population. Alleles that may play a role in the rate of virus speed by effecting the immune response may be different from those found to be associated with a particular disease. We feel that the only truly informative data, in this regard, can be generated from a relative precise determination of the time of infection (to study disease progression) and adequate numbers of individuals with specific diseases to study specific disease association. If such data can be generated we will have a much better understanding of the pathogenetic process(es) of HIV-1 infection. JF - AIDS research and human retroviruses AU - Mann, D L AU - Carrington, M AU - O'Donnell, M AU - Miller, T AU - Goedert, J AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, MD 21702-1201. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 1345 EP - 1346 VL - 8 IS - 8 SN - 0889-2229, 0889-2229 KW - HLA Antigens KW - 0 KW - Index Medicus KW - AIDS/HIV KW - Phenotype KW - Alleles KW - Humans KW - Disease Susceptibility -- immunology KW - Genetic Predisposition to Disease KW - Male KW - Leukocyte Count KW - CD4-Positive T-Lymphocytes KW - HIV Infections -- immunology KW - HIV Infections -- genetics KW - HLA Antigens -- analysis KW - HIV-1 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73386616?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+research+and+human+retroviruses&rft.atitle=HLA+phenotype+is+a+factor+in+determining+rate+of+disease+progression+and+outcome+in+HIV-1-infected+individuals.&rft.au=Mann%2C+D+L%3BCarrington%2C+M%3BO%27Donnell%2C+M%3BMiller%2C+T%3BGoedert%2C+J&rft.aulast=Mann&rft.aufirst=D&rft.date=1992-08-01&rft.volume=8&rft.issue=8&rft.spage=1345&rft.isbn=&rft.btitle=&rft.title=AIDS+research+and+human+retroviruses&rft.issn=08892229&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-28 N1 - Date created - 1993-01-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Clues to cancer etiology from studies of farmers. AN - 73261434; 1411362 AB - This article summarizes cancer risks among farmers to clarify the magnitude of the problem and to suggest directions for future research. Significant excesses occurred for Hodgkin's disease, multiple myeloma, leukemia, skin melanomas, and cancers of the lip, stomach, and prostate. Nonsignificant increases in risk were also noted for non-Hodgkin's lymphoma and cancers of connective tissue and brain. These excesses occurred against a background of substantial deficits among farmers for total mortality and mortality from many specific diseases. The tumors vary in frequency, histology, and prognosis and do not fall into any obvious grouping. Two commonalities may be important. Several of the tumors excessive among farmers appear to be rising in the general population and are excessive among patients with naturally occurring or medically induced immunodeficiencies. Therefore epidemiologic studies on specific exposures among farmers may help explain the rising trend of certain cancers in developed countries and provide clues to mechanisms of action for environmental carcinogens. JF - Scandinavian journal of work, environment & health AU - Blair, A AU - Zahm, S H AU - Pearce, N E AU - Heineman, E F AU - Fraumeni, J F AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 209 EP - 215 VL - 18 IS - 4 SN - 0355-3140, 0355-3140 KW - Carcinogens, Environmental KW - 0 KW - Index Medicus KW - Risk KW - Carcinogens, Environmental -- adverse effects KW - Humans KW - Male KW - Female KW - Cause of Death KW - Occupational Exposure KW - Agricultural Workers' Diseases -- mortality KW - Neoplasms -- mortality KW - Agricultural Workers' Diseases -- etiology KW - Cross-Cultural Comparison KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73261434?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scandinavian+journal+of+work%2C+environment+%26+health&rft.atitle=Clues+to+cancer+etiology+from+studies+of+farmers.&rft.au=Blair%2C+A%3BZahm%2C+S+H%3BPearce%2C+N+E%3BHeineman%2C+E+F%3BFraumeni%2C+J+F&rft.aulast=Blair&rft.aufirst=A&rft.date=1992-08-01&rft.volume=18&rft.issue=4&rft.spage=209&rft.isbn=&rft.btitle=&rft.title=Scandinavian+journal+of+work%2C+environment+%26+health&rft.issn=03553140&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-04 N1 - Date created - 1992-11-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of thioacetamide-induced hepatocellular necrosis by prostaglandins is associated with novel histologic changes. AN - 73250900; 1406079 AB - Cytoprotective effects of the prostaglandins 16,16-dimethyl PGE2 (dmPGE2) and PGF2 alpha tromethamine (PGF2 alpha) were evaluated in the rat model of acute hepatocellular necrosis induced by thioacetamide (TAA). dmPGE2 (100 micrograms/kg SC 8 hourly) did not induce a significant increase in survival when started after the onset of TAA-induced fulminant hepatic failure. However, priming with dmPGE2 (100 micrograms/kg SC 30 min before TAA) reduced TAA-induced elevations in serum ALT (684 +/- 68 (SEM) vs 274 +/- 135 IU/1, p less than 0.01). This phenomenon did not occur if dmPGE2 was administered after TAA or by the IP route. Modulation of TAA-induced centrizonal hepatocellular necrosis by dmPGE2 was associated with a striking increase in centrizonal ballooning of hepatocytes (p less than 0.01), and, as assessed by stereology, less hepatocellular necrosis and degenerative changes. PGF2 alpha, which in contrast to dmPGE2 does not act via cAMP, had no effect on TAA-induced changes in serum ALT or hepatic histology. These findings suggest that dmPGE2 decreases hepatocellular necrosis by activating surface membrane adenylate cyclase and consequently stimulating cAMP. Ballooning of hepatocytes could occur secondary to these membrane events and appears to be a marker of dmPGE2-induced cytoprotection in this model. JF - Liver AU - Bergasa, N V AU - Borque, M J AU - Wahl, L M AU - Rabin, L AU - Jones, E A AD - Liver Diseases Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 168 EP - 174 VL - 12 IS - 4 Pt 1 SN - 0106-9543, 0106-9543 KW - Thioacetamide KW - 075T165X8M KW - Dinoprost KW - B7IN85G1HY KW - dinoprost tromethamine KW - CT6BBQ5A68 KW - Alanine Transaminase KW - EC 2.6.1.2 KW - 16,16-Dimethylprostaglandin E2 KW - M790V82VAC KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Necrosis KW - Alanine Transaminase -- blood KW - Male KW - Hepatic Encephalopathy -- drug therapy KW - Liver -- pathology KW - Liver -- drug effects KW - Dinoprost -- therapeutic use KW - Dinoprost -- analogs & derivatives KW - Hepatic Encephalopathy -- pathology KW - 16,16-Dimethylprostaglandin E2 -- therapeutic use KW - Hepatic Encephalopathy -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73250900?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Liver&rft.atitle=Modulation+of+thioacetamide-induced+hepatocellular+necrosis+by+prostaglandins+is+associated+with+novel+histologic+changes.&rft.au=Bergasa%2C+N+V%3BBorque%2C+M+J%3BWahl%2C+L+M%3BRabin%2C+L%3BJones%2C+E+A&rft.aulast=Bergasa&rft.aufirst=N&rft.date=1992-08-01&rft.volume=12&rft.issue=4+Pt+1&rft.spage=168&rft.isbn=&rft.btitle=&rft.title=Liver&rft.issn=01069543&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-13 N1 - Date created - 1992-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cerebrospinal fluid and serum levels of neuron-specific enolase in patients with schizophrenia. AN - 73250717; 1357702 AB - Some patients with schizophrenia appear to have brain abnormalities, including enlarged third and lateral ventricles and reduced volumes of temporal lobe structures. These abnormalities could be attributed to a developmental abnormality or a neurodegenerative process. Neuron-specific enolase (NSE), a protein that is found primarily in neurons and neuroendocrine cells, has been used as an index of neuronal damage or degeneration. Levels of NSE in cerebrospinal fluid (CSF) and serum from 50 patients with acute and chronic schizophrenia were compared with those in normal and neurological control subjects. A double-antibody, solid phase iodinated radioimmunoassay was used to determine NSE levels. There was no evidence of elevated levels in patients with schizophrenia, whereas control subjects with neurological illnesses had increased levels of NSE in CSF. Because NSE is rapidly cleared from CSF, however, elevated levels could have been missed. Unmedicated patients tended to have lower levels than medicated patients. JF - Psychiatry research AU - Egan, M F AU - el-Mallakh, R S AU - Suddath, R L AU - Lohr, J B AU - Bracha, H S AU - Wyatt, R J AD - Neuropsychiatry Branch, National Institute of Mental Health, Washington, DC. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 187 EP - 195 VL - 43 IS - 2 SN - 0165-1781, 0165-1781 KW - Antipsychotic Agents KW - 0 KW - Phosphopyruvate Hydratase KW - EC 4.2.1.11 KW - Index Medicus KW - Magnetic Resonance Imaging KW - Psychiatric Status Rating Scales KW - Humans KW - Brain -- pathology KW - Adult KW - Tomography, X-Ray Computed KW - Chronic Disease KW - Antipsychotic Agents -- adverse effects KW - Male KW - Female KW - Neurocognitive Disorders -- diagnosis KW - Neurocognitive Disorders -- cerebrospinal fluid KW - Neurocognitive Disorders -- psychology KW - Schizophrenia -- diagnosis KW - Blood-Brain Barrier -- physiology KW - Schizophrenic Psychology KW - Schizophrenia -- drug therapy KW - Neurocognitive Disorders -- drug therapy KW - Schizophrenia -- cerebrospinal fluid KW - Phosphopyruvate Hydratase -- cerebrospinal fluid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73250717?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychiatry+research&rft.atitle=Cerebrospinal+fluid+and+serum+levels+of+neuron-specific+enolase+in+patients+with+schizophrenia.&rft.au=Egan%2C+M+F%3Bel-Mallakh%2C+R+S%3BSuddath%2C+R+L%3BLohr%2C+J+B%3BBracha%2C+H+S%3BWyatt%2C+R+J&rft.aulast=Egan&rft.aufirst=M&rft.date=1992-08-01&rft.volume=43&rft.issue=2&rft.spage=187&rft.isbn=&rft.btitle=&rft.title=Psychiatry+research&rft.issn=01651781&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-23 N1 - Date created - 1992-11-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutagenesis induced by bacterial UmuDC proteins and their plasmid homologues. AN - 73236097; 1406263 AB - The popular image of a world full of pollutants mutating DNA is only partly true since there are relatively few agents which can subtly and directly change base coding; for example, some alkylating agents alter guanine so that it pairs like adenine. Many more mutagens are less subtle and simply destroy coding altogether rather than changing it. Such mutagens include ultraviolet light, X-rays, DNA cross-linkers and other agents which make DNA breaks or large adducts. In Escherichia coli, mutagenesis by these agents occurs during a DNA repair process which increases cell survival but with an inherent possibility of changing the original sequence. Such mutagenic DNA repair is, in part, encoded by the E. coli umuDC operon. This article reviews the structure, function, regulation and evolution of the umuDC operon and similar genes found both in other species and on naturally occurring plasmids. JF - Molecular microbiology AU - Woodgate, R AU - Sedgwick, S G AD - Section on Viruses and Cellular Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 2213 EP - 2218 VL - 6 IS - 16 SN - 0950-382X, 0950-382X KW - umu KW - Bacterial Proteins KW - 0 KW - Escherichia coli Proteins KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - UmuD protein, E coli KW - Index Medicus KW - Phenotype KW - DNA Repair KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Bacterial Proteins -- genetics KW - Escherichia coli -- genetics KW - Plasmids KW - Mutagenesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73236097?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+microbiology&rft.atitle=Mutagenesis+induced+by+bacterial+UmuDC+proteins+and+their+plasmid+homologues.&rft.au=Woodgate%2C+R%3BSedgwick%2C+S+G&rft.aulast=Woodgate&rft.aufirst=R&rft.date=1992-08-01&rft.volume=6&rft.issue=16&rft.spage=2213&rft.isbn=&rft.btitle=&rft.title=Molecular+microbiology&rft.issn=0950382X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-29 N1 - Date created - 1992-10-29 N1 - Date revised - 2017-01-13 N1 - Gene symbol - umu N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - D2 or not D2? AN - 73207241; 1326905 JF - Alcoholism, clinical and experimental research AU - Karp, R W AD - Division of Basic Research, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 786 EP - 787 VL - 16 IS - 4 SN - 0145-6008, 0145-6008 KW - Receptors, Dopamine KW - 0 KW - Receptors, Dopamine D2 KW - Index Medicus KW - Rats KW - Liver Cirrhosis, Alcoholic -- genetics KW - Animals KW - Liver Cirrhosis, Alcoholic -- physiopathology KW - Synaptic Transmission -- genetics KW - Risk Factors KW - Humans KW - Synaptic Transmission -- physiology KW - Receptors, Dopamine -- physiology KW - Alleles KW - Receptors, Dopamine -- genetics KW - Alcoholism -- physiopathology KW - Alcoholism -- genetics KW - Alcoholism -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73207241?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%2C+clinical+and+experimental+research&rft.atitle=D2+or+not+D2%3F&rft.au=Karp%2C+R+W&rft.aulast=Karp&rft.aufirst=R&rft.date=1992-08-01&rft.volume=16&rft.issue=4&rft.spage=786&rft.isbn=&rft.btitle=&rft.title=Alcoholism%2C+clinical+and+experimental+research&rft.issn=01456008&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-20 N1 - Date created - 1992-10-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synergy of carbamazepine and valproic acid in affective illness: case report and review of the literature. AN - 73188824; 1527232 AB - Carbamazepine and valproic acid are anticonvulsants with mood-stabilizing properties. Basic and clinical research suggest that these medications used together may have synergistic anticonvulsant effects. Psychotropic synergy of the combination has yet to be explored systematically. We present the case of a patient with rapid-cycling bipolar disorder studied under double-blind conditions whose hypomanias and depressions were refractory to either carbamazepine or valproic acid alone, but responded dramatically to the combination. The superior response to the combination appeared to be due to pharmacodynamic rather than pharmacokinetic effects. The clinical and theoretical aspects of the use of carbamazepine and valproic acid in combination are discussed. JF - Journal of clinical psychopharmacology AU - Ketter, T A AU - Pazzaglia, P J AU - Post, R M AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 276 EP - 281 VL - 12 IS - 4 SN - 0271-0749, 0271-0749 KW - Carbamazepine KW - 33CM23913M KW - Valproic Acid KW - 614OI1Z5WI KW - Index Medicus KW - Drug Therapy, Combination KW - Double-Blind Method KW - Humans KW - Middle Aged KW - Drug Synergism KW - Male KW - Bipolar Disorder -- drug therapy KW - Carbamazepine -- therapeutic use KW - Valproic Acid -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73188824?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+psychopharmacology&rft.atitle=Synergy+of+carbamazepine+and+valproic+acid+in+affective+illness%3A+case+report+and+review+of+the+literature.&rft.au=Ketter%2C+T+A%3BPazzaglia%2C+P+J%3BPost%2C+R+M&rft.aulast=Ketter&rft.aufirst=T&rft.date=1992-08-01&rft.volume=12&rft.issue=4&rft.spage=276&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+psychopharmacology&rft.issn=02710749&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Variability in alkaloid profiles in neotropical poison frogs (Dendrobatidae): genetic versus environmental determinants. AN - 73187408; 1523680 AB - Dendrobatid frogs produce a diverse set of alkaloids, whose profiles appear characteristic of frogs of each species or, in the case of variable species, of each population. In the case of one widespread species, Dendrobates auratus, alkaloid profiles in extracts of skin are markedly different in three populations, one from a Pacific island, Isla Taboga, Panama, one from central mountains in Panama, and the third from the Caribbean coast in Costa Rica. The first contains three major classes of dendrobatid alkaloids, the histrionicotoxins, the pumiliotoxin-A class and the decahydroquinolines. The second contains mainly histrionicotoxins, pumiliotoxin-A class alkaloids and one indolizidine. The third contains histrionicotoxins, a homopumiliotoxin, one decahydroquinoline, and a variety of indolizidines, quinolizidines and pyrrolizidines. Frogs from Isla Taboga or a nearby island were introduced into the Manoa Valley, Oahu, Hawaii, in 1932. Remarkably, although alkaloids of the pumiliotoxin-A class and one decahydroquinoline are still major constituents in skin extracts of Hawaiian frogs descended from the 1932 founding population, histrionicotoxins are absent and a novel tricyclic alkaloid is present. Offspring of wild-caught parents from Hawaii, Panama or Costa Rica raised in indoor terrariums on a diet of crickets and fruit flies do not contain detectable amounts of skin alkaloids. Offspring raised in large outside terrariums in Hawaii and fed mainly wild-caught termites and fruit flies do contain the same profile of alkaloids as their wild-caught parents in Hawaii, but at reduced levels. The genetic, environmental and dietary determinants of alkaloid profiles in dendrobatid frogs remain obscure, in particular the underlying cause for total absence in terrarium-reared frogs. JF - Toxicon : official journal of the International Society on Toxinology AU - Daly, J W AU - Secunda, S I AU - Garraffo, H M AU - Spande, T F AU - Wisnieski, A AU - Nishihira, C AU - Cover, J F AD - Laboratory of Bioorganic Chemistry, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 887 EP - 898 VL - 30 IS - 8 SN - 0041-0101, 0041-0101 KW - Alkaloids KW - 0 KW - Poisons KW - Index Medicus KW - Panama KW - Ecology KW - Skin -- chemistry KW - Animals KW - Costa Rica KW - Hawaii KW - Diet KW - Ranidae -- metabolism KW - Alkaloids -- chemistry KW - Poisons -- chemistry KW - Genetics, Population KW - Alkaloids -- isolation & purification KW - Poisons -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73187408?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicon+%3A+official+journal+of+the+International+Society+on+Toxinology&rft.atitle=Variability+in+alkaloid+profiles+in+neotropical+poison+frogs+%28Dendrobatidae%29%3A+genetic+versus+environmental+determinants.&rft.au=Daly%2C+J+W%3BSecunda%2C+S+I%3BGarraffo%2C+H+M%3BSpande%2C+T+F%3BWisnieski%2C+A%3BNishihira%2C+C%3BCover%2C+J+F&rft.aulast=Daly&rft.aufirst=J&rft.date=1992-08-01&rft.volume=30&rft.issue=8&rft.spage=887&rft.isbn=&rft.btitle=&rft.title=Toxicon+%3A+official+journal+of+the+International+Society+on+Toxinology&rft.issn=00410101&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-09 N1 - Date created - 1992-10-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Angiotensin AT2 receptors regulate cerebral blood flow in rats. AN - 73171003; 1520859 AB - LARGE cerebral arteries have been reported to contain angiotensin receptors that are exclusively of the AT2 subtype. We measured the effect of the AT2 receptor selective ligand PD 123319 on cerebral blood flow (CBF) in rats, using laser-doppler flowmetry. PD 123319 (1-10 mg kg-1) dose-dependently inhibited the increase in CBF, when the blood pressure was increased by a norepinephrine infusion. However, PD 123319 did not alter baseline CBF at normal blood pressures. Therefore PD 123319 appears to interfere with the autoregulatory mechanisms of CBF. The participation of AT2 receptors in the regulation of CBF confirms a physiological role for this receptor subtype, and may give clues for future treatment of various cerebrovascular disorders. JF - Neuroreport AU - Strömberg, C AU - Näveri, L AU - Saavedra, J M AD - Section on Pharmacology, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 703 EP - 704 VL - 3 IS - 8 SN - 0959-4965, 0959-4965 KW - Angiotensin Receptor Antagonists KW - 0 KW - Imidazoles KW - Pyridines KW - Receptors, Angiotensin KW - Angiotensin II KW - 11128-99-7 KW - PD 123319 KW - 130663-39-7 KW - Sodium Chloride KW - 451W47IQ8X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Hypertension -- chemically induced KW - Imidazoles -- pharmacology KW - Hypertension -- physiopathology KW - Dose-Response Relationship, Drug KW - Hypertension -- prevention & control KW - Pyridines -- pharmacology KW - Male KW - Angiotensin II -- metabolism KW - Receptors, Angiotensin -- physiology KW - Norepinephrine -- pharmacology KW - Cerebrovascular Circulation -- physiology KW - Cerebrovascular Circulation -- drug effects KW - Blood Pressure -- drug effects KW - Angiotensin II -- pharmacology KW - Receptors, Angiotensin -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73171003?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroreport&rft.atitle=Angiotensin+AT2+receptors+regulate+cerebral+blood+flow+in+rats.&rft.au=Str%C3%B6mberg%2C+C%3BN%C3%A4veri%2C+L%3BSaavedra%2C+J+M&rft.aulast=Str%C3%B6mberg&rft.aufirst=C&rft.date=1992-08-01&rft.volume=3&rft.issue=8&rft.spage=703&rft.isbn=&rft.btitle=&rft.title=Neuroreport&rft.issn=09594965&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-15 N1 - Date created - 1992-10-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - An examination of the association between maximum-tolerated dose and carcinogenicity in 326 long-term studies in rats and mice. AN - 73153376; 1516777 AB - The association between rodent carcinogenicity and maximum-tolerated dose (MTD) was evaluated in 326 long-term carcinogenicity studies in mice and rats. Others investigating this association have focused primarily on positive studies, but our investigation considered all experimental outcomes. We found that chemicals with low MTDs were somewhat more likely to be rodent carcinogens than chemicals with high MTDs, but this association was limited primarily to gavage studies. Overall, the MTD was not a reliable predictor of whether or not a chemical would be a rodent carcinogen. Our investigation confirms that comparisons of carcinogenic potencies based only on positive studies may result in artifactually elevated estimates of the underlying association between chemical toxicity and rodent carcinogenicity and thus may also inflate the estimated interspecies correlation in carcinogenic response. Nevertheless, the results of our study are consistent with the frequently cited 75% concordance in carcinogenicity outcome between rats and mice. This concordance is quite high, particularly since 80% is approximately the maximum level of observable interspecies concordance achievable for a set of chemicals with relatively low carcinogenic potency, because of the variability in observed tumor responses that can induce false negative or false positive outcomes in either of the two species. Thus, the underlying qualitative interspecies correlation in carcinogenic response between rats and mice may be greater than is commonly recognized. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Haseman, J K AU - Seilkop, S K AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 207 EP - 213 VL - 19 IS - 2 SN - 0272-0590, 0272-0590 KW - Carcinogens KW - 0 KW - Index Medicus KW - Rats KW - Animals KW - Dose-Response Relationship, Drug KW - Carcinogenicity Tests KW - Mice KW - Species Specificity KW - Male KW - Female KW - Carcinogens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73153376?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=An+examination+of+the+association+between+maximum-tolerated+dose+and+carcinogenicity+in+326+long-term+studies+in+rats+and+mice.&rft.au=Haseman%2C+J+K%3BSeilkop%2C+S+K&rft.aulast=Haseman&rft.aufirst=J&rft.date=1992-08-01&rft.volume=19&rft.issue=2&rft.spage=207&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-02 N1 - Date created - 1992-10-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - N-methyl-D-aspartate exposure blocks glutamate toxicity in cultured cerebellar granule cells. AN - 73146442; 1355259 AB - Exposure of cultured cerebellar granule cells to glutamate results in a concentration-dependent (EC50 = 22.7 +/- 0.4 microM) and delayed (24-72 hr) neurotoxicity, which is blocked by the specific N-methyl-D-aspartate (NMDA) receptor antagonists 2-amino-5-phosphovalerate and MK-801 but is unaffected by the non-NMDA receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione and 6,7-dinitroquinoxaline-2,3-dione. Although glutamate toxicity in these cells is mediated by the NMDA subtype of glutamate receptor, pretreatment of cerebellar granule cells with subtoxic concentrations of NMDA markedly antagonizes the neurotoxic actions of glutamate, with an IC50 of 55 +/- 4 microM. The neuroprotective effect of NMDA requires a preincubation time of approximately 120 min to be fully manifested and does not require the presence of NMDA during glutamate exposure. These data demonstrate that NMDA receptors mediate both neurotoxicity and neuroprotection in cerebellar granule cells. Among four glutamate receptor agonists tested (NMDA, quisqualate, ibotenate, and kainate), only NMDA was able to provide a robust neuroprotection against glutamate toxicity. Quisqualate was neither neurotoxic nor neuroprotective, whereas ibotenate, which was nontoxic by itself, induced a small degree of neuroprotection. In contrast, kainate, which was neurotoxic to cerebellar granule cells, also provided considerable neuroprotection against glutamate toxicity. Because preincubation of cerebellar granule cells with NMDA fails to alter NMDA receptor-mediated phosphoinositide hydrolysis or the specific binding of [3H]MK-801 to NMDA receptors, it appears that the neuroprotective effects of NMDA are not due to NMDA receptor desensitization. JF - Molecular pharmacology AU - Chuang, D M AU - Gao, X M AU - Paul, S M AD - Section on Molecular Neurobiology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 210 EP - 216 VL - 42 IS - 2 SN - 0026-895X, 0026-895X KW - Culture Media KW - 0 KW - Excitatory Amino Acid Antagonists KW - Glutamates KW - Receptors, Glutamate KW - Receptors, N-Methyl-D-Aspartate KW - Receptors, Neurotransmitter KW - Tritium KW - 10028-17-8 KW - Ibotenic Acid KW - 2552-55-8 KW - Aspartic Acid KW - 30KYC7MIAI KW - Glutamic Acid KW - 3KX376GY7L KW - Ouabain KW - 5ACL011P69 KW - N-Methylaspartate KW - 6384-92-5 KW - Quisqualic Acid KW - 8OC22C1B99 KW - Magnesium KW - I38ZP9992A KW - Glucose KW - IY9XDZ35W2 KW - Kainic Acid KW - SIV03811UC KW - Index Medicus KW - Sensitivity and Specificity KW - Animals KW - Neurons -- drug effects KW - Receptors, Neurotransmitter -- drug effects KW - Cytoplasmic Granules -- metabolism KW - Ibotenic Acid -- pharmacology KW - Aspartic Acid -- pharmacokinetics KW - Rats KW - Receptors, Neurotransmitter -- physiology KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Receptors, N-Methyl-D-Aspartate -- drug effects KW - Magnesium -- pharmacology KW - Cytoplasmic Granules -- drug effects KW - Ouabain -- metabolism KW - Kainic Acid -- pharmacology KW - Neurons -- metabolism KW - Quisqualic Acid -- pharmacology KW - Rats, Inbred Strains KW - Glucose -- pharmacology KW - Cells, Cultured KW - Cerebellum -- cytology KW - N-Methylaspartate -- pharmacology KW - Glutamates -- metabolism KW - Cerebellum -- drug effects KW - Glutamates -- toxicity KW - Cerebellum -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73146442?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=N-methyl-D-aspartate+exposure+blocks+glutamate+toxicity+in+cultured+cerebellar+granule+cells.&rft.au=Chuang%2C+D+M%3BGao%2C+X+M%3BPaul%2C+S+M&rft.aulast=Chuang&rft.aufirst=D&rft.date=1992-08-01&rft.volume=42&rft.issue=2&rft.spage=210&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=0026895X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-30 N1 - Date created - 1992-09-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Early onset of drinking as a risk factor for lifetime alcohol-related problems. AN - 73144518; 1511233 AB - Heavy drinking among students has been a major public health concern over the past decade. A nationally representative 1988 survey on drinking practices and related problems examined the effect of age of of onset of drinking on lifetime alcohol-related problems. Prevalence estimates were obtained for major demographic subgroups of the population. Results and implications are discussed in the context of minimum legal drinking age. JF - British journal of addiction AU - Chou, S P AU - Pickering, R P AD - National Institute on Alcohol Abuse and Alcoholism, Division of Biometry and Epidemiology, Rockville, MD 20857. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 1199 EP - 1204 VL - 87 IS - 8 SN - 0952-0481, 0952-0481 KW - Index Medicus KW - Cross-Sectional Studies KW - Risk Factors KW - Humans KW - Adult KW - Incidence KW - Aged KW - Middle Aged KW - Adolescent KW - United States -- epidemiology KW - Male KW - Female KW - Alcoholism -- epidemiology KW - Alcohol Drinking -- psychology KW - Personality Development KW - Alcohol Drinking -- epidemiology KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73144518?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+addiction&rft.atitle=Early+onset+of+drinking+as+a+risk+factor+for+lifetime+alcohol-related+problems.&rft.au=Chou%2C+S+P%3BPickering%2C+R+P&rft.aulast=Chou&rft.aufirst=S&rft.date=1992-08-01&rft.volume=87&rft.issue=8&rft.spage=1199&rft.isbn=&rft.btitle=&rft.title=British+journal+of+addiction&rft.issn=09520481&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-01 N1 - Date created - 1992-10-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Enhanced hydroxyl radical generation by 2'-methyl analog of MPTP: suppression by clorgyline and deprenyl. AN - 73138445; 1323883 AB - Sodium salicylate was infused through a microdialysis probe placed in the striatum of anesthetized rats in order to assay the formation of hydroxyl radical (.OH) in the extracellular fluid in vivo. In addition to causing sustained dopamine release, intrastriatal infusion of the 2'-methyl analog of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (2'CH3-MPTP) increased the formation of 2,3-dihydroxybenzoic acid (2,3-DHBA), the nonenzymatic .OH adduct of salicylate in the brain dialysate. Inhibition of monoamine oxidase (MAO) by clorgyline and deprenyl completely blocked the formation of 2,3-DHBA and the sustained dopamine overflow induced by 2'-CH3-MPTP. The results indicate that the enhanced formation of cytotoxic .OH by 2'-CH3-MPTP is suppressed by MAO inhibitors. These data support the hypothesis that the protective effect of MAO inhibitors on the neurotoxicity induced by MPTP analogues may be due not only to the inhibition of MPTP metabolism by MAO but also the blockade of the formation of .OH free radicals. An enhanced generation of cytotoxic .OH free radicals in the striatum which in turn leads to oxidant damage may be relevant to the development of parkinsonism-like changes in animals produced by MPTP analogues. JF - Synapse (New York, N.Y.) AU - Chiueh, C C AU - Huang, S J AU - Murphy, D L AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 346 EP - 348 VL - 11 IS - 4 SN - 0887-4476, 0887-4476 KW - Free Radicals KW - 0 KW - Hydroxides KW - 1-methyl-4-(2'-methylphenyl)-1,2,3,6-tetrahydropyridine KW - 102417-86-7 KW - Selegiline KW - 2K1V7GP655 KW - Hydroxyl Radical KW - 3352-57-6 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Clorgyline KW - LYJ16FZU9Q KW - Index Medicus KW - Rats KW - Animals KW - Dialysis KW - Selegiline -- pharmacology KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- analogs & derivatives KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- metabolism KW - Clorgyline -- pharmacology KW - Hydroxides -- metabolism KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- antagonists & inhibitors KW - Hydroxides -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73138445?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Synapse+%28New+York%2C+N.Y.%29&rft.atitle=Enhanced+hydroxyl+radical+generation+by+2%27-methyl+analog+of+MPTP%3A+suppression+by+clorgyline+and+deprenyl.&rft.au=Chiueh%2C+C+C%3BHuang%2C+S+J%3BMurphy%2C+D+L&rft.aulast=Chiueh&rft.aufirst=C&rft.date=1992-08-01&rft.volume=11&rft.issue=4&rft.spage=346&rft.isbn=&rft.btitle=&rft.title=Synapse+%28New+York%2C+N.Y.%29&rft.issn=08874476&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-14 N1 - Date created - 1992-09-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Development of renal toxicity in F344 rats gavaged with mercuric chloride for 2 weeks, or 2, 4, 6, 15, and 24 months. AN - 73127496; 1354752 AB - Both sexes of F344 rats were gavaged with maximal tolerated doses of mercuric chloride for periods from 2 wk to up to 2 yr to investigate chronic nephrotoxicity and potential carcinogenicity. The toxicity of mercuric chloride was excessive after 2 wk of exposure to doses ranging from 1.25 to 20 mg/kg, compromising renal function by selectively destroying cells of the proximal tubules, and eliciting marked elevations in urinary biomarker enzymes diagnostic for acute renal tubule necrosis. In the 2-wk studies, urinary alkaline phosphatase and aspartate amino-transferase were most sensitive to renal mercury toxicity among a panel of six enzymes, exhibiting twofold increases above controls at the 5.0 mg/kg dose, before changes in the other enzymes occurred. Urinary lactate dehydrogenase was the most responsive enzyme, with up to 11-fold increases in activity above controls. In response to mercuric chloride exposure of 5.0 mg/kg for 2-6 mo, the greatest and most persistent increases in elevation of urinary enzyme activities were exhibited by alkaline phosphatase and gamma-glutamyl transferase, which increased two-to threefold above controls. At this interval, the maximal severity of the renal lesions in both sexes of rats was graded as minimal to mild. Beyond 6 mo none of the urinary enzymes measured in this study was adequate as biomarkers of nephrotoxicity, although the severity of the renal lesions had progressed. Mercury accumulated in a dose-related fashion primarily in the kidney, and to a lesser extent in the liver. The severity of the renal lesions was increased by continued exposure to mercuric chloride, as tissue concentrations of mercury rose in proportion to dose. Mercuric chloride treatment for 2 yr clearly exacerbated the severity of the spontaneous nephrotoxicity prevalent in aging F344 rats. The excessive mortality that occurred in the male rats was probably due to a combination of these factors. No renal tumors were detected in rats, possibly because the potential for their development was reduced; however, direct tissue contact with mercury induced squamous-cell papillomas of the forestomach in both sexes. JF - Journal of toxicology and environmental health AU - Dieter, M P AU - Boorman, G A AU - Jameson, C W AU - Eustis, S L AU - Uraih, L C AD - National Institutes of Health, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 319 EP - 340 VL - 36 IS - 4 SN - 0098-4108, 0098-4108 KW - Mercuric Chloride KW - 53GH7MZT1R KW - gamma-Glutamyltransferase KW - EC 2.3.2.2 KW - Aspartate Aminotransferases KW - EC 2.6.1.1 KW - Alkaline Phosphatase KW - EC 3.1.3.1 KW - Acid Phosphatase KW - EC 3.1.3.2 KW - Leucyl Aminopeptidase KW - EC 3.4.11.1 KW - Mercury KW - FXS1BY2PGL KW - Index Medicus KW - Aspartate Aminotransferases -- urine KW - Animals KW - Alkaline Phosphatase -- urine KW - Dose-Response Relationship, Drug KW - Brain Chemistry KW - Mercury -- analysis KW - Kidney -- drug effects KW - Tissue Distribution KW - Kidney -- chemistry KW - Liver -- chemistry KW - Drug Administration Routes KW - Acid Phosphatase -- urine KW - Rats KW - Rats, Inbred F344 KW - Leucyl Aminopeptidase -- urine KW - Body Weight -- drug effects KW - Hyperparathyroidism -- chemically induced KW - Time Factors KW - gamma-Glutamyltransferase -- urine KW - Male KW - Female KW - Organ Size -- drug effects KW - Kidney -- anatomy & histology KW - Mercuric Chloride -- pharmacokinetics KW - Kidney Diseases -- metabolism KW - Kidney Diseases -- enzymology KW - Mercuric Chloride -- toxicity KW - Kidney Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73127496?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+toxicology+and+environmental+health&rft.atitle=Development+of+renal+toxicity+in+F344+rats+gavaged+with+mercuric+chloride+for+2+weeks%2C+or+2%2C+4%2C+6%2C+15%2C+and+24+months.&rft.au=Dieter%2C+M+P%3BBoorman%2C+G+A%3BJameson%2C+C+W%3BEustis%2C+S+L%3BUraih%2C+L+C&rft.aulast=Dieter&rft.aufirst=M&rft.date=1992-08-01&rft.volume=36&rft.issue=4&rft.spage=319&rft.isbn=&rft.btitle=&rft.title=Journal+of+toxicology+and+environmental+health&rft.issn=00984108&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-22 N1 - Date created - 1992-09-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Structure, expression, and regulation of the major noncollagenous matrix proteins of bone. AN - 73113156; 1499220 AB - The noncollagenous proteins (NCPs) that predominate the bone matrix have recently been the focus of intense investigation because of their potential influence on cell attachment, Ca2+ and hydroxyapatite binding, and the mineralization of bone tissue. With the advent of molecular biology, all of the major NCPs of bone have been cloned and their amino acid sequences completely determined. While each of the proteins has distinct structural properties, some proteins appear to be part of gene families. Examples include the small proteoglycans, decorin and biglycan, as well as the gamma carboxyglutamic acid proteins, such as matrix gla protein and osteocalcin (bone gla protein). Some of the NCPs that are clearly not members of any known gene family still share several common characteristics. One such example of this "convergent evolution" is bone sialoprotein and osteopontin. Both are highly posttranslationally modified glycoproteins that share the cell attachment amino acid sequence RGD (arginine-glycine-aspartic acid), which facilitates the attachment of bone cells in vitro, yet they are clearly not related genetically. Using cDNAs and antisera as probes, the precise temporal localization of NCP expression has been determined, and it has been shown that NCPs are produced in skeletal, and in most cases, nonskeletal tissue as well. This observation implies that the functions of the NCPs are not necessarily limited to bone tissue. Many of the promoters for these genes have been isolated and functional domains determined by a combination of chloramphenicol acetyltransferase assay, gel shift, and footprint analyses. The most extensively studied promoter in the NCP category is osteocalcin, whose sensitivity to 1,25-dihydroxycholecalciferol has been delineated in detail. Future studies on the individual and cooperative activities of the NCPs in bone are likely to involve site-directed mutagenesis of cloned DNA and a combination of in vitro and in vivo functional analyses. JF - Clinical orthopaedics and related research AU - Young, M F AU - Kerr, J M AU - Ibaraki, K AU - Heegaard, A M AU - Robey, P G AD - Bone Research Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 275 EP - 294 IS - 281 SN - 0009-921X, 0009-921X KW - BGN protein, human KW - 0 KW - Biglycan KW - Calcium-Binding Proteins KW - DCN protein, human KW - Decorin KW - Extracellular Matrix Proteins KW - Glycoproteins KW - IBSP protein, human KW - Integrin-Binding Sialoprotein KW - Osteonectin KW - Phosphoproteins KW - Platelet Membrane Glycoproteins KW - Proteins KW - Proteoglycans KW - SPP1 protein, human KW - Sialoglycoproteins KW - Thrombospondins KW - bone acidic glycoprotein-75, human KW - matrix Gla protein KW - Osteocalcin KW - 104982-03-8 KW - Osteopontin KW - 106441-73-0 KW - Abridged Index Medicus KW - Index Medicus KW - Space life sciences KW - Phosphoproteins -- genetics KW - Sialoglycoproteins -- genetics KW - Humans KW - Phosphoproteins -- physiology KW - Proteoglycans -- physiology KW - Platelet Membrane Glycoproteins -- genetics KW - Osteocalcin -- physiology KW - Glycoproteins -- genetics KW - Sialoglycoproteins -- physiology KW - Platelet Membrane Glycoproteins -- physiology KW - Proteoglycans -- genetics KW - Osteocalcin -- genetics KW - Genetic Techniques KW - Osteonectin -- genetics KW - Calcium-Binding Proteins -- physiology KW - Calcium-Binding Proteins -- genetics KW - Osteonectin -- physiology KW - Glycoproteins -- physiology KW - Proteins -- chemistry KW - Gene Expression KW - Proteins -- genetics KW - Proteins -- physiology KW - Bone Matrix -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73113156?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+orthopaedics+and+related+research&rft.atitle=Structure%2C+expression%2C+and+regulation+of+the+major+noncollagenous+matrix+proteins+of+bone.&rft.au=Young%2C+M+F%3BKerr%2C+J+M%3BIbaraki%2C+K%3BHeegaard%2C+A+M%3BRobey%2C+P+G&rft.aulast=Young&rft.aufirst=M&rft.date=1992-08-01&rft.volume=&rft.issue=281&rft.spage=275&rft.isbn=&rft.btitle=&rft.title=Clinical+orthopaedics+and+related+research&rft.issn=0009921X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-14 N1 - Date created - 1992-09-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Classical conditioning and protein kinase C activation regulate the same single potassium channel in Hermissenda crassicornis photoreceptors. AN - 73112041; 1496012 AB - The patch-clamp technique was used to study the effects of classical conditioning and protein kinase C (PKC) activation on K+ channels of identified neurons in the snail Hermissenda crassicornis. Here we present evidence that classical conditioning and PKC activation similarly modify the same K+ channel. K+ channels were recorded in cells from animals with different training experience. The 64-pS K+ channel appeared with significantly lower frequency in the conditioned group compared to the frequencies in control animals (naive and unpaired). In addition, when present, the 64-pS channel exhibited a lower percentage of open time and an increased interval between opening bursts in cells from conditioned animals. The 42-pS K+ channel was observed with about the same frequency in all three groups, and its percentage of open time was invariant, regardless of the animal's experience. Incubation of the photoreceptor with the PKC activator phorbol 12,13-dibutyrate (PDBu) led to a profound decrease in the percentage of open time of the 64-pS K+ channel, from 35.7% in the control group to 2.5% in the PDBu-treated group. The inactive phorbol 4 alpha-phorbol 12-myristate 13-acetate had no effect. The use of the PKC inhibitor H-7 significantly blocked the phorbol effect. Inside-out patches obtained from phorbol preincubated cells likewise showed the same effect of PDBu on K+ channels, but the effect was not observed when phorbol was added after the cell-free patches were obtained from nontreated cells. By contrast, the percentage of open time of the 42-pS K+ channel remained unchanged after phorbol treatment. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Etcheberrigaray, R AU - Matzel, L D AU - Lederhendler, I I AU - Alkon, D L AD - Neural Systems Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08/01/ PY - 1992 DA - 1992 Aug 01 SP - 7184 EP - 7188 VL - 89 IS - 15 SN - 0027-8424, 0027-8424 KW - Isoquinolines KW - 0 KW - Piperazines KW - Potassium Channels KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine KW - 84477-87-2 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Isoquinolines -- pharmacology KW - Animals KW - Enzyme Activation KW - In Vitro Techniques KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Membrane Potentials -- drug effects KW - Piperazines -- pharmacology KW - Phorbol 12,13-Dibutyrate -- pharmacology KW - Protein Kinase C -- metabolism KW - Protein Kinase C -- antagonists & inhibitors KW - Conditioning, Classical -- physiology KW - Snails -- physiology KW - Potassium Channels -- physiology KW - Photoreceptor Cells -- physiology KW - Potassium Channels -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73112041?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Classical+conditioning+and+protein+kinase+C+activation+regulate+the+same+single+potassium+channel+in+Hermissenda+crassicornis+photoreceptors.&rft.au=Etcheberrigaray%2C+R%3BMatzel%2C+L+D%3BLederhendler%2C+I+I%3BAlkon%2C+D+L&rft.aulast=Etcheberrigaray&rft.aufirst=R&rft.date=1992-08-01&rft.volume=89&rft.issue=15&rft.spage=7184&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-04 N1 - Date created - 1992-09-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: FEBS Lett. 1990 Jul 2;267(1):25-8 [1694792] Science. 1982 Feb 5;215(4533):693-5 [7058334] J Neurophysiol. 1991 Apr;65(4):796-807 [2051204] Behav Neural Biol. 1990 Sep;54(2):131-45 [2241759] Biochem Biophys Res Commun. 1986 Feb 13;134(3):1215-22 [2418836] Neurosci Lett. 1987 Jul 9;78(1):101-6 [2441331] Biochim Biophys Acta. 1988 Sep 1;943(3):419-27 [2458133] J Neurosci. 1988 Nov;8(11):4069-78 [2846795] Proc Natl Acad Sci U S A. 1985 Apr;82(8):2538-42 [3157991] Science. 1984 Nov 30;226(4678):1037-45 [6093258] Pflugers Arch. 1981 Aug;391(2):85-100 [6270629] FEBS Lett. 1991 Feb 25;279(2):256-60 [1900473] J Exp Biol. 1991 Mar;156:619-23 [2051138] J Neurosci. 1990 May;10(5):1699-706 [2159060] J Neurosci. 1990 Jul;10(7):2300-7 [2376776] Nature. 1986 Jan 16-22;319(6050):220-3 [2418358] Science. 1987 Jan 16;235(4786):345-8 [2432663] J Neurochem. 1988 Sep;51(3):903-17 [2457656] J Neurophysiol. 1989 May;61(5):971-81 [2542473] Behav Brain Res. 1989 Oct 1;35(1):75-80 [2803546] Biophys J. 1988 Nov;54(5):955-60 [2853980] J Neurosci. 1986 May;6(5):1325-31 [3711982] Behav Neural Biol. 1985 Sep;44(2):278-300 [4062781] J Exp Biol. 1984 Sep;112:95-112 [6150967] Erratum In: Proc Natl Acad Sci U S A 1992 Nov 15;89(22):11107 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Monoclonal antibody C242-Pseudomonas exotoxin A. A specific and potent immunotoxin with antitumor activity on a human colon cancer xenograft in nude mice. AN - 73110894; 1644913 AB - Two immunotoxins were constructed by chemically coupling the monoclonal antibody C242 to Pseudomonas exotoxin A (PE) or a modified form, NlysPE40, that lacks the cell binding domain of PE. Monoclonal antibody C242 recognizes a specific sialylated carbohydrate epitope on a high molecular weight membrane glycoprotein present on cells of human colon, pancreatic, and cervical cancers. C242-PE and C242-NlysPE40 were very cytotoxic for cells expressing this antigen with 50% inhibition of protein synthesis occurring on Colo205 cells at 0.2 ng/ml (0.9 pM) for C242-PE and 6.0 ng/ml (31 pM) for C242-NlysPE40. The two immunotoxins also exhibited a strong antitumor effect on a human colon cancer xenograft grown in nude mice. The specificity and potency of these two C242 immunotoxins warrant their further development for the treatment of cancer. JF - The Journal of clinical investigation AU - Debinski, W AU - Karlsson, B AU - Lindholm, L AU - Siegall, C B AU - Willingham, M C AU - FitzGerald, D AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 405 EP - 411 VL - 90 IS - 2 SN - 0021-9738, 0021-9738 KW - Antibodies, Monoclonal KW - 0 KW - Antibodies, Neoplasm KW - Antigens, Tumor-Associated, Carbohydrate KW - Bacterial Toxins KW - Exotoxins KW - Immunotoxins KW - Neoplasm Proteins KW - Oligodeoxyribonucleotides KW - Recombinant Fusion Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Neoplasm Proteins -- biosynthesis KW - Humans KW - Immunotherapy KW - Adenocarcinoma -- therapy KW - Amino Acid Sequence KW - Mice KW - Mice, Nude KW - Antibody Affinity KW - Neoplasm Transplantation KW - Base Sequence KW - Tumor Cells, Cultured KW - Oligodeoxyribonucleotides -- chemistry KW - In Vitro Techniques KW - Molecular Sequence Data KW - Transplantation, Heterologous KW - Immunotoxins -- chemistry KW - Exotoxins -- administration & dosage KW - Colonic Neoplasms -- therapy KW - Antigens, Tumor-Associated, Carbohydrate -- immunology KW - Exotoxins -- toxicity KW - Antibodies, Neoplasm -- administration & dosage KW - Antibodies, Monoclonal -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73110894?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+clinical+investigation&rft.atitle=Monoclonal+antibody+C242-Pseudomonas+exotoxin+A.+A+specific+and+potent+immunotoxin+with+antitumor+activity+on+a+human+colon+cancer+xenograft+in+nude+mice.&rft.au=Debinski%2C+W%3BKarlsson%2C+B%3BLindholm%2C+L%3BSiegall%2C+C+B%3BWillingham%2C+M+C%3BFitzGerald%2C+D%3BPastan%2C+I&rft.aulast=Debinski&rft.aufirst=W&rft.date=1992-08-01&rft.volume=90&rft.issue=2&rft.spage=405&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+clinical+investigation&rft.issn=00219738&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-09 N1 - Date created - 1992-09-09 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Br J Cancer. 1989 Dec;60(6):845-51 [2557879] Biochemistry. 1973 Aug 14;12(17):3266-73 [4581787] Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3358-62 [2014255] Cancer Res. 1991 Mar 1;51(5):1529-36 [1997194] Cancer Res. 1990 Dec 15;50(24):7750-3 [2253218] J Biol Chem. 1989 Aug 25;264(24):14256-61 [2503515] Proc Natl Acad Sci U S A. 1986 Mar;83(5):1320-4 [3006045] Peptides. 1986 Mar-Apr;7(2):241-6 [2942845] J Biol Chem. 1988 Jul 5;263(19):9470-5 [3132465] Cell. 1987 Jan 16;48(1):129-36 [3098436] Proc Natl Acad Sci U S A. 1989 Nov;86(21):8545-9 [2510169] J Biol Chem. 1989 Sep 15;264(26):15157-60 [2504717] Cancer Res. 1989 Jul 1;49(13):3562-7 [2499420] Proc Natl Acad Sci U S A. 1988 May;85(9):2939-43 [3283735] Science. 1987 Nov 20;238(4830):1098-104 [3317828] Acta Pathol Microbiol Immunol Scand A. 1987 Jul;95(4):177-83 [3303832] Cell. 1986 Dec 5;47(5):641-8 [3536124] J Immunol Methods. 1984 Aug 3;72(1):77-89 [6086763] Proc Natl Acad Sci U S A. 1978 Jul;75(7):3405-9 [80012] Eur J Biochem. 1979 Nov;101(2):395-9 [574817] Arch Biochem Biophys. 1959 May;82(1):70-7 [13650640] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of a tyrosine kinase activity associated with the high-affinity interleukin 2 receptor complex. AN - 73110564; 1497623 AB - The IL-2 receptor complex is minimally composed of two genetically unrelated subunits of relative molecular masses 55 and 75 kDa respectively. Structural information deduced from the cDNA sequences of either subunit have not revealed significant information as to the basis of the mechanisms of IL-2 receptor signal transduction. Nevertheless, IL-2 stimulates the activation of one or more tyrosine kinases requiring the functional participation of the p75 member of the receptor complex. Here we have developed the methods to isolate the receptor complex with an associated tyrosine protein kinase. Extracts of membrane glycoproteins from activated normal human T lymphocytes and cell lines demonstrated catalytic activation of tyrosine kinase activity when stimulated with IL-2. Purification of the receptor complex with biotinylated IL-2 revealed the presence of two dominant phosphotyrosyl-proteins of approximate molecular masses 58 and 97 kDa. Denaturation gel electrophoresis followed by renaturation of proteins associated with the IL-2 receptor complex demonstrated that the 97 kDa protein had catalytic autophosphorylation activity. The results indicate that the 58 and 97 kDa phosphotyrosyl-proteins can be found to co-precipitate with the IL-2 receptor complex and that the 97 kDa protein was demonstrated to have protein kinase activity. The association of such kinases with receptors devoid of catalytic structure may represent a unique paradigm of growth-factor receptor mechanisms. JF - The Biochemical journal AU - Garcia, G G AU - Evans, G A AU - Michiel, D F AU - Farrar, W L AD - Biological Carcinogenesis and Development Program, NCI-Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1992/08/01/ PY - 1992 DA - 1992 Aug 01 SP - 851 EP - 856 VL - 285 ( Pt 3) SN - 0264-6021, 0264-6021 KW - Interleukin-2 KW - 0 KW - Phosphoproteins KW - Receptors, Interleukin-2 KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Index Medicus KW - Interleukin-2 -- pharmacology KW - Phosphorylation KW - Enzyme Activation KW - Humans KW - Phosphoproteins -- analysis KW - Electrophoresis, Gel, Two-Dimensional KW - Chemical Precipitation KW - T-Lymphocytes -- enzymology KW - Molecular Weight KW - Cell Line KW - Phosphoproteins -- metabolism KW - Receptors, Interleukin-2 -- metabolism KW - Receptors, Interleukin-2 -- isolation & purification KW - Protein-Tyrosine Kinases -- isolation & purification KW - Protein-Tyrosine Kinases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73110564?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Biochemical+journal&rft.atitle=Characterization+of+a+tyrosine+kinase+activity+associated+with+the+high-affinity+interleukin+2+receptor+complex.&rft.au=Garcia%2C+G+G%3BEvans%2C+G+A%3BMichiel%2C+D+F%3BFarrar%2C+W+L&rft.aulast=Garcia&rft.aufirst=G&rft.date=1992-08-01&rft.volume=285+%28+Pt+3%29&rft.issue=&rft.spage=851&rft.isbn=&rft.btitle=&rft.title=The+Biochemical+journal&rft.issn=02646021&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-10 N1 - Date created - 1992-09-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1991 Jun 14;252(5012):1523-8 [2047859] Mol Cell Biol. 1991 Jan;11(1):568-72 [1986248] Cell. 1990 Apr 20;61(2):203-12 [2158859] Proc Natl Acad Sci U S A. 1990 Jan;87(1):11-5 [2296573] Cell. 1990 Mar 23;60(6):941-51 [2317865] J Immunol Methods. 1988 May 9;109(2):277-85 [2452204] J Immunol. 1989 Oct 15;143(8):2530-3 [2477446] Cell. 1989 Sep 22;58(6):1023-4 [2550142] Biochem Biophys Res Commun. 1989 Oct 31;164(2):788-95 [2554900] J Biol Chem. 1989 Dec 5;264(34):20723-9 [2555369] Cell. 1989 Dec 1;59(5):837-45 [2590941] J Immunol Methods. 1989 Aug 15;122(1):33-41 [2668418] Science. 1989 May 5;244(4904):551-6 [2785715] J Biol Chem. 1989 Jul 25;264(21):12562-7 [2787319] J Immunol. 1989 Aug 1;143(3):870-6 [2787350] J Biol Chem. 1988 May 25;263(15):6956-9 [3259228] Nature. 1984 Oct 18-24;311(5987):626-31 [6090948] Cell. 1990 Aug 10;62(3):481-92 [1696179] Cytokine. 1991 Sep;3(5):428-38 [1751780] EMBO J. 1991 Feb;10(2):317-25 [1825055] J Exp Med. 1990 Mar 1;171(3):637-44 [2106566] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A signature element distinguishes sibling and independent mutations in a shuttle vector plasmid. AN - 73108549; 1644298 AB - We have developed a new shuttle vector plasmid for studying mutagenesis in mammalian cells that permits proof of independence of identical mutations. Mutations occur more frequently at some sites in a gene than in others, and in a collection of mutant plasmids from a single transfection of mammalian cells the same mutation may appear several times. However, those arising from independent events cannot be distinguished from siblings of an initial event. The new vector system (pSP189) is a population of plasmids, each of which contains an 8-bp 'signature sequence'. This sequence confers a unique identification tag to each plasmid and allows individual members to be identified by a distinctive signature. The plasmid also carries the Escherichia coli bacterial supF gene as a marker for mutagenesis, as well as sequences which support replication in primate (including human) cells and E. coli. We have used the pSP189 system to generate a UV-induced spectrum of mutations in supF following replication in a single plate of human DNA-repair-deficient cells (xeroderma pigmentosum, complementation group A). With the signature sequence, we were able to determine whether identical mutations derived from the transfection were of independent or sibling origin. There were eight identical mutations at the strongest hotspot, all of which had different signature sequences. Only one of these events would have been reported in previous experiments. This plasmid reduces the effort required to generate a spectrum of mutations caused by a DNA-damaging agent and allows a more accurate assessment of mutational hotspot intensity. JF - Gene AU - Parris, C N AU - Seidman, M M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/08/01/ PY - 1992 DA - 1992 Aug 01 SP - 1 EP - 5 VL - 117 IS - 1 SN - 0378-1119, 0378-1119 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Ultraviolet Rays KW - Base Sequence KW - Humans KW - Molecular Sequence Data KW - Cell Line, Transformed KW - Genetic Vectors -- radiation effects KW - Xeroderma Pigmentosum -- genetics KW - Plasmids -- radiation effects KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73108549?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene&rft.atitle=A+signature+element+distinguishes+sibling+and+independent+mutations+in+a+shuttle+vector+plasmid.&rft.au=Parris%2C+C+N%3BSeidman%2C+M+M&rft.aulast=Parris&rft.aufirst=C&rft.date=1992-08-01&rft.volume=117&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Gene&rft.issn=03781119&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-08 N1 - Date created - 1992-09-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Poliovirus induces indoleamine-2,3-dioxygenase and quinolinic acid synthesis in macaque brain. AN - 73108020; 1322853 AB - Accumulation of the neurotoxin quinolinic acid within the brain occurs in a broad spectrum of patients with inflammatory neurologic disease and may be of neuropathologic significance. The production of quinolinic acid was postulated to reflect local induction of indoleamine 2,3-dioxygenase by cytokines in reactive cells and inflammatory cell infiltrates within the central nervous system. To test this hypothesis, macaques received an intraspinal injection of poliovirus as a model of localized inflammatory neurologic disease. Seventeen days later, spinal cord indoleamine 2,3-dioxygenase activity and quinolinic acid concentrations in spinal cord and cerebrospinal fluid were both increased in proportion to the degree of inflammatory responses and neurologic damage in the spinal cord, as well as the severity of motor paralysis. The absolute concentrations of quinolinic acid achieved in spinal cord and cerebrospinal fluid exceeded levels reported to kill spinal cord neurons in vitro. Smaller increases in indoleamine 2,3-dioxygenase activity and quinolinic acid concentrations also occurred in parietal cortex, a poliovirus target area. In frontal cortex, which is not a target for poliovirus, indoleamine 2,3-dioxygenase was not affected. A monoclonal antibody to human indoleamine 2,3-dioxygenase was used to visualize indoleamine 2,3-dioxygenase predominantly in grey matter of poliovirus-infected spinal cord, in conjunction with local inflammatory lesions. Macrophage/monocytes in vitro synthesized [13C6]quinolinic acid from [13C6]L-tryptophan, particularly when stimulated by interferon-gamma. Spinal cord slices from poliovirus-inoculated macaques in vitro also converted [13C6]L-tryptophan to [13C6]quinolinic acid. We conclude that local synthesis of quinolinic acid from L-tryptophan within the central nervous system follows the induction of indoleamine-2,3-dioxygenase, particularly within macrophage/microglia. In view of this link between immune stimulation and the synthesis of neurotoxic amounts of quinolinic acid, we propose that attenuation of local inflammation, strategies to reduce the synthesis of neuroactive kynurenine pathway metabolites, or drugs that interfere with the neurotoxicity of quinolinic acid offer new approaches to therapy in inflammatory neurologic disease. JF - FASEB journal : official publication of the Federation of American Societies for Experimental Biology AU - Heyes, M P AU - Saito, K AU - Jacobowitz, D AU - Markey, S P AU - Takikawa, O AU - Vickers, J H AD - Section on Analytical Biochemistry, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 2977 EP - 2989 VL - 6 IS - 11 SN - 0892-6638, 0892-6638 KW - Quinolinic Acids KW - 0 KW - Interferon-gamma KW - 82115-62-6 KW - Tryptophan KW - 8DUH1N11BX KW - Tryptophan Oxygenase KW - EC 1.13.11.11 KW - Quinolinic Acid KW - F6F0HK1URN KW - Index Medicus KW - Animals KW - Macaca KW - Interferon-gamma -- pharmacology KW - Enzyme Induction KW - Tryptophan -- metabolism KW - Immunohistochemistry KW - Poliovirus KW - Tryptophan Oxygenase -- biosynthesis KW - Poliomyelitis -- metabolism KW - Quinolinic Acids -- metabolism KW - Brain -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73108020?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FASEB+journal+%3A+official+publication+of+the+Federation+of+American+Societies+for+Experimental+Biology&rft.atitle=Poliovirus+induces+indoleamine-2%2C3-dioxygenase+and+quinolinic+acid+synthesis+in+macaque+brain.&rft.au=Heyes%2C+M+P%3BSaito%2C+K%3BJacobowitz%2C+D%3BMarkey%2C+S+P%3BTakikawa%2C+O%3BVickers%2C+J+H&rft.aulast=Heyes&rft.aufirst=M&rft.date=1992-08-01&rft.volume=6&rft.issue=11&rft.spage=2977&rft.isbn=&rft.btitle=&rft.title=FASEB+journal+%3A+official+publication+of+the+Federation+of+American+Societies+for+Experimental+Biology&rft.issn=08926638&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-09 N1 - Date created - 1992-09-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Gene- and strand-specific damage and repair in Chinese hamster ovary cells treated with 4-nitroquinoline 1-oxide. AN - 73102084; 1638532 AB - 4-Nitroquinoline 1-oxide (4NQO) is a model chemical carcinogen that has often been referred to as a UV mimetic agent. Previous studies have indicated that UV-induced pyrimidine dimers are repaired preferentially and strand-specifically in actively transcribing genes. In the current study we have examined the gene-specific and strand-specific repair of 4NQO in Chinese hamster ovary B-11 cells treated with 2.5 microM 4NQO. The methodology used for detecting adducts involved the treatment of DNA from 4NQO-exposed cells with uvrABC excinuclease, which incises DNA at adduct sites, followed by denaturing gel electrophoresis of DNA, Southern hybridization, and probing for the sequence of interest. We examined the active and inactive coding regions of the DHFR gene, the active adenine phosphoribosyltransferase gene, relatively inactive c-fos oncogene, and the mitochondrial genome for 4NQO adducts. Initial 4NQO adduct levels found in these genes varied from 1.10 to 1.52 adducts/10 kilobases. Little difference in repair was found between active coding and inactive regions of the DHFR gene, or between DHFR, adenine phosphoribosyltransferase, and c-fos genes, which are transcribed at different levels. Approximately 71% of 4NQO adducts were repaired within 24 h in all gene sequences examined. During this same time period, approximately 51% of adducts were repaired from the genome overall, as determined by comparing the removal of bound radiolabeled 4NQO to total DNA. The results indicate that 4NQO adducts, unlike UV light-induced cyclobutane pyrimidine dimers (UV dimers), are not preferentially repaired in transcriptionally active genes. However, there may be regions of the genome that are not repaired with the same efficiency as the specific genes examined here. In addition, little to no difference was observed in the repair of 4NQO adducts in the transcribed and nontranscribed strands of the DHFR gene, a finding which is also in contrast to results with UV dimers. Interestingly, 4NQO adducts, unlike UV dimers, were removed from the mitochondrial genome, suggesting that repair of select lesions occurs in this organelle. Thus, there appear to be some differences in the repair pathways operating for 4NQO adducts and UV dimers, particularly with respect to gene- and strand-specific DNA repair. JF - Cancer research AU - Snyderwine, E G AU - Bohr, V A AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/08/01/ PY - 1992 DA - 1992 Aug 01 SP - 4183 EP - 4189 VL - 52 IS - 15 SN - 0008-5472, 0008-5472 KW - APRT KW - DHFR KW - c-fos KW - DNA Probes KW - 0 KW - DNA, Mitochondrial KW - Escherichia coli Proteins KW - 4-Nitroquinoline-1-oxide KW - 56-57-5 KW - DNA KW - 9007-49-2 KW - Tetrahydrofolate Dehydrogenase KW - EC 1.5.1.3 KW - Adenine Phosphoribosyltransferase KW - EC 2.4.2.7 KW - Endodeoxyribonucleases KW - EC 3.1.- KW - endodeoxyribonuclease uvrABC KW - EC 3.1.25.- KW - Index Medicus KW - Animals KW - Ultraviolet Rays KW - Transcription, Genetic -- drug effects KW - DNA -- drug effects KW - DNA, Mitochondrial -- drug effects KW - Transfection KW - Blotting, Southern KW - DNA -- genetics KW - Genes -- drug effects KW - Restriction Mapping KW - CHO Cells KW - Cricetinae KW - DNA, Mitochondrial -- genetics KW - 4-Nitroquinoline-1-oxide -- pharmacology KW - DNA Repair KW - DNA Damage KW - Adenine Phosphoribosyltransferase -- genetics KW - Endodeoxyribonucleases -- metabolism KW - Genes, fos -- drug effects KW - Tetrahydrofolate Dehydrogenase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73102084?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Gene-+and+strand-specific+damage+and+repair+in+Chinese+hamster+ovary+cells+treated+with+4-nitroquinoline+1-oxide.&rft.au=Snyderwine%2C+E+G%3BBohr%2C+V+A&rft.aulast=Snyderwine&rft.aufirst=E&rft.date=1992-08-01&rft.volume=52&rft.issue=15&rft.spage=4183&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-28 N1 - Date created - 1992-08-28 N1 - Date revised - 2017-01-13 N1 - Gene symbol - APRT; DHFR; c-fos N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Abnormal structure and expression of the p53 gene in human ovarian carcinoma cell lines. AN - 73100534; 1638534 AB - In an effort to analyze molecular mechanisms of human ovarian carcinogenesis, we studied the structure and expression of the p53 gene in different cell lines established from human ovarian carcinomas. In all six lines (PA-1, Caov-3 and -4, OVCAR-3, SK-OV-3, and Kuramochi), p53 abnormalities were detected. In the SK-OV-3 cell line, Southern analysis suggested the presence of sequence deletions/rearrangements in at least one allele of the p53 gene, and transcripts were not detectable by either Northern or polymerase chain reaction analysis. Sequence analysis of the entire coding region of the p53 gene revealed point mutations resulting in codon changes of a highly conserved region of the protein in four cell lines, Caov-3 and -4, OVCAR-3, and Kuramochi. In the Caov-3 cell line, the point mutation resulted in chain termination at codon 136. Quantitation of p53 protein by immunoprecipitation analysis revealed a 6-fold higher than control cell level in PA-1. By contrast, p53 protein was not detectable in lines Caov-3 and SK-OV-3. We conclude that altered levels of p53 gene expression and/or mutant forms of the p53 gene product are associated with all human ovarian cancer cells tested. JF - Cancer research AU - Yaginuma, Y AU - Westphal, H AD - Laboratory of Mammalian Genes and Development, National Institute of Child Health and Human Development, NIH, Bethesda, Maryland 20892. Y1 - 1992/08/01/ PY - 1992 DA - 1992 Aug 01 SP - 4196 EP - 4199 VL - 52 IS - 15 SN - 0008-5472, 0008-5472 KW - p53 KW - DNA, Neoplasm KW - 0 KW - Oligodeoxyribonucleotides KW - RNA, Messenger KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Placenta -- chemistry KW - Humans KW - Gene Expression KW - RNA, Messenger -- genetics KW - DNA, Neoplasm -- isolation & purification KW - Pregnancy KW - Cloning, Molecular KW - DNA -- isolation & purification KW - Promoter Regions, Genetic KW - Base Sequence KW - Blotting, Southern KW - Polymerase Chain Reaction -- methods KW - DNA -- genetics KW - Molecular Sequence Data KW - DNA, Neoplasm -- genetics KW - RNA, Messenger -- isolation & purification KW - Cell Line KW - Female KW - Genes, p53 KW - Ovarian Neoplasms -- genetics KW - Transcription, Genetic KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73100534?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Abnormal+structure+and+expression+of+the+p53+gene+in+human+ovarian+carcinoma+cell+lines.&rft.au=Yaginuma%2C+Y%3BWestphal%2C+H&rft.aulast=Yaginuma&rft.aufirst=Y&rft.date=1992-08-01&rft.volume=52&rft.issue=15&rft.spage=4196&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-28 N1 - Date created - 1992-08-28 N1 - Date revised - 2017-01-13 N1 - Gene symbol - p53 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Endothelial leukocyte adhesion molecule-1 in endotoxin-induced uveitis. AN - 73099851; 1379217 AB - Expression of endothelial leukocyte adhesion molecule-1 (ELAM-1) on endothelial cells leads to the attachment of polymorphonuclear leukocytes. The sequential expression of ELAM-1 and major histocompatibility complex (MHC) class II antigen was examined in the eyes of 59 Lewis rats with endotoxin-induced uveitis (EIU) after the injection of Salmonella typhimurium endotoxin. The eyes were enucleated at 2-hr intervals. Hematoxylin and eosin-stained paraffin-embedded sections and immunohistochemically stained cryostat sections were graded by two masked observers. The MHC class II antigen was expressed on cells in the iris and ciliary body 4 hr after injection of endotoxin and on the corneal endothelium, 8 hr postinjection. It was found that ELAM-1 was expressed first on cells of the ciliary body and iris 10 hr after the injection of endotoxin and on the corneal endothelium, 22 hr postinjection. Clinical and histopathologic disease developed 16 hr postinjection. Adherence of polymorphonuclear cells to the corneal endothelium was observed at the time of ELAM-1 expression. In conclusion, expression of ELAM-1 on ocular tissue occurred in EIU and appeared to promote polymorphonuclear cell accumulation in the anterior segment of the eye. JF - Investigative ophthalmology & visual science AU - Whitcup, S M AU - Wakefield, D AU - Li, Q AU - Nussenblatt, R B AU - Chan, C C AD - Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 2626 EP - 2630 VL - 33 IS - 9 SN - 0146-0404, 0146-0404 KW - Antibodies, Monoclonal KW - 0 KW - Bacterial Toxins KW - Cell Adhesion Molecules KW - E-Selectin KW - Endotoxins KW - Enterotoxins KW - Histocompatibility Antigens Class II KW - Membrane Glycoproteins KW - Receptors, Immunologic KW - salmonella toxin KW - Index Medicus KW - Animals KW - Rats, Inbred Lew KW - Endothelium, Corneal -- metabolism KW - Endothelium, Corneal -- immunology KW - Rats KW - Neutrophils -- metabolism KW - Histocompatibility Antigens Class II -- metabolism KW - Receptors, Immunologic -- metabolism KW - Anterior Eye Segment -- metabolism KW - Salmonella KW - Immunoenzyme Techniques KW - Female KW - Cell Adhesion KW - Uveitis, Anterior -- chemically induced KW - Uveitis, Anterior -- immunology KW - Cell Adhesion Molecules -- metabolism KW - Uveitis, Anterior -- metabolism KW - Membrane Glycoproteins -- immunology KW - Membrane Glycoproteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73099851?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Investigative+ophthalmology+%26+visual+science&rft.atitle=Endothelial+leukocyte+adhesion+molecule-1+in+endotoxin-induced+uveitis.&rft.au=Whitcup%2C+S+M%3BWakefield%2C+D%3BLi%2C+Q%3BNussenblatt%2C+R+B%3BChan%2C+C+C&rft.aulast=Whitcup&rft.aufirst=S&rft.date=1992-08-01&rft.volume=33&rft.issue=9&rft.spage=2626&rft.isbn=&rft.btitle=&rft.title=Investigative+ophthalmology+%26+visual+science&rft.issn=01460404&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-31 N1 - Date created - 1992-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of colony-stimulating factor receptor expression on hematopoietic progenitor cells: proposed mechanism for growth factor synergism. AN - 73097375; 1379087 AB - In many cells systems, the cellular interaction between two or more humoral factors leads to a synergistic response in terms of cellular growth and function. In particular, the growth and differentiation of hematopoietic progenitor cells involves numerous synergistic interactions between colony-stimulating factors (CSFs) that individually stimulate hematopoiesis (granulocyte-CSF, granulocyte-macrophage-CSF, and interleukin-3 [IL-3]), as well as between these factors and other cytokines that individually have no proliferative effect on progenitor cell growth (IL-1 and IL-6). The present study investigated whether hematopoietic growth factor (HGF) synergy could be mediated by upregulation of CSF receptors. Synergistic effects on bone marrow (BM) progenitor cell colony formation, regardless of the combination of factors used, were consistently preceded by increased CSF receptor expression on highly enriched BM progenitor cells, but not on unfractionated BM cells. Induction of CSF receptors preceded detectable differentiation and did not require cell division because nocodazole, an inhibitor of mitosis, blocked CSF-mediated cell proliferation, but not receptor upregulation. Furthermore, combinations of cytokines that did not synergize also failed to affect the level of CSF receptors on BM progenitors. These results have led us to propose a model for HGF synergy whereby one mechanism of action the investigated synergistic cytokines might be the ability to induce increased expression of CSF receptors. JF - Blood AU - Jacobsen, S E AU - Ruscetti, F W AU - Dubois, C M AU - Wine, J AU - Keller, J R AD - Laboratory of Molecular Immunoregulation, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1992/08/01/ PY - 1992 DA - 1992 Aug 01 SP - 678 EP - 687 VL - 80 IS - 3 SN - 0006-4971, 0006-4971 KW - Growth Substances KW - 0 KW - Interleukin-1 KW - Interleukin-3 KW - Interleukin-6 KW - Iodine Radioisotopes KW - Receptors, Colony-Stimulating Factor KW - Recombinant Proteins KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - Granulocyte-Macrophage Colony-Stimulating Factor KW - 83869-56-1 KW - Thymidine KW - VC2W18DGKR KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Interleukin-1 -- pharmacology KW - Recombinant Proteins -- pharmacology KW - Bone Marrow -- physiology KW - Interleukin-3 -- pharmacology KW - Cell Division -- drug effects KW - Mice KW - Interleukin-6 -- pharmacology KW - Radioligand Assay KW - Mice, Inbred BALB C KW - Autoradiography KW - Granulocyte Colony-Stimulating Factor -- pharmacology KW - Granulocyte-Macrophage Colony-Stimulating Factor -- pharmacology KW - DNA Replication -- drug effects KW - Thymidine -- metabolism KW - Bone Marrow Cells KW - Granulocyte Colony-Stimulating Factor -- metabolism KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Drug Synergism KW - Granulocyte-Macrophage Colony-Stimulating Factor -- metabolism KW - Receptors, Colony-Stimulating Factor -- biosynthesis KW - Growth Substances -- pharmacology KW - Receptors, Colony-Stimulating Factor -- metabolism KW - Hematopoietic Stem Cells -- physiology KW - Hematopoietic Stem Cells -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73097375?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Blood&rft.atitle=Induction+of+colony-stimulating+factor+receptor+expression+on+hematopoietic+progenitor+cells%3A+proposed+mechanism+for+growth+factor+synergism.&rft.au=Jacobsen%2C+S+E%3BRuscetti%2C+F+W%3BDubois%2C+C+M%3BWine%2C+J%3BKeller%2C+J+R&rft.aulast=Jacobsen&rft.aufirst=S&rft.date=1992-08-01&rft.volume=80&rft.issue=3&rft.spage=678&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-31 N1 - Date created - 1992-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interferon-gamma gene expression in human B-cell lines: induction by interleukin-2, protein kinase C activators, and possible effect of hypomethylation on gene regulation. AN - 73092329; 1322203 AB - Human interferon-gamma (IFN-gamma) is an important immunomodulatory protein produced predominantly by T cells and large granular lymphocytes (LGLs). Whereas large amounts of data have been accumulated regarding IFN gamma gene expression in these two cell types, little information about IFN gamma expression in other cell types exists. In this study, we have analyzed the production of IFN gamma by the Epstein-Barr virus (EBV)-positive B-cell line, JLP(c), derived from a patient with Burkitt's lymphoma, and another human B-cell line, PA682BM-1, which was derived from an acquired immunodeficiency syndrome patient. Southern blot analysis indicates the presence of an Ig heavy chain gene rearrangement, but no rearrangement of the T-cell receptor beta chain gene or IFN gamma gene in these B-cell lines. Both cell lines were found to express surface IgD and other B-cell surface markers, thus confirming their B-cell lineage. Analysis for surface Ig, cytoplasmic Ig, and secreted Ig indicates that the two cell lines are in relatively early stages of the B-cell differentiation pathway. We now report that PA682BM-1 can be triggered by the protein kinase C (PKC) activators, phorbol 12-myristate 13-acetate (PMA) and (-)Indolactam-v, to secrete IFN gamma, whereas JLP(c) cells spontaneously produce low levels of IFN gamma that can be enhanced by PKC activators and interleukin-2 (IL-2). After activation of the cell lines with IL-2, (-)Indolactam-v, and PMA, increases in cytoplasmic messenger RNAs (mRNAs) of IFN gamma and the IL-2 receptor chains were also observed. The induction of IFN gamma mRNA and protein by IL-2 was completely blocked by a monoclonal antibody to IL-2 receptor p75 (beta chain), but not by the monoclonal antibody to p55 (alpha chain). Analysis of IFN gamma genomic DNA indicates that the gene is not amplified, but that hypomethylation in the 5' noncoding region of the IFN gamma gene has occurred in the B-cell line from the Burkitt's lymphoma patient that spontaneously produces IFN gamma. This finding suggests that the methylation state of the promoter region may play an important role in the control of IFN gamma gene expression in B cells. JF - Blood AU - Pang, Y AU - Norihisa, Y AU - Benjamin, D AU - Kantor, R R AU - Young, H A AD - Laboratory of Experimental Immunology, BRMP, NCI-FCRDC, Frederick, MD 21702-1201. Y1 - 1992/08/01/ PY - 1992 DA - 1992 Aug 01 SP - 724 EP - 732 VL - 80 IS - 3 SN - 0006-4971, 0006-4971 KW - Antigens, Surface KW - 0 KW - Carcinogens KW - DNA, Neoplasm KW - Immunoglobulin Heavy Chains KW - Indoles KW - Interleukin-1 KW - Interleukin-2 KW - Interleukin-6 KW - Lactams KW - Recombinant Proteins KW - Interleukin-4 KW - 207137-56-2 KW - Interferon-gamma KW - 82115-62-6 KW - indolactam V KW - 8CIY9O1323 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Gene Expression -- drug effects KW - Carcinogens -- pharmacology KW - Acquired Immunodeficiency Syndrome -- complications KW - Burkitt Lymphoma -- etiology KW - Interleukin-1 -- pharmacology KW - Humans KW - Burkitt Lymphoma -- genetics KW - Genes, Immunoglobulin KW - Interleukin-6 -- pharmacology KW - Immunoglobulin Heavy Chains -- genetics KW - Blotting, Southern KW - Flow Cytometry KW - Antigens, Surface -- analysis KW - Recombinant Proteins -- pharmacology KW - Enzyme Activation KW - Interleukin-4 -- pharmacology KW - Gene Rearrangement KW - Gene Rearrangement, beta-Chain T-Cell Antigen Receptor KW - B-Lymphocytes -- immunology KW - Burkitt Lymphoma -- immunology KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Lactams -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Indoles -- pharmacology KW - Methylation KW - Cell Line KW - Protein Kinase C -- metabolism KW - Interleukin-2 -- pharmacology KW - Interferon-gamma -- genetics KW - DNA, Neoplasm -- genetics KW - DNA, Neoplasm -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73092329?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Blood&rft.atitle=Interferon-gamma+gene+expression+in+human+B-cell+lines%3A+induction+by+interleukin-2%2C+protein+kinase+C+activators%2C+and+possible+effect+of+hypomethylation+on+gene+regulation.&rft.au=Pang%2C+Y%3BNorihisa%2C+Y%3BBenjamin%2C+D%3BKantor%2C+R+R%3BYoung%2C+H+A&rft.aulast=Pang&rft.aufirst=Y&rft.date=1992-08-01&rft.volume=80&rft.issue=3&rft.spage=724&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-31 N1 - Date created - 1992-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Methotrexate pharmacokinetics following administration of recombinant carboxypeptidase-G2 in rhesus monkeys. AN - 73092099; 1634927 AB - Carboxypeptidase-G2 (CPDG2) is a bacterial enzyme that rapidly hydrolyzes methotrexate (MTX) into inactive metabolites. As an alternative form of rescue after high-dose MTX (HDMTX), CPDG2 has more potential advantages than standard leucovorin (LV) rescue. In this study, the plasma pharmacokinetics of MTX with and without CPDG2 were evaluated in adult rhesus monkeys. The plasma pharmacokinetics of MTX were determined in groups of animals that had received a 300-mg/m2 loading dose of MTX followed by a 60-mg/m2/h infusion during an 18-hour period. One group received CPDG2 at the end of the infusion, and the other group served as a control. Two additional animals with high titers of anti-CPDG2 antibody also were studied. During infusion, the steady-state MTX plasma concentration was 11.3 +/- 4.8 mumol/L. Without CPDG2, the postinfusion plasma MTX concentration remained above 0.1 mumol/L for more than 6 hours. After the administration of 50 U/kg of CPDG2, plasma MTX concentrations decreased to nontoxic levels (less than 0.05 mumol/L) within 30 minutes. The initial half-life (t1/2 alpha) of MTX decreased from 5.8 +/- 2.1 minutes to 0.7 +/- 0.02 minutes after enzyme administration. The postinfusion area under the plasma concentration time curve of MTX was 301 +/- 171 mumol/L/min without CPDG2 compared with 19.6 +/- 6.1 mumol/L/min with CPDG2. The immunogenicity studies performed indicated that although animals developed anti-CPDG2 antibodies, none of them manifested allergic symptoms. The effectiveness of CPDG2 was diminished but not eliminated in animals with high titers of anti-CPDG2 antibody. CPDG2 is capable of rapidly decreasing plasma MTX concentrations to nontoxic levels. The administration of CPDG2 seems safe, well tolerated, and it may be useful as an alternative to LV rescue. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Adamson, P C AU - Balis, F M AU - McCully, C L AU - Godwin, K S AU - Poplack, D G AD - Pediatric Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 1359 EP - 1364 VL - 10 IS - 8 SN - 0732-183X, 0732-183X KW - Recombinant Proteins KW - 0 KW - gamma-Glutamyl Hydrolase KW - EC 3.4.19.9 KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Animals KW - Feasibility Studies KW - Drug Interactions KW - Recombinant Proteins -- pharmacology KW - Recombinant Proteins -- immunology KW - Recombinant Proteins -- pharmacokinetics KW - Antibody Formation KW - Macaca mulatta KW - Male KW - Methotrexate -- pharmacokinetics KW - gamma-Glutamyl Hydrolase -- pharmacology KW - gamma-Glutamyl Hydrolase -- pharmacokinetics KW - gamma-Glutamyl Hydrolase -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73092099?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Methotrexate+pharmacokinetics+following+administration+of+recombinant+carboxypeptidase-G2+in+rhesus+monkeys.&rft.au=Adamson%2C+P+C%3BBalis%2C+F+M%3BMcCully%2C+C+L%3BGodwin%2C+K+S%3BPoplack%2C+D+G&rft.aulast=Adamson&rft.aufirst=P&rft.date=1992-08-01&rft.volume=10&rft.issue=8&rft.spage=1359&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=0732183X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-25 N1 - Date created - 1992-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Gonadotropin-releasing hormone-induced calcium signaling in clonal pituitary gonadotrophs. AN - 73090225; 1379169 AB - In agonist-stimulated clonal pituitary gonadotrophs (alpha T3-1 cells), cytoplasmic calcium ([Ca2+]i) exhibited rapid and prominent peak increases, followed by lower, but sustained, elevations for up to 15 min. The [Ca2+]i response to GnRH was rapidly inhibited by prior addition of a potent GnRH antagonist. In the absence of extracellular Ca2+ the initial peak [Ca2+]i response was only slightly decreased, but the prolonged increase in [Ca2+]i was abolished, indicating that the peak is derived largely from intracellular calcium mobilization and the sustained phase from Ca2+ influx. Application of the endoplasmic reticulum Ca(2+)-ATPase blocker thapsigargin caused progressive and dose-dependent elevation of [Ca2+]i and decreased the peak amplitude of the GnRH-induced Ca2+ response. On the other hand, addition of dihydropyridine calcium channel antagonists before or after GnRH treatment prevented or terminated the plateau phase, respectively, consistent with entry of Ca2+ through L-type voltage-sensitive Ca2+ channels (VSCC) as the major Ca2+ influx pathway during GnRH action. The presence of L-type VSCC in alpha T3-1 cells was further indicated by the ability of elevated extracellular K+ levels and the dihydropyridine calcium channel agonist Bay K 8644 to elevate [Ca2+]i in an extracellular calcium-dependent manner. These actions of depolarization and Bay K 8644 were inhibited by nifedipine, with an IC50 of 10 nM. High extracellular K(+)- and GnRH-induced Ca2+ entry was also attenuated by phorbol esters and permeant diacylglycerols, indicating that protein kinase-C exerts inhibitory modulation of VSCC activity. In contrast to normal pituitary gonadotrophs, in which GnRH induces a frequency-modulated oscillatory [Ca2+]i response, single alpha T3-1 cells exhibited a nonoscillatory amplitude-modulated signal during agonist stimulation. The [Ca2+]i responses observed in alpha T3-1 gonadotrophs indicate that the immortalized cells retain functional GnRH receptors and their coupling to the Ca2+ signaling pathway. Ca2+ influx through L-type channels maintains the plateau phase of the [Ca2+]i response during agonist stimulation and is inhibited by activation of protein kinase-C. JF - Endocrinology AU - Merelli, F AU - Stojilković, S S AU - Iida, T AU - Krsmanovic, L Z AU - Zheng, L AU - Mellon, P L AU - Catt, K J AD - Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 925 EP - 932 VL - 131 IS - 2 SN - 0013-7227, 0013-7227 KW - Calcium Channel Blockers KW - 0 KW - Calcium Channels KW - Dihydropyridines KW - Terpenes KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 KW - Ionomycin KW - 56092-81-0 KW - Thapsigargin KW - 67526-95-8 KW - 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester KW - 71145-03-4 KW - Calcium-Transporting ATPases KW - EC 3.6.3.8 KW - Nifedipine KW - I9ZF7L6G2L KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Potassium KW - RWP5GA015D KW - Calcium KW - SY7Q814VUP KW - Abridged Index Medicus KW - Index Medicus KW - Nifedipine -- pharmacology KW - Endoplasmic Reticulum -- enzymology KW - Dihydropyridines -- pharmacology KW - Calcium Channels -- metabolism KW - Calcium Channel Blockers -- pharmacology KW - 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Potassium -- pharmacology KW - Ionomycin -- pharmacology KW - Calcium-Transporting ATPases -- antagonists & inhibitors KW - Terpenes -- pharmacology KW - Cell Line KW - Calcium -- metabolism KW - Signal Transduction -- drug effects KW - Gonadotropin-Releasing Hormone -- antagonists & inhibitors KW - Calcium -- pharmacology KW - Pituitary Gland -- metabolism KW - Gonadotropin-Releasing Hormone -- pharmacology KW - Pituitary Gland -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73090225?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrinology&rft.atitle=Gonadotropin-releasing+hormone-induced+calcium+signaling+in+clonal+pituitary+gonadotrophs.&rft.au=Merelli%2C+F%3BStojilkovi%C4%87%2C+S+S%3BIida%2C+T%3BKrsmanovic%2C+L+Z%3BZheng%2C+L%3BMellon%2C+P+L%3BCatt%2C+K+J&rft.aulast=Merelli&rft.aufirst=F&rft.date=1992-08-01&rft.volume=131&rft.issue=2&rft.spage=925&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-02 N1 - Date created - 1992-09-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of a stage selector element in the human gamma-globin gene promoter that fosters preferential interaction with the 5' HS2 enhancer when in competition with the beta-promoter. AN - 73084165; 1639067 AB - The erythroid-specific enhancer within hypersensitivity site 2 (HS2) of the human beta-globin locus control region is required for high level globin gene expression. We investigated interaction between HS2 and the gamma- and beta-promoters using reporter constructs in transient assays in human erythroleukemia (K562) cells. The beta-promoter, usually silent in K562 cells, was activated by HS2. This activity was abolished when a gamma-promoter was linked in cis. Analysis of truncation mutants suggested that sequences conveying the competitive advantage of the gamma-promoter for HS2 included those between positions -53 and -35 relative to the transcriptional start site. This sequence, when used to replace the corresponding region of the beta-promoter, increased beta-promoter activity 10-fold when linked to HS2. The modified beta-promoter was also capable of competing with a gamma-promoter modified internally in the -53 to -35 region, when the two promoters were linked to HS2 in a single plasmid. The corresponding sequences from the Galago gamma-promoter, a species which lacks fetal gamma-gene expression, were inactive in analogous assays. We have identified and partially purified a nuclear protein found in human (fetal stage) erythroleukemia cells, but present in much lower concentration in murine (adult stage) erythroleukemia cells, that binds the -53 to -35 sequence of the gamma-promoter. We speculate that this region of the gamma-promoter functions as a stage selector element in the regulation of hemoglobin switching in humans. JF - The EMBO journal AU - Jane, S M AU - Ney, P A AU - Vanin, E F AU - Gumucio, D L AU - Nienhuis, A W AD - National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 2961 EP - 2969 VL - 11 IS - 8 SN - 0261-4189, 0261-4189 KW - Recombinant Fusion Proteins KW - 0 KW - Globins KW - 9004-22-2 KW - Luciferases KW - EC 1.13.12.- KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - Animals KW - Humans KW - Luciferases -- metabolism KW - Gene Expression KW - Mice KW - Chloramphenicol O-Acetyltransferase -- metabolism KW - Binding Sites KW - Recombinant Fusion Proteins -- metabolism KW - Mutagenesis, Site-Directed KW - Gene Expression Regulation, Neoplastic KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Base Sequence KW - Leukemia, Experimental KW - Transfection KW - Kinetics KW - Restriction Mapping KW - Binding, Competitive KW - Molecular Sequence Data KW - Leukemia, Myelogenous, Chronic, BCR-ABL Positive KW - Cell Nucleus -- physiology KW - Luciferases -- genetics KW - Cell Line KW - Promoter Regions, Genetic KW - Enhancer Elements, Genetic KW - Globins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73084165?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+EMBO+journal&rft.atitle=Identification+of+a+stage+selector+element+in+the+human+gamma-globin+gene+promoter+that+fosters+preferential+interaction+with+the+5%27+HS2+enhancer+when+in+competition+with+the+beta-promoter.&rft.au=Jane%2C+S+M%3BNey%2C+P+A%3BVanin%2C+E+F%3BGumucio%2C+D+L%3BNienhuis%2C+A+W&rft.aulast=Jane&rft.aufirst=S&rft.date=1992-08-01&rft.volume=11&rft.issue=8&rft.spage=2961&rft.isbn=&rft.btitle=&rft.title=The+EMBO+journal&rft.issn=02614189&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-28 N1 - Date created - 1992-08-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1979 Jul 12;280(5718):164-5 [95354] Cell. 1984 Jul;37(3):889-901 [6540146] Anal Biochem. 1976 May 7;72:248-54 [942051] Genes Dev. 1989 Mar;3(3):314-23 [2721958] Proc Natl Acad Sci U S A. 1989 Apr;86(8):2554-8 [2704733] Proc Natl Acad Sci U S A. 1989 Sep;86(18):7033-7 [2476809] Cell. 1988 Oct 7;55(1):17-26 [3167976] Proc Natl Acad Sci U S A. 1988 Sep;85(17):6267-71 [3166139] Genes Dev. 1989 Dec;3(12A):1860-73 [2620826] Genes Dev. 1989 Dec;3(12A):1845-59 [2620825] Proc Natl Acad Sci U S A. 1986 Jun;83(12):4312-6 [3459175] Cell. 1986 Jul 4;46(1):89-94 [3719696] J Clin Invest. 1987 Aug;80(2):374-80 [3611352] Mol Cell Biol. 1987 Jan;7(1):398-402 [3561396] Proc Natl Acad Sci U S A. 1987 Jul;84(14):4786-90 [3474625] Proc Natl Acad Sci U S A. 1985 Oct;82(19):6384-8 [3879975] EMBO J. 1985 Jul;4(7):1715-23 [2992937] Nature. 1986 Feb 20-26;319(6055):685-9 [3951540] Mol Cell Biol. 1987 Nov;7(11):4024-9 [2828925] Cell. 1987 Dec 24;51(6):975-85 [3690667] J Biol Chem. 1987 Dec 15;262(35):17051-7 [2445753] Nature. 1985 Mar 28-Apr 3;314(6009):377-80 [3982505] Mol Cell Biol. 1987 Feb;7(2):725-37 [3821727] Biochemistry. 1987 Nov 17;26(23):7234-8 [3322397] Proc Natl Acad Sci U S A. 1984 Nov;81(22):7161-5 [6438633] Blood. 1991 Sep 1;78(5):1355-63 [1878596] Genes Dev. 1991 Aug;5(8):1387-94 [1714415] Blood. 1991 Oct 1;78(7):1853-63 [1912570] Nature. 1991 Mar 21;350(6315):252-4 [1706482] Nucleic Acids Res. 1990 Sep 25;18(18):5465-72 [2216720] Nature. 1990 Dec 20-27;348(6303):749-52 [2175398] Nucleic Acids Res. 1989 Jan 11;17(1):37-54 [2911469] J Mol Biol. 1988 Sep 20;203(2):439-55 [3199442] Cell. 1989 Mar 24;56(6):969-77 [2924354] Genes Dev. 1988 Jul;2(7):863-73 [3209071] Nature. 1989 Mar 23;338(6213):352-5 [2922063] Genes Dev. 1990 Jun;4(6):993-1006 [2116990] Mol Cell Biol. 1990 Mar;10(3):1116-25 [2304460] Nature. 1990 Mar 22;344(6264):309-13 [2314472] Genes Dev. 1990 Mar;4(3):380-9 [1692558] Nature. 1990 Jan 4;343(6253):92-6 [2104960] Proc Natl Acad Sci U S A. 1990 Jan;87(2):668-72 [2300555] Proc Natl Acad Sci U S A. 1980 Jun;77(6):3509-13 [6932034] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] Methods Enzymol. 1980;65(1):499-560 [6246368] Nucleic Acids Res. 1981 Dec 11;9(23):6505-25 [6275366] Blood. 1975 Mar;45(3):321-34 [163658] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Specific antibody to the thyrotropin receptor identifies multiple receptor forms in membranes of cells transfected with wild-type receptor complementary deoxyribonucleic acid: characterization of their relevance to receptor synthesis, processing, structure, and function. AN - 73083816; 1639025 AB - An antibody to a peptide of the TSH receptor, residues 352-366 which are not present in gonadotropin receptors, specifically identifies three major forms of the receptor on Western blots of detergent-solubilized membrane preparations from Cos-7 cells transfected with full-length rat and human TSH receptor cDNA: 230, 180, and 95-100 kilodaltons (kDa), based on simultaneously run protein standards. The 95- to 100-kDa protein is absent in cells transfected with a mutant receptor with no signal peptide and is sensitive to endoglycosidase-F. Its size is consistent with the sum of amino acids predicted from its cDNA sequence (84 kDa after subtracting the signal peptide) plus its carbohydrate content (14 kDa estimated from glycosylation mutants). It alone is absent in two deletion mutants that have lost TSH binding and activity after transfection: M1 missing residues 37-121 and M2 missing residues 110-307. It, thus, appears to be the processed glycosylated functional receptor on the cell surface. The 230-kDa protein is a nonprocessed form of the receptor, as evidenced by its insensitivity to endoglycosidase-F and its continued presence in cells transfected with a mutant receptor with no signal peptide. It is the primary form identified in rat FRTL-5 thyroid cells that have a functioning TSH receptor; it is not present in rat FRT thyroid cells with no functioning TSH receptor or receptor RNA. It appears, therefore, to be a early synthetic form of the functional TSH receptor. The 180-kDa protein is endoglycosidase-F sensitive and appears to be a processed intermediate between the 230-kDa early synthetic form and the 95- to 100-kDa functional receptor, rather than a dimer of the latter. Thus, with decreases in size appropriate to a receptor monomer, it remains present in membranes from the M1 and M2 deletion mutants that contain the 230-kDa protein but are missing the 95- to 100-kDa receptor form in association with lost TSH binding and activity after transfection. Minor receptor forms (54 kDa in rat receptor transfectants, 54 and 48 kDa in human receptor transfectants) appear to be degraded forms of the processed and glycosylated 95- to 100-kDa receptor. The presence or absence of reducing agents in the detergent solubilization mixture does not change the pattern or amount of the receptor forms recognized by the antibody, including the 54-kDa form; however, boiling does.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Endocrinology AU - Ban, T AU - Kosugi, S AU - Kohn, L D AD - Cell Regulation Section, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 815 EP - 829 VL - 131 IS - 2 SN - 0013-7227, 0013-7227 KW - Antibodies KW - 0 KW - Detergents KW - Receptors, Thyrotropin KW - DNA KW - 9007-49-2 KW - Mannosyl-Glycoprotein Endo-beta-N-Acetylglucosaminidase KW - EC 3.2.1.96 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Antibodies -- immunology KW - Humans KW - Amino Acid Sequence KW - Glycosylation KW - Molecular Weight KW - Structure-Activity Relationship KW - Rats KW - Oxidation-Reduction KW - Mutagenesis, Site-Directed KW - Antibody Specificity KW - Hot Temperature KW - Blotting, Western KW - Mannosyl-Glycoprotein Endo-beta-N-Acetylglucosaminidase -- metabolism KW - Molecular Sequence Data KW - Receptors, Thyrotropin -- chemistry KW - Receptors, Thyrotropin -- physiology KW - Transfection KW - DNA -- genetics KW - Cell Membrane -- chemistry KW - Receptors, Thyrotropin -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73083816?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrinology&rft.atitle=Specific+antibody+to+the+thyrotropin+receptor+identifies+multiple+receptor+forms+in+membranes+of+cells+transfected+with+wild-type+receptor+complementary+deoxyribonucleic+acid%3A+characterization+of+their+relevance+to+receptor+synthesis%2C+processing%2C+structure%2C+and+function.&rft.au=Ban%2C+T%3BKosugi%2C+S%3BKohn%2C+L+D&rft.aulast=Ban&rft.aufirst=T&rft.date=1992-08-01&rft.volume=131&rft.issue=2&rft.spage=815&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-02 N1 - Date created - 1992-09-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ultraviolet mutagenesis in human lymphocytes: the effect of cellular transformation. AN - 73074994; 1322318 AB - We have assessed the role of cellular transformation in ultraviolet (uv)-induced mutagenic events in human cells. To maintain uniformity of genetic background and to eliminate the effect of DNA repair, primary nontransformed lymphocytes (T-cells) and Epstein-Barr virus-transformed lymphocytes (B-cells) from one patient (XP12Be) with the DNA repair-deficient disorder xeroderma pigmentosum (group A) were transfected with the mutagenesis shuttle vector pZ189. Parallel control experiments were performed with primary, nontransformed lymphocytes from a normal individual and with a repair-proficient Epstein-Barr virus-transformed lymphocyte line (KR6058). pZ189 was treated with uv and introduced into the four cell lines by electroporation. Plasmid survival and mutations inactivating the marker supF suppressor tRNA gene in the recovered pZ189 were scored by transforming an indicator strain of Escherichia coli. Plasmid survival was reduced and mutation frequency elevated equally with both XP-A cell lines compared to both normal cell lines. Base sequence analysis of more than 250 independent plasmids showed that while the G:C----A:T base substitution mutation was found in at least 60% of plasmids with single or tandem mutations with all four cell lines, the frequency with the transformed XP-A (93%) cells was significantly higher (P less than 0.01) than that with the nontransformed XP-A cells (77%). In addition, with the transformed XP-A cells, there were significantly fewer plasmids with transversions and with mutations at a transversion hotspot (base pair 134) than with plasmids recovered from nontransformed XP-A cells. Interleukin-2 and phytohemagglutinin (used to maintain growth of the nontransformed lymphocytes) treatment of transformed XP12Be cells did not change overall plasmid survival or mutation frequency, but increased the transversion frequency and induced a mutational hotspot (at base pair 159), while another mutational hotspot (at base pair 123) disappeared. Thus we have demonstrated that in repair-deficient human cells, cellular transformation, while not affecting overall postuv plasmid survival and mutation frequency, does increase the susceptibility to G:C----A:T transition mutations, a type of mutation associated with uv-induced neoplasia. JF - Experimental cell research AU - Parris, C N AU - Kraemer, K H AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 462 EP - 469 VL - 201 IS - 2 SN - 0014-4827, 0014-4827 KW - Interleukin-2 KW - 0 KW - Phytohemagglutinins KW - Index Medicus KW - Interleukin-2 -- pharmacology KW - Ultraviolet Rays KW - Base Sequence KW - Transfection KW - Humans KW - Genetic Vectors KW - Molecular Sequence Data KW - Mutation KW - Herpesvirus 4, Human KW - Cell Line KW - Mutagenesis KW - Lymphocytes -- pathology KW - Xeroderma Pigmentosum -- physiopathology KW - Lymphocytes -- radiation effects KW - Lymphocytes -- drug effects KW - Cell Transformation, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73074994?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Experimental+cell+research&rft.atitle=Ultraviolet+mutagenesis+in+human+lymphocytes%3A+the+effect+of+cellular+transformation.&rft.au=Parris%2C+C+N%3BKraemer%2C+K+H&rft.aulast=Parris&rft.aufirst=C&rft.date=1992-08-01&rft.volume=201&rft.issue=2&rft.spage=462&rft.isbn=&rft.btitle=&rft.title=Experimental+cell+research&rft.issn=00144827&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-03 N1 - Date created - 1992-09-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synthesis, characterization, and some immunological properties of conjugates composed of the detoxified lipopolysaccharide of Vibrio cholerae O1 serotype Inaba bound to cholera toxin. AN - 73072829; 1639490 AB - Protection against cholera has been correlated with the level of serum vibriocidal antibodies. The specificity of these vibriocidal antibodies was mostly to the lipopolysaccharide (LPS). We synthesized conjugates of detoxified LPS with cholera toxin (CT) and other proteins in order to elicit serum LPS antibodies with vibriocidal activity. Treatment with hydrazine (deacylated LPS) reduced the endotoxic properties of the LPS to clinically acceptable levels and resulted in a molecule larger and more antigenic than the saccharide produced by acid hydrolysis. More immunogenic conjugates resulted from multipoint compared with single-point attachment of the deacylated LPS to the protein. The conjugates containing CT had low levels of pyrogen and no toxic activity upon Chinese hamster ovary cells and elicited booster responses of vibriocidal and CT antibodies when injected subcutaneously as saline solutions into mice; the vibriocidal titers were similar to those elicited by comparable doses of cellular vaccines. We suggest how serum vibriocidal antibodies might prevent cholera. JF - Infection and immunity AU - Gupta, R K AU - Szu, S C AU - Finkelstein, R A AU - Robbins, J B AD - Laboratory of Developmental and Molecular Immunity, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 3201 EP - 3208 VL - 60 IS - 8 SN - 0019-9567, 0019-9567 KW - Antibodies, Bacterial KW - 0 KW - Cholera Vaccines KW - Lipopolysaccharides KW - Vaccines, Synthetic KW - Cholera Toxin KW - 9012-63-9 KW - Index Medicus KW - Animals KW - Antibodies, Bacterial -- analysis KW - Antibodies, Bacterial -- immunology KW - Rabbits KW - Mice KW - Mice, Inbred BALB C KW - Female KW - Cholera Toxin -- immunology KW - Lipopolysaccharides -- immunology KW - Cholera Vaccines -- immunology KW - Vibrio cholerae -- immunology KW - Vaccines, Synthetic -- immunology KW - Lipopolysaccharides -- toxicity KW - Cholera Toxin -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73072829?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+immunity&rft.atitle=Synthesis%2C+characterization%2C+and+some+immunological+properties+of+conjugates+composed+of+the+detoxified+lipopolysaccharide+of+Vibrio+cholerae+O1+serotype+Inaba+bound+to+cholera+toxin.&rft.au=Gupta%2C+R+K%3BSzu%2C+S+C%3BFinkelstein%2C+R+A%3BRobbins%2C+J+B&rft.aulast=Gupta&rft.aufirst=R&rft.date=1992-08-01&rft.volume=60&rft.issue=8&rft.spage=3201&rft.isbn=&rft.btitle=&rft.title=Infection+and+immunity&rft.issn=00199567&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-28 N1 - Date created - 1992-08-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Vaccine. 1990 Oct;8(5):469-72 [2251873] J Immunol. 1970 Aug;105(2):431-41 [5433700] Infect Immun. 1991 Mar;59(3):977-82 [1705246] Infect Immun. 1991 Nov;59(11):4266-70 [1937784] Infect Immun. 1986 Aug;53(2):272-7 [2426198] Bull Johns Hopkins Hosp. 1965 Mar;116:152-60 [14280312] Am J Public Health Nations Health. 1954 Dec;44(12):1572-9 [13207484] Biochem J. 1952 Jan;50(3):298-303 [14915949] J Infect Dis. 1991 Aug;164(2):407-11 [1856488] Infect Immun. 1991 Dec;59(12):4450-8 [1937803] J Infect Dis. 1991 Jun;163(6):1235-42 [2037789] J Clin Microbiol. 1986 Aug;24(2):203-9 [3528211] Infect Immun. 1987 May;55(5):1116-20 [3552989] J Biol Stand. 1986 Jan;14(1):25-33 [2420803] J Immunol. 1986 Aug 15;137(4):1181-6 [3016088] Infect Immun. 1986 Nov;54(2):448-55 [3095243] J Infect Dis. 1988 Aug;158(2):301-11 [3042872] Infect Immun. 1988 Jan;56(1):142-8 [2447017] Infect Immun. 1989 Dec;57(12):3823-7 [2807549] J Med Microbiol. 1987 Feb;23(1):9-18 [3820275] J Bacteriol. 1985 Feb;161(2):795-8 [3968044] J Infect Dis. 1990 May;161(5):821-32 [2182727] Lancet. 1990 Feb 3;335(8684):270-3 [1967730] Infect Immun. 1990 Apr;58(4):1030-7 [2108085] Infect Immun. 1990 Jul;58(7):2352-60 [1694826] Infect Immun. 1990 Jul;58(7):2309-12 [2365462] Adv Exp Med Biol. 1990;256:189-97 [2327294] Carbohydr Res. 1982 Mar 1;100:341-9 [7083255] J Immunol. 1984 Jun;132(6):2736-41 [6233359] Infect Immun. 1984 Feb;43(2):515-22 [6693169] Infect Immun. 1979 Nov;26(2):528-33 [546785] Biochim Biophys Acta. 1979 May 1;584(2):346-52 [86366] J Infect Dis. 1977 Aug;136 Suppl:S105-12 [197173] Immunochemistry. 1978 Sep;15(9):611-4 [738758] Lancet. 1973 Jun 2;1(7814):1232-5 [4122575] J Infect Dis. 1974 Oct;130(4):325-33 [4443613] Infect Immun. 1976 Mar;13(3):735-40 [1270131] Eur J Biochem. 1974 Oct 2;48(2):319-23 [4375034] J Infect Dis. 1972 Oct;126(4):401-7 [4627648] J Infect Dis. 1972 Jul;126(1):41-7 [5038023] J Infect Dis. 1970 May;121(5):505-13 [4986889] J Infect Dis. 1971 Aug;124(2):223-6 [4942061] J Infect Dis. 1971 Oct;124(4):359-66 [5143844] Proc Natl Acad Sci U S A. 1991 Mar 1;88(5):1641-5 [2000374] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Bipartite signal for read-through suppression in murine leukemia virus mRNA: an eight-nucleotide purine-rich sequence immediately downstream of the gag termination codon followed by an RNA pseudoknot. AN - 73058503; 1629968 AB - The pol gene of murine leukemia virus and other mammalian type C retroviruses is expressed by read-through suppression of an in-frame UAG codon which separates the gag and pol coding regions. In this study, we have analyzed the sequence requirements for read-through suppression by placing different portions of wild-type and mutant viral sequences from the gag-pol junction between reporter genes and testing transcripts of these constructs for suppression in reticulocyte lysates. We find that the read-through signal is contained within the first 57 nucleotides on the 3' side of the UAG codon. Our results indicate that the identities of six conserved bases in the eight-nucleotide, purine-rich sequence immediately downstream of the UAG codon are critical for suppression, as is the existence of a pseudoknot structure spanning the next 49 nucleotides. Thus, read-through suppression depends on a complex, bipartite signal in the mRNA. JF - Journal of virology AU - Feng, Y X AU - Yuan, H AU - Rein, A AU - Levin, J G AD - Laboratory of Molecular Virology and Carcinogenesis, NCI-Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 5127 EP - 5132 VL - 66 IS - 8 SN - 0022-538X, 0022-538X KW - gag KW - pol KW - Codon KW - 0 KW - Fusion Proteins, gag-pol KW - RNA, Messenger KW - RNA, Viral KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - Base Sequence KW - Codon -- genetics KW - Reticulocytes -- metabolism KW - Molecular Sequence Data KW - Fusion Proteins, gag-pol -- genetics KW - Transcription, Genetic KW - Nucleic Acid Conformation KW - Signal Transduction KW - Genes, pol KW - Cloning, Molecular KW - Terminator Regions, Genetic KW - Suppression, Genetic KW - Moloney murine leukemia virus -- genetics KW - RNA, Viral -- genetics KW - RNA, Messenger -- genetics KW - Genes, gag UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73058503?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Bipartite+signal+for+read-through+suppression+in+murine+leukemia+virus+mRNA%3A+an+eight-nucleotide+purine-rich+sequence+immediately+downstream+of+the+gag+termination+codon+followed+by+an+RNA+pseudoknot.&rft.au=Feng%2C+Y+X%3BYuan%2C+H%3BRein%2C+A%3BLevin%2C+J+G&rft.aulast=Feng&rft.aufirst=Y&rft.date=1992-08-01&rft.volume=66&rft.issue=8&rft.spage=5127&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-14 N1 - Date created - 1992-08-14 N1 - Date revised - 2017-01-13 N1 - Gene symbol - gag; pol N1 - SuppNotes - Cited By: Cell. 1989 May 19;57(4):537-47 [2720781] J Virol. 1989 May;63(5):2405-10 [2784837] Nucleic Acids Res. 1985 Mar 11;13(5):1717-31 [4000943] Trends Biochem Sci. 1990 Apr;15(4):143-7 [1692647] J Virol. 1990 Jun;64(6):2642-52 [2186174] Virus Genes. 1990 Jul;4(2):121-36 [2402881] Virology. 1984 Apr 15;134(1):196-207 [6200992] J Virol. 1984 Jan;49(1):214-22 [6197537] Nature. 1981 Oct 15-21;293(5833):543-8 [6169994] Virology. 1977 May 1;78(1):11-34 [67705] Cell. 1978 Jan;13(1):189-99 [202399] EMBO J. 1984 Feb;3(2):351-6 [16453503] J Biol Chem. 1991 Sep 5;266(25):16257-60 [1832153] J Virol. 1984 Feb;49(2):471-8 [6319746] J Virol. 1980 May;34(2):464-73 [7373716] Nature. 1991 Sep 19;353(6341):273-6 [1832744] Proc Natl Acad Sci U S A. 1990 Nov;87(22):8860-3 [2247457] Proc Natl Acad Sci U S A. 1992 Jan 15;89(2):713-7 [1309954] Adv Virus Res. 1992;41:193-239 [1575083] J Mol Biol. 1991 Aug 20;220(4):889-902 [1880803] Proc Natl Acad Sci U S A. 1991 Aug 15;88(16):6991-5 [1871115] Virology. 1991 Jul;183(1):313-9 [2053284] J Mol Biol. 1991 Mar 20;218(2):365-73 [2010914] Proc Natl Acad Sci U S A. 1991 Jan 1;88(1):174-8 [1986362] J Virol. 1988 Oct;62(10):3574-80 [2843660] Cell. 1988 Nov 4;55(3):447-58 [2846182] Cell. 1989 Jul 14;58(1):9-12 [2473840] J Virol. 1986 Oct;60(1):267-74 [2427747] Nucleic Acids Res. 1989 Aug 11;17(15):5933-45 [2549503] J Virol. 1989 Jun;63(6):2870-3 [2542597] Proc Natl Acad Sci U S A. 1985 Mar;82(6):1618-22 [3885215] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interaction of the human papillomavirus type 16 E6 oncoprotein with wild-type and mutant human p53 proteins. AN - 73053400; 1321290 AB - The E6 oncoproteins encoded by the cancer-associated human papillomaviruses (HPVs) can associate with and promote the degradation of wild-type p53 in vitro. To gain further insight into this process, the ability of HPV-16 E6 to complex with and promote the degradation of mutant forms of p53 was studied. A correlation between binding and the targeted degradation of p53 was established. Mutant p53 proteins that bound HPV-16 E6 were targeted for degradation, whereas those that did not complex HPV-16 E6 were not degraded. Since the HPV-16 E6-promoted degradation involves the ubiquitin-dependent proteolysis pathway, specific mutations were made in the amino terminus of p53 to examine whether the E6 targeted degradation involved the N-end rule pathway. No requirement for destabilizing amino acids at the N terminus of p53 was found, nor was evidence found that HPV-16 E6 could provide this determinant in trans, indicating that the N-terminal rule pathway is not involved in the E6-promoted degradation of p53. JF - Journal of virology AU - Scheffner, M AU - Takahashi, T AU - Huibregtse, J M AU - Minna, J D AU - Howley, P M AD - Laboratory of Tumor Virus Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 5100 EP - 5105 VL - 66 IS - 8 SN - 0022-538X, 0022-538X KW - E6 protein, Human papillomavirus type 16 KW - 0 KW - Oligodeoxyribonucleotides KW - Oncogene Proteins, Viral KW - Repressor Proteins KW - Tumor Suppressor Protein p53 KW - Index Medicus KW - Protein Biosynthesis KW - Polymerase Chain Reaction KW - Animals KW - Humans KW - Reticulocytes -- metabolism KW - Papillomaviridae -- metabolism KW - Rabbits KW - Papillomaviridae -- genetics KW - Amino Acid Sequence KW - Binding Sites KW - Mutagenesis, Site-Directed KW - Oncogene Proteins, Viral -- genetics KW - Tumor Suppressor Protein p53 -- genetics KW - Tumor Suppressor Protein p53 -- metabolism KW - Oncogene Proteins, Viral -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73053400?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Interaction+of+the+human+papillomavirus+type+16+E6+oncoprotein+with+wild-type+and+mutant+human+p53+proteins.&rft.au=Scheffner%2C+M%3BTakahashi%2C+T%3BHuibregtse%2C+J+M%3BMinna%2C+J+D%3BHowley%2C+P+M&rft.aulast=Scheffner&rft.aufirst=M&rft.date=1992-08-01&rft.volume=66&rft.issue=8&rft.spage=5100&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-14 N1 - Date created - 1992-08-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1979 Mar 15;278(5701):261-3 [218111] Mol Cell Biol. 1981 Feb;1(2):101-10 [6100960] Oncogene. 1991 May;6(5):873-5 [1646990] Proc Natl Acad Sci U S A. 1991 Jul 1;88(13):5523-7 [1648218] Mol Carcinog. 1991;4(3):171-5 [1648361] J Virol. 1991 Dec;65(12):6671-6 [1658367] EMBO J. 1991 Dec;10(13):4129-35 [1661671] EMBO J. 1990 May;9(5):1595-602 [1691710] J Virol. 1991 Jan;65(1):292-8 [1845889] Nature. 1991 Jan 10;349(6305):132-8 [1846030] Proc Natl Acad Sci U S A. 1991 Jan 1;88(1):139-43 [1846034] Lancet. 1990 May 19;335(8699):1171-4 [1971033] Oncogene. 1990 Oct;5(10):1603-10 [1979160] Cell. 1991 May 31;65(5):765-74 [2040013] Cell. 1990 May 18;61(4):697-708 [2111732] Oncogene. 1990 Jul;5(7):945-52 [2142762] J Virol. 1990 Mar;64(3):1353-6 [2154613] Cell. 1990 Dec 21;63(6):1129-36 [2175676] New Biol. 1990 Mar;2(3):227-34 [2177651] EMBO J. 1988 Jun;7(6):1815-20 [2458921] J Biol Chem. 1989 Oct 5;264(28):16700-12 [2506181] J Virol. 1989 Mar;63(3):1247-55 [2536832] J Virol. 1989 Mar;63(3):1465-9 [2536847] EMBO J. 1989 Dec 1;8(12):3905-10 [2555178] Med Microbiol Immunol. 1987;176(5):245-56 [2821369] Cell. 1988 May 20;53(4):539-47 [2836062] Cell. 1988 Jul 15;54(2):275-83 [2839300] Nature. 1988 Jul 14;334(6178):124-9 [2968522] Proc Natl Acad Sci U S A. 1986 Jul;83(13):4680-4 [3014503] J Virol. 1987 Apr;61(4):962-71 [3029430] Cell. 1984 Aug;38(1):119-26 [6088057] Cell. 1982 Feb;28(2):387-94 [6277513] Mol Cell Biol. 1983 Dec;3(12):2143-50 [6318085] Nature. 1991 Jun 6;351(6326):453-6 [2046748] J Virol. 1990 Feb;64(2):723-30 [2153238] Nature. 1990 Jul 19;346(6281):287-91 [2165217] Science. 1990 Oct 5;250(4977):113-6 [2218501] J Virol. 1989 Oct;63(10):4417-21 [2476573] J Virol. 1989 Feb;63(2):965-9 [2536119] Science. 1989 Feb 17;243(4893):934-7 [2537532] EMBO J. 1989 Dec 20;8(13):4099-105 [2556261] Virology. 1988 Jul;165(1):321-5 [2838969] Oncogene Res. 1988 Sep;3(2):167-75 [2852339] Nature. 1985 Mar 7-13;314(6006):111-4 [2983228] J Biol Chem. 1988 Feb 25;263(6):2693-8 [3343227] Cell. 1979 May;17(1):43-52 [222475] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutational analysis of the core, spacer, and initiator regions of vaccinia virus intermediate-class promoters. AN - 73053187; 1629951 AB - Activation of vaccinia virus late gene transcription is dependent on DNA replication and the expression of three genes: A1L, A2L, and G8R (J. G. Keck, C. J. Baldick, Jr., and B. Moss, Cell 61:801-809, 1990). To fully characterize the promoter elements of these trans-activator genes, we prepared more than 140 plasmid vectors containing natural and mutated DNA segments ligated to the Escherichia coli lacZ or chloramphenicol acetyltransferase reporter gene. Expression of the reporter genes occurred when the plasmids were transfected into vaccinia virus-infected cells and was enhanced when DNA replication was prevented, indicating that the A1L, A2L, and G8R promoters belong to the intermediate regulatory class. Deletional mutagenesis demonstrated that the regulatory elements of all three promoters extended between 20 and 30 nucleotides upstream of their RNA start sites. Single-base substitutions of the G8R promoter revealed two critical elements located from -26 to -13 (the core element) and -1 to +3 (the initiator element). Mutations in these regions drastically affected expression, as determined by beta-galactosidase and mRNA analyses. Additional mutations defined the TAAA sequence as the critical initiator element. The length, but not the nucleotide sequence, of the segment between the core and initiator regions was crucial. The requirement for the spacer to be 10 or 11 nucleotides was consistent with a single turn of a double helix. The A1L and A2L promoters resembled the G8R promoter, and mutations in the conserved bases had the predicted effects on expression. We concluded that the three intermediate promoters are composed of a 14-bp A+T-rich core sequence separated by one turn of the double helix from the TAAA initiator element. JF - Journal of virology AU - Baldick, C J AU - Keck, J G AU - Moss, B AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 4710 EP - 4719 VL - 66 IS - 8 SN - 0022-538X, 0022-538X KW - A1L KW - A2L KW - G8R KW - DNA, Ribosomal KW - 0 KW - Oligodeoxyribonucleotides KW - RNA, Viral KW - Trans-Activators KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Transfection KW - Humans KW - Restriction Mapping KW - Polymerase Chain Reaction -- methods KW - Molecular Sequence Data KW - Transcription, Genetic KW - RNA, Viral -- isolation & purification KW - RNA, Viral -- genetics KW - DNA Replication KW - Cell Line KW - Cloning, Molecular KW - Vaccinia virus -- genetics KW - Promoter Regions, Genetic KW - Trans-Activators -- genetics KW - Genes, Viral KW - DNA, Ribosomal -- genetics KW - Genes, Regulator UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73053187?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Mutational+analysis+of+the+core%2C+spacer%2C+and+initiator+regions+of+vaccinia+virus+intermediate-class+promoters.&rft.au=Baldick%2C+C+J%3BKeck%2C+J+G%3BMoss%2C+B&rft.aulast=Baldick&rft.aufirst=C&rft.date=1992-08-01&rft.volume=66&rft.issue=8&rft.spage=4710&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-14 N1 - Date created - 1992-08-14 N1 - Date revised - 2017-01-13 N1 - Gene symbol - A1L; A2L; G8R N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1989 Aug;86(16):6126-30 [2548200] J Virol. 1989 Oct;63(10):4224-33 [2476568] Virology. 1987 May;158(1):206-10 [3472413] Anal Biochem. 1987 Apr;162(1):156-9 [2440339] EMBO J. 1986 Aug;5(8):1951-7 [3019674] Proc Natl Acad Sci U S A. 1985 Jan;82(1):19-23 [3855541] EMBO J. 1987 Dec 1;6(12):3787-94 [2828037] J Virol. 1988 Jun;62(6):1889-97 [2835495] EMBO J. 1988 Nov;7(11):3487-92 [2850166] EMBO J. 1986 May;5(5):1071-6 [3013615] J Virol. 1986 Nov;60(2):436-49 [3021979] Nucleic Acids Res. 1986 Apr 11;14(7):3003-16 [3008103] J Virol. 1989 Jan;63(1):226-32 [2462059] J Mol Biol. 1989 Dec 20;210(4):771-84 [2515287] J Mol Biol. 1989 Dec 20;210(4):749-69 [2515286] J Virol. 1988 Jan;62(1):297-304 [3334746] Anal Biochem. 1986 Feb 1;152(2):232-8 [3516005] Proc Natl Acad Sci U S A. 1987 Sep;84(17):6069-73 [3476927] Cell. 1987 Jul 17;50(2):163-9 [3594569] J Virol. 1987 Jan;61(1):75-80 [3783825] J Virol. 1985 Apr;54(1):30-7 [3973982] J Virol. 1990 Jun;64(6):3019-24 [2335825] Proc Natl Acad Sci U S A. 1990 Feb;87(4):1536-40 [1968253] Annu Rev Biochem. 1990;59:661-88 [2197987] Cell. 1990 Jun 1;61(5):801-9 [2344616] J Biol Chem. 1991 Aug 15;266(23):15539-44 [1869571] EMBO J. 1991 Sep;10(9):2553-8 [1651230] J Biol Chem. 1991 Jan 25;266(3):1355-8 [1988424] Cell. 1991 Apr 5;65(1):105-13 [2013091] J Virol. 1991 Jul;65(7):3715-20 [2041091] J Virol. 1990 Dec;64(12):6063-9 [2243387] J Biol Chem. 1988 May 5;263(13):6220-5 [2834368] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A block in full-length transcript maturation in cells nonpermissive for B19 parvovirus. AN - 73049885; 1385833 AB - Vertebrate parvoviruses share a similar genomic organization, with the capsid proteins encoded by genes on the right side and nonstructural proteins encoded by genes on the left side. The temporal and cell-specific appearances of these two types of gene products are regulated by a variety of genetic mechanisms. Rodent parvovirus structural proteins, for example, are encoded by a separate promoter which is positively regulated by nonstructural-gene products. In contrast, for the human B19 parvovirus, the analogous structural-gene promoter is nonfunctional, and both left- and right-side transcripts originate from a single promoter and are highly processed. Using a combination of sensitive RNA analyses of wild-type and mutant templates, we have found that the relative abundance of these alternatively processed transcripts appears to be governed by unique postinitiation events. In permissive cells, the steady-state level of right-side structural-gene transcripts predominates over that of left-side nonstructural-gene transcripts. In nonpermissive cells transfected with the B19 virus genome, nonstructural-gene transcripts predominate. Removal of 3' processing signals located in the middle of the viral genome increases transcription of the far right side. Disruption of a polyadenylation signal in this region makes readthrough of full-length right-side transcripts possible. These results suggest that the abundance of B19 virus RNAs is determined by active 3' processing and is coupled to DNA template replication. JF - Journal of virology AU - Liu, J M AU - Green, S W AU - Shimada, T AU - Young, N S AD - Clinical Hematology Branch, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 4686 EP - 4692 VL - 66 IS - 8 SN - 0022-538X, 0022-538X KW - Capsid Proteins KW - 0 KW - DNA, Viral KW - Oligodeoxyribonucleotides KW - Oligonucleotides, Antisense KW - RNA, Viral KW - Viral Core Proteins KW - Viral Nonstructural Proteins KW - Index Medicus KW - Animals KW - Blotting, Northern KW - HeLa Cells KW - Humans KW - Transcription, Genetic KW - Mutagenesis, Site-Directed KW - Promoter Regions, Genetic KW - Base Sequence KW - Transfection KW - Restriction Mapping KW - Polymerase Chain Reaction -- methods KW - Molecular Sequence Data KW - Templates, Genetic KW - Cell Line KW - Parvoviridae -- genetics KW - Capsid -- genetics KW - Viral Core Proteins -- genetics KW - RNA, Viral -- genetics KW - Parvoviridae -- physiology KW - DNA, Viral -- genetics KW - DNA Replication UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73049885?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=A+block+in+full-length+transcript+maturation+in+cells+nonpermissive+for+B19+parvovirus.&rft.au=Liu%2C+J+M%3BGreen%2C+S+W%3BShimada%2C+T%3BYoung%2C+N+S&rft.aulast=Liu&rft.aufirst=J&rft.date=1992-08-01&rft.volume=66&rft.issue=8&rft.spage=4686&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-14 N1 - Date created - 1992-08-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Blood. 1990 Nov 15;76(10):1997-2004 [2146978] Virology. 1991 Jul;183(1):133-42 [2053277] J Biol Chem. 1989 Jun 15;264(17):10057-64 [2722860] Virology. 1989 Oct;172(2):659-64 [2800343] Semin Hematol. 1988 Apr;25(2):159-72 [2838911] J Clin Invest. 1987 May;79(5):1486-92 [3033026] Blood. 1987 Aug;70(2):384-91 [3038211] Science. 1987 Jun 5;236(4806):1237-45 [3296191] J Gen Virol. 1987 Mar;68 ( Pt 3):601-14 [3546593] J Virol. 1986 Jun;58(3):921-36 [3701931] J Virol. 1984 Oct;52(1):266-76 [6090703] Cell. 1981 Dec;27(2 Pt 1):279-88 [6277501] Cell. 1982 Aug;30(1):173-83 [6290076] Cell. 1980 Jun;20(2):293-301 [6771018] Cell. 1980 Jun;20(2):303-12 [6771019] Nature. 1981 Mar 12;290(5802):113-8 [7207591] Cell. 1978 Jul;14(3):725-31 [210957] Virology. 1991 Nov;185(1):39-47 [1926783] Virology. 1991 May;182(1):361-4 [2024472] J Virol. 1990 Jan;64(1):387-96 [2293668] J Virol. 1989 Jun;63(6):2422-6 [2657097] Gene. 1989 Apr 15;77(1):51-9 [2744487] J Virol. 1988 Aug;62(8):2884-9 [2969055] N Engl J Med. 1987 Jul 30;317(5):287-94 [3037373] Adv Virus Res. 1987;33:91-174 [3296697] J Virol. 1987 Aug;61(8):2395-406 [3599180] Science. 1986 Aug 22;233(4766):883-6 [3738514] Nature. 1982 Jul 15;298(5871):240-4 [6283379] J Virol. 1983 Jun;46(3):937-43 [6602221] Cell. 1980 Jun;20(2):313-9 [6771020] Blood. 1992 Jan 1;79(1):18-24 [1728307] Genes Dev. 1991 Feb;5(2):244-53 [1995416] Blood. 1990 Feb 1;75(3):603-10 [2404522] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ultraviolet light irradiation increases cellular diacylglycerol and induces translocation of diacylglycerol kinase in murine keratinocytes. AN - 73048760; 1321202 AB - Cellular lipid metabolism can provide a variety of mediators of signal transduction, including diacylglycerols and inositol phosphates. These factors may be involved in the control of epidermal differentiation and proliferation because they are modulated by extracellular calcium, which also regulates the maturation phenotype of cultured keratinocytes. The effect of non-cytotoxic exposures to ultraviolet light on lipid metabolism was studied in cultured murine keratinocytes. Ultraviolet treatment of cultured murine keratinocytes growing in 0.05 mM Ca++ did not significantly change the total amount of [3H]inositol phosphates at 0.5, 8 or 24 h post-irradiation. Irradiated cells responded to an increase from 0.05 mM Ca++ to 1.4 mM Ca++ medium with increased formation of inositol phosphates suggesting irradiation did not alter the normal inositol lipid turnover in response to the Ca++ signal for terminal differentiation. Irradiation (20-120 J/m2 of UVB) induced a dose-dependent increase in the cellular level of diacylglycerols as measured at 24 h post-irradiation, without changing the turnover of other phospholipids including phosphatidylcholine and phosphatidylethanolamine. The increased cellular levels of diacylglycerols following ultraviolet exposure were accompanied by changes in the activity of diacylglycerol kinase (DAG-kinase). The cytosolic DAG-kinase activity was decreased whereas the DAG-kinase activity in the membrane fraction was increased. These results suggest that ultraviolet irradiation increases the level of diacylglycerols via changes in de novo metabolism through a DAG-kinase pathway. Elevated diacylglycerol may influence signal-transduction pathways mediated by cellular lipids and contribute to some keratinocyte responses to ultraviolet light. JF - The Journal of investigative dermatology AU - Punnonen, K AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 221 EP - 226 VL - 99 IS - 2 SN - 0022-202X, 0022-202X KW - Diglycerides KW - 0 KW - Membrane Lipids KW - Phospholipids KW - Phosphotransferases KW - EC 2.7.- KW - Diacylglycerol Kinase KW - EC 2.7.1.107 KW - Index Medicus KW - Translocation, Genetic -- radiation effects KW - Animals KW - Cells, Cultured KW - Phospholipids -- analysis KW - Mice KW - Diglycerides -- analysis KW - Chromatography, Thin Layer KW - Signal Transduction -- radiation effects KW - Phosphotransferases -- genetics KW - Ultraviolet Rays KW - Membrane Lipids -- radiation effects KW - Keratinocytes -- chemistry KW - Keratinocytes -- enzymology KW - Membrane Lipids -- metabolism KW - Keratinocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73048760?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+investigative+dermatology&rft.atitle=Ultraviolet+light+irradiation+increases+cellular+diacylglycerol+and+induces+translocation+of+diacylglycerol+kinase+in+murine+keratinocytes.&rft.au=Punnonen%2C+K%3BYuspa%2C+S+H&rft.aulast=Punnonen&rft.aufirst=K&rft.date=1992-08-01&rft.volume=99&rft.issue=2&rft.spage=221&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+investigative+dermatology&rft.issn=0022202X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-20 N1 - Date created - 1992-08-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Basis for receptor specificity of nonecotropic murine leukemia virus surface glycoprotein gp70SU. AN - 73043934; 1321266 AB - Murine leukemia viruses (MuLVs) initiate infection of NIH 3T3 cells by binding of the viral envelope (Env) protein to a cell surface receptor. Interference assays have shown that MuLVs can be divided into four groups, each using a distinct receptor: ecotropic, polytropic, amphotropic, and 10A1. In this study, we have attempted to map the determinants within viral Env proteins by constructing chimeric env genes. Chimeras were made in all six pairwise combinations between Moloney MCF (a polytropic MuLV), amphotropic MuLV, and 10A1, using a conserved EcoRI site in the middle of the Env coding region. The receptor specificity of each chimera was determined by using an interference assay. We found that amphotropic receptor specificity of each chimera was determined by using an interference assay. We found that amphotropic receptor specificity seems to map to the N-terminal portion of surface glycoprotein gp70SU. The difference between amphotropic and 10A1 receptor specificity can be attributed to one or more of only six amino acid differences in this region. Nearly all other cases showed evidence of interaction between Env domains in the generation of receptor specificity. Thus, a chimera composed exclusively of MCF and amphotropic sequences was found to exhibit 10A1 receptor specificity. None of the chimeras were able to infect cells by using the MCF receptor; however, two chimeras containing the C-terminal portion of MCF gp70SU could bind to this receptor, while they were able to infect cells via the amphotropic receptor. This result raises the possibility that receptor binding maps to the C-terminal portion of MCF gp70SU but requires MCF N-terminal sequences for a functional interaction with the MCF receptor. JF - Journal of virology AU - Ott, D AU - Rein, A AD - Laboratory of Molecular Virology and Carcinogenesis, NCI-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 4632 EP - 4638 VL - 66 IS - 8 SN - 0022-538X, 0022-538X KW - Receptors, Virus KW - 0 KW - Retroviridae Proteins, Oncogenic KW - Viral Envelope Proteins KW - Index Medicus KW - Animals KW - 3T3 Cells KW - Chimera KW - Sequence Homology, Nucleic Acid KW - Molecular Sequence Data KW - CHO Cells KW - Mice KW - Amino Acid Sequence KW - Cricetinae KW - Leukemia Virus, Murine -- physiology KW - Retroviridae Proteins, Oncogenic -- genetics KW - Receptors, Virus -- physiology KW - Leukemia Virus, Murine -- genetics KW - Viral Envelope Proteins -- metabolism KW - Retroviridae Proteins, Oncogenic -- metabolism KW - Viral Envelope Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73043934?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Basis+for+receptor+specificity+of+nonecotropic+murine+leukemia+virus+surface+glycoprotein+gp70SU.&rft.au=Ott%2C+D%3BRein%2C+A&rft.aulast=Ott&rft.aufirst=D&rft.date=1992-08-01&rft.volume=66&rft.issue=8&rft.spage=4632&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-14 N1 - Date created - 1992-08-14 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M33470; GENBANK; M55596; M33469; M55597 N1 - SuppNotes - Cited By: Virology. 1991 Aug;183(2):545-54 [1853560] Virology. 1984 Jul 15;136(1):144-52 [6330990] J Virol. 1989 Jan;63(1):273-80 [2535733] Cell. 1986 May 9;45(3):365-74 [3009025] Virology. 1986 Jul 30;152(2):343-54 [3014723] Virology. 1966 Aug;29(4):642-53 [4287699] J Virol. 1980 Mar;33(3):983-92 [6154154] J Virol. 1984 Feb;49(2):452-8 [6198530] J Virol. 1981 Sep;39(3):777-91 [6270351] J Virol. 1983 Jan;45(1):1-9 [6296423] J Virol. 1982 Oct;44(1):19-31 [7143566] J Virol. 1992 Mar;66(3):1468-75 [1310758] J Virol. 1990 Feb;64(2):757-66 [2153240] J Virol. 1985 Jan;53(1):32-9 [2981357] Proc Natl Acad Sci U S A. 1988 Nov;85(22):8420-4 [3141927] Virology. 1973 Apr;52(2):456-67 [4705382] Nature. 1981 Oct 15-21;293(5833):543-8 [6169994] Virology. 1982 Jul 15;120(1):251-7 [6285602] J Virol. 1991 Aug;65(8):4026-32 [2072445] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanistic aspects of signaling through Ras in NIH 3T3 cells. AN - 73101039; 1496380 AB - Serum and growth factors can increase the proportion of Ras in the active guanosine triphosphate (GTP)-bound form. Growth factors might stimulate guanine nucleotide exchange or decrease the activity of the guanosine triphosphatase-activating proteins GAP and neurofibromin (NF1). In NIH 3T3 cells that overexpress the mutant Ras protein His116, which releases bound guanine nucleotide at a constitutively high rate and retains sensitivity to GAP and NF1, the proportion of GTP bound to the His116 protein was not altered by serum or platelet-derived growth factor. However, these mitogens increased the proportion of Ras in the GTP-bound form in cells that overexpressed control Ras proteins with a normal intrinsic rate of guanine nucleotide release. The amount of GTP-bound His116 or control Ras proteins was higher in cells at low density than in cells at high density, which have more GAP-like activity. The lower proportion of GTP-bound Ras in NIH 3T3 cells at high density may result from increased GAP-like activity. By contrast, serum and platelet-derived growth factors appear to stimulate guanine nucleotide exchange. JF - Science (New York, N.Y.) AU - Zhang, K AU - Papageorge, A G AU - Lowy, D R AD - Laboratory of Cellular Oncology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/07/31/ PY - 1992 DA - 1992 Jul 31 SP - 671 EP - 674 VL - 257 IS - 5070 SN - 0036-8075, 0036-8075 KW - c-ras KW - GTPase-Activating Proteins KW - 0 KW - Growth Substances KW - Neurofibromin 1 KW - Platelet-Derived Growth Factor KW - Proteins KW - ras GTPase-Activating Proteins KW - Histidine KW - 4QD397987E KW - Guanosine Triphosphate KW - 86-01-1 KW - Methionine KW - AE28F7PNPL KW - Proto-Oncogene Proteins p21(ras) KW - EC 3.6.5.2 KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Platelet-Derived Growth Factor -- pharmacology KW - Gene Expression KW - Mice KW - Mutagenesis KW - Proteins -- pharmacology KW - Blood KW - Cell Line, Transformed KW - Proto-Oncogene Proteins p21(ras) -- metabolism KW - Growth Substances -- pharmacology KW - Genes, ras -- physiology KW - Signal Transduction -- genetics KW - Proto-Oncogene Proteins p21(ras) -- chemistry KW - Fibroblasts -- metabolism KW - Proto-Oncogene Proteins p21(ras) -- genetics KW - Guanosine Triphosphate -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73101039?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft.atitle=Mechanistic+aspects+of+signaling+through+Ras+in+NIH+3T3+cells.&rft.au=Zhang%2C+K%3BPapageorge%2C+A+G%3BLowy%2C+D+R&rft.aulast=Zhang&rft.aufirst=K&rft.date=1992-07-31&rft.volume=257&rft.issue=5070&rft.spage=671&rft.isbn=&rft.btitle=&rft.title=Science+%28New+York%2C+N.Y.%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-04 N1 - Date created - 1992-09-04 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of protein phosphatases blocks myogenesis by first altering MyoD binding activity. AN - 73081346; 1321827 AB - To examine the role of protein phosphatases in skeletal muscle differentiation, C2C12 myoblasts were treated with okadaic acid, a potent in vitro inhibitor of protein phosphatases 1 and 2A which regulate various cellular events in intact cells. We now show that okadaic acid treatment of the mouse myoblast C2C12 cell line reversibly altered the morphology of the cells and blocked differentiation. At a molecular level, it extinguished expression of the myogenic determination genes, MyoD1 and myogenin, but induced the expression of an inhibitor of differentiation, Id. Analysis of the MyoD1 promoter showed that inhibition of MyoD1 expression by okadaic acid occurs at the transcriptional level. These changes occur 10-20 h after okadaic acid treatment. However, within 1 h of treatment the ability of muscle extracts to support a specific MyoD-dependent gel mobility shift using a MyoD DNA binding site is lost. These data suggest that protein phosphatases play an important role during myogenic differentiation. JF - The Journal of biological chemistry AU - Kim, S J AU - Kim, K Y AU - Tapscott, S J AU - Winokur, T S AU - Park, K AU - Fujiki, H AU - Weintraub, H AU - Roberts, A B AD - Laboratory of Chemoprevention, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/07/25/ PY - 1992 DA - 1992 Jul 25 SP - 15140 EP - 15145 VL - 267 IS - 21 SN - 0021-9258, 0021-9258 KW - DNA-Binding Proteins KW - 0 KW - Ethers, Cyclic KW - Muscle Proteins KW - MyoD Protein KW - RNA, Messenger KW - Okadaic Acid KW - 1W21G5Q4N2 KW - DNA KW - 9007-49-2 KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Phosphoprotein Phosphatases KW - EC 3.1.3.16 KW - Index Medicus KW - Animals KW - DNA -- metabolism KW - Cell Differentiation KW - Mice KW - Ethers, Cyclic -- pharmacology KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Promoter Regions, Genetic KW - Base Sequence KW - RNA, Messenger -- metabolism KW - Transfection KW - Molecular Sequence Data KW - Muscles -- enzymology KW - Cell Line KW - Muscles -- drug effects KW - Phosphoprotein Phosphatases -- antagonists & inhibitors KW - Muscle Proteins -- metabolism KW - Muscle Proteins -- genetics KW - Muscle Development KW - DNA-Binding Proteins -- genetics KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73081346?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Inhibition+of+protein+phosphatases+blocks+myogenesis+by+first+altering+MyoD+binding+activity.&rft.au=Kim%2C+S+J%3BKim%2C+K+Y%3BTapscott%2C+S+J%3BWinokur%2C+T+S%3BPark%2C+K%3BFujiki%2C+H%3BWeintraub%2C+H%3BRoberts%2C+A+B&rft.aulast=Kim&rft.aufirst=S&rft.date=1992-07-25&rft.volume=267&rft.issue=21&rft.spage=15140&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-26 N1 - Date created - 1992-08-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evidence for GTP-binding protein involvement in the tyrosine phosphorylation of the T cell receptor zeta chain. AN - 73077685; 1386076 AB - The zeta subunit of the T cell receptor (TCR) is a prominent substrate for a TCR-activated tyrosine kinase. Tyrosine phosphorylation of the zeta subunit in response to antibody-mediated receptor cross-linking was synergized in permeabilized T cells by either of two non-hydrolyzable GTP analogues, guanosine 5'-[gamma-thio]triphosphate (GTP gamma S) or guanosine 5'-[beta, gamma-imido]triphosphate Gpp(NH)p. ATP analogues did not significantly affect antibody-induced tyrosine phosphorylation. Unlike the GTP analogues, the GDP analogue guanosine 5'-[beta-thio]diphosphate (GDP beta S) did not enhance phosphorylation of zeta. The effect induced by the GTP analogues required TCR occupancy and was independent of protein kinase C. Taken together these observations implicate a GTP-binding protein in the modulation of TCR-induced tyrosine phosphorylation. JF - The Journal of biological chemistry AU - Cenciarelli, C AU - Hohman, R J AU - Atkinson, T P AU - Gusovsky, F AU - Weissman, A M AD - Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07/25/ PY - 1992 DA - 1992 Jul 25 SP - 14527 EP - 14530 VL - 267 IS - 21 SN - 0021-9258, 0021-9258 KW - Receptors, Antigen, T-Cell, gamma-delta KW - 0 KW - Thionucleotides KW - Guanosine Diphosphate KW - 146-91-8 KW - 6-thioguanosine 5'-diphosphate KW - 16541-19-8 KW - Guanylyl Imidodiphosphate KW - 34273-04-6 KW - Guanosine 5'-O-(3-Thiotriphosphate) KW - 37589-80-3 KW - Tyrosine KW - 42HK56048U KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Guanylyl Imidodiphosphate -- metabolism KW - Blotting, Western KW - Tumor Cells, Cultured KW - Phosphorylation KW - Guanosine Diphosphate -- metabolism KW - Electrophoresis, Polyacrylamide Gel KW - Guanosine Diphosphate -- analogs & derivatives KW - Thionucleotides -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Guanosine 5'-O-(3-Thiotriphosphate) -- metabolism KW - Mice KW - GTP-Binding Proteins -- physiology KW - Tyrosine -- metabolism KW - Receptors, Antigen, T-Cell, gamma-delta -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73077685?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Evidence+for+GTP-binding+protein+involvement+in+the+tyrosine+phosphorylation+of+the+T+cell+receptor+zeta+chain.&rft.au=Cenciarelli%2C+C%3BHohman%2C+R+J%3BAtkinson%2C+T+P%3BGusovsky%2C+F%3BWeissman%2C+A+M&rft.aulast=Cenciarelli&rft.aufirst=C&rft.date=1992-07-25&rft.volume=267&rft.issue=21&rft.spage=14527&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-26 N1 - Date created - 1992-08-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of cis-regulatory elements in the myelin proteolipid protein (PLP) gene. AN - 73074474; 1378839 AB - Regulatory elements of the proteolipid protein (PLP) gene were identified physically by footprinting and gel mobility shift assays and functionally by transfecting glial cell lines with PLP-chloramphenicol acetyltransferase chimeric genes. In both human and rat glial cells, only several hundred base pairs of upstream sequence were sufficient for high level activity of the human PLP promoter. This region contains five sites that contact nuclear proteins in vitro. More distal recognition sites may exist, as regions upstream of -524 displayed silencing activity indicative of a negative regulatory element. A series of site directed mutations revealed one essential positive element (ATGGA at -118) which is found in other genes encoding myelin proteins. Our combined biochemical and functional analyses indicate that the key cis sites for maximal tissue-specific expression of PLP in cultured glial cells are clustered near the promoter. Within this cluster are several conserved motifs that may coordinate the regulation of myelin-specific genes. JF - The Journal of biological chemistry AU - Berndt, J A AU - Kim, J G AU - Hudson, L D AD - Laboratory of Viral and Molecular Pathogenesis, National Institute of Neurologic Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07/25/ PY - 1992 DA - 1992 Jul 25 SP - 14730 EP - 14737 VL - 267 IS - 21 SN - 0021-9258, 0021-9258 KW - PLP KW - Myelin Proteins KW - 0 KW - Myelin Proteolipid Protein KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - Neuroglia -- cytology KW - Animals KW - HeLa Cells KW - Humans KW - Gene Expression KW - DNA Fingerprinting KW - Rats KW - Neuroglia -- metabolism KW - Mutagenesis, Site-Directed KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Promoter Regions, Genetic KW - Base Sequence KW - Chimera KW - Transfection KW - Cells, Cultured KW - Molecular Sequence Data KW - Methylation KW - Regulatory Sequences, Nucleic Acid KW - Myelin Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73074474?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Identification+of+cis-regulatory+elements+in+the+myelin+proteolipid+protein+%28PLP%29+gene.&rft.au=Berndt%2C+J+A%3BKim%2C+J+G%3BHudson%2C+L+D&rft.aulast=Berndt&rft.aufirst=J&rft.date=1992-07-25&rft.volume=267&rft.issue=21&rft.spage=14730&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-26 N1 - Date created - 1992-08-26 N1 - Date revised - 2017-01-13 N1 - Gene symbol - PLP N1 - Genetic sequence - M93105; GENBANK; M86615; M86618; M86619; M86616; M86617; X62322; M63383; M95057; M86620 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of P-glycoprotein phosphorylation and drug transport by sodium butyrate. AN - 73081851; 1352990 AB - P-Glycoprotein (Pgp) expression in cell lines derived from tumors arising from cells which normally express Pgp can be increased by sodium butyrate and other differentiating agents. Although the Pgp level increased 25-fold after sodium butyrate treatment in SW620 human colon carcinoma cells, the intracellular accumulation of vinblastine, adriamycin, and actinomycin D increased rather than decreased. In contrast, colchicine showed the expected decrease in accumulation, as a result of increased efflux. Likewise, treatment of a Pgp-expressing multidrug-resistant SW620 subline with sodium butyrate resulted in active interference with Pgp function. This effect was partially reversed by phorbol esters with a resulting decrease in the accumulation of vinblastine, adriamycin, and actinomycin D. Sodium butyrate, while increasing Pgp levels, inhibited the phosphorylation of Pgp. Time course studies revealed a tight relationship between decreased Pgp phosphorylation and increased vinblastine accumulation after sodium butyrate treatment. Either treatment with phorbol esters or withdrawal of sodium butyrate increased Pgp phosphorylation while decreasing vinblastine accumulation. These studies suggest that the specificity of Pgp transport can be modulated by phosphorylation and that vinblastine, adriamycin, or actinomycin D transport, but not that of colchicine, is diminished after dephosphorylation by sodium butyrate. JF - Biochemistry AU - Bates, S E AU - Currier, S J AU - Alvarez, M AU - Fojo, A T AD - Medicine Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07/21/ PY - 1992 DA - 1992 Jul 21 SP - 6366 EP - 6372 VL - 31 IS - 28 SN - 0006-2960, 0006-2960 KW - Butyrates KW - 0 KW - Membrane Glycoproteins KW - P-Glycoprotein KW - Phorbol Esters KW - Phosphoproteins KW - Butyric Acid KW - 107-92-6 KW - Dactinomycin KW - 1CC1JFE158 KW - Vinblastine KW - 5V9KLZ54CY KW - Doxorubicin KW - 80168379AG KW - Colchicine KW - SML2Y3J35T KW - Index Medicus KW - Vinblastine -- metabolism KW - Humans KW - Biological Transport -- drug effects KW - Colchicine -- metabolism KW - Phorbol Esters -- pharmacology KW - Dactinomycin -- metabolism KW - Doxorubicin -- metabolism KW - Phosphorylation KW - In Vitro Techniques KW - Cell Line KW - Phosphoproteins -- metabolism KW - Butyrates -- pharmacology KW - Drug Resistance KW - Membrane Glycoproteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73081851?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=Modulation+of+P-glycoprotein+phosphorylation+and+drug+transport+by+sodium+butyrate.&rft.au=Bates%2C+S+E%3BCurrier%2C+S+J%3BAlvarez%2C+M%3BFojo%2C+A+T&rft.aulast=Bates&rft.aufirst=S&rft.date=1992-07-21&rft.volume=31&rft.issue=28&rft.spage=6366&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-25 N1 - Date created - 1992-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Methionine enkephalin accumulates in plasma but not in brain or cerebrospinal fluid of rats with acute toxic hepatitis. AN - 73325900; 1436641 AB - In order to determine whether acute toxic hepatitis in the rat is associated with an accumulation of methionine enkephalin in plasma and increased blood-to-brain transfer of methionine enkephalin, immunoreactive methionine enkephalin levels were determined by radioimmunoassay in plasma, cerebrospinal fluid and whole brain samples from rats with thioacetamide induced acute toxic hepatitis. Thioacetamide treatment was associated with an 8.7-fold increase in plasma immunoreactive methionine enkephalin levels (P less than or equal to 0.005) 24 h after treatment. However, this marked elevation in plasma immunoreactive methionine enkephalin levels was not associated with an increase in whole brain or cerebrospinal fluid immunoreactive methionine enkephalin levels. These data suggest that increased plasma-to-brain transfer of methionine enkephalin does not occur in this model of acute toxic hepatitis. JF - Neuroscience letters AU - Swain, M G AU - Heyes, M P AU - Vergalla, J AU - Jones, E A AD - Liver Diseases Section, NIDDK, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/07/20/ PY - 1992 DA - 1992 Jul 20 SP - 243 EP - 246 VL - 141 IS - 2 SN - 0304-3940, 0304-3940 KW - Thioacetamide KW - 075T165X8M KW - Enkephalin, Methionine KW - 58569-55-4 KW - Index Medicus KW - Rats KW - Acute Disease KW - Animals KW - Rats, Sprague-Dawley KW - Liver -- pathology KW - Liver -- drug effects KW - Thioacetamide -- pharmacology KW - Male KW - Enkephalin, Methionine -- blood KW - Chemical and Drug Induced Liver Injury -- blood KW - Enkephalin, Methionine -- cerebrospinal fluid KW - Chemical and Drug Induced Liver Injury -- cerebrospinal fluid KW - Enkephalin, Methionine -- metabolism KW - Brain -- metabolism KW - Chemical and Drug Induced Liver Injury -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73325900?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+letters&rft.atitle=Methionine+enkephalin+accumulates+in+plasma+but+not+in+brain+or+cerebrospinal+fluid+of+rats+with+acute+toxic+hepatitis.&rft.au=Swain%2C+M+G%3BHeyes%2C+M+P%3BVergalla%2C+J%3BJones%2C+E+A&rft.aulast=Swain&rft.aufirst=M&rft.date=1992-07-20&rft.volume=141&rft.issue=2&rft.spage=243&rft.isbn=&rft.btitle=&rft.title=Neuroscience+letters&rft.issn=03043940&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-11 N1 - Date created - 1992-12-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - N-methyl-D-aspartate receptor-mediated neuroprotection in cerebellar granule cells requires new RNA and protein synthesis. AN - 73070281; 1385875 AB - Cerebellar granule cells are susceptible to the excitotoxin glutamate, which acts at N-methyl-D-aspartate (NMDA) receptors, as well as the neurotoxin 1-methyl-4-phenylpyridinium ion (MPP+), the active cytotoxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Paradoxically, preincubation of cultured cerebellar granule cells with low concentrations of NMDA or glutamate markedly antagonizes the neurotoxicity resulting from subsequent exposure to toxic concentrations of either MPP+ or glutamate. The neuroprotective effects of NMDA and glutamate against MPP+ toxicity are observed at agonist concentrations as low as 1 microM, are blocked by specific NMDA receptor antagonists, and require at least 30 min to develop fully. Moreover, NMDA receptor-mediated neuroprotection is prevented by the RNA synthesis inhibitor actinomycin D or the protein synthesis inhibitor cycloheximide. Thus, in cerebellar granule cells activation of NMDA receptors by glutamate can result in either neurotoxicity or neuroprotection, depending on the apparent degree of receptor stimulation. NMDA receptor-mediated neuroprotection requires new RNA and protein synthesis and therefore appears to be mediated by the expression of a neuroprotective protein(s). These data demonstrate the presence of an active NMDA receptor-mediated and transcriptionally directed neuroprotective mechanism in cerebellar granule cells. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Marini, A M AU - Paul, S M AD - Section on Molecular Pharmacology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1992/07/15/ PY - 1992 DA - 1992 Jul 15 SP - 6555 EP - 6559 VL - 89 IS - 14 SN - 0027-8424, 0027-8424 KW - Glutamates KW - 0 KW - Nerve Tissue Proteins KW - Receptors, N-Methyl-D-Aspartate KW - N-Methylaspartate KW - 6384-92-5 KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Cell Survival -- drug effects KW - 1-Methyl-4-phenylpyridinium -- toxicity KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - In Vitro Techniques KW - N-Methylaspartate -- toxicity KW - Gene Expression KW - Glutamates -- toxicity KW - Time Factors KW - Nerve Tissue Proteins -- physiology KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Cerebellum -- cytology KW - Receptors, N-Methyl-D-Aspartate -- drug effects KW - Cerebellum -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73070281?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=N-methyl-D-aspartate+receptor-mediated+neuroprotection+in+cerebellar+granule+cells+requires+new+RNA+and+protein+synthesis.&rft.au=Marini%2C+A+M%3BPaul%2C+S+M&rft.aulast=Marini&rft.aufirst=A&rft.date=1992-07-15&rft.volume=89&rft.issue=14&rft.spage=6555&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-18 N1 - Date created - 1992-08-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: FASEB J. 1990 Jul;4(10):2789-97 [2165013] Nature. 1991 Jan 31;349(6308):414-8 [1846943] Neurosci Lett. 1989 Apr 24;99(1-2):113-8 [2568605] Neurosci Lett. 1988 Aug 15;91(1):47-52 [2845308] Annu Rev Neurosci. 1988;11:81-96 [3129982] J Neurosci. 1988 Jun;8(6):2153-63 [3385492] J Neurosci. 1988 Jun;8(6):2164-71 [3385493] Brain Res. 1984 Jan 2;290(1):77-86 [6140986] Nature. 1976 Sep 16;263(5574):244-6 [8731] Biochem Biophys Res Commun. 1991 Dec 31;181(3):1442-8 [1764096] Proc Natl Acad Sci U S A. 1990 Feb;87(3):1193-7 [2153974] Neuroscience. 1990;37(1):251-8 [2173814] J Neurosci. 1989 Oct;9(10):3665-72 [2571685] Neuron. 1988 Oct;1(8):623-34 [2908446] Science. 1988 Jun 3;240(4857):1328-31 [3131879] Proc Natl Acad Sci U S A. 1982 Dec;79(24):7919-23 [6130529] J Biol Chem. 1951 Nov;193(1):265-75 [14907713] Eur J Pharmacol. 1991 Feb 26;194(1):131-2 [1676372] J Neurochem. 1990 May;54(5):1509-16 [1691274] J Pharmacol Exp Ther. 1991 Jan;256(1):402-11 [1846423] Brain Res. 1988 Jun 7;451(1-2):205-12 [2472189] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antitumor activity and immune responses induced by a recombinant carcinoembryonic antigen-vaccinia virus vaccine. AN - 73043914; 1619682 AB - Human carcinoembryonic antigen (CEA) is a 180-kd glycoprotein expressed in human colorectal, gastric, pancreatic, breast, and non-small-cell lung carcinomas. Previous studies have demonstrated enhanced immune responses to other antigens presented with vaccinia virus proteins via a recombinant vaccinia virus construct. In addition, we have developed a recombinant CEA-vaccinia virus construct, designated rV(WR)-CEA, and have demonstrated humoral anti-CEA responses in mice after immunization with that virus. The goals of this study were (a) to construct a recombinant CEA-vaccinia vaccine in a less virulent vaccinia strain that is potentially safe and effective for treatment of patients whose tumors express CEA and (b) to evaluate the ability of the recombinant CEA-vaccinia vaccine to prevent and reverse tumor growth in mice and to elicit cell-mediated and humoral anti-CEA immune responses. Using the New York City strain of vaccinia virus, which is used in smallpox vaccination and is more attenuated for humans than rV(WR), we derived a recombinant CEA-vaccinia construct, designated rV(NYC)-CEA. The ability of this construct to induce antitumor immunity was evaluated in mice receiving subcutaneous injections of murine colon adenocarcinoma cells expressing the human CEA gene. Administration of rV(NYC)-CEA in mice induced strong anti-CEA antibody responses, as well as CEA-specific cell-mediated responses, including delayed-type hypersensitivity, lymphoproliferative, and cytotoxic responses. Vaccination of mice with the rV(NYC)-CEA rendered them resistant to the growth of subsequently transplanted CEA-expressing tumors. Moreover, when mice were vaccinated 7 days after tumor cell injection, tumor growth was either greatly reduced or eliminated. No toxic effects were observed in any of the mice. These studies demonstrate that antitumor activity can be induced with the use of a recombinant CEA-vaccinia virus construct derived from an attenuated vaccinia strain, and they reveal the range of cell-mediated and humoral responses induced by this recombinant vaccine. JF - Journal of the National Cancer Institute AU - Kantor, J AU - Irvine, K AU - Abrams, S AU - Kaufman, H AU - DiPietro, J AU - Schlom, J AD - Laboratory of Tumor Immunology and Biology, National Cancer Institute, Bethesda, Md 20892. Y1 - 1992/07/15/ PY - 1992 DA - 1992 Jul 15 SP - 1084 EP - 1091 VL - 84 IS - 14 SN - 0027-8874, 0027-8874 KW - Antibodies, Neoplasm KW - 0 KW - Carcinoembryonic Antigen KW - Vaccines, Synthetic KW - Index Medicus KW - Animals KW - Humans KW - Antibodies, Neoplasm -- immunology KW - T-Lymphocytes, Cytotoxic -- immunology KW - Mice KW - Immunity, Cellular -- immunology KW - Cytotoxicity, Immunologic -- immunology KW - Vaccination KW - Hypersensitivity, Delayed -- immunology KW - Neoplasm Transplantation KW - Blotting, Western KW - Tumor Cells, Cultured KW - Lymphocyte Activation -- immunology KW - Antibody Formation -- immunology KW - Mice, Inbred C57BL KW - T-Lymphocytes -- immunology KW - Female KW - Vaccinia virus -- immunology KW - Carcinoembryonic Antigen -- immunology KW - Vaccines, Synthetic -- immunology KW - Vaccines, Synthetic -- administration & dosage KW - Adenocarcinoma -- immunology KW - Adenocarcinoma -- prevention & control KW - Colonic Neoplasms -- prevention & control KW - Colonic Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73043914?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Antitumor+activity+and+immune+responses+induced+by+a+recombinant+carcinoembryonic+antigen-vaccinia+virus+vaccine.&rft.au=Kantor%2C+J%3BIrvine%2C+K%3BAbrams%2C+S%3BKaufman%2C+H%3BDiPietro%2C+J%3BSchlom%2C+J&rft.aulast=Kantor&rft.aufirst=J&rft.date=1992-07-15&rft.volume=84&rft.issue=14&rft.spage=1084&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-03 N1 - Date created - 1992-08-03 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Natl Cancer Inst. 1992 Jul 15;84(14):1059-61 [1619675] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Parity and primary liver cancer among young women. AN - 73024073; 1619686 JF - Journal of the National Cancer Institute AU - Hsing, A W AU - McLaughlin, J K AU - Hoover, R N AU - Co Chien, H T AU - Blot, W J AU - Fraumeni, J F AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, Md. 20892. Y1 - 1992/07/15/ PY - 1992 DA - 1992 Jul 15 SP - 1118 EP - 1119 VL - 84 IS - 14 SN - 0027-8874, 0027-8874 KW - Contraceptives, Oral KW - 0 KW - Index Medicus KW - Population KW - United States KW - Fertility KW - Research Methodology KW - Metabolic Effects KW - Estrogens--changes KW - Population Dynamics KW - Physiology KW - Contraceptive Methods--side effects KW - Oral Contraceptives--side effects KW - Hormones KW - Developed Countries KW - Liver Neoplasms KW - Demographic Factors KW - Diseases KW - Family Planning KW - Parity KW - North America KW - Americas KW - Endocrine System KW - Studies KW - Methodological Studies KW - Matched Groups KW - Pregnancy KW - Case Control Studies KW - Northern America KW - Neoplasms KW - Control Groups KW - Contraception KW - Reproduction KW - Fertility Measurements KW - Biology KW - Contraceptives, Oral -- adverse effects KW - Risk Factors KW - Humans KW - Adult KW - Case-Control Studies KW - Middle Aged KW - Female KW - Liver Neoplasms -- chemically induced KW - Liver Neoplasms -- epidemiology KW - Liver Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73024073?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Parity+and+primary+liver+cancer+among+young+women.&rft.au=Hsing%2C+A+W%3BMcLaughlin%2C+J+K%3BHoover%2C+R+N%3BCo+Chien%2C+H+T%3BBlot%2C+W+J%3BFraumeni%2C+J+F&rft.aulast=Hsing&rft.aufirst=A&rft.date=1992-07-15&rft.volume=84&rft.issue=14&rft.spage=1118&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-03 N1 - Date created - 1992-08-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutagenesis of T cell antigen receptor zeta chain tyrosine residues. Effects on tyrosine phosphorylation and lymphokine production. AN - 73051315; 1535630 AB - Occupancy of the T cell antigen receptor triggers a complex set of events that culminate in cellular activation. It is clear that tyrosine kinases play important roles in this process. The zeta subunit of the T cell antigen receptor is a 16-kDa transmembrane structure that exists primarily as a disulfide-linked homodimer. On receptor activation, a subset of zeta molecules undergo tyrosine phosphorylation. To evaluate this process and the role of zeta phosphorylation in T cell activation, site-specific mutagenesis of the intracytoplasmic tyrosines of zeta has been carried out. Analysis of cells expressing these mutant zeta subunits demonstrated that multiple tyrosines underwent phosphorylation in response to receptor engagement, and that the four most carboxyl tyrosines were most crucial to this process. Despite abnormalities in phosphorylation induced by the mutations, lymphokine production in these transfectants was unaffected. Hence, although zeta is a prominent substrate for a receptor-activated tyrosine kinase, neither the mutation of individual tyrosines nor the alteration of the phosphorylation state of the molecule substantively affected the coupling of T cell receptor activation to lymphokine production. These findings raise questions regarding the role of zeta phosphorylation in T cell activation. JF - The Journal of biological chemistry AU - Frank, S J AU - Cenciarelli, C AU - Niklinska, B B AU - Letourneur, F AU - Ashwell, J D AU - Weissman, A M AD - Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07/05/ PY - 1992 DA - 1992 Jul 05 SP - 13656 EP - 13660 VL - 267 IS - 19 SN - 0021-9258, 0021-9258 KW - Interleukin-2 KW - 0 KW - Receptors, Antigen, T-Cell, gamma-delta KW - Tyrosine KW - 42HK56048U KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Lymphocyte Activation KW - Animals KW - Hybridomas KW - Phosphorylation KW - Transfection KW - Mice KW - Precipitin Tests KW - T-Lymphocytes -- immunology KW - Mutagenesis, Site-Directed KW - Receptors, Antigen, T-Cell, gamma-delta -- genetics KW - Interleukin-2 -- biosynthesis KW - Tyrosine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73051315?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Mutagenesis+of+T+cell+antigen+receptor+zeta+chain+tyrosine+residues.+Effects+on+tyrosine+phosphorylation+and+lymphokine+production.&rft.au=Frank%2C+S+J%3BCenciarelli%2C+C%3BNiklinska%2C+B+B%3BLetourneur%2C+F%3BAshwell%2C+J+D%3BWeissman%2C+A+M&rft.aulast=Frank&rft.aufirst=S&rft.date=1992-07-05&rft.volume=267&rft.issue=19&rft.spage=13656&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-05 N1 - Date created - 1992-08-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: J Biol Chem 1992 Sep 25;267(27):19752 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Physiological abnormalities in hereditary hyperekplexia. AN - 85273721; pmid-1642471 AB - Five patients from a kindred with hereditary hyperekplexia had physiological testing. The surface-recorded electromyographic pattern of audiogenic muscle jerks was identical to that of the normal acoustic startle reflex. Testing at graded stimulus intensities indicated an increase in the gain of the acoustic startle reflex. Nose-tap stimuli resulted in short-latency generalized electromyographic bursts that were similar to the R1 component of the blink reflex. Electrical stimulation of peripheral nerves elicited a pattern of generalized muscle jerks that was similar to that of the acoustic startle reflex. Somatosensory evoked potentials, brainstem auditory evoked potentials, and cortical auditory evoked potentials were normal. The primary physiological abnormality in hereditary hyperekplexia is widespread elevated gain of vestigial withdrawal reflexes in the brainstem and possibly the spinal cord, most likely resulting from increased excitability of reticular neurons. JF - Annals of Neurology AU - Matsumoto, J AU - Fuhr, P AU - Nigro, M AU - Hallett, M AD - Human Motor Control Section, Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. PY - 1992 SP - 41 EP - 50 VL - 32 IS - 1 SN - 0364-5134, 0364-5134 KW - Reference Values KW - Spinal Cord KW - Startle Reaction KW - Human KW - Electromyography KW - Child KW - Sensation KW - Child, Preschool KW - Infant KW - Needles KW - Movement Disorders KW - Adult KW - Neural Conduction KW - Middle Age KW - Acoustic Stimulation KW - Reflex KW - Adolescent KW - Time Factors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85273721?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+Neurology&rft.atitle=Physiological+abnormalities+in+hereditary+hyperekplexia.&rft.au=Matsumoto%2C+J%3BFuhr%2C+P%3BNigro%2C+M%3BHallett%2C+M&rft.aulast=Matsumoto&rft.aufirst=J&rft.date=1992-07-01&rft.volume=32&rft.issue=1&rft.spage=41&rft.isbn=&rft.btitle=&rft.title=Annals+of+Neurology&rft.issn=03645134&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Ethanol dependence and withdrawal selectively alter localized cerebral glucose utilization. AN - 85231841; pmid-1515942 AB - The 2-deoxyglucose technique was used to determine local cerebral glucose utilization (LCGU) in over 50 brain regions of rats physically dependent upon ethanol and compared to those of acutely intoxicated and those undergoing an overt ethanol-withdrawal syndrome. Dependent-intoxicated rats (average blood ethanol concentration 64 mM) had decreased LCGU in 13/54 regions, including those associated with the limbic system, cerebellum, and motor system. The ethanol withdrawal syndrome was associated with 17/50 gray regions showing an increase, including regions involved with motor function, auditory system, and mammillary bodies-anterior thalamus-cingulate cortex pathway. The most pronounced differences between these groups occurred in regions associated with motor function, cerebellar function, anterior thalamus, and median raphe. Comparisons between dependent-intoxicated and acutely intoxicated rats (average blood ethanol concentration 66 mM) revealed that acute intoxication was associated with a relatively greater reduction in LCGU in regions involved with sensory-related functions, mammillary bodies, and median raphe. With the development of dependence, adaptation occurred in these regions except for inferior colliculus and median raphe. Dependence was also associated with a relative decrease in LCGU in white matter, limbic system, and extrapyramidal motor system. JF - Brain Research AU - Eckardt, M J AU - Campbell, G A AU - Marietta, C A AU - Majchrowicz, E AU - Rawlings, R R AU - Weight, F F AD - Laboratory of Clinical Studies, DICBR, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. PY - 1992 SP - 244 EP - 250 VL - 584 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Rats KW - Rats, Inbred Strains KW - Substance Withdrawal Syndrome KW - Brain Chemistry KW - Animal KW - Glucose KW - Substance-Related Disorders KW - Deoxyglucose KW - Autoradiography KW - Male KW - Ethanol UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85231841?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+Research&rft.atitle=Ethanol+dependence+and+withdrawal+selectively+alter+localized+cerebral+glucose+utilization.&rft.au=Eckardt%2C+M+J%3BCampbell%2C+G+A%3BMarietta%2C+C+A%3BMajchrowicz%2C+E%3BRawlings%2C+R+R%3BWeight%2C+F+F&rft.aulast=Eckardt&rft.aufirst=M&rft.date=1992-07-01&rft.volume=584&rft.issue=1-2&rft.spage=244&rft.isbn=&rft.btitle=&rft.title=Brain+Research&rft.issn=00068993&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Intensive therapy with cisplatin, interleukin-2 and interferon-alpha-2a in patients with metastatic melanoma. A phase II Study. AN - 75541645; 1343617 AB - Based upon their individual clinical activity and combined effects in animal models or in vitro, we wished to evaluate a regimen of cisplatin, interferon-alpha, and IL-2 in patients with metastatic melanoma. Phase II pilot study. Referral-based US Government clinical research unit. Nine patients with metastatic malignant melanoma. Cisplatin 75-100 mg/m2 was administered intravenously over 30 minutes on days 1 and 8. Interferon-alpha 2a 5 Mu/m2 body surface area (BSA) was given subcutaneously for 4 days beginning 1 day before each dose of cisplatin. Beginning on day 15 and day 22, IL-2 was administered by intravenous continuous infusion at 3 Mu/m2 BSA/d for 96 hours and by daily intravenous bolus concurrent with daily subcutaneous doses of interferon-alpha 2a. Antitumor response and toxicities. The study was stopped due to renal and hematopoietic toxicity and severe, delayed nausea and vomiting associated with the cisplatin-interferon treatment. Three of 9 patients achieved a partial response (duration 2.5, 4, 14+ months), and an additional patient had a 50% reduction in measurable tumor volume before undergoing resection of residual disease. Overall response rate was 45%. This regimen was associated with excessive toxicity, and the lack of complete responses in a patient cohort with favorable characteristics for response (good performance status, predominance of skin and lymph node metastatic sites) suggests that it had no advantage over less toxic treatment regimens. National Cancer Institute/Cancer Therapy Evaluation Program T89-0137. JF - The Online journal of current clinical trials AU - Sznol, M AU - Steis, R G AU - Smith, J W AU - Janik, J E AU - Sharfman, W H AU - Urba, W J AU - Fenton, R G AU - Creekmore, S P AU - Beveridge, J AU - Longo, D L AD - Clinical Research Branch, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21701. Y1 - 1992/07/01/ PY - 1992 DA - 1992 Jul 01 VL - Doc No 9 KW - Interferon-alpha KW - 0 KW - Interleukin-2 KW - Recombinant Proteins KW - interferon alfa-2a KW - 47RRR83SK7 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Nausea -- chemically induced KW - Combined Modality Therapy KW - Humans KW - Vomiting -- chemically induced KW - Adult KW - Aged KW - Middle Aged KW - Male KW - Female KW - Cisplatin -- therapeutic use KW - Interleukin-2 -- adverse effects KW - Interferon-alpha -- therapeutic use KW - Interferon-alpha -- adverse effects KW - Melanoma -- secondary KW - Interleukin-2 -- therapeutic use KW - Melanoma -- therapy KW - Cisplatin -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75541645?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Online+journal+of+current+clinical+trials&rft.atitle=Intensive+therapy+with+cisplatin%2C+interleukin-2+and+interferon-alpha-2a+in+patients+with+metastatic+melanoma.+A+phase+II+Study.&rft.au=Sznol%2C+M%3BSteis%2C+R+G%3BSmith%2C+J+W%3BJanik%2C+J+E%3BSharfman%2C+W+H%3BUrba%2C+W+J%3BFenton%2C+R+G%3BCreekmore%2C+S+P%3BBeveridge%2C+J%3BLongo%2C+D+L&rft.aulast=Sznol&rft.aufirst=M&rft.date=1992-07-01&rft.volume=Doc+No+9&rft.issue=&rft.spage=%5B3841+words%3B+32+paragraphs%5D&rft.isbn=&rft.btitle=&rft.title=The+Online+journal+of+current+clinical+trials&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-03-17 N1 - Date created - 1994-03-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alkylation of DNA by 1,3-dialkyl-3-acyltriazenes: correlation of biological activity with chemical behavior. AN - 73218601; 1391620 AB - The reactions of calf thymus DNA with four 1,3-dialkyl-3-acyltriazenes were studied alone or in the presence of pig liver esterase in pH 7.4 phosphate buffer for varying lengths of time. The best alkylating agent in the absence of esterase was determined to be 1,3-dimethyl-3-carbethoxytriazene (DMC), followed in order by 1-(2-hydroxyethyl)-3-methyl-3-carbethoxytriazene (HMC), 1-(2-hydroxyethyl)-3-methyl-3-acetyltriazene (HMA), and 1-(2- chloroethyl)-3-methyl-3-carbethoxytriazene (CMC). This order is the same as that for the rate of decomposition of the various acyltriazenes in pH 7.5 phosphate buffer. The extent of calf thymus DNA alkylation by CMC was found to be dependent on both the reaction buffer and the ionic strength of the medium. Alkylation by CMC alone in low ionic strength glycine buffer produced large quantities of 7-(2-chloroethyl)guanine and 7-(2-hydroxyethyl)guanine. The products of DNA alkylation observed at neutral pH are consistent with N(2)-N(3) heterolysis of the triazene, resulting in the N(1) alkyldiazonium ion as the sole alkylating species. In the presence of esterase, CMC showed an enhanced rate of product formation. Furthermore, the product distribution shifted dramatically from mainly hydroxyethylation to predominantly methylation. CMC is postulated to undergo initial enzymatic deacylation, leading to two different alkyldiazonium ions which competitively alkylate DNA. HMC, on the other hand, was little affected by the esterase. The enzyme-catalyzed reaction showed a small increase in methylation and a smaller decrease in hydroxyethylation.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Chemical research in toxicology AU - Kroeger-Koepke, M B AU - Michejda, C J AU - Smith, R H AD - Molecular Aspects of Drug Design Section, NCI-Frederick Cancer Research and Development Center, Maryland 21702. PY - 1992 SP - 541 EP - 547 VL - 5 IS - 4 SN - 0893-228X, 0893-228X KW - Alkylating Agents KW - 0 KW - Triazenes KW - DNA KW - 9007-49-2 KW - Esterases KW - EC 3.1.- KW - Index Medicus KW - Animals KW - Cattle KW - Esterases -- metabolism KW - Kinetics KW - Catalysis KW - Triazenes -- metabolism KW - Alkylating Agents -- metabolism KW - DNA -- metabolism KW - Triazenes -- chemistry KW - DNA -- chemistry KW - Alkylating Agents -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73218601?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=Alkylation+of+DNA+by+1%2C3-dialkyl-3-acyltriazenes%3A+correlation+of+biological+activity+with+chemical+behavior.&rft.au=Kroeger-Koepke%2C+M+B%3BMichejda%2C+C+J%3BSmith%2C+R+H&rft.aulast=Kroeger-Koepke&rft.aufirst=M&rft.date=1992-07-01&rft.volume=5&rft.issue=4&rft.spage=541&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-04 N1 - Date created - 1992-11-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - CONF T1 - Agricultural chemical utilization and human health. AN - 73218240; 1396466 AB - The public is justifiably concerned about the human health effects of agricultural chemicals. The many gaps in information about the mechanisms of toxic action, human exposures, and the nature and extent of human health effects are large. Very few older pesticides, in particular, have been tested for human health effects. Workers who produce, harvest, store, transport, process, and prepare food and fibers are exposed to many chemicals that are potentially hazardous and that are used in agriculture. The occupational health of these workers has not been adequately studied, and protective efforts have sometimes been minimal. Valid and accurate risk assessment is best based on sound information about how chemicals, in this case agricultural chemicals, are involved in toxic events--their mechanisms of action. These health effects include tumor promotion, chronic and acute neurotoxicity, immunotoxicity, and reproductive and developmental toxicity. Another key part of risk assessment is exposure assessment. Fundamental studies of the toxicology of target organisms and nontarget organisms exposed to agricultural chemicals are needed to discover and develop better solutions to the problems of agricultural pest control, including better formulations, optimal application rates and public education in safety and alternative agricultural practices. The large number of pesticides that have never been adequately tested for effects on human health is particularly worrisome in light of emerging information about delayed nervous system effects. JF - Environmental health perspectives AU - Mushak, E W AU - Piver, W T Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 269 EP - 274 VL - 97 KW - Agrochemicals KW - 0 KW - Biomarkers KW - Index Medicus KW - Research -- education KW - Humans KW - Research Design KW - Health Status Indicators KW - Environmental Exposure -- adverse effects KW - Agrochemicals -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73218240?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=Environmental+health+perspectives&rft.atitle=Agricultural+chemical+utilization+and+human+health.&rft.au=Mushak%2C+E+W%3BPiver%2C+W+T&rft.aulast=Mushak&rft.aufirst=E&rft.date=1992-07-01&rft.volume=97&rft.issue=&rft.spage=269&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-26 N1 - Date created - 1992-10-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modeling cyanide release from nitriles: prediction of cytochrome P450 mediated acute nitrile toxicity. AN - 73214882; 1391621 AB - A mechanism-based model for prediction of acute nitrile toxicity was developed using octanol-water partition coefficients (log P) and estimated rates of alpha-hydrogen atom abstraction as variables. Relative rates of hydrogen atom abstraction were derived from differences in heats of formation for ground-state and radical geometries and radical ionization potentials. Calculated energies of activation for all potential sites of oxidation for a given nitrile were used to estimate partitioning of metabolites among multiple oxidative pathways. logP and the resulting corrected rate constants for alpha-carbon oxidation were effective variables in an acute toxicity model of structurally diverse nitriles. The pharmacokinetics of substrate disposition is discussed in the context of multiple metabolic pathways. Structure-toxicity relationships are also discussed. JF - Chemical research in toxicology AU - Grogan, J AU - DeVito, S C AU - Pearlman, R S AU - Korzekwa, K R AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. PY - 1992 SP - 548 EP - 552 VL - 5 IS - 4 SN - 0893-228X, 0893-228X KW - Cyanides KW - 0 KW - Nitriles KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Thermodynamics KW - Cytochrome P-450 Enzyme System -- metabolism KW - Models, Chemical KW - Cyanides -- metabolism KW - Nitriles -- metabolism KW - Nitriles -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73214882?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=Modeling+cyanide+release+from+nitriles%3A+prediction+of+cytochrome+P450+mediated+acute+nitrile+toxicity.&rft.au=Grogan%2C+J%3BDeVito%2C+S+C%3BPearlman%2C+R+S%3BKorzekwa%2C+K+R&rft.aulast=Grogan&rft.aufirst=J&rft.date=1992-07-01&rft.volume=5&rft.issue=4&rft.spage=548&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-04 N1 - Date created - 1992-11-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cancer risk following exposure to Thorotrast: overview in relation to a case report. AN - 73185726; 1522013 AB - Radioactive measurements and histopathologic findings are described in a patient administered Thorotrast, a radiographic contrast agent, 36 y prior to death and compared with cancer risks noted in epidemiologic studies. This person [designated as U.S. Uranium Registry (USUR) Case 1001] had prearranged for donation of her body to the USUR and the National Cancer Institute for study. Elevated levels of radioactivity were noted in those organs in which excess cancers have been reported in epidemiologic surveys of Thorotrast-exposed subjects. Hepatic tissue in USUR Case 1001 was estimated to have received an average lifetime absorbed dose of 16.2 Gy, based on radiochemical analyses, consistent with the high risks for liver tumors reported in all studied populations. Thorotrast was present throughout the bone marrow of USUR Case 1001, who died secondary to complications of refractory anemia with excess blasts (RAEB). Elevated risks for acute myeloid leukemia have been noted in Thorotrast patients, and more recently, cases of RAEB and RAEB in transformation have been reported. The thorium decay series includes the bone-seeking radionuclides 224Ra and 228Ra, which have been associated with high risks for osteosarcomas, although the association between Thorotrast and bone cancer is not as convincing. The skeleton of USUR Case 1001, however, contained significant levels of radioactivity. Other tissues evaluated in USUR Case 1001 included lung, eye, kidney, and breast, which did not contain elevated levels of radioactivity. JF - Health physics AU - Travis, L B AU - Kathren, R L AU - Boice, J D AD - Radiation Epidemiology Branch, National Cancer Institute, National Institutes of Health, U.S. Department of Health and Human Services, Rockville, MD 20852. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 89 EP - 97 VL - 63 IS - 1 SN - 0017-9078, 0017-9078 KW - Contrast Media KW - 0 KW - Thorium Dioxide KW - 9XA7X17UQC KW - Index Medicus KW - Risk KW - Humans KW - Leukemia, Radiation-Induced -- etiology KW - Aged KW - Leukemia, Myeloid -- etiology KW - Liver Neoplasms -- etiology KW - Time Factors KW - Female KW - Contrast Media -- adverse effects KW - Thorium Dioxide -- adverse effects KW - Neoplasms, Radiation-Induced -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73185726?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+physics&rft.atitle=Cancer+risk+following+exposure+to+Thorotrast%3A+overview+in+relation+to+a+case+report.&rft.au=Travis%2C+L+B%3BKathren%2C+R+L%3BBoice%2C+J+D&rft.aulast=Travis&rft.aufirst=L&rft.date=1992-07-01&rft.volume=63&rft.issue=1&rft.spage=89&rft.isbn=&rft.btitle=&rft.title=Health+physics&rft.issn=00179078&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-15 N1 - Date created - 1992-10-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Amphibian tumors: a comparison of anurans and urodeles. AN - 73181722; 1520844 AB - Anuran and urodele amphibians develop spontaneous neoplasms in all major organ systems with the integumentary system a frequent target. Anurans and urodeles have spontaneous viral-associated tumors, the biological behavior of which is temperature-related. Anurans seem to have a greater frequency of spontaneous neoplasms than do urodeles and respond to chemical carcinogens in a manner analogous to mammalian species. Urodeles have greater cell regenerative capabilities than do anurans and paradoxically, are more refractory than anurans or mammalian species to chemical carcinogens in their proliferating regenerative blastema. JF - In vivo (Athens, Greece) AU - Anver, M R AD - PRI/DynCorp, Inc., National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702-1201. PY - 1992 SP - 435 EP - 437 VL - 6 IS - 4 SN - 0258-851X, 0258-851X KW - Carcinogens KW - 0 KW - Index Medicus KW - Animals KW - Species Specificity KW - Neoplasms -- veterinary KW - Urodela KW - Neoplasms -- pathology KW - Neoplasms -- chemically induced KW - Neoplasms -- epidemiology KW - Anura UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73181722?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=In+vivo+%28Athens%2C+Greece%29&rft.atitle=Amphibian+tumors%3A+a+comparison+of+anurans+and+urodeles.&rft.au=Anver%2C+M+R&rft.aulast=Anver&rft.aufirst=M&rft.date=1992-07-01&rft.volume=6&rft.issue=4&rft.spage=435&rft.isbn=&rft.btitle=&rft.title=In+vivo+%28Athens%2C+Greece%29&rft.issn=0258851X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-15 N1 - Date created - 1992-10-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - External gamma-ray counting of selected tissues from a Thorotrast patient. AN - 73179141; 1522008 AB - Results of gamma-ray measurements of selected tissues from a patient who was injected with Thorotrast almost 36 y ago are reported. The purposes of this study were: 1) to determine the relative tissue distribution and activities of specific radionuclides in the 232Th decay chain, specifically 228Ra (as measured by 228Ac), 212Pb, and 224Ra (measured directly and as measured by 212Pb), and 2) to evaluate the level of radioactive disequilibrium among the daughter products. The spleen and liver had the highest concentrations of radioactivity. Bone also appears to be a long-term sink for 232Th daughter products based on estimates from a small portion of one rib. Larynx and esophagus contained measurable activity, which may have been due to their proximity to the "Thorotrastoma." Radioactivity in the remaining measured tissues were low, as expected. Secular equilibrium could be demonstrated in bone, pancreas, larynx, esophagus, and breast. Significant disequilibrium was observed for spleen, liver, kidney, and red blood cells. Radioactivity measurements reported here will be useful in estimating radiation doses to selected tissues. Such dose estimates are valuable in refining current risk estimates (e.g., liver) and in identifying tissues at risk for further epidemiologic studies. These results, while consistent with other published studies, should be interpreted with caution since measurements were made on only one patient. JF - Health physics AU - Mays, C W AU - Aamodt, R L AU - Inn, K G AU - Brown, D R AU - Greenberg, R R AU - Iyengar, V G AU - Schima, F J AU - Slaback, L S AU - Tracy, J W AU - Lynch, T P AD - National Cancer Institute, National Institutes of Health, Rockville, MD 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 33 EP - 40 VL - 63 IS - 1 SN - 0017-9078, 0017-9078 KW - Contrast Media KW - 0 KW - Thorium Dioxide KW - 9XA7X17UQC KW - Index Medicus KW - Spleen -- metabolism KW - Humans KW - Liver -- metabolism KW - Aged KW - Tissue Distribution KW - Radioactivity KW - Bone and Bones -- metabolism KW - Time Factors KW - Female KW - Thorium Dioxide -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73179141?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+physics&rft.atitle=External+gamma-ray+counting+of+selected+tissues+from+a+Thorotrast+patient.&rft.au=Mays%2C+C+W%3BAamodt%2C+R+L%3BInn%2C+K+G%3BBrown%2C+D+R%3BGreenberg%2C+R+R%3BIyengar%2C+V+G%3BSchima%2C+F+J%3BSlaback%2C+L+S%3BTracy%2C+J+W%3BLynch%2C+T+P&rft.aulast=Mays&rft.aufirst=C&rft.date=1992-07-01&rft.volume=63&rft.issue=1&rft.spage=33&rft.isbn=&rft.btitle=&rft.title=Health+physics&rft.issn=00179078&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-15 N1 - Date created - 1992-10-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comprehensive evaluation of a Thorotrast patient: an overview. AN - 73174256; 1522002 AB - For several decades, thousands of people received Thorotrast during the course of angiography and other radiologic procedures. Eventually, as the hazards of this radioactive, radiographic contrast agent became apparent, research was initiated to further evaluate its associated adverse effects. In 1988 and 1989, Charles W. Mays, together with colleagues at a variety of sites, developed a detailed protocol for the comprehensive postmortem evaluation of one subject who had been administered Thorotrast 36 y previously. This case represents the first holistic approach to the analysis of Thorotrast in a whole body, simultaneously assembling clinical and autopsy findings with dosimetric, radiochemical, autoradiographic, and molecular evaluations. JF - Health physics AU - Travis, L B AU - Kathren, R L AU - Mays, D AU - Mays, C W AD - Epidemiology and Biostatistics Program, National Cancer Institute, National Institutes of Health, Rockville, MD 20852. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 10 EP - 12 VL - 63 IS - 1 SN - 0017-9078, 0017-9078 KW - Contrast Media KW - 0 KW - Thorium Dioxide KW - 9XA7X17UQC KW - Index Medicus KW - Humans KW - Aged KW - Tissue Distribution KW - Time Factors KW - Female KW - Contrast Media -- adverse effects KW - Thorium Dioxide -- pharmacokinetics KW - Contrast Media -- pharmacokinetics KW - Thorium Dioxide -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73174256?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+physics&rft.atitle=Comprehensive+evaluation+of+a+Thorotrast+patient%3A+an+overview.&rft.au=Travis%2C+L+B%3BKathren%2C+R+L%3BMays%2C+D%3BMays%2C+C+W&rft.aulast=Travis&rft.aufirst=L&rft.date=1992-07-01&rft.volume=63&rft.issue=1&rft.spage=10&rft.isbn=&rft.btitle=&rft.title=Health+physics&rft.issn=00179078&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-15 N1 - Date created - 1992-10-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Possible roles for nitric oxide in AIDS and associated pathology. AN - 73168170; 1513271 AB - The endogenous free radical, nitric oxide (NO), plays a neurotransmitter-like role in vascular endothelium, a second-messenger role in N-methyl-D-aspartate (NMDA)-responsive neurons in the central nervous system (CNS), a neurotoxic role after its release from these neurons, and a cytotoxic role after its release by macrophages. NO also derives from exogenous sources, such as the nitrite inhalants, amyl, butyl and isobutyl nitrite. There is evidence that abuse of nitrite inhalants can affect immunomodulation, and epidemiological studies suggest that such abuse may be a cofactor in the pathogenesis of acquired immunodeficiency syndrome (AIDS). Hitherto, however, the potential role of NO in such pathogenesis has not been examined. This paper presents some current evidence that implicates both endogenous and exogenous sources of NO in AIDS and associated pathology. JF - Medical hypotheses AU - Morgan, M J AU - Kimes, A S AU - London, E D AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 189 EP - 193 VL - 38 IS - 3 SN - 0306-9877, 0306-9877 KW - Free Radicals KW - 0 KW - Neurotoxins KW - Nitrites KW - Nitric Oxide KW - 31C4KY9ESH KW - Index Medicus KW - AIDS/HIV KW - Nitrites -- adverse effects KW - Humans KW - Pneumonia, Pneumocystis -- etiology KW - Homosexuality KW - Neurotoxins -- adverse effects KW - Administration, Inhalation KW - Male KW - Sarcoma, Kaposi -- etiology KW - Acquired Immunodeficiency Syndrome -- pathology KW - Acquired Immunodeficiency Syndrome -- complications KW - Nitric Oxide -- metabolism KW - Acquired Immunodeficiency Syndrome -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73168170?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Medical+hypotheses&rft.atitle=Possible+roles+for+nitric+oxide+in+AIDS+and+associated+pathology.&rft.au=Morgan%2C+M+J%3BKimes%2C+A+S%3BLondon%2C+E+D&rft.aulast=Morgan&rft.aufirst=M&rft.date=1992-07-01&rft.volume=38&rft.issue=3&rft.spage=189&rft.isbn=&rft.btitle=&rft.title=Medical+hypotheses&rft.issn=03069877&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-25 N1 - Date created - 1992-09-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Med Hypotheses 1993 Feb;40(2):142 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Primary chemotherapy for locally advanced uterine cervical carcinoma. AN - 73155117; 1514836 AB - From September 1985 to May 1991, thirty consecutive patients with locally advanced cervical carcinoma stage IB-II (FIGO) with high risk factors of local treatment failure were treated with Epirubicin and Cisplatinum combination as primary chemotherapy. Twenty-five patients were evaluated for response, operability and survival. This combination chemotherapy could induce remarkable clinical complete response of 68% (17/25) and partial response of 28% (7/25), but only 18 patients were permitted for surgery, therefore operability rate was 72% (18/25). Pathological examination revealed complete response at 24% (6/25) and partial response was 48% (12/25) due to the presence of residual tumor at the cervix and dissected lymph nodes. The average number of lymph node dissected was II (range 0-26), which have been usually found in stage IIB-III patients. This combination chemotherapy did not allow to complicate surgery in these circumstances. Toxicities were mild except only leukopenia which was moderate to severe degree (WHO, grading). No death related to treatment has been found. The median time of follow up was 19 months (range 4-72), 24 patients still living, 22 without disease and 2 with diseases at the cervix and bone. The result of pilot study has suggested a beneficial role of primary chemotherapy in this type of malignancy. However, these data require further confirmation and longer follow up before a definite conclusion can be made regarding cure rate and prolong disease free-survival in locally-advanced uterine cervical carcinoma. JF - Gan to kagaku ryoho. Cancer & chemotherapy AU - Cheirsilpa, A AU - Kosiyatrakul, T AU - Benjachai, W AU - Tangkrutt, S AU - Puriphat, S AD - Division of Medical Oncology, National Cancer Institute, Bangkok, Thailand. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 1224 EP - 1232 VL - 19 IS - 8 Suppl SN - 0385-0684, 0385-0684 KW - Antiemetics KW - 0 KW - Epirubicin KW - 3Z8479ZZ5X KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Drug Administration Schedule KW - Humans KW - Vomiting -- chemically induced KW - Aged KW - Epirubicin -- adverse effects KW - Cisplatin -- administration & dosage KW - Nausea -- chemically induced KW - Antiemetics -- administration & dosage KW - Survival Rate KW - Adult KW - Middle Aged KW - Follow-Up Studies KW - Cisplatin -- adverse effects KW - Epirubicin -- administration & dosage KW - Female KW - Alopecia -- chemically induced KW - Uterine Cervical Neoplasms -- drug therapy KW - Uterine Cervical Neoplasms -- mortality KW - Carcinoma, Squamous Cell -- mortality KW - Adenocarcinoma -- mortality KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Adenocarcinoma -- drug therapy KW - Carcinoma, Squamous Cell -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73155117?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gan+to+kagaku+ryoho.+Cancer+%26+chemotherapy&rft.atitle=Primary+chemotherapy+for+locally+advanced+uterine+cervical+carcinoma.&rft.au=Cheirsilpa%2C+A%3BKosiyatrakul%2C+T%3BBenjachai%2C+W%3BTangkrutt%2C+S%3BPuriphat%2C+S&rft.aulast=Cheirsilpa&rft.aufirst=A&rft.date=1992-07-01&rft.volume=19&rft.issue=8+Suppl&rft.spage=1224&rft.isbn=&rft.btitle=&rft.title=Gan+to+kagaku+ryoho.+Cancer+%26+chemotherapy&rft.issn=03850684&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-29 N1 - Date created - 1992-09-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sympathoadrenal contribution to plasma dopa (3,4-dihydroxyphenylalanine) in rats. AN - 73146295; 1325324 AB - 1. To determine the sources of dopa (3,4-dihydroxyphenylalanine) in plasma, we measured regional arteriovenous differences, tissue concentrations and urinary excretion of dopa during systemic intravenous infusions of I-[3H]dopa into anaesthetized intact rats and rats pretreated with the sympathetic neurotoxin, 6-hydroxydopamine. 2. In intact rats, large arteriovenous increments in plasma dopa concentrations were noted in the femoral (47%) and adrenal (141%) beds, with a small arterial-portal venous increment (11%), whereas in the kidney there was a substantial (47%) arteriovenous decrement in plasma dopa levels. Skeletal muscle appeared to be a major source of dopa in arterial plasma. 3. Treatment with 6-hydroxydopamine abolished the afferent-efferent increment of plasma dopa concentrations in the femoral bed. The arteriovenous decrement of plasma dopa concentrations in the kidney was preserved, and the arteriovenous increment in the adrenal bed was decreased by about half. Arterial plasma dopa levels fell by 41%. 4. Regional extraction percentages of I-[3H]dopa were used to estimate the clearances and rates of appearance (spillovers) of dopa in plasma. Dopa spillover was detected in the femoral, renal, splanchnic and adrenal beds, with skeletal muscle accounting for about 44% and the kidneys accounting for about 18% of dopa in arterial plasma. Whereas chemical sympathectomy decreased the femoral and renal spillover of dopa by 90% or more, arterial dopa levels and estimated dopa spillover into arterial plasma were decreased by only about 45%. 5. The kidneys accounted for 22% of dopa clearance from arterial plasma. From the renal extraction of I-[3H]dopa and the urinary excretion of [3H]dopamine, it was estimated that 77% of dopa removed in the kidneys was excreted as dopamine in intact animals and 69% was excreted as dopamine in sympathectomized animals. Conversely, about 80% of urinary endogenous dopamine was derived from plasma dopa, regardless of 6-hydroxydopamine treatment. 6. The results indicate that endogenous dopa in arterial plasma is derived substantially but not exclusively from sympathetic nerve endings that are destroyed by 6-hydroxydopamine, especially in skeletal muscle and the kidneys. Regional dopa spillover therefore probably reflects regional catecholamine biosynthesis. In rats, urinary dopamine is derived mainly from renal decarboxylation of circulating dopa. JF - Clinical science (London, England : 1979) AU - Grossman, E AU - Hoffman, A AU - Armando, I AU - Abassi, Z AU - Kopin, I J AU - Goldstein, D S AD - Hypertension-Endocrine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 65 EP - 74 VL - 83 IS - 1 SN - 0143-5221, 0143-5221 KW - Dihydroxyphenylalanine KW - 63-84-3 KW - Oxidopamine KW - 8HW4YBZ748 KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Kidney -- metabolism KW - Arteries KW - Muscles -- metabolism KW - Sympathectomy, Chemical KW - Femoral Artery KW - Dopamine -- urine KW - Male KW - Adrenal Glands -- metabolism KW - Dihydroxyphenylalanine -- biosynthesis KW - Sympathetic Nervous System -- metabolism KW - Dihydroxyphenylalanine -- blood KW - Adrenal Glands -- blood supply UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73146295?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+science+%28London%2C+England+%3A+1979%29&rft.atitle=Sympathoadrenal+contribution+to+plasma+dopa+%283%2C4-dihydroxyphenylalanine%29+in+rats.&rft.au=Grossman%2C+E%3BHoffman%2C+A%3BArmando%2C+I%3BAbassi%2C+Z%3BKopin%2C+I+J%3BGoldstein%2C+D+S&rft.aulast=Grossman&rft.aufirst=E&rft.date=1992-07-01&rft.volume=83&rft.issue=1&rft.spage=65&rft.isbn=&rft.btitle=&rft.title=Clinical+science+%28London%2C+England+%3A+1979%29&rft.issn=01435221&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-06 N1 - Date created - 1992-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Systemically administered antifungal agents. A review of their clinical pharmacology and therapeutic applications. AN - 73116016; 1379913 AB - Systemic antifungal agents express great diversity in their pharmacokinetic profiles, mechanisms of action, and toxicities. Understanding the diverse pharmacokinetic properties of systemic antifungals is critical to their appropriate application. Amphotericin B, drug of choice for most invasive mycoses, has unique pharmacokinetic properties, binding initially to serum lipoproteins and redistributing from blood to tissues. Dosing recommendations are based on the specific infection and the status of the host. Lipid formulations of amphotericin B may be able to attenuate some of its toxicities. Flucytosine is a water-soluble, fluorinated pyrimidine that possesses excellent bioavailability. It is administered only in combination with amphotericin B because of frequent development of secondary drug resistance, and is associated with dose-dependent bone marrow suppression. The antifungal azoles are relatively well tolerated, have broad spectrum antifungal activity, and are fungistatic in vitro. Ketoconazole and itraconazole are highly bound to plasma proteins, are extensively metabolised by the liver, and are relatively insoluble in aqueous solution. By comparison, fluconazole is only weakly bound to serum proteins, is relatively stable to metabolic conversion, and is water soluble. Fluconazole penetrates the cerebrospinal fluid well and is approved for primary and suppressive therapy of cryptococcal meningitis in AIDS patients. The echinocandins have a narrow spectrum of antifungal activity, being effective only against Candida spp. JF - Drugs AU - Lyman, C A AU - Walsh, T J AD - Pediatric Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 9 EP - 35 VL - 44 IS - 1 SN - 0012-6667, 0012-6667 KW - Antifungal Agents KW - 0 KW - Azoles KW - Drugs, Investigational KW - Amphotericin B KW - 7XU7A7DROE KW - Flucytosine KW - D83282DT06 KW - Index Medicus KW - AIDS/HIV KW - Drugs, Investigational -- therapeutic use KW - Drugs, Investigational -- pharmacokinetics KW - Flucytosine -- pharmacology KW - Drugs, Investigational -- pharmacology KW - Azoles -- therapeutic use KW - Azoles -- pharmacology KW - Humans KW - Drug Resistance, Microbial KW - Amphotericin B -- pharmacology KW - Amphotericin B -- therapeutic use KW - Flucytosine -- therapeutic use KW - Antifungal Agents -- pharmacokinetics KW - Antifungal Agents -- pharmacology KW - Mycoses -- drug therapy KW - Fungi -- drug effects KW - Antifungal Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73116016?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drugs&rft.atitle=Systemically+administered+antifungal+agents.+A+review+of+their+clinical+pharmacology+and+therapeutic+applications.&rft.au=Lyman%2C+C+A%3BWalsh%2C+T+J&rft.aulast=Lyman&rft.aufirst=C&rft.date=1992-07-01&rft.volume=44&rft.issue=1&rft.spage=9&rft.isbn=&rft.btitle=&rft.title=Drugs&rft.issn=00126667&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-17 N1 - Date created - 1992-09-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Photodynamic therapy for thoracic malignancies. AN - 73105962; 1386470 AB - Photodynamic therapy (PDT) is an experimental form of cancer therapy which employs photoactivation of a sensitizing chemical by light of a given wavelength via the production of toxic oxygen species. PDT causes local destruction of cancer, and relies on a therapeutic index between normal and malignant tissue since the latter seems to selectively retain the sensitizer. PDT has both direct tumoricidal effects as well as indirect effects on tumor vasculature causing an early hemorrhagic necrosis of tissue. The treatment has been used for the treatment of endobronchial obstruction by primary and metastatic tumors. Most recently, trials are being performed to evaluate this therapy as a surgical adjunct in the treatment of pleural malignancies such as mesothelioma. JF - Seminars in surgical oncology AU - Pass, H I AU - Pogrebniak, H AD - Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 217 EP - 225 VL - 8 IS - 4 SN - 8756-0437, 8756-0437 KW - Antineoplastic Agents KW - 0 KW - Deuteroporphyrins KW - Hematoporphyrins KW - hydroxyethylvinyldeuteroporphyrin KW - 82647-38-9 KW - Dihematoporphyrin Ether KW - 97067-70-4 KW - Index Medicus KW - Humans KW - Hematoporphyrins -- therapeutic use KW - Laser Therapy KW - Antineoplastic Agents -- therapeutic use KW - Deuteroporphyrins -- therapeutic use KW - Lung Neoplasms -- diagnosis KW - Hematoporphyrin Photoradiation KW - Lung Neoplasms -- drug therapy KW - Pleural Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73105962?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+surgical+oncology&rft.atitle=Photodynamic+therapy+for+thoracic+malignancies.&rft.au=Pass%2C+H+I%3BPogrebniak%2C+H&rft.aulast=Pass&rft.aufirst=H&rft.date=1992-07-01&rft.volume=8&rft.issue=4&rft.spage=217&rft.isbn=&rft.btitle=&rft.title=Seminars+in+surgical+oncology&rft.issn=87560437&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-28 N1 - Date created - 1992-08-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A pilot study of suramin in the treatment of progressive refractory follicular lymphomas. AN - 73103852; 1498080 AB - Ten patients with progressive follicular lymphomas (seven with follicular mixed lymphomas, three with follicular, small cleaved cell lymphomas) with clinical indications for systemic therapy received parenteral suramin. Each had failed from one to six prior chemotherapeutic regimens and three had in addition received prior radiation therapy. All had measurable disease and nine of the ten had documented bone marrow involvement at the start of therapy. Suramin was administered at an initial infusion rate of 350 mg/m2/day, which was then modified on the basis of subsequent weekly plasma suramin concentrations in order to reach a final plasma concentrations of 250-350 micrograms/ml. Treatment cycles were repeated at eight week intervals. Nine of ten patients are evaluable for response. Five of nine evaluable patients achieved a partial remission as defined by a greater than 50% decrease in the sum of the product of all measurable lesions. Sites of response include: Peripheral (five patients) and central (four patients) adenopathy, disappearance of biopsy-proven skin involvement (one patient), malignant pleural effusions (one patient) and shrinkage of an enlarged spleen (two patients). Disappearance of B symptoms occurred in the one responder with these symptoms. Response duration varied from 3 to 9 months (mean 5.6 months) with time to subsequent systemic therapy varying from 5 to 12 months (mean 8 months). Drug related toxicity included the development of polyradiculopathy (one case), liver function abnormalities (three cases), thrombocytopenia (five cases), vortex keratopathy (two cases) and bacterial infection (two cases). We conclude that suramin has significant activity against follicular lymphomas refractory to standard chemotherapy and that its precise role in the treatment of lymphoproliferative neoplasms in general warrants further investigation. JF - Annals of oncology : official journal of the European Society for Medical Oncology AU - La Rocca, R V AU - Cooper, M R AU - Stein, C A AU - Kohler, D AU - Uhrich, M AU - Weinberger, E AU - Myers, C E AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 571 EP - 573 VL - 3 IS - 7 SN - 0923-7534, 0923-7534 KW - Suramin KW - 6032D45BEM KW - Index Medicus KW - Humans KW - Adult KW - Pilot Projects KW - Suramin -- adverse effects KW - Lymphoma, Follicular -- drug therapy KW - Suramin -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73103852?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+oncology+%3A+official+journal+of+the+European+Society+for+Medical+Oncology&rft.atitle=A+pilot+study+of+suramin+in+the+treatment+of+progressive+refractory+follicular+lymphomas.&rft.au=La+Rocca%2C+R+V%3BCooper%2C+M+R%3BStein%2C+C+A%3BKohler%2C+D%3BUhrich%2C+M%3BWeinberger%2C+E%3BMyers%2C+C+E&rft.aulast=La+Rocca&rft.aufirst=R&rft.date=1992-07-01&rft.volume=3&rft.issue=7&rft.spage=571&rft.isbn=&rft.btitle=&rft.title=Annals+of+oncology+%3A+official+journal+of+the+European+Society+for+Medical+Oncology&rft.issn=09237534&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-11 N1 - Date created - 1992-09-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of DNA repair in malignant neoplastic transformation of human mammary epithelial cells in culture. AN - 73100507; 1638679 AB - Epithelial cells derived from normal human mammary tissue were examined for capacity to repair radiation-induced chromatin DNA damage. Repair capacity was estimated by quantifying chromatid aberrations in metaphase cells arrested 0.5-1.5 h after X-irradiation during G2. The parental cells at passage 12 had 19 chromatid breaks and 16 gaps per 100 metaphase cells, representing efficient repair. Of two continuous cell lines, derived after benzo[a]pyrene treatment, A1 maintained the efficient repair phenotype through passage 50, while a subline of A1 developed the repair-deficient phenotype characterized by a 3- to 5-fold higher frequency of chromatid breaks or gaps. This line was transformed to tumorigenic cells by HaMSV and SV40 T antigen. The second continuous line B5 and derivatives had 102-165 chromatid breaks and 87-134 gaps per 100 metaphases (deficient repair phenotype). This line was transformed to tumorigenic cells by KiMSV. As reported previously for human epidermal keratinocytes, acquisition of this repair-deficient phenotype appears to be an early requisite step in the malignant neoplastic transformation of human cells in culture. JF - Carcinogenesis AU - Sanford, K K AU - Price, F M AU - Rhim, J S AU - Stampfer, M R AU - Parshad, R AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 1137 EP - 1141 VL - 13 IS - 7 SN - 0143-3334, 0143-3334 KW - Chromatin KW - 0 KW - Index Medicus KW - G2 Phase -- radiation effects KW - Chromatin -- radiation effects KW - Epithelial Cells KW - Cells, Cultured KW - Humans KW - Epithelium -- physiology KW - Adult KW - Metaphase KW - Epithelium -- radiation effects KW - Female KW - Breast -- radiation effects KW - DNA Repair KW - DNA Damage KW - Cell Transformation, Neoplastic -- radiation effects KW - Breast -- cytology KW - Chromosome Aberrations KW - Breast -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73100507?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Role+of+DNA+repair+in+malignant+neoplastic+transformation+of+human+mammary+epithelial+cells+in+culture.&rft.au=Sanford%2C+K+K%3BPrice%2C+F+M%3BRhim%2C+J+S%3BStampfer%2C+M+R%3BParshad%2C+R&rft.aulast=Sanford&rft.aufirst=K&rft.date=1992-07-01&rft.volume=13&rft.issue=7&rft.spage=1137&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-28 N1 - Date created - 1992-08-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of lymphocytes infiltrating human breast cancer: specific immune reactivity detected by measuring cytokine secretion. AN - 73096897; 1637779 AB - Primary breast cancers from 19 patients and draining lymph nodes from nine of them (seven containing metastatic tumor) were used in growing tumor-infiltrating lymphocytes (TIL) in culture. TIL were studied for proliferation, phenotype, cytotoxicity, and the ability to secrete cytokines in response to autologous tumor. Lymphocytes from primary breast tumors proliferated in 15 of 19 cultures, a median of 6.7 x 10(3)-fold in 65 days. For eight of nine patients, lymphocytes derived from draining lymph nodes proliferated in culture, a median of 110-fold in 49 days. Breast TIL became predominantly CD4+ cells over time in culture and were 73% CD4+ and 21% CD8+ (means) at 63 days (median). Lymph node lymphocytes were 63% CD4+ at 51 days. TIL were poorly lytic in 4-hour 51Cr release assays. Lysis of autologous tumor occurred in only one of 12 breast TIL and one of nine lymph node cultures. This lysis was low (15% at effector:target = 40:1) and was nonspecific (non-major-histocompatibility-complex restricted). Cytokine secretion was tested by co-culturing TIL with autologous or allogeneic tumors for 24 hours. Cytokines were measured in culture supernatants by enzyme-linked immunosorbent assay or radioimmunoassay. TIL from three of 11 patients specifically secreted granulocyte macrophage-colony-stimulating factor, tumor necrosis factor-alpha and interferon-gamma when stimulated by autologous tumor and not by a panel of four to five allogeneic breast cancers. Cytokine secretion has made possible the identification of lymphocytes infiltrating breast cancers with specific immune reactivity. This finding will guide the development of new immunotherapies for patients with breast cancer. JF - Journal of immunotherapy : official journal of the Society for Biological Therapy AU - Schwartzentruber, D J AU - Solomon, D AU - Rosenberg, S A AU - Topalian, S L AD - Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 1 EP - 12 VL - 12 IS - 1 SN - 1053-8550, 1053-8550 KW - Cytokines KW - 0 KW - HLA Antigens KW - HLA-D Antigens KW - Histocompatibility Antigens Class I KW - Index Medicus KW - HLA-D Antigens -- analysis KW - Tumor Cells, Cultured KW - Lymphatic Metastasis KW - Cells, Cultured KW - Cell Division -- immunology KW - Humans KW - HLA Antigens -- immunology KW - Cytotoxicity Tests, Immunologic KW - Histocompatibility Antigens Class I -- analysis KW - Immunophenotyping KW - Immunohistochemistry KW - Female KW - Breast Neoplasms -- immunology KW - Lymphocytes, Tumor-Infiltrating -- secretion KW - Lymphocytes, Tumor-Infiltrating -- immunology KW - Breast Neoplasms -- pathology KW - Cytokines -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73096897?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunotherapy+%3A+official+journal+of+the+Society+for+Biological+Therapy&rft.atitle=Characterization+of+lymphocytes+infiltrating+human+breast+cancer%3A+specific+immune+reactivity+detected+by+measuring+cytokine+secretion.&rft.au=Schwartzentruber%2C+D+J%3BSolomon%2C+D%3BRosenberg%2C+S+A%3BTopalian%2C+S+L&rft.aulast=Schwartzentruber&rft.aufirst=D&rft.date=1992-07-01&rft.volume=12&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunotherapy+%3A+official+journal+of+the+Society+for+Biological+Therapy&rft.issn=10538550&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-31 N1 - Date created - 1992-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A role for behavioral sensitization in uncontrolled ethanol intake. AN - 73090560; 1637498 AB - The processes that underlie the transition from controlled to uncontrolled consumption of ethanol are unknown. Behavioral sensitization is proposed as one of these processes and occurs with repeated administration of psychomotor stimulants whereby both behavioral and neurochemical responses to the drugs are progressively enhanced. Because ethanol shares some actions in common with these drugs, chronic exposure to ethanol may intensify its reinforcing properties. The effect of ethanol on several behavioral models suggests that behavioral sensitization may develop especially in the presence of environmental cues. Thus, a research opportunity exists to study factors that contribute to an increasing probability of progressively higher ethanol consumption. Knowledge of these factors will lead to a better understanding of why some people drink uncontrollably. JF - Alcohol (Fayetteville, N.Y.) AU - Hunt, W A AU - Lands, W E AD - Division of Basic Research, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857. PY - 1992 SP - 327 EP - 328 VL - 9 IS - 4 SN - 0741-8329, 0741-8329 KW - Index Medicus KW - Environment KW - Animals KW - Humans KW - Alcoholism -- physiopathology KW - Behavior -- physiology KW - Alcohol Drinking KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73090560?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcohol+%28Fayetteville%2C+N.Y.%29&rft.atitle=A+role+for+behavioral+sensitization+in+uncontrolled+ethanol+intake.&rft.au=Hunt%2C+W+A%3BLands%2C+W+E&rft.aulast=Hunt&rft.aufirst=W&rft.date=1992-07-01&rft.volume=9&rft.issue=4&rft.spage=327&rft.isbn=&rft.btitle=&rft.title=Alcohol+%28Fayetteville%2C+N.Y.%29&rft.issn=07418329&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-03 N1 - Date created - 1992-09-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chemical modification and irreversible inhibition of striatal A2a adenosine receptors. AN - 73089495; 1635550 AB - The ligand recognition site of A2a-adenosine receptors in rabbit striatal membranes was probed using non-site-directed labeling reagents and specific affinity labels. Exposure of membranes to diethylpyrocarbonate at a concentration of 2.5 mM, followed by washing, was found to inhibit the binding of [3H]CGS 21680 and [3H]xanthine amine congener to A2a receptors, by 86 and 30%, respectively. Protection from diethylpyrocarbonate inactivation by an adenosine receptor agonist, 5'-N-ethylcarboxamidoadenosine, and an antagonist, theophylline, suggested the presence of two histidyl residues on the receptor, one associated with agonist binding and the other with antagonist binding. Binding of [3H]CGS 21680 or [3H]xanthine amine congener was partially restored after incubation with 250 mM hydroxylamine, further supporting histidine as the modification site. Preincubation with disulfide-reactive reagents, dithiothreitol or sodium dithionite, at greater than 5 mM inhibited radioligand binding, indicating the presence of essential disulfide bridges in A2a receptors, whereas the concentration of mercaptoethanol required to inhibit binding was greater than 50 mM. A number of isothiocyanate-bearing affinity labels derived from the A2a-selective agonist 2-[(2-aminoethylamino) carbonylethylphenylethylamino]-5'-N- ethylcarboxamidoadenosine (APEC) were synthesized and found to inhibit A2a receptor binding in rabbit and bovine striatal membranes. Binding to rabbit A1 receptors was not inhibited. Preincubation with the affinity label 4-isothiocyanatophenylaminothiocarbonyl-APEC (100 nM) diminished the Bmax for [3H]CGS 21680 binding by 71%, and the Kd was unaffected, suggesting a direct modification of the ligand binding site. Reversal of 4-isothiocyanatophenylaminothiocarbonyl-APEC inhibition of [3H]CGS 21680 binding with hydroxylamine suggested that the site of modification by the isothiocyanate is a cysteine residue. A bromoacetyl derivative of APEC was ineffective as an affinity label at submicromolar concentrations. JF - Molecular pharmacology AU - Jacobson, K A AU - Stiles, G L AU - Ji, X D AD - Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 123 EP - 133 VL - 42 IS - 1 SN - 0026-895X, 0026-895X KW - Affinity Labels KW - 0 KW - Hydroxylamines KW - Phenethylamines KW - Purinergic Antagonists KW - Receptors, Purinergic KW - Xanthines KW - 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine KW - 120225-54-9 KW - Hydroxylamine KW - 2FP81O2L9Z KW - Adenosine-5'-(N-ethylcarboxamide) KW - 35920-39-9 KW - 8-(4-((2-aminoethyl)aminocarbonylmethyloxy)phenyl)-1,3-dipropylxanthine KW - 96865-92-8 KW - Theophylline KW - C137DTR5RG KW - Adenosine KW - K72T3FS567 KW - Diethyl Pyrocarbonate KW - LMR3LZG146 KW - Index Medicus KW - Animals KW - Adenosine -- analogs & derivatives KW - Xanthines -- metabolism KW - Rabbits KW - Amino Acid Sequence KW - Radioligand Assay KW - Receptors, Purinergic -- drug effects KW - Receptors, Purinergic -- metabolism KW - Phenethylamines -- metabolism KW - Adenosine -- pharmacology KW - Theophylline -- pharmacology KW - Diethyl Pyrocarbonate -- pharmacology KW - Molecular Sequence Data KW - Receptors, Purinergic -- chemistry KW - Hydroxylamines -- pharmacology KW - Drug Antagonism KW - Adenosine -- metabolism KW - Corpus Striatum -- metabolism KW - Corpus Striatum -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73089495?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=Chemical+modification+and+irreversible+inhibition+of+striatal+A2a+adenosine+receptors.&rft.au=Jacobson%2C+K+A%3BStiles%2C+G+L%3BJi%2C+X+D&rft.aulast=Jacobson&rft.aufirst=K&rft.date=1992-07-01&rft.volume=42&rft.issue=1&rft.spage=123&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=0026895X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-21 N1 - Date created - 1992-08-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Pharmacol Exp Ther. 1991 Oct;259(1):286-94 [1920121] Biochem Pharmacol. 1990 Aug 15;40(4):835-42 [2143656] Methods Enzymol. 1977;47:431-42 [22021] Mol Pharmacol. 1992 Feb;41(2):352-9 [1311411] Med Res Rev. 1992 Sep;12(5):423-71 [1513184] Neurochem Int. 1991;18(2):207-13 [20504695] Mol Pharmacol. 1988 Dec;34(6):724-8 [3200248] J Biol Chem. 1988 Nov 25;263(33):17522-6 [3182861] FEBS Lett. 1985 May 6;184(1):30-5 [2985445] Naunyn Schmiedebergs Arch Pharmacol. 1988 Jan;337(1):64-8 [2835689] Proc Natl Acad Sci U S A. 1989 Sep;86(17):6572-6 [2771944] J Med Chem. 1989 May;32(5):1043-51 [2709373] J Pharmacol Exp Ther. 1989 Dec;251(3):888-93 [2600819] J Mol Recognit. 1989 Dec;2(4):170-8 [2561548] Science. 1989 May 5;244(4904):569-72 [2541503] Physiol Rev. 1990 Jul;70(3):761-845 [2194223] Mol Pharmacol. 1991 Jul;40(1):1-7 [1857334] Bioconjug Chem. 1991 Mar-Apr;2(2):77-88 [1868116] Mol Pharmacol. 1991 Feb;39(2):130-5 [1899902] Mol Pharmacol. 1991 Nov;40(5):639-47 [1944235] Biochem Pharmacol. 1991 Mar 1;41(5):735-42 [1998528] FEBS Lett. 1990 Oct 29;273(1-2):6-10 [2121544] Biochem Biophys Res Commun. 1990 Dec 31;173(3):1169-78 [2125216] J Clin Invest. 1990 Apr;85(4):1150-7 [2156895] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Parkinsonism-inducing neurotoxin MPP+: uptake and toxicity in nonneuronal COS cells expressing dopamine transporter cDNA. AN - 73084197; 1642464 AB - Expression of a cloned dopamine transporter complementary DNA in COS cells allows these primate kidney cells to accumulate the parkinsonism-inducing neurotoxin metabolite MPP+ (1-methyl-4-phenylpyridinium) avidly, and MPP+ toxicity results. By documenting that the dopamine transporter can confer MPP+ sensitivity to nonneural cells, these results highlight the key role that this transporter could play in mechanisms underlying parkinsonism. JF - Annals of neurology AU - Kitayama, S AU - Shimada, S AU - Uhl, G R AD - Laboratory of Molecular Neurobiology, Addiction Research Center/National Institute on Drug Abuse, Johns Hopkins University School of Medicine, Baltimore, MD. 21224. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 109 EP - 111 VL - 32 IS - 1 SN - 0364-5134, 0364-5134 KW - Carrier Proteins KW - 0 KW - Dopamine Plasma Membrane Transport Proteins KW - Membrane Glycoproteins KW - Membrane Transport Proteins KW - Nerve Tissue Proteins KW - Neurotoxins KW - DNA KW - 9007-49-2 KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Index Medicus KW - Animals KW - Neurotoxins -- pharmacokinetics KW - Neurotoxins -- poisoning KW - Nerve Tissue Proteins -- genetics KW - Cell Line KW - Parkinson Disease, Secondary -- chemically induced KW - Kidney -- metabolism KW - 1-Methyl-4-phenylpyridinium -- pharmacokinetics KW - DNA -- metabolism KW - Carrier Proteins -- genetics KW - 1-Methyl-4-phenylpyridinium -- poisoning KW - Kidney -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73084197?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+neurology&rft.atitle=Parkinsonism-inducing+neurotoxin+MPP%2B%3A+uptake+and+toxicity+in+nonneuronal+COS+cells+expressing+dopamine+transporter+cDNA.&rft.au=Kitayama%2C+S%3BShimada%2C+S%3BUhl%2C+G+R&rft.aulast=Kitayama&rft.aufirst=S&rft.date=1992-07-01&rft.volume=32&rft.issue=1&rft.spage=109&rft.isbn=&rft.btitle=&rft.title=Annals+of+neurology&rft.issn=03645134&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-01 N1 - Date created - 1992-09-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Drug abuse related emergency room episodes in the United States. AN - 73079165; 1643400 AB - Drug-related hospital emergency room cases provide one measure of the morbidity associated with drug abuse. Over time, they indicate if problems associated with particular drugs are increasing or decreasing. These trends may be influenced by a number of factors including increased prevalence of use, increased dosages, increased potency, increased frequency of use, the aging of drug addicts, the use of more dangerous routes of administration, and the combined use of two or more drugs. The primary source of this information in the United States is the Drug Abuse Warning Network (DAWN). This paper will present statistics on the drug-related emergencies reported to the DAWN system for 1989 and 1990. In addition to numbers of drug-related emergencies, this paper includes the population based rates for drug-related emergencies in 1990. JF - British journal of addiction AU - Kopstein, A AD - Division of Epidemiology and Prevention Research, National Institute on Drug Abuse, Rockville, Maryland 20852. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 1071 EP - 1075 VL - 87 IS - 7 SN - 0952-0481, 0952-0481 KW - Psychotropic Drugs KW - 0 KW - Street Drugs KW - Index Medicus KW - Cross-Sectional Studies KW - Humans KW - Adult KW - Incidence KW - Middle Aged KW - Child KW - Adolescent KW - United States -- epidemiology KW - Male KW - Female KW - Street Drugs -- adverse effects KW - Substance-Related Disorders -- complications KW - Emergency Service, Hospital -- utilization KW - Psychotropic Drugs -- adverse effects KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73079165?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+addiction&rft.atitle=Drug+abuse+related+emergency+room+episodes+in+the+United+States.&rft.au=Kopstein%2C+A&rft.aulast=Kopstein&rft.aufirst=A&rft.date=1992-07-01&rft.volume=87&rft.issue=7&rft.spage=1071&rft.isbn=&rft.btitle=&rft.title=British+journal+of+addiction&rft.issn=09520481&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-10 N1 - Date created - 1992-09-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Addiction. 1993 Feb;88(2):281-3 [8292181] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phthalate ester effects on rat Sertoli cell function in vitro: effects of phthalate side chain and age of animal. AN - 73077105; 1321518 AB - Mono(2-ethylhexyl) phthalate (MEHP), the active metabolite of the testicular toxicant di(2-ethylhexyl) phthalate, inhibits FSH-stimulated rat Sertoli cell cAMP accumulation, stimulates basal lactate production, and decreases intracellular ATP levels in vitro. Dibutyl phthalate and dipentyl phthalate but not diethyldimethyl or dipropyl are also age-dependent testicular toxicants in vivo. We therefore examined the effect of animal age and phthalate monoester on the Sertoli cell FSH-stimulated cAMP accumulation, lactate secretion, and ATP levels in order to determine if these effects are part of the mechanism of action of phthalate esters in vivo. MEHP, monobutyl and monopentyl phthalates but not the monoethyl, monomethyl, or monopropyl phthalates inhibited FSH-stimulated cAMP accumulation, a segregation which matches the in vivo toxicity potential of these agents. MEHP and monopentyl, but not monobutyl phthalates, also stimulated Sertoli cell lactate secretion. The effect of the active phthalates on FSH-stimulated cAMP accumulation and lactate secretion is not dependent on age of animal over a range of 13-80 days, suggesting that the age-related toxicity in vivo may be related to differences in metabolism and disposition rather than tissue sensitivity. Since the ED50 of MEHP inhibition of cAMP accumulation and lactate secretion is similar, these two effects may be related to a common initial effect of the active phthalates. Inhibition of intracellular ATP levels is specific for MEHP and is lost with age (greater than 28 days of age) and thus is not likely to be an essential part of the in vivo mechanism of action of phthalate diesters. JF - Toxicology and applied pharmacology AU - Heindel, J J AU - Powell, C J AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 116 EP - 123 VL - 115 IS - 1 SN - 0041-008X, 0041-008X KW - Lactates KW - 0 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Follicle Stimulating Hormone KW - 9002-68-0 KW - Diethylhexyl Phthalate KW - C42K0PH13C KW - Cyclic AMP KW - E0399OZS9N KW - mono-(2-ethylhexyl)phthalate KW - FU2EWB60RT KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Lactates -- metabolism KW - Cells, Cultured KW - Adenosine Triphosphate -- metabolism KW - Cyclic AMP -- metabolism KW - Follicle Stimulating Hormone -- pharmacology KW - Male KW - Sertoli Cells -- secretion KW - Sertoli Cells -- drug effects KW - Sertoli Cells -- cytology KW - Diethylhexyl Phthalate -- toxicity KW - Aging KW - Diethylhexyl Phthalate -- chemistry KW - Diethylhexyl Phthalate -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73077105?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Phthalate+ester+effects+on+rat+Sertoli+cell+function+in+vitro%3A+effects+of+phthalate+side+chain+and+age+of+animal.&rft.au=Heindel%2C+J+J%3BPowell%2C+C+J&rft.aulast=Heindel&rft.aufirst=J&rft.date=1992-07-01&rft.volume=115&rft.issue=1&rft.spage=116&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=0041008X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-18 N1 - Date created - 1992-08-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Drug treatment of canine acral lick. An animal model of obsessive-compulsive disorder. AN - 73063547; 1385694 AB - Canine acral lick dermatitis is a naturally occurring disorder in which excessive licking of paws or flank can produce ulcers and infection that require medical treatment. Forty-two dogs with severe chronic canine acral lick dermatitis were treated in three double-blind crossover comparisons of clomipramine hydrochloride/desipramine hydrochloride, fluoxetine hydrochloride/fenfluramine hydrochloride, and sertraline hydrochloride/placebo. The serotonin uptake blocking drugs were clinically effective, while the other drugs were not. Based on phenomenology and pharmacological response, we propose canine acral lick dermatitis as an animal model of obsessive-compulsive disorder. JF - Archives of general psychiatry AU - Rapoport, J L AU - Ryland, D H AU - Kriete, M AD - Child Psychiatry Branch, National Institute of Mental Health, Bethesda, Md. 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 517 EP - 521 VL - 49 IS - 7 SN - 0003-990X, 0003-990X KW - Neurotransmitter Uptake Inhibitors KW - 0 KW - Fluoxetine KW - 01K63SUP8D KW - Fenfluramine KW - 2DS058H2CF KW - Serotonin KW - 333DO1RDJY KW - 1-Naphthylamine KW - 9753I242R5 KW - Clomipramine KW - NUV44L116D KW - Sertraline KW - QUC7NX6WMB KW - Desipramine KW - TG537D343B KW - Abridged Index Medicus KW - Index Medicus KW - Ulcer -- drug therapy KW - Animals KW - Double-Blind Method KW - Humans KW - Fenfluramine -- therapeutic use KW - Clomipramine -- therapeutic use KW - 1-Naphthylamine -- analogs & derivatives KW - Ulcer -- veterinary KW - Desipramine -- therapeutic use KW - Dogs KW - Fluoxetine -- therapeutic use KW - Follow-Up Studies KW - 1-Naphthylamine -- therapeutic use KW - Obsessive-Compulsive Disorder -- physiopathology KW - Serotonin -- physiology KW - Dermatitis -- veterinary KW - Obsessive-Compulsive Disorder -- drug therapy KW - Grooming -- drug effects KW - Grooming -- physiology KW - Dog Diseases -- drug therapy KW - Disease Models, Animal KW - Neurotransmitter Uptake Inhibitors -- therapeutic use KW - Dermatitis -- drug therapy KW - Dog Diseases -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73063547?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+general+psychiatry&rft.atitle=Drug+treatment+of+canine+acral+lick.+An+animal+model+of+obsessive-compulsive+disorder.&rft.au=Rapoport%2C+J+L%3BRyland%2C+D+H%3BKriete%2C+M&rft.aulast=Rapoport&rft.aufirst=J&rft.date=1992-07-01&rft.volume=49&rft.issue=7&rft.spage=517&rft.isbn=&rft.btitle=&rft.title=Archives+of+general+psychiatry&rft.issn=0003990X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-12 N1 - Date created - 1992-08-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selective interaction of beta 2- and alpha 2-adrenergic receptors with stimulatory and inhibitory guanine nucleotide-binding proteins. AN - 73063101; 1321955 AB - In Chinese hamster ovary cells expressing recombinant beta 2-adrenergic receptors, isoproterenol enhanced cholera toxin-catalyzed ADP-ribosylation of the large form of G5 alpha. The effect was stereoselectively blocked by the enantiomers of propranolol, indicating receptor mediation. The ADP-ribosylated form of Gs alpha-subunit was resolved into a triplet in gradient gels. beta 2-Adrenergic receptors increased both the labelling and the apparent mass of the slower migrating forms of large Gs alpha, as determined by autoradiography and immunoblotting, suggesting that Gs alpha, can incorporate more than one ADP-ribose per molecule. In cells coexpressing similar amounts of beta 2-adrenergic, alpha 2-adrenergic, and m1 muscarinic receptors, beta 2 receptors stimulated the ADP-ribosylation of only large Gs and alpha 2 receptors that of only Gi; muscarinic receptors had no apparent effect. Thus, in native membranes there appears to be a selectivity for the interaction between adrenergic receptor subtypes and Gs alpha or Gi alpha subunits. JF - Molecular pharmacology AU - Ogino, Y AU - Fraser, C M AU - Costa, T AD - Laboratory of Theoretical and Physical Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 6 EP - 9 VL - 42 IS - 1 SN - 0026-895X, 0026-895X KW - Receptors, Adrenergic, alpha KW - 0 KW - Receptors, Adrenergic, beta KW - Recombinant Proteins KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Cholera Toxin KW - 9012-63-9 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Isoproterenol KW - L628TT009W KW - Index Medicus KW - Animals KW - Blotting, Western KW - Recombinant Proteins -- metabolism KW - Electrophoresis, Polyacrylamide Gel KW - Humans KW - Cholera Toxin -- pharmacology KW - CHO Cells KW - Autoradiography KW - Adenosine Diphosphate Ribose -- metabolism KW - Isoproterenol -- pharmacology KW - Cricetinae KW - Receptors, Adrenergic, beta -- metabolism KW - GTP-Binding Proteins -- metabolism KW - Receptors, Adrenergic, alpha -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73063101?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=Selective+interaction+of+beta+2-+and+alpha+2-adrenergic+receptors+with+stimulatory+and+inhibitory+guanine+nucleotide-binding+proteins.&rft.au=Ogino%2C+Y%3BFraser%2C+C+M%3BCosta%2C+T&rft.aulast=Ogino&rft.aufirst=Y&rft.date=1992-07-01&rft.volume=42&rft.issue=1&rft.spage=6&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=0026895X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-21 N1 - Date created - 1992-08-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Recombinant anti-erbB2 immunotoxins containing Pseudomonas exotoxin. AN - 73055343; 1352878 AB - Immunotoxins were made using five different murine monoclonal antibodies to the human erbB2 gene product and LysPE40, a 40-kDa recombinant form of Pseudomonas exotoxin (PE) lacking its cell-binding domain. All five conjugates were specifically cytotoxic to cancer cell lines overexpressing erbB2 protein. The most active conjugate was e23-LysPE40, generated by chemical crosslinking of anti-erbB2 monoclonal antibody e23 to LysPE40. In addition, a recombinant immunotoxin, e23(Fv)PE40, was constructed that consists of the light-chain variable domain of e23 connected through a peptide linker to its heavy-chain variable domain, which in turn is fused to PE40. The recombinant protein was made in Escherichia coli, purified to near homogeneity, and shown to selectively kill cells expressing the erbB2 protooncogene. To improve the cytotoxic activity of e23(Fv)PE40, PE40 was replaced with a variant, PE38KDEL, in which the carboxyl end of PE is changed from Arg-Glu-Asp-Leu-Lys to Lys-Asp-Glu-Leu and amino acids 365-380 of PE are deleted. The e23(Fv)PE38KDEL protein inhibits the growth of tumors formed by the human gastric cancer cell line N87 in immunodeficient mice. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Batra, J K AU - Kasprzyk, P G AU - Bird, R E AU - Pastan, I AU - King, C R AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/07/01/ PY - 1992 DA - 1992 Jul 01 SP - 5867 EP - 5871 VL - 89 IS - 13 SN - 0027-8424, 0027-8424 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Immunotoxins KW - Oligodeoxyribonucleotides KW - Proto-Oncogene Proteins KW - Receptors, Cell Surface KW - Recombinant Fusion Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Receptor, ErbB-2 KW - EC 2.7.10.1 KW - Index Medicus KW - Animals KW - Antibody-Dependent Cell Cytotoxicity KW - Immunotherapy KW - Amino Acid Sequence KW - Mice KW - Mice, Nude KW - Recombinant Fusion Proteins -- toxicity KW - Structure-Activity Relationship KW - Neoplasm Transplantation KW - Cytotoxicity, Immunologic KW - Base Sequence KW - Tumor Cells, Cultured KW - Oligodeoxyribonucleotides -- chemistry KW - In Vitro Techniques KW - Stomach Neoplasms -- therapy KW - Molecular Sequence Data KW - Bacterial Toxins -- chemistry KW - Bacterial Toxins -- toxicity KW - Pseudomonas aeruginosa KW - Immunotoxins -- chemistry KW - Receptors, Cell Surface -- immunology KW - Proto-Oncogene Proteins -- immunology KW - Exotoxins -- toxicity KW - Exotoxins -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73055343?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Recombinant+anti-erbB2+immunotoxins+containing+Pseudomonas+exotoxin.&rft.au=Batra%2C+J+K%3BKasprzyk%2C+P+G%3BBird%2C+R+E%3BPastan%2C+I%3BKing%2C+C+R&rft.aulast=Batra&rft.aufirst=J&rft.date=1992-07-01&rft.volume=89&rft.issue=13&rft.spage=5867&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-14 N1 - Date created - 1992-08-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1991 Nov 22;254(5035):1173-7 [1683495] Nature. 1970 Aug 15;227(5259):680-5 [5432063] Mol Cell Biol. 1991 Apr;11(4):2200-5 [2005905] Proc Natl Acad Sci U S A. 1990 Feb;87(3):1066-70 [2105495] Nature. 1989 Jun 1;339(6223):394-7 [2498664] J Biol Chem. 1989 Aug 25;264(24):14256-61 [2503515] Br J Cancer. 1988 Oct;58(4):453-7 [2849975] Science. 1987 Jul 10;237(4811):178-82 [2885917] Proc Natl Acad Sci U S A. 1987 Oct;84(20):7159-63 [2890160] EMBO J. 1987 Mar;6(3):605-10 [3034598] J Biol Chem. 1988 Jul 5;263(19):9470-5 [3132465] Cancer Res. 1987 Nov 15;47(22):6123-5 [3664511] Science. 1987 Jan 9;235(4785):177-82 [3798106] Cancer Res. 1992 May 15;52(10):2771-6 [1349849] Proc Natl Acad Sci U S A. 1991 Oct 1;88(19):8616-20 [1924323] Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3358-62 [2014255] Science. 1989 May 12;244(4905):707-12 [2470152] Proc Natl Acad Sci U S A. 1989 Nov;86(21):8545-9 [2510169] Lancet. 1986 Apr 5;1(8484):765-7 [2870269] Science. 1985 Sep 6;229(4717):974-6 [2992089] Cell. 1987 Jan 16;48(1):129-36 [3098436] Science. 1987 Nov 20;238(4830):1098-104 [3317828] J Biol Chem. 1991 Sep 15;266(26):17376-81 [1910044] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Adaptive control with feedback strategies for suramin dosing. AN - 73052884; 1623689 AB - Suramin, a drug used in the treatment of parasitic diseases, is currently being evaluated in clinical trials as an antineoplastic agent. The use of therapeutic drug monitoring and adaptive control with feedback in clinical trials of suramin was initially motivated by an association between acute neurologic toxicity and plasma suramin concentrations in excess of 350 micrograms/ml. We have prospectively examined the performance of both two- and three-compartment population pharmacokinetic models in controlling plasma suramin concentrations and have found that a three-compartment model best describes this drug. No correlation was found between the clearance of suramin and creatinine clearance, as had been previously hypothesized. The low systemic clearance of suramin and the number of parameters required to describe the three-compartment model suggest the need for a bayesian approach to the estimation of individual pharmacokinetics. JF - Clinical pharmacology and therapeutics AU - Cooper, M R AU - Lieberman, R AU - La Rocca, R V AU - Gernt, P R AU - Weinberger, M S AU - Headlee, D J AU - Kohler, D R AU - Goldspiel, B R AU - Peck, C C AU - Myers, C E AD - Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 11 EP - 23 VL - 52 IS - 1 SN - 0009-9236, 0009-9236 KW - Antineoplastic Agents KW - 0 KW - Suramin KW - 6032D45BEM KW - Creatinine KW - AYI8EX34EU KW - Abridged Index Medicus KW - Index Medicus KW - Software KW - Prospective Studies KW - Infusions, Intravenous KW - Humans KW - Bayes Theorem KW - Nervous System Diseases -- blood KW - Creatinine -- pharmacokinetics KW - Nervous System Diseases -- chemically induced KW - Models, Biological KW - Drug Monitoring -- methods KW - Suramin -- adverse effects KW - Antineoplastic Agents -- administration & dosage KW - Adrenal Gland Neoplasms -- blood KW - Suramin -- pharmacokinetics KW - Suramin -- administration & dosage KW - Adrenal Gland Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73052884?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+pharmacology+and+therapeutics&rft.atitle=Adaptive+control+with+feedback+strategies+for+suramin+dosing.&rft.au=Cooper%2C+M+R%3BLieberman%2C+R%3BLa+Rocca%2C+R+V%3BGernt%2C+P+R%3BWeinberger%2C+M+S%3BHeadlee%2C+D+J%3BKohler%2C+D+R%3BGoldspiel%2C+B+R%3BPeck%2C+C+C%3BMyers%2C+C+E&rft.aulast=Cooper&rft.aufirst=M&rft.date=1992-07-01&rft.volume=52&rft.issue=1&rft.spage=11&rft.isbn=&rft.btitle=&rft.title=Clinical+pharmacology+and+therapeutics&rft.issn=00099236&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-10 N1 - Date created - 1992-08-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Population-based monitoring of an urban HIV/AIDS epidemic. Magnitude and trends in the District of Columbia. AN - 73046291; 1619741 AB - To assess the extent of the human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS) epidemic in the District of Columbia and demonstrate an approach to monitoring HIV infection and projecting AIDS incidence at a community level. Backcalculation methods to reconstruct HIV incidence from AIDS incidence in subgroups. Results were compared with directly measured HIV seroprevalence in selected sentinel populations: childbearing women, civilian applicants for military service, and hospital patients admitted for conditions unrelated to HIV infection. Between the start of the epidemic in 1980 and January 1, 1991, one in 57 District of Columbia men aged 20 to 64 years was diagnosed with AIDS. Unlike the plateau projected for the nation, AIDS incidence for the District of Columbia was projected to increase by 34% between 1990 and 1994. Models of HIV infection incidence suggested two broad epidemic waves of approximately equal size. The first occurred in men who have sex with men and peaked during the period from 1982 through 1983. The second began in the mid-1980s in injecting drug users and heterosexuals. We estimated that among District of Columbia residents aged 20 to 64 years, 0.3% of white women, 2.9% of white men, 1.6% of black women, and 4.9% of black men were living with HIV infection as of January 1, 1991. These estimates are broadly consistent with survey data: among black childbearing women in their 20s, HIV prevalence doubled to 2% between the fall of 1989 and the spring of 1991; from military applicant data, we estimated that over 5% of black men born from 1951 through 1967 were HIV-positive; in the sentinel hospital, HIV prevalence rates among male patients aged 25 to 34 years were 11.3% in white men and 16.9% in black men. Backcalculation and surveys yielded quantitatively consistent estimates of HIV prevalence. Many injecting drug users and heterosexuals in the District of Columbia were infected after January 1, 1986. Similar monitoring of the epidemic in other localities is needed to focus efforts to reduce the incidence of HIV transmission. JF - JAMA AU - Rosenberg, P S AU - Levy, M E AU - Brundage, J F AU - Petersen, L R AU - Karon, J M AU - Fears, T R AU - Gardner, L I AU - Gail, M H AU - Goedert, J J AU - Blattner, W A AD - Epidemiologic Methods Section, National Cancer Institute, Rockville, Md 20892. PY - 1992 SP - 495 EP - 503 VL - 268 IS - 4 SN - 0098-7484, 0098-7484 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - HIV Seroprevalence -- trends KW - Humans KW - Models, Statistical KW - Pregnancy KW - Population Surveillance KW - Military Personnel KW - Adult KW - District of Columbia -- epidemiology KW - Incidence KW - Middle Aged KW - Substance Abuse, Intravenous -- complications KW - African Continental Ancestry Group KW - Female KW - Male KW - Acquired Immunodeficiency Syndrome -- ethnology KW - Acquired Immunodeficiency Syndrome -- epidemiology KW - Urban Health -- statistics & numerical data KW - HIV Infections -- ethnology KW - Disease Outbreaks KW - HIV Infections -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73046291?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=JAMA&rft.atitle=Population-based+monitoring+of+an+urban+HIV%2FAIDS+epidemic.+Magnitude+and+trends+in+the+District+of+Columbia.&rft.au=Rosenberg%2C+P+S%3BLevy%2C+M+E%3BBrundage%2C+J+F%3BPetersen%2C+L+R%3BKaron%2C+J+M%3BFears%2C+T+R%3BGardner%2C+L+I%3BGail%2C+M+H%3BGoedert%2C+J+J%3BBlattner%2C+W+A&rft.aulast=Rosenberg&rft.aufirst=P&rft.date=1992-07-01&rft.volume=268&rft.issue=4&rft.spage=495&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-31 N1 - Date created - 1992-07-31 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: JAMA. 1993 Jan 27;269(4):472-3 [8481178] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Disruption of a silencer domain by a retrotransposon. AN - 73044117; 1321064 AB - A galactose-inducible Ty element carrying the HIS3 gene has been used as an insertional mutagen to generate alpha-factor resistant mutants. This collection of Ty-induced mutations includes insertions into the gene for the alpha-factor receptor (STE2), several nonspecific STE genes, and mutations that lead to the expression of the normally silent HML alpha locus. The hml alpha "on" mutations fall into two classes, those that disrupt trans-acting regulators involved in silencing HML alpha and a novel class of mutations that activate HML alpha by insertion at that locus. The hml alpha::Ty "on" mutations illustrate the unusual ability of these retrotransposons to activate genes by overcoming gene silencing mechanisms. The hml alpha::Ty "on" mutations include examples of multimeric Ty arrays. Single Ty and solo delta insertion derivatives of these Ty multimers restore the ability of the silencing mechanism to repress HML alpha. JF - Genetics AU - Mastrangelo, M F AU - Weinstock, K G AU - Shafer, B K AU - Hedge, A M AU - Garfinkel, D J AU - Strathern, J N AD - Laboratory of Eukaryotic Gene Expression, NCI-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 519 EP - 529 VL - 131 IS - 3 SN - 0016-6731, 0016-6731 KW - HIS3 KW - HML&agr; KW - MAR KW - MAT KW - SIR KW - STE KW - DNA Transposable Elements KW - 0 KW - Peptides KW - Receptors, Cell Surface KW - Receptors, Mating Factor KW - Receptors, Peptide KW - Transcription Factors KW - Mating Factor KW - 61194-02-3 KW - Index Medicus KW - Saccharomyces cerevisiae -- genetics KW - Phenotype KW - Genes, Fungal KW - Blotting, Southern KW - Electrophoresis, Gel, Pulsed-Field KW - Receptors, Cell Surface -- genetics KW - Mutagenesis, Insertional KW - Gene Expression Regulation, Fungal KW - Regulatory Sequences, Nucleic Acid KW - Peptides -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73044117?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genetics&rft.atitle=Disruption+of+a+silencer+domain+by+a+retrotransposon.&rft.au=Mastrangelo%2C+M+F%3BWeinstock%2C+K+G%3BShafer%2C+B+K%3BHedge%2C+A+M%3BGarfinkel%2C+D+J%3BStrathern%2C+J+N&rft.aulast=Mastrangelo&rft.aufirst=M&rft.date=1992-07-01&rft.volume=131&rft.issue=3&rft.spage=519&rft.isbn=&rft.btitle=&rft.title=Genetics&rft.issn=00166731&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-18 N1 - Date created - 1992-08-18 N1 - Date revised - 2017-01-13 N1 - Gene symbol - HIS3; HML&agr;; MAR; MAT; SIR; STE N1 - SuppNotes - Cited By: Cell. 1989 Nov 17;59(4):637-47 [2684414] Cell. 1990 Feb 23;60(4):649-64 [2406028] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2120-4 [3281162] Cell. 1987 Dec 4;51(5):721-32 [3315231] Methods Enzymol. 1987;154:164-75 [3323810] J Mol Biol. 1984 Oct 5;178(4):815-34 [6092645] Nature. 1981 Jan 22;289(5795):239-44 [6256655] Cell. 1982 Nov;31(1):183-92 [6297747] Cold Spring Harb Symp Quant Biol. 1983;47 Pt 2:989-98 [6345082] J Mol Biol. 1984 Jul 5;176(3):307-31 [6379190] Cell. 1981 Nov;27(1 Pt 2):15-23 [7034964] Genetics. 1979 Sep;93(1):13-35 [16118901] Genetics. 1977 Mar;85(3):395-405 [17248736] Genetics. 1979 Dec;93(4):877-901 [397913] Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9392-6 [1946350] Genes Dev. 1991 Apr;5(4):605-15 [2010086] Nature. 1989 Dec 14;342(6251):749-57 [2513489] EMBO J. 1989 Jul;8(7):2067-75 [2551674] Mol Cell Biol. 1989 Nov;9(11):4621-30 [2689860] Cell. 1985 Mar;40(3):491-500 [2982495] Mol Cell Biol. 1988 Jan;8(1):210-25 [3275867] Genetics. 1987 May;116(1):9-22 [3297920] Mol Cell Biol. 1987 Oct;7(10):3713-22 [3316986] Cell. 1985 May;41(1):41-8 [3888409] Mol Cell Biol. 1985 Aug;5(8):1878-86 [3915783] Cell. 1982 Sep;30(2):567-78 [6215985] Nature. 1981 Jan 22;289(5795):244-50 [6256656] Cell. 1981 Aug;25(2):517-24 [6269749] Methods Enzymol. 1983;101:202-11 [6310324] Genetics. 1983 Jun;104(2):219-34 [6345265] J Cell Biol. 1980 Jun;85(3):811-22 [6993497] J Mol Biol. 1981 Apr 15;147(3):357-72 [7031257] Mol Cell Biol. 1982 Jan;2(1):11-20 [7050665] EMBO J. 1985 Oct;4(10):2643-8 [16453635] Genetics. 1976 Jun;83(2):245-58 [17248712] Genetics. 1979 Sep;93(1):37-50 [17248968] Cell. 1979 Oct;18(2):309-19 [387260] Mol Cell Biol. 1991 Feb;11(2):1069-79 [1990267] Genetics. 1988 Sep;120(1):95-108 [2851484] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Skeletal hyperostosis in patients receiving chronic, very-low-dose isotretinoin. AN - 73043576; 1626958 AB - We conducted a prospective roentgenographic survey of patients participating in a randomized, placebo-controlled, multicenter clinical trial that evaluated the effectiveness of chronic, very-low-dose (approximately 0.14 mg/kg per day for 3 years) isotretinoin in preventing the subsequent occurrences of new basal cell carcinoma in patients with previous basal cell carcinoma. To assess potential skeletal changes, a sample of 269 patients from among a total of 981 enrollees were randomly selected for comparative roentgenographic review. Baseline and 36-month roentgenograms of the cervical and thoracic spine of each patient were read side by side by a radiologist, masked to treatment group, who noted both the presence and extent of abnormalities at each vertebral level at baseline and the progression of existing or occurrence of new abnormalities at previously unaffected levels at 36 months. In comparison with the placebo group, significantly more patients in the isotretinoin group exhibited progression of existing hyperostotic abnormalities (40% vs 18%; P less than .001) and new hyperostotic involvement at previously unaffected vertebral levels (8% vs 1%; P = .015). Our findings indicate that chronic, very-low-dose isotretinoin can induce hyperostotic axial skeletal changes similar to those reported in patients taking higher doses. JF - Archives of dermatology AU - Tangrea, J A AU - Kilcoyne, R F AU - Taylor, P R AU - Helsel, W E AU - Adrianza, M E AU - Hartman, A M AU - Edwards, B K AU - Peck, G L AD - Division of Cancer Prevention and Control, National Cancer Institute, National Institutes of Health, Bethesda, Md. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 921 EP - 925 VL - 128 IS - 7 SN - 0003-987X, 0003-987X KW - Isotretinoin KW - EH28UP18IF KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Thoracic Vertebrae -- diagnostic imaging KW - Aged KW - Skin Neoplasms -- prevention & control KW - Neoplasm Recurrence, Local -- prevention & control KW - Carcinoma, Basal Cell -- prevention & control KW - Prospective Studies KW - Cervical Vertebrae -- diagnostic imaging KW - Adult KW - Middle Aged KW - Radiography KW - Female KW - Male KW - Isotretinoin -- administration & dosage KW - Hyperostosis, Diffuse Idiopathic Skeletal -- diagnostic imaging KW - Isotretinoin -- adverse effects KW - Hyperostosis, Diffuse Idiopathic Skeletal -- chemically induced KW - Isotretinoin -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73043576?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+dermatology&rft.atitle=Skeletal+hyperostosis+in+patients+receiving+chronic%2C+very-low-dose+isotretinoin.&rft.au=Tangrea%2C+J+A%3BKilcoyne%2C+R+F%3BTaylor%2C+P+R%3BHelsel%2C+W+E%3BAdrianza%2C+M+E%3BHartman%2C+A+M%3BEdwards%2C+B+K%3BPeck%2C+G+L&rft.aulast=Tangrea&rft.aufirst=J&rft.date=1992-07-01&rft.volume=128&rft.issue=7&rft.spage=921&rft.isbn=&rft.btitle=&rft.title=Archives+of+dermatology&rft.issn=0003987X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-13 N1 - Date created - 1992-08-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Arch Dermatol. 1992 Dec;128(12):1650 [1308126] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Soft tissue sarcoma and tobacco use: data from a prospective cohort study of United States veterans. AN - 73041322; 1617125 AB - A report of an increased risk of soft tissue sarcoma (STS) among users of smokeless tobacco led us to evaluate this association and the role of other types of tobacco in a prospective cohort mortality-study of United States veterans. A total of 248,046 veterans provided tobacco-use histories on a mail questionnaire in 1954 or 1957. Data on subsequent tobacco use were not collected. By 1980, 119 deaths from STS had occurred among the cohort members. Veterans who had ever chewed tobacco or used snuff had a nonsignificant 40 percent excess of STS (95 percent confidence interval [CI] = 0.8-2.6; 21 deaths) in comparison with veterans who had never used any tobacco products. Risk was limited to former users (relative risk [RR] = 1.5) with no excess seen among current users (RR = 0.9). Frequent former users had higher risk (RR = 1.9) than infrequent users (RR = 1.3). Risk was slightly higher in persons who started using smokeless tobacco at younger ages, but did not increase with duration of use or with late age at cessation of use. Most veterans who used chewing tobacco or snuff also used some other form of tobacco. No STS deaths occurred among the 2,308 veterans who used smokeless tobacco only. An unexpected finding of the study was the significant excess of STS deaths among cigarette smokers (RR = 1.8, CI = 1.1-2.9). Risk was higher among ex-smokers (RR = 2.2) than among current smokers (RR = 1.5) and was not related to number of cigarettes per day, age started smoking, duration, or pack-years.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Cancer causes & control : CCC AU - Zahm, S H AU - Heineman, E F AU - Vaught, J B AD - Occupational Studies Section, National Cancer Institute, Rockville, MD 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 371 EP - 376 VL - 3 IS - 4 SN - 0957-5243, 0957-5243 KW - Index Medicus KW - Prospective Studies KW - Aged, 80 and over KW - Risk Factors KW - Humans KW - Cohort Studies KW - Adult KW - Smoking -- adverse effects KW - Aged KW - Middle Aged KW - United States -- epidemiology KW - Veterans KW - Plants, Toxic KW - Mouth Neoplasms -- mortality KW - Soft Tissue Neoplasms -- mortality KW - Sarcoma -- mortality KW - Pharyngeal Neoplasms -- etiology KW - Mouth Neoplasms -- etiology KW - Tobacco, Smokeless -- adverse effects KW - Soft Tissue Neoplasms -- etiology KW - Pharyngeal Neoplasms -- mortality KW - Sarcoma -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73041322?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+causes+%26+control+%3A+CCC&rft.atitle=Soft+tissue+sarcoma+and+tobacco+use%3A+data+from+a+prospective+cohort+study+of+United+States+veterans.&rft.au=Zahm%2C+S+H%3BHeineman%2C+E+F%3BVaught%2C+J+B&rft.aulast=Zahm&rft.aufirst=S&rft.date=1992-07-01&rft.volume=3&rft.issue=4&rft.spage=371&rft.isbn=&rft.btitle=&rft.title=Cancer+causes+%26+control+%3A+CCC&rft.issn=09575243&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-04 N1 - Date created - 1992-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reduced mRNA levels for the multidrug-resistance genes in cAMP-dependent protein kinase mutant cell lines. AN - 73041049; 1352302 AB - We have previously shown that in Chinese hamster ovary (CHO) cells, a mutant cell line with a defective regulatory subunit (RI) for the cAMP-dependent protein kinase (Abraham et al: Mol. Cell. Biol., 7:3098-3106, 1987), and a transfectant cell line expressing the same mutant kinase, showed increased sensitivity to a number of drugs that are known to be substrates for the multidrug transporter (P-glycoprotein). In the current study we have investigated the mechanism by which cAMP-dependent protein kinase controls drug resistance. We report here that the sensitivity of the kinase defective CHO cell lines to multiple drugs results from decreased RNA levels for the multidrug-resistance gene. Similar results were obtained with mouse Y1 adrenal cells. Wild-type Y1 cells had high levels of P-glycoprotein due to expression of both the mdr1b and mdr2 genes, whereas the cAMP-dependent protein kinase mutant Kin 8 cells had decreased RNA levels for these genes. A Kin 8 transfectant with restored cAMP-dependent protein kinase activity recovered mdr expression, indicating a cause and effect relationship between the protein kinase mutations and mdr expression. No changes in nuclear run-off assays could be detected, suggesting a non-transcriptional mechanism of regulation. Wild-type Y1 cells are more drug sensitive despite having higher levels of P-glycoprotein than the mutant cells. This paradoxical result may be explained by the higher rate of synthesis of steroids by the wild-type Y1 cells, which appear to be inhibitors of P-glycoprotein transport activity. JF - Journal of cellular physiology AU - Chin, K V AU - Chauhan, S S AU - Abraham, I AU - Sampson, K E AU - Krolczyk, A J AU - Wong, M AU - Schimmer, B AU - Pastan, I AU - Gottesman, M M AD - Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 87 EP - 94 VL - 152 IS - 1 SN - 0021-9541, 0021-9541 KW - mdr KW - Cytotoxins KW - 0 KW - Membrane Glycoproteins KW - P-Glycoprotein KW - RNA, Messenger KW - Steroids KW - Verapamil KW - CJ0O37KU29 KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinases KW - EC 2.7.- KW - Quinidine KW - ITX08688JL KW - Colchicine KW - SML2Y3J35T KW - Index Medicus KW - Animals KW - Cricetulus KW - Transcription, Genetic KW - Mice KW - Cytotoxins -- pharmacology KW - Verapamil -- pharmacology KW - Precipitin Tests KW - Polymerase Chain Reaction KW - Base Sequence KW - Colchicine -- pharmacology KW - Transfection KW - Cells, Cultured KW - Molecular Sequence Data KW - Quinidine -- pharmacology KW - Female KW - Steroids -- metabolism KW - Cricetinae KW - Ovary -- chemistry KW - Adrenal Glands -- metabolism KW - Adrenal Glands -- cytology KW - RNA, Messenger -- analysis KW - RNA, Messenger -- genetics KW - Ovary -- metabolism KW - RNA, Messenger -- metabolism KW - Ovary -- cytology KW - Cyclic AMP -- pharmacology KW - Protein Kinases -- genetics KW - Mutation -- genetics KW - Adrenal Glands -- chemistry KW - Membrane Glycoproteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73041049?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cellular+physiology&rft.atitle=Reduced+mRNA+levels+for+the+multidrug-resistance+genes+in+cAMP-dependent+protein+kinase+mutant+cell+lines.&rft.au=Chin%2C+K+V%3BChauhan%2C+S+S%3BAbraham%2C+I%3BSampson%2C+K+E%3BKrolczyk%2C+A+J%3BWong%2C+M%3BSchimmer%2C+B%3BPastan%2C+I%3BGottesman%2C+M+M&rft.aulast=Chin&rft.aufirst=K&rft.date=1992-07-01&rft.volume=152&rft.issue=1&rft.spage=87&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+physiology&rft.issn=00219541&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-04 N1 - Date created - 1992-08-04 N1 - Date revised - 2017-01-13 N1 - Gene symbol - mdr N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Elevated level of nuclear protein kinase C in multidrug-resistant MCF-7 human breast carcinoma cells. AN - 73039706; 1617646 AB - Previous studies have demonstrated elevated levels of protein kinase C (PKC) activity in multidrug-resistant human breast carcinoma MCF-7/ADR cells compared to control drug-sensitive MCF-7/WT cells (R.L. Fine, J. Patel, and B.A. Chabner, Proc. Natl. Acad. Sci. USA, 85:582-586, 1988). In our present studies, immunohistochemical localization analysis using a polyclonal PKC antibody recognizing the alpha, beta, and gamma subtypes of PKC demonstrates that immunoreactivity is enhanced in MCF-7/ADR cells, with pronounced staining noted in the nuclear region. Other studies with purified nuclei isolated from MCF-7/ADR cells also show a marked increase in the intensity of immunostaining for PKC when compared to nuclei prepared from control MCF-7/WT cells. Western blot analysis of proteins extracted from purified nuclear preparations further establishes an increase in PKC enzyme protein associated with the nuclear fraction of MCF-7/ADR cells. Subcellular fractionation studies also indicate that MCF-7/ADR cells have 4-8 times higher nuclear PKC activity compared to that of control MCF-7/WT cells. MCF-7/ADR cells also possess 3-5-fold elevated cytosolic PKC activity, while a less than 2-fold increase is found in PKC activity associated with the plasma membrane fraction of MCF-7/ADR cells. Examination of these extracts with PKC isotype-specific antisera, as well as by DEAE-cellulose chromatography, reveals that nuclei prepared from MCF-7/ADR cells contain markedly elevated amounts of a slightly altered form of PKC alpha. These results suggest that elevated levels of a modified form of PKC alpha at the nucleus may play a role in modulating nuclear events to promote the development of multidrug resistance in MCF-7 cells. JF - Cancer research AU - Lee, S A AU - Karaszkiewicz, J W AU - Anderson, W B AD - Laboratory of Cellular Oncology, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/07/01/ PY - 1992 DA - 1992 Jul 01 SP - 3750 EP - 3759 VL - 52 IS - 13 SN - 0008-5472, 0008-5472 KW - Doxorubicin KW - 80168379AG KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Blotting, Western KW - Tumor Cells, Cultured KW - Doxorubicin -- pharmacology KW - Chromatography, DEAE-Cellulose KW - Humans KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Amino Acid Sequence KW - Immunohistochemistry KW - Female KW - Protein Kinase C -- analysis KW - Cell Nucleus -- enzymology KW - Breast Neoplasms -- pathology KW - Drug Resistance KW - Breast Neoplasms -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73039706?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Elevated+level+of+nuclear+protein+kinase+C+in+multidrug-resistant+MCF-7+human+breast+carcinoma+cells.&rft.au=Lee%2C+S+A%3BKaraszkiewicz%2C+J+W%3BAnderson%2C+W+B&rft.aulast=Lee&rft.aufirst=S&rft.date=1992-07-01&rft.volume=52&rft.issue=13&rft.spage=3750&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-04 N1 - Date created - 1992-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effect of acculturation on drinking attitudes among Japanese in Japan and Japanese Americans in Hawaii and California. AN - 73034768; 1619931 AB - Data from a joint Japan-U.S. collaborative study were examined to determine the relationship of acculturation to drinking attitudes among Japanese in Japan and Japanese Americans in Hawaii and California. Drinking attitudes (i.e., self-reported acceptable or appropriate levels of drinking) among ethnic groups differed significantly for the nine situations studied: (1) at a bar with friends, (2) at a party at someone else's house, (3) as a parent, spending time with small children, (4) during working hours, (5) visiting in-laws, (6) with friends at home, (7) with friends after work, (8) with people at sports events and (9) before driving a car. Factor analysis was used to determine the differences in drinking attitudes among these ethnic groups. Japanese and Japanese Americans differentiated drinking situations into different categories. The major difference between the two groups was that the Japanese associated spending time with small children with a situation appropriate for drinking, such as being with friends at home, whereas Japanese Americans associated spending time with small children with a situation inappropriate for drinking, such as before driving. JF - Journal of studies on alcohol AU - Tsunoda, T AU - Parrish, K M AU - Higuchi, S AU - Stinson, F S AU - Kono, H AU - Ogata, M AU - Harford, T C AD - National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 369 EP - 377 VL - 53 IS - 4 SN - 0096-882X, 0096-882X KW - Index Medicus KW - California KW - Alcoholic Intoxication -- psychology KW - Humans KW - Adult KW - Social Values KW - Hawaii KW - Aged KW - Middle Aged KW - Adolescent KW - Male KW - Japan KW - Female KW - Asian Americans -- psychology KW - Acculturation KW - Cross-Cultural Comparison KW - Alcohol Drinking -- psychology KW - Attitude KW - Social Environment UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73034768?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+studies+on+alcohol&rft.atitle=The+effect+of+acculturation+on+drinking+attitudes+among+Japanese+in+Japan+and+Japanese+Americans+in+Hawaii+and+California.&rft.au=Tsunoda%2C+T%3BParrish%2C+K+M%3BHiguchi%2C+S%3BStinson%2C+F+S%3BKono%2C+H%3BOgata%2C+M%3BHarford%2C+T+C&rft.aulast=Tsunoda&rft.aufirst=T&rft.date=1992-07-01&rft.volume=53&rft.issue=4&rft.spage=369&rft.isbn=&rft.btitle=&rft.title=Journal+of+studies+on+alcohol&rft.issn=0096882X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-31 N1 - Date created - 1992-07-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cloning of the outer membrane high-affinity Fe(III)-pyochelin receptor of Pseudomonas aeruginosa. AN - 73031911; 1320609 AB - Pseudomonas aeruginosa produces the phenolic siderophore pyochelin under iron-limiting conditions. In this study, an Fe(III)-pyochelin transport-negative (Fpt-) strain, IA613, was isolated and characterized. 55Fe(III)-pyochelin transport assays determined that no Fe(III)-pyochelin associated with the Fpt- IA613 cells while a significant amount associated with KCN-poisoned Fpt+ cells. A P. aeruginosa genomic library was constructed in the IncP cosmid pLAFR1. The genomic library was mobilized into IA613, and a recombinant cosmid, pCC41, which complemented the Fpt- phenotype of IA613, was isolated. pCC41 contained a 28-kb insert of P. aeruginosa DNA, and the Fpt(-)-complementing region was localized to a 3.6-kb BamHI-EcoRI fragment by deletion and subcloning of the insert. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis of IA613 revealed that it lacked a 75-kDa outer membrane protein present in Fpt+ strains. IA613 strains bearing plasmid pRML303, which carries the 3.6-kb BamHI-EcoRI fragment of pCC41, expressed the 75-kDa outer membrane protein and demonstrated a 55Fe(III)-pyochelin transport phenotype identical to that of a wild-type Fpt+ strain. Minicell analysis demonstrated that the 3.6-kb BamHI-EcoRI fragment of pCC41 encoded a protein of approximately 75 kDa. The results presented here and in a previous report (D. E. Heinrichs, L. Young, and K. Poole, Infect. Immun. 59:3680-3684, 1991) lead to the conclusion that the 75-kDa outer membrane protein is the high-affinity receptor for Fe(III)-pyochelin in P. aeruginosa. JF - Journal of bacteriology AU - Ankenbauer, R G AD - Laboratory of Microbial Structure and Function, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 59840. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 4401 EP - 4409 VL - 174 IS - 13 SN - 0021-9193, 0021-9193 KW - Bacterial Outer Membrane Proteins KW - 0 KW - DNA, Bacterial KW - FPTA protein, Pseudomonas KW - Iron Chelating Agents KW - Phenols KW - Receptors, Cell Surface KW - Recombinant Proteins KW - Thiazoles KW - pyochelin KW - 69772-54-9 KW - Iron KW - E1UOL152H7 KW - Index Medicus KW - Electrophoresis, Polyacrylamide Gel KW - DNA, Bacterial -- isolation & purification KW - Escherichia coli -- genetics KW - Plasmids KW - Molecular Weight KW - Cloning, Molecular KW - Phenotype KW - Recombinant Proteins -- isolation & purification KW - Recombinant Proteins -- metabolism KW - DNA, Bacterial -- genetics KW - Kinetics KW - Restriction Mapping KW - Iron Chelating Agents -- metabolism KW - Cell Membrane -- metabolism KW - Receptors, Cell Surface -- metabolism KW - Receptors, Cell Surface -- isolation & purification KW - Pseudomonas aeruginosa -- metabolism KW - Pseudomonas aeruginosa -- genetics KW - Bacterial Outer Membrane Proteins -- genetics KW - Phenols -- metabolism KW - Bacterial Outer Membrane Proteins -- isolation & purification KW - Bacterial Outer Membrane Proteins -- metabolism KW - Receptors, Cell Surface -- genetics KW - Iron -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73031911?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+bacteriology&rft.atitle=Cloning+of+the+outer+membrane+high-affinity+Fe%28III%29-pyochelin+receptor+of+Pseudomonas+aeruginosa.&rft.au=Ankenbauer%2C+R+G&rft.aulast=Ankenbauer&rft.aufirst=R&rft.date=1992-07-01&rft.volume=174&rft.issue=13&rft.spage=4401&rft.isbn=&rft.btitle=&rft.title=Journal+of+bacteriology&rft.issn=00219193&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-07 N1 - Date created - 1992-08-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Bacteriol. 1979 Jan;137(1):357-64 [104968] Infect Immun. 1982 Apr;36(1):17-23 [6804387] J Bacteriol. 1979 Dec;140(3):902-10 [118160] Proc Natl Acad Sci U S A. 1979 Apr;76(4):1648-52 [377280] J Bacteriol. 1976 Sep;127(3):1370-5 [783142] Mol Microbiol. 1991 Mar;5(3):647-55 [1646376] J Clin Invest. 1990 Oct;86(4):1030-7 [2170442] Microbiol Rev. 1989 Dec;53(4):517-30 [2531838] Gene. 1988 Oct 15;70(1):191-7 [2853689] J Clin Microbiol. 1986 Mar;23(3):560-2 [2937804] J Bacteriol. 1987 Aug;169(8):3638-46 [2956250] Infect Immun. 1986 Mar;51(3):896-900 [3081447] Infect Immun. 1987 Sep;55(9):2021-5 [3114141] J Bacteriol. 1988 Nov;170(11):5364-7 [3141387] Antibiot Chemother (1971). 1985;36:1-12 [3159335] Microb Pathog. 1988 Sep;5(3):197-205 [3216778] Biotechniques. 1988 Oct;6(9):839, 841-3 [3273192] J Gen Microbiol. 1966 May;43(2):159-271 [5963505] Infect Immun. 1983 May;40(2):665-9 [6302002] J Bacteriol. 1984 Jun;158(3):1115-21 [6427188] J Bacteriol. 1980 Jan;141(1):199-204 [6766439] Proc Natl Acad Sci U S A. 1981 Jul;78(7):4256-60 [6794030] J Bacteriol. 1982 Aug;151(2):783-7 [6807961] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7347-51 [7012838] J Bacteriol. 1978 Oct;136(1):381-90 [101518] Infect Immun. 1979 Dec;26(3):925-32 [160892] FEBS Lett. 1975 Oct 15;58(1):254-8 [773686] Infect Immun. 1991 Oct;59(10):3680-4 [1910015] Biotechniques. 1990 Nov;9(5):565-6, 568 [2268423] Plasmid. 1989 Mar;21(2):99-112 [2740456] Infect Immun. 1986 Jun;52(3):885-91 [2940187] J Bacteriol. 1987 Jul;169(7):3365-8 [3036785] J Bacteriol. 1988 Nov;170(11):5344-51 [3141386] Infect Immun. 1985 Apr;48(1):130-8 [3156815] Infect Immun. 1985 Jul;49(1):132-40 [3159677] J Bacteriol. 1974 May;118(2):442-53 [4208134] Gene. 1982 Jun;18(3):289-96 [6290332] Biochemistry. 1984 Oct 9;23(21):5076-80 [6437446] J Bacteriol. 1980 May;142(2):581-7 [6769903] J Bacteriol. 1979 Apr;138(1):193-200 [108250] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytogenetic studies of mice exposed to styrene by inhalation. AN - 73026204; 1377343 AB - The data for the in vivo genotoxicity of styrene (STY) are equivocal. To evaluate the clastogenicity and sister-chromatid exchange (SCE)-inducing potential of STY in vivo under carefully controlled conditions, B6C3F1 female mice were exposed by inhalation for 6 h/day for 14 consecutive days to either 0, 125, 250 or 500 ppm STY. One day after the final exposure, peripheral blood, spleen, and lungs were removed and cells were cultured for the analysis of micronucleus (MN) induction using the cytochalasin B-block method, chromosome breakage, and SCE induction. Peripheral blood smears were also made for scoring MN in erythrocytes. There was a significant concentration-related elevation of SCE frequency in lymphocytes from the spleen and the peripheral blood as well as in cells from the lung. However, no statistically significant concentration-related increases were found in the frequency of chromosome aberrations in the cultured splenocytes or lung cells, and no significant increases in MN frequencies were observed in binucleated splenocytes or normochromatic erythrocytes in peripheral blood smears. JF - Mutation research AU - Kligerman, A D AU - Allen, J W AU - Bryant, M F AU - Campbell, J A AU - Collins, B W AU - Doerr, C L AU - Erexson, G L AU - Kwanyuen, P AU - Morgan, D L AD - U.S. Environmental Protection Agency, National Institute of Environmental Health Sciences, Research Triangle Park, NC. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 35 EP - 43 VL - 280 IS - 1 SN - 0027-5107, 0027-5107 KW - Styrenes KW - 0 KW - Cytochalasin B KW - 3CHI920QS7 KW - Styrene KW - 44LJ2U959V KW - Index Medicus KW - Animals KW - Mutagenicity Tests KW - Micronucleus Tests KW - Sister Chromatid Exchange KW - Cytochalasin B -- pharmacology KW - Mice KW - Administration, Inhalation KW - Female KW - Styrenes -- administration & dosage KW - Chromosome Aberrations KW - Styrenes -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73026204?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+research&rft.atitle=Cytogenetic+studies+of+mice+exposed+to+styrene+by+inhalation.&rft.au=Kligerman%2C+A+D%3BAllen%2C+J+W%3BBryant%2C+M+F%3BCampbell%2C+J+A%3BCollins%2C+B+W%3BDoerr%2C+C+L%3BErexson%2C+G+L%3BKwanyuen%2C+P%3BMorgan%2C+D+L&rft.aulast=Kligerman&rft.aufirst=A&rft.date=1992-07-01&rft.volume=280&rft.issue=1&rft.spage=35&rft.isbn=&rft.btitle=&rft.title=Mutation+research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-28 N1 - Date created - 1992-07-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Delayed L-phenylalanine infusion allows for simultaneous kinetic analysis and improved evaluation of specific-to-nonspecific fluorine-18-dopa uptake in brain. AN - 73025645; 1613582 AB - The accumulation of 3-O-methyl-6-[18F]fluoro-L-DOPA (18F-30M-DOPA) in the brain from the circulation is responsible for most of the nonspecific background during 18F-DOPA positron emission tomography scanning. To increase the sensitivity of 18F-DOPA for imaging presynaptic dopamine systems, we took advantage of 18F-30M-DOPA's rapid clearance from the brain (T1/2 approximately 15-20 min). The infusion of the unlabeled amino acid L-phenylalanine, starting 75 min after 18F-DOPA administration, prevents 18F-30M-DOPA entrance into the brain through competition at the large amino acid transport system of the blood brain barrier. This method produces high specific-to-nonspecific contrast images of 18F accumulation beginning 15-30 min after onset of amino acid infusion and better sensitivity to small changes in 18F-DOPA uptake while still allowing for kinetic analysis of the data in the early time points. Kinetic and anatomical data were found to be strongly correlated. JF - Journal of nuclear medicine : official publication, Society of Nuclear Medicine AU - Doudet, D J AU - McLellan, C A AU - Aigner, T G AU - Wyatt, R J AU - Cohen, R M AD - Section on Clinical Brain Imaging, LCM, NIMH, IRP Bethesda, Maryland. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 1383 EP - 1389 VL - 33 IS - 7 SN - 0161-5505, 0161-5505 KW - 3-O-methyl-6-fluoro-dopa KW - 107257-16-9 KW - fluorodopa F 18 KW - 2C598205QX KW - Phenylalanine KW - 47E5O17Y3R KW - Dihydroxyphenylalanine KW - 63-84-3 KW - Carbidopa KW - MNX7R8C5VO KW - Index Medicus KW - Corpus Striatum -- diagnostic imaging KW - Animals KW - Cerebral Cortex -- drug effects KW - Cerebral Cortex -- metabolism KW - Carbidopa -- pharmacology KW - Corpus Striatum -- metabolism KW - Tomography, Emission-Computed KW - Corpus Striatum -- drug effects KW - Macaca mulatta KW - Time Factors KW - Cerebral Cortex -- diagnostic imaging KW - MPTP Poisoning KW - Brain -- drug effects KW - Dihydroxyphenylalanine -- metabolism KW - Brain -- metabolism KW - Phenylalanine -- administration & dosage KW - Brain -- diagnostic imaging KW - Dihydroxyphenylalanine -- pharmacokinetics KW - Dihydroxyphenylalanine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73025645?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+nuclear+medicine+%3A+official+publication%2C+Society+of+Nuclear+Medicine&rft.atitle=Delayed+L-phenylalanine+infusion+allows+for+simultaneous+kinetic+analysis+and+improved+evaluation+of+specific-to-nonspecific+fluorine-18-dopa+uptake+in+brain.&rft.au=Doudet%2C+D+J%3BMcLellan%2C+C+A%3BAigner%2C+T+G%3BWyatt%2C+R+J%3BCohen%2C+R+M&rft.aulast=Doudet&rft.aufirst=D&rft.date=1992-07-01&rft.volume=33&rft.issue=7&rft.spage=1383&rft.isbn=&rft.btitle=&rft.title=Journal+of+nuclear+medicine+%3A+official+publication%2C+Society+of+Nuclear+Medicine&rft.issn=01615505&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-28 N1 - Date created - 1992-07-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - L-histidinol: preclinical therapeutic studies in combination with antitumor agents and pharmacokinetic studies in mice. AN - 73016518; 1617631 AB - Therapeutic studies were conducted with L-histidinol, in combination with cyclophosphamide, bischloroethylnitrosourea, 5-fluorouracil, phenylalanine mustard, or cis-platinum(II)diammine dichloride, in several transplantable tumors in mice. These tumor types included murine L1210 P388 leukemias, M5076 sarcoma, mammary 16/C adenocarcinoma, human LOX melanoma, and colon HT-29 adenocarcinoma. Therapeutic benefits of adding L-histidinol to a regimen, compared to the regimen alone, were marginal. Pharmacokinetic studies indicated a rapid clearance of L-histidinol following a bolus dose (250 mg/kg i.p.), peak plasma concentration of 200 micrograms/ml (1.4 mM), and beta phase t1/2 of 12.6 min. Maximum tolerable plasma steady state concentrations with a 24-h infusion (2000 mg/kg/24 h) were no greater than 25 micrograms/ml (0.18 mM). JF - Cancer research AU - Zaharko, D AU - Plowman, J AU - Waud, W AU - Dykes, D AU - Malspeis, L AD - Pharmacology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/07/01/ PY - 1992 DA - 1992 Jul 01 SP - 3604 EP - 3609 VL - 52 IS - 13 SN - 0008-5472, 0008-5472 KW - Histidinol KW - 501-28-0 KW - Cyclophosphamide KW - 8N3DW7272P KW - Cisplatin KW - Q20Q21Q62J KW - Carmustine KW - U68WG3173Y KW - Index Medicus KW - Neoplasm Transplantation KW - Cyclophosphamide -- administration & dosage KW - Animals KW - Leukemia P388 -- drug therapy KW - Humans KW - Mice, Inbred C57BL KW - Mice, Inbred C3H KW - Transplantation, Heterologous KW - Mice KW - Leukemia L1210 -- drug therapy KW - Carmustine -- administration & dosage KW - Cisplatin -- administration & dosage KW - Histidinol -- administration & dosage KW - Neoplasms, Experimental -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Histidinol -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73016518?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=L-histidinol%3A+preclinical+therapeutic+studies+in+combination+with+antitumor+agents+and+pharmacokinetic+studies+in+mice.&rft.au=Zaharko%2C+D%3BPlowman%2C+J%3BWaud%2C+W%3BDykes%2C+D%3BMalspeis%2C+L&rft.aulast=Zaharko&rft.aufirst=D&rft.date=1992-07-01&rft.volume=52&rft.issue=13&rft.spage=3604&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-04 N1 - Date created - 1992-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Somatostatin content increases following norepinephrine depletion in frontal cortex of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated mice. AN - 73013837; 1351925 AB - The effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on somatostatin (SS)-containing neurons were examined by measuring dopamine, norepinephrine (NE), SS, and SS mRNA in striatum and frontal cortex of C57/B16 mice at various times following treatment with MPTP-HCl (96 mg/kg i.p.). MPTP caused a 70% depletion of dopamine in striatum by 1 day and a 40% depletion of NE in frontal cortex within 3 days. SS content was increased in frontal cortex 4 days later, but not in striatum; there were no changes in SS mRNA. Maprotiline, a specific NE-uptake blocker, prevented both the depletion of NE and the increase of SS in frontal cortex due to MPTP administration. These results support the possibility that NE can regulate SS in frontal cortex and are discussed in terms of the decrease of SS seen in parkinsonian patients with dementia. JF - Journal of neurochemistry AU - Mitsuo, K AU - Schwartz, J P AD - Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 267 EP - 272 VL - 59 IS - 1 SN - 0022-3042, 0022-3042 KW - RNA, Messenger KW - 0 KW - Maprotiline KW - 2U1W68TROF KW - Somatostatin KW - 51110-01-1 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Animals KW - Maprotiline -- pharmacology KW - RNA, Messenger -- metabolism KW - Mice, Inbred C57BL KW - Dopamine -- metabolism KW - Mice KW - Male KW - Somatostatin -- genetics KW - Norepinephrine -- metabolism KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- pharmacology KW - Frontal Lobe -- metabolism KW - Somatostatin -- metabolism KW - Norepinephrine -- deficiency UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73013837?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=Somatostatin+content+increases+following+norepinephrine+depletion+in+frontal+cortex+of+1-methyl-4-phenyl-1%2C2%2C3%2C6-tetrahydropyridine-treated+mice.&rft.au=Mitsuo%2C+K%3BSchwartz%2C+J+P&rft.aulast=Mitsuo&rft.aufirst=K&rft.date=1992-07-01&rft.volume=59&rft.issue=1&rft.spage=267&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-24 N1 - Date created - 1992-07-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vivo evidence that lithium inactivates Gi modulation of adenylate cyclase in brain. AN - 73013616; 1319465 AB - In vivo microdialysis of cyclic AMP from prefrontal cortex complemented by ex vivo measures was used to investigate the possibility that lithium produces functional changes in G proteins that could account for its effects on adenylate cyclase activity. Four weeks of lithium administration (serum lithium concentration of 0.85 +/- 0.05 mM; n = 11) significantly increased the basal cyclic AMP content in dialysate from prefrontal cortex of anesthetized rats. Forskolin infused through the probe increased dialysate cyclic AMP, but the magnitude of this increase was unaffected by chronic lithium administration. Inactivation of the inhibitory guanine nucleotide binding protein Gi with pertussis toxin increased dialysate cyclic AMP in control rats, as did stimulation with cholera toxin (which activates the stimulatory guanine nucleotide binding protein Gs). The effect of pertussis toxin was abolished following chronic lithium, whereas the increase in cyclic AMP after cholera toxin was enhanced. In vitro pertussis toxin-catalyzed ADP ribosylation of alpha i (and alpha o) was increased by 20% in prefrontal cortex from lithium-treated rats, but the alpha i and alpha s contents (as determined by immunoblot) as well as the cholera toxin-catalyzed ADP ribosylation of alpha s were unchanged. Taken together, these results suggest that chronic lithium administration may interfere with the dissociation of Gi into its active components and thereby remove a tonic inhibitory influence on adenylate cyclase, with resultant enhanced basal and cholera toxin-stimulated adenylate cyclase activity. JF - Journal of neurochemistry AU - Masana, M I AU - Bitran, J A AU - Hsiao, J K AU - Potter, W Z AD - Section on Clinical Pharmacology, Experimental Therapeutics Branch, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 200 EP - 205 VL - 59 IS - 1 SN - 0022-3042, 0022-3042 KW - Adenylate Cyclase Toxin KW - 0 KW - Virulence Factors, Bordetella KW - Colforsin KW - 1F7A44V6OU KW - Cholera Toxin KW - 9012-63-9 KW - Lithium KW - 9FN79X2M3F KW - Cyclic AMP KW - E0399OZS9N KW - Pertussis Toxin KW - EC 2.4.2.31 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Virulence Factors, Bordetella -- pharmacology KW - Animals KW - Colforsin -- pharmacology KW - Cyclic AMP -- metabolism KW - Cholera Toxin -- pharmacology KW - Male KW - Dialysis -- methods KW - Brain -- enzymology KW - GTP-Binding Proteins -- antagonists & inhibitors KW - Adenylyl Cyclases -- metabolism KW - GTP-Binding Proteins -- physiology KW - Lithium -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73013616?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=In+vivo+evidence+that+lithium+inactivates+Gi+modulation+of+adenylate+cyclase+in+brain.&rft.au=Masana%2C+M+I%3BBitran%2C+J+A%3BHsiao%2C+J+K%3BPotter%2C+W+Z&rft.aulast=Masana&rft.aufirst=M&rft.date=1992-07-01&rft.volume=59&rft.issue=1&rft.spage=200&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-24 N1 - Date created - 1992-07-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of hair coloring products and the risk of lymphoma, multiple myeloma, and chronic lymphocytic leukemia. AN - 73012297; 1609918 AB - Hair coloring products are widely used and contain components that are mutagenic and carcinogenic. An association between occupational exposure to hair coloring products and hematopoietic cancers has been reported, but the risk for these cancers among users has not been carefully evaluated. We conducted a population-based, case-control study with telephone interviews from 385 with telephone interviews from 385 non-Hodgkin's lymphoma cases, 70 Hodgkin's disease cases, 72 multiple myeloma cases, 56 chronic lymphocytic leukemia cases, and 1432 controls. Among women, use was associated with odds ratios of 1.5 for non-Hodgkin's lymphoma, 1.7 for Hodgkin's disease, 1.8 for multiple myeloma, and 1.0 for chronic lymphocytic leukemia. Risk was higher for permanent hair coloring products than for semi- or nonpermanent products, particularly for dark colors. Long duration and early age of first use tended to increase risk, but the patterns were inconsistent. Use was much less common in men and did not significantly increase risk. The use of hair coloring products appears to increase the risk of non-Hodgkin's lymphoma. Multiple myeloma and Hodgkin's disease were also associated, although based on far fewer subjects. If these results represent a causal association, use of hair coloring products would account for 35% of non-Hodgkin's lymphoma cases in exposed women and 20% in all women. JF - American journal of public health AU - Zahm, S H AU - Weisenburger, D D AU - Babbitt, P A AU - Saal, R C AU - Vaught, J B AU - Blair, A AD - Occupational Studies Section, National Cancer Institute, Rockville, MD 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 990 EP - 997 VL - 82 IS - 7 SN - 0090-0036, 0090-0036 KW - Hair Dyes KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Causality KW - Odds Ratio KW - Age Factors KW - Humans KW - Nebraska -- epidemiology KW - Registries KW - Health Status Indicators KW - Logistic Models KW - Adult KW - Case-Control Studies KW - Incidence KW - Interviews as Topic KW - Middle Aged KW - Time Factors KW - Female KW - Male KW - Multiple Myeloma -- chemically induced KW - Lymphoma -- epidemiology KW - Leukemia, Lymphocytic, Chronic, B-Cell -- epidemiology KW - Lymphoma -- classification KW - Hair Dyes -- classification KW - Multiple Myeloma -- epidemiology KW - Leukemia, Lymphocytic, Chronic, B-Cell -- chemically induced KW - Lymphoma -- chemically induced KW - Hair Dyes -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73012297?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+public+health&rft.atitle=Use+of+hair+coloring+products+and+the+risk+of+lymphoma%2C+multiple+myeloma%2C+and+chronic+lymphocytic+leukemia.&rft.au=Zahm%2C+S+H%3BWeisenburger%2C+D+D%3BBabbitt%2C+P+A%3BSaal%2C+R+C%3BVaught%2C+J+B%3BBlair%2C+A&rft.aulast=Zahm&rft.aufirst=S&rft.date=1992-07-01&rft.volume=82&rft.issue=7&rft.spage=990&rft.isbn=&rft.btitle=&rft.title=American+journal+of+public+health&rft.issn=00900036&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-23 N1 - Date created - 1992-07-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Lancet. 1979 Sep 8;2(8141):536 [90265] Lancet. 1979 Nov 17;2(8151):1070-1 [91802] Curr Probl Dermatol. 1978;7:196-204 [752455] Br J Cancer. 1977 Oct;36(4):467-78 [588414] J Natl Cancer Inst. 1977 Nov;59(5):1423-5 [909104] J Natl Cancer Inst. 1979 Feb;62(2):277-83 [283264] Epidemiology. 1990 Sep;1(5):349-56 [2078610] Mod Pathol. 1988 Jan;1(1):29-34 [3266335] Am J Public Health. 1988 May;78(5):570-1 [3354743] Am J Pathol. 1987 Apr;127(1):1-8 [3494405] Int J Epidemiol. 1989 Mar;18(1):283 [2722380] Drug Chem Toxicol. 1984;7(6):573-86 [6534733] Cancer Res. 1987 Jun 1;47(11):2978-81 [3567914] Int J Epidemiol. 1985 Dec;14(4):549-54 [4086141] Pathol Annu. 1990;25 Pt 1:99-115 [2404252] Lancet. 1990 Aug 25;336(8713):474-81 [1974997] Eur J Cancer. 1990 Apr;26(4):500-8 [2141517] Am J Epidemiol. 1990 Oct;132(4):746-8 [2403115] J Clin Epidemiol. 1990;43(1):87-91 [2319285] J Natl Cancer Inst. 1984 May;72(5):1051-7 [6585583] J Natl Cancer Inst. 1983 Mar;70(3):443-6 [6572734] Am J Ind Med. 1984;6(2):97-102 [6465143] Br J Cancer. 1983 Dec;48(6):853-7 [6652026] Am J Epidemiol. 1983 Jan;117(1):76-85 [6823955] J Natl Cancer Inst. 1981 Mar;66(3):591-602 [6937712] J Natl Cancer Inst. 1980 Oct;65(4):735-8 [6932526] Am J Ind Med. 1982;3(2):169-71 [7137173] Am J Epidemiol. 1981 Apr;113(4):464-73 [7211828] Br J Cancer. 1981 Feb;43(2):236-9 [7470387] Lancet. 1979 Nov 17;2(8151):1070 [91801] Lancet. 1979 Jun 30;1(8131):1390-3 [87844] Comment In: Am J Public Health. 1993 Apr;83(4):598-9 [8460749] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Presentation of three different viral peptides, HTLV-1 Tax, HCMV gB, and influenza virus M1, is determined by common structural features of the HLA-A2.1 molecule. AN - 73010626; 1607654 AB - To determine whether similar or dissimilar molecular features of class I molecules are involved in the presentation of structurally distinct peptides, we have investigated the influence of different pockets of the HLA-A2.1 molecule on the presentation of three different viral peptides. HTLV-I Tax peptide 12-19, HCMV gB 619-628, and influenza M1 58-66 are minimal peptides that induce HLA-A2.1-restricted noncross-reactive CTL. A detailed analysis of the structural features of HLA-A2.1 that are involved in peptide presentation was undertaken using a panel of 11 HLA-A2 mutants with single amino acid substitutions within pockets present in the peptide binding site. Nine of the 11 mutants affected presentation of each of the three peptides, whereas the other two mutants had negative effects on presentation of only two of these viral peptides. These results indicate that common structural features in HLA-A2 determine the binding of different peptides, and help to provide a plausible explanation for how structurally diverse peptides bind to HLA-A2. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Utz, U AU - Koenig, S AU - Coligan, J E AU - Biddison, W E AD - Molecular Immunology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health (NIH), Bethesda, MD 20892. Y1 - 1992/07/01/ PY - 1992 DA - 1992 Jul 01 SP - 214 EP - 221 VL - 149 IS - 1 SN - 0022-1767, 0022-1767 KW - Antigens, Viral KW - 0 KW - Gene Products, tax KW - HLA-A2 Antigen KW - M-protein, influenza virus KW - M1 protein, Influenza A virus KW - Peptides KW - Viral Envelope Proteins KW - Viral Matrix Proteins KW - glycoprotein B, Simplexvirus KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Mutagenesis, Site-Directed KW - Cytotoxicity, Immunologic KW - Viral Envelope Proteins -- immunology KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Gene Products, tax -- immunology KW - Viral Matrix Proteins -- immunology KW - Structure-Activity Relationship KW - Binding Sites KW - Antigens, Viral -- metabolism KW - Peptides -- immunology KW - Human T-lymphotropic virus 1 -- immunology KW - Antigen-Presenting Cells -- immunology KW - HLA-A2 Antigen -- metabolism KW - HLA-A2 Antigen -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73010626?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Presentation+of+three+different+viral+peptides%2C+HTLV-1+Tax%2C+HCMV+gB%2C+and+influenza+virus+M1%2C+is+determined+by+common+structural+features+of+the+HLA-A2.1+molecule.&rft.au=Utz%2C+U%3BKoenig%2C+S%3BColigan%2C+J+E%3BBiddison%2C+W+E&rft.aulast=Utz&rft.aufirst=U&rft.date=1992-07-01&rft.volume=149&rft.issue=1&rft.spage=214&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-21 N1 - Date created - 1992-07-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phase I study of taxol and granulocyte colony-stimulating factor in patients with refractory ovarian cancer. AN - 73010258; 1376773 AB - To increase the taxol dose beyond the current standard dose intensity of 175 mg/m2 per 21 days in patients with refractory ovarian cancer. Fifteen patients who had platinum-refractory or recurrent advanced-stage ovarian cancer were treated with taxol in a phase I trial and were given granulocyte-colony stimulating factor (G-CSF). Taxol was administered at doses of 170, 200, 250, and 300 mg/m2 every 3 weeks. G-CSF was given as a daily subcutaneous injection that started 24 hours after the completion of the taxol infusion. Four patients required either taxol dose reduction or delay. The dose-limiting toxicity (DLT) was peripheral neuropathy, and it occurred at 300 mg/m2. This toxicity was manifested clinically as a stocking-and-glove sensory disturbance that primarily affected proprioception, and was associated with objective changes on nerve conduction studies in affected individuals. Mucositis was rarely observed. Substantial myelosuppression was observed, but was not dose-limiting. Five of 14 assessable patients experienced an objective response to therapy, with another five individuals who experienced a 30% to 45% reduction in tumor mass. Taxol can be safely administered in doses up to 250 mg/m2 with G-CSF support, which may make it possible to study taxol dose intensification. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Sarosy, G AU - Kohn, E AU - Stone, D A AU - Rothenberg, M AU - Jacob, J AU - Adamo, D O AU - Ognibene, F P AU - Cunnion, R E AU - Reed, E AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 1165 EP - 1170 VL - 10 IS - 7 SN - 0732-183X, 0732-183X KW - Alkaloids KW - 0 KW - Antineoplastic Agents, Phytogenic KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - Paclitaxel KW - P88XT4IS4D KW - Index Medicus KW - Drug Evaluation KW - Humans KW - Carcinoma -- drug therapy KW - Adult KW - Treatment Outcome KW - Aged KW - Middle Aged KW - Female KW - Granulocyte Colony-Stimulating Factor -- therapeutic use KW - Bone Marrow Diseases -- prevention & control KW - Bone Marrow Diseases -- chemically induced KW - Antineoplastic Agents, Phytogenic -- adverse effects KW - Alkaloids -- adverse effects KW - Antineoplastic Agents, Phytogenic -- administration & dosage KW - Ovarian Neoplasms -- drug therapy KW - Alkaloids -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73010258?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Phase+I+study+of+taxol+and+granulocyte+colony-stimulating+factor+in+patients+with+refractory+ovarian+cancer.&rft.au=Sarosy%2C+G%3BKohn%2C+E%3BStone%2C+D+A%3BRothenberg%2C+M%3BJacob%2C+J%3BAdamo%2C+D+O%3BOgnibene%2C+F+P%3BCunnion%2C+R+E%3BReed%2C+E&rft.aulast=Sarosy&rft.aufirst=G&rft.date=1992-07-01&rft.volume=10&rft.issue=7&rft.spage=1165&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=0732183X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-23 N1 - Date created - 1992-07-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Elevation of interleukin-6 in response to a chronic inflammatory stimulus in mice: inhibition by indomethacin. AN - 73006999; 1611085 AB - Intraperitoneal (i.p.) injection of a mineral oil such as pristane induces a chronic inflammatory response in mice. This is characterized by a large influx of macrophages and other inflammatory cells into the peritoneal cavity for months after injection of the oil. By using the B9 cell bioassay, it was found that injection of pristane caused a marked and prolonged elevation of interleukin-6 (IL-6) levels in the peritoneal cavities of the mice. IL-6 was undetectable (less than 15 U/mL) in the peritoneal fluids of unprimed mice and during the first week after injecting pristane. From 4 to 20 weeks, the concentration of IL-6 increased to an apparent plateau with concentrations ranging from 200 to 2,000 U/mL. Increasing the dose of pristane did not substantially increase the peritoneal levels of IL-6 established at 20 weeks after pristane treatment. At later times (by day 250), the level decreased to 263 +/- 217 U/mL. However, mice that developed plasma cell tumors around day 300 showed high levels of IL-6 in the ascites fluid (650 to 2,400 U/mL). Serum levels of IL-6 were also elevated in pristane-primed mice but were substantially lower than those found in the peritoneal cavity. Chronic administration of the nonsteroidal anti-inflammatory drug indomethacin decreased the levels of IL-6 by 75% to 80%. Experiments performed in vitro showed that pristane-elicited macrophages secreted low levels of IL-6 constitutively and high levels of IL-6 in the presence of lipopolysaccharide. Both IL-6 and prostaglandin E2 production were inhibited by addition of indomethacin to macrophage cultures in vitro. Treatment of mice with pristane may provide a model system for studying the inflammatory pathways that control IL-6 levels in vivo. The relevance of these results to elucidation of the role of IL-6 in plasma cell tumorigenesis is discussed. JF - Blood AU - Shacter, E AU - Arzadon, G K AU - Williams, J AD - Laboratory of Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/07/01/ PY - 1992 DA - 1992 Jul 01 SP - 194 EP - 202 VL - 80 IS - 1 SN - 0006-4971, 0006-4971 KW - Interleukin-6 KW - 0 KW - Lipopolysaccharides KW - Terpenes KW - pristane KW - 26HZV48DT1 KW - Dinoprostone KW - K7Q1JQR04M KW - Indomethacin KW - XXE1CET956 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Peritoneal Cavity -- cytology KW - Lipopolysaccharides -- administration & dosage KW - Terpenes -- administration & dosage KW - Dinoprostone -- biosynthesis KW - Dose-Response Relationship, Drug KW - Mice KW - Ascitic Fluid -- metabolism KW - Mice, Inbred BALB C KW - Time Factors KW - Interleukin-6 -- metabolism KW - Inflammation -- metabolism KW - Indomethacin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73006999?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Blood&rft.atitle=Elevation+of+interleukin-6+in+response+to+a+chronic+inflammatory+stimulus+in+mice%3A+inhibition+by+indomethacin.&rft.au=Shacter%2C+E%3BArzadon%2C+G+K%3BWilliams%2C+J&rft.aulast=Shacter&rft.aufirst=E&rft.date=1992-07-01&rft.volume=80&rft.issue=1&rft.spage=194&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-29 N1 - Date created - 1992-07-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hematopoietic stem cell depletion by restorative growth factor regimens during repeated high-dose cyclophosphamide therapy. AN - 73002362; 1377055 AB - We studied the effects of six cycles of repeated cyclophosphamide (CTX) therapy followed by restorative therapy with either granulocyte-macrophage colony-stimulating factor (GM-CSF) or G-CSF on the hematopoietic stem cell compartment. Stem cell function was assessed by serially transferring bone marrow cells from CTX-CSF-treated mice into lethally irradiated recipient mice. Bone marrow cells from mice that initially received either G-CSF or GM-CSF after CTX therapy more rapidly lost the ability to repopulate the recipient lymphoid organs, showed a dramatic loss of hematopoietic progenitors, a more rapid loss of CFU-S capacity, and a 40% to 50% reduction in marrow repopulating ability (MRA). Interleukin-1 (IL-1) appeared to have little effect on the CTX-treated mice when used alone. However, when administered before the CTX-CSF regimen, IL-1 prevented the stem cell depletion as determined by CFU-C, CFU-S, and MRA through the serial transplantation procedures. These results support the hypothesis that repeated treatments with myelosuppressive drugs followed by stimulation with the CSFs may induce damage to the host stem cell compartment, and further suggest that pretreatment with IL-1 before CTX therapy may prevent this stem cell damage. JF - Blood AU - Hornung, R L AU - Longo, D L AD - Biological Carcinogenesis & Development Program, Program Resources, Inc/DynCorp, National Cancer Institute-Frederick Cancer Research & Development Center 21702-1201. Y1 - 1992/07/01/ PY - 1992 DA - 1992 Jul 01 SP - 77 EP - 83 VL - 80 IS - 1 SN - 0006-4971, 0006-4971 KW - Antigens, Ly KW - 0 KW - Interleukin-1 KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - Granulocyte-Macrophage Colony-Stimulating Factor KW - 83869-56-1 KW - Cyclophosphamide KW - 8N3DW7272P KW - Abridged Index Medicus KW - Index Medicus KW - Bone Marrow Cells KW - Animals KW - Dose-Response Relationship, Drug KW - Antigens, Ly -- analysis KW - Mice, Inbred C57BL KW - Mice KW - Time Factors KW - Bone Marrow -- drug effects KW - Radiation Chimera KW - Female KW - Bone Marrow Transplantation KW - Granulocyte-Macrophage Colony-Stimulating Factor -- administration & dosage KW - Cyclophosphamide -- administration & dosage KW - Interleukin-1 -- administration & dosage KW - Hematopoiesis -- drug effects KW - Granulocyte Colony-Stimulating Factor -- administration & dosage KW - Hematopoietic Stem Cells -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73002362?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Blood&rft.atitle=Hematopoietic+stem+cell+depletion+by+restorative+growth+factor+regimens+during+repeated+high-dose+cyclophosphamide+therapy.&rft.au=Hornung%2C+R+L%3BLongo%2C+D+L&rft.aulast=Hornung&rft.aufirst=R&rft.date=1992-07-01&rft.volume=80&rft.issue=1&rft.spage=77&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-29 N1 - Date created - 1992-07-29 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Blood. 1992 Jul 1;80(1):3-7 [1377052] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of the murine homologue of the cell cycle control protein p34cdc2 in T lymphocytes. AN - 72999757; 1637418 AB - The mammalian homologue of the cdc2 gene of the fission yeast Schizosaccharomyces pombe encodes a p34cdc2 cyclin-dependent kinase that regulates the cell cycle of a wide variety of cell types. Resting murine T lymphocytes contained no detectable p34cdc2 protein, histone kinase activity, or specific mRNA for the cdc2 gene. Activation of the T cells by immobilized anti-CD3 resulted in the expression of specific mRNA late in the G1 phase of the cell cycle, and p34cdc2 protein was detectable at or near G1/S. At this point in the cell cycle, the protein was phosphorylated at tyrosine and displayed no H1 histone kinase activity. As the cells progressed through the cycle, the amount of specific mRNA and p34cdc2 increased, and H1 histone kinase activity was detectable when the cells were blocked at G2/M by nocodazole. The activation of T cells by phorbol dibutyrate induced the expression of IL-2R but failed to induce the synthesis of IL-2 or the expression of cdc2-specific mRNA. Under these conditions, the activated cells failed to enter the S phase of the cell cycle. Because the presence of IL-2 added exogenously during activation by phorbol dibutyrate resulted in the expression of cdc2-specific mRNA and progression through the cell cycle, either IL-2 or the interaction with IL-2R may be involved in the expression of cdc2 and regulation of the G1/S transition. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Kim, Y H AU - Proust, J J AU - Buchholz, M J AU - Chrest, F J AU - Nordin, A A AD - Clinical Immunology Section, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224. Y1 - 1992/07/01/ PY - 1992 DA - 1992 Jul 01 SP - 17 EP - 23 VL - 149 IS - 1 SN - 0022-1767, 0022-1767 KW - Proto-Oncogene Proteins KW - 0 KW - Proto-Oncogene Proteins c-myb KW - RNA, Messenger KW - Receptors, Interleukin-2 KW - Receptors, Transferrin KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Protein Kinases KW - EC 2.7.- KW - CDC2 Protein Kinase KW - EC 2.7.11.22 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Genes, myc KW - Gene Expression KW - Amino Acid Sequence KW - Mice KW - RNA, Messenger -- genetics KW - Receptors, Interleukin-2 -- genetics KW - Phorbol 12,13-Dibutyrate -- pharmacology KW - Protein Kinases -- metabolism KW - Blotting, Western KW - Cells, Cultured KW - Receptors, Transferrin -- genetics KW - In Vitro Techniques KW - Mice, Inbred C57BL KW - Molecular Sequence Data KW - Proto-Oncogene Proteins -- genetics KW - Lymphocyte Activation KW - CDC2 Protein Kinase -- genetics KW - T-Lymphocytes -- physiology KW - Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72999757?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Expression+of+the+murine+homologue+of+the+cell+cycle+control+protein+p34cdc2+in+T+lymphocytes.&rft.au=Kim%2C+Y+H%3BProust%2C+J+J%3BBuchholz%2C+M+J%3BChrest%2C+F+J%3BNordin%2C+A+A&rft.aulast=Kim&rft.aufirst=Y&rft.date=1992-07-01&rft.volume=149&rft.issue=1&rft.spage=17&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-21 N1 - Date created - 1992-07-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of ultraviolet radiation on murine epidermal Langerhans cells: doses of ultraviolet radiation that modulate ICAM-1 (CD54) expression and inhibit Langerhans cell function cause delayed cytotoxicity in vitro. AN - 72994537; 1351507 AB - Low doses (100 J/m2) of ultraviolet B (UVB) radiation from sunlamp fluorescent FS20 tubes inhibit the ability of freshly isolated murine epidermal Langerhans cells (LC) to support anti-CD3 MoAb-induced T-cell mitogenesis and selectively inhibit the upregulation of ICAM-1 expression by LC without causing appreciable cytotoxicity in short-term (less than or equal to 24 h) incubations (J Immunol 146:3347-3355, 1991). In the present study, epidermal cells (EC) were exposed to UVB radiation or were sham-irradiated and cultured for 24, 48, or 72 h when LC were recovered, enumerated, and assayed for simultaneous expression of I-A antigens and ICAM-1 by flow cytometry. UVB-irradiated LC that had been cultured for 24 h exhibited levels of I-A antigens comparable to those on unirradiated LC but expressed substantially less ICAM-1. After 48 and 72 h, cultured UVB-irradiated LC expressed somewhat lower levels of I-A antigens and markedly less ICAM-1 than unirradiated controls. Although similar numbers of LC were recovered from cultures initiated with UVB-irradiated and unirradiated epidermal cells after 24 h, far fewer identifiable LC were recovered from cultures seeded with irradiated cells at 48 and 72 h (approximately 50 and approximately 10% of control, respectively). The effect of UVB radiation on the survival of LC in vitro was not reversible with exogenous TNF alpha (125 U/ml) alone or granulocyte/macrophage colony-stimulating factor (5 ng/ml) and IL-1 (50 U/ml) in combination, although these cytokines had modest effects on the expression of I-A antigens and ICAM-1 by cultured UVB-irradiated LC. Results of survival studies performed with enriched LC preparations demonstrated that UVB radiation was clearly cytotoxic for LC and did not merely downregulate surface expression of I-A antigens or alter LC buoyant density. Exposure of LC to radiation from blacklight fluorescent (UVA) tubes (0.25 J/cm2) in the presence of 8-methoxypsoralen (1 micrograms/ml; PUVA) or monochromatic UVC radiation (20 J/m2) also inhibited LC accessory cell function. Results of survival studies performed with EC that had been exposed to PUVA or UVC radiation before culture were similar to those of studies performed with UVB-irradiated cells, although PUVA- and UVC-induced LC cytotoxicity was much more pronounced 48 h after culture initiation than UVB-induced cytotoxicity. UVA radiation alone augmented LC recovery at 24 and 48 h, but did not influence I-A antigen or ICAM-1 expression.(ABSTRACT TRUNCATED AT 400 WORDS) JF - The Journal of investigative dermatology AU - Tang, A AU - Udey, M C AD - Dermatology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 83 EP - 89 VL - 99 IS - 1 SN - 0022-202X, 0022-202X KW - Cell Adhesion Molecules KW - 0 KW - Cytokines KW - Histocompatibility Antigens Class II KW - Intercellular Adhesion Molecule-1 KW - 126547-89-5 KW - Index Medicus KW - Animals KW - Cell Adhesion Molecules -- genetics KW - Cytokines -- pharmacology KW - PUVA Therapy KW - Mice KW - Dose-Response Relationship, Radiation KW - Mice, Inbred BALB C KW - Gene Expression Regulation -- radiation effects KW - Cell Survival -- drug effects KW - Antigen-Presenting Cells -- physiology KW - Histocompatibility Antigens Class II -- physiology KW - Antigen-Presenting Cells -- radiation effects KW - Cell Survival -- radiation effects KW - Female KW - Langerhans Cells -- radiation effects KW - Ultraviolet Rays KW - Langerhans Cells -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72994537?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+investigative+dermatology&rft.atitle=Effects+of+ultraviolet+radiation+on+murine+epidermal+Langerhans+cells%3A+doses+of+ultraviolet+radiation+that+modulate+ICAM-1+%28CD54%29+expression+and+inhibit+Langerhans+cell+function+cause+delayed+cytotoxicity+in+vitro.&rft.au=Tang%2C+A%3BUdey%2C+M+C&rft.aulast=Tang&rft.aufirst=A&rft.date=1992-07-01&rft.volume=99&rft.issue=1&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+investigative+dermatology&rft.issn=0022202X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-22 N1 - Date created - 1992-07-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Statistical methods for short-term tests in genetic toxicology: the first fifteen years. AN - 72993418; 1376440 AB - Short-term tests (STTs) for detecting and assessing genotoxic or mutagenic effects have catalyzed the development of biostatistical methods for more than one decade. Most notably, the Ames Salmonella/microsome assay created statistical methodology with a range of applications going beyond genotoxicity. Early approaches with parametric statistical methods appeared to be insufficient and have been replaced by non-parametric ones requiring less restrictive distributional assumptions. There have also been successful attempts to use biomathematical models for establishing dose-response relationships. Overdispersion has been recognized as a major problem for the evaluation of mutagenic count data and methods to cope with it have became available. A theory of generalized linear modelling is emerging to combine dose-response modeling with much less restrictive distributional assumptions, while allowing the inclusion of concomitant factors arising from the experimental conditions. The methodological survey below reviews the present state of this development and is intended to promote further research into biostatistical issues and methods of analysis. Appropriate methods for the design and analysis of STTs are discussed. The progress for the Ames assay was only partially transmitted to the analysis of the large number of other short-term assays. Several such assays are reviewed with respect to their present state of statistical evaluation. JF - Mutation research AU - Edler, L AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 11 EP - 33 VL - 277 IS - 1 SN - 0027-5107, 0027-5107 KW - Index Medicus KW - Animals KW - Models, Genetic KW - Models, Statistical KW - Mutagenicity Tests KW - Statistics as Topic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72993418?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+research&rft.atitle=Statistical+methods+for+short-term+tests+in+genetic+toxicology%3A+the+first+fifteen+years.&rft.au=Edler%2C+L&rft.aulast=Edler&rft.aufirst=L&rft.date=1992-07-01&rft.volume=277&rft.issue=1&rft.spage=11&rft.isbn=&rft.btitle=&rft.title=Mutation+research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-16 N1 - Date created - 1992-07-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - NMDA receptors: role in ethanol withdrawal seizures. AN - 73068719; 1321581 JF - Annals of the New York Academy of Sciences AU - Hoffman, P L AU - Grant, K A AU - Snell, L D AU - Reinlib, L AU - Iorio, K AU - Tabakoff, B AD - Laboratory of Physiologic and Pharmacologic Studies, National Institute on Alcohol Abuse and Alcoholism Rockville, Maryland 20852. Y1 - 1992/06/28/ PY - 1992 DA - 1992 Jun 28 SP - 52 EP - 60 VL - 654 SN - 0077-8923, 0077-8923 KW - Receptors, GABA-A KW - 0 KW - Receptors, N-Methyl-D-Aspartate KW - Index Medicus KW - Animals KW - Receptors, GABA-A -- physiology KW - Humans KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Substance Withdrawal Syndrome -- physiopathology KW - Seizures -- physiopathology KW - Alcoholism -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73068719?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=NMDA+receptors%3A+role+in+ethanol+withdrawal+seizures.&rft.au=Hoffman%2C+P+L%3BGrant%2C+K+A%3BSnell%2C+L+D%3BReinlib%2C+L%3BIorio%2C+K%3BTabakoff%2C+B&rft.aulast=Hoffman&rft.aufirst=P&rft.date=1992-06-28&rft.volume=654&rft.issue=&rft.spage=52&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-17 N1 - Date created - 1992-08-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Conditioned sensitization to the psychomotor stimulant cocaine. AN - 73067394; 1632592 JF - Annals of the New York Academy of Sciences AU - Post, R M AU - Weiss, S R AU - Fontana, D AU - Pert, A AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1992/06/28/ PY - 1992 DA - 1992 Jun 28 SP - 386 EP - 399 VL - 654 SN - 0077-8923, 0077-8923 KW - Cocaine KW - I5Y540LHVR KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Substance-Related Disorders -- physiopathology KW - Animals KW - Humans KW - Dopamine -- metabolism KW - Substance-Related Disorders -- psychology KW - Conditioning (Psychology) KW - Brain -- drug effects KW - Motor Activity -- drug effects KW - Cocaine -- pharmacology KW - Cocaine -- administration & dosage KW - Brain -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73067394?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=Conditioned+sensitization+to+the+psychomotor+stimulant+cocaine.&rft.au=Post%2C+R+M%3BWeiss%2C+S+R%3BFontana%2C+D%3BPert%2C+A&rft.aulast=Post&rft.aufirst=R&rft.date=1992-06-28&rft.volume=654&rft.issue=&rft.spage=386&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-17 N1 - Date created - 1992-08-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The role of solvent viscosity in the dynamics of protein conformational changes. AN - 73016715; 1615323 AB - Nanosecond lasers were used to measure the rate of conformational changes in myoglobin after ligand dissociation at ambient temperatures. At low solvent viscosities the rate is independent of viscosity, but at high viscosities it depends on approximately the inverse first power of the viscosity. Kramers theory for unimolecular rate processes can be used to explain this result if the friction term is modified to include protein as well as solvent friction. The theory and experiment suggest that the dominant factor in markedly reducing the rate of conformational changes in myoglobin at low temperatures (less than 200 K) is the very high viscosity (greater than 10(7) centipoise) of the glycerol-water solvent. That is, at low temperatures conformational substates may not be "frozen" so much as "stuck." JF - Science (New York, N.Y.) AU - Ansari, A AU - Jones, C M AU - Henry, E R AU - Hofrichter, J AU - Eaton, W A AD - Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06/26/ PY - 1992 DA - 1992 Jun 26 SP - 1796 EP - 1798 VL - 256 IS - 5065 SN - 0036-8075, 0036-8075 KW - Myoglobin KW - 0 KW - Solvents KW - Carbon Monoxide KW - 7U1EE4V452 KW - Index Medicus KW - Hot Temperature KW - Viscosity KW - Spectrophotometry, Atomic KW - Lasers KW - Protein Conformation KW - Myoglobin -- chemistry KW - Solvents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73016715?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft.atitle=The+role+of+solvent+viscosity+in+the+dynamics+of+protein+conformational+changes.&rft.au=Ansari%2C+A%3BJones%2C+C+M%3BHenry%2C+E+R%3BHofrichter%2C+J%3BEaton%2C+W+A&rft.aulast=Ansari&rft.aufirst=A&rft.date=1992-06-26&rft.volume=256&rft.issue=5065&rft.spage=1796&rft.isbn=&rft.btitle=&rft.title=Science+%28New+York%2C+N.Y.%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-24 N1 - Date created - 1992-07-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Risk of leukemia after chemotherapy and radiation treatment for breast cancer. AN - 72966855; 1594016 AB - Few studies have evaluated the late effects of adjuvant chemotherapy for breast cancer. Moreover, the relation between the risk of leukemia and the amount of drug given and the interaction of chemotherapy with radiotherapy have not been described in detail. We conducted a case-control study in a cohort of 82,700 women given a diagnosis of breast cancer from 1973 to 1985 in five areas of the United States. Detailed information about therapy was obtained for 90 patients with leukemia and 264 matched controls. The dose of radiation to the active marrow was estimated from individual radiotherapy records (mean dose, 7.5 Gy). The risk of acute nonlymphocytic leukemia was significantly increased after regional radiotherapy alone (relative risk, 2.4), alkylating agents alone (relative risk, 10.0), and combined radiation and drug therapy (relative risk, 17.4). Dose-dependent risks were observed after radiotherapy and treatment with melphalan and cyclophosphamide. Melphalan was 10 times more leukemogenic than cyclophosphamide (relative risk, 31.4 vs. 3.1). There was little increase in the risk associated with total cyclophosphamide doses of less than 20,000 mg. Although leukemia occurs in few patients with breast cancer, significantly elevated risks were linked to treatments with regional radiation and alkylating agents. Melphalan is a more potent leukemogen than cyclophosphamide or radiotherapy. Low risks were associated with the levels of cyclophosphamide in common use today. Systemic drug therapy combined with radiotherapy that delivers high doses to the marrow appears to enhance the risk of leukemia. JF - The New England journal of medicine AU - Curtis, R E AU - Boice, J D AU - Stovall, M AU - Bernstein, L AU - Greenberg, R S AU - Flannery, J T AU - Schwartz, A G AU - Weyer, P AU - Moloney, W C AU - Hoover, R N AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, Md. 20892. Y1 - 1992/06/25/ PY - 1992 DA - 1992 Jun 25 SP - 1745 EP - 1751 VL - 326 IS - 26 SN - 0028-4793, 0028-4793 KW - Alkylating Agents KW - 0 KW - Cyclophosphamide KW - 8N3DW7272P KW - Melphalan KW - Q41OR9510P KW - Abridged Index Medicus KW - Index Medicus KW - Dose-Response Relationship, Drug KW - Humans KW - Leukemia, Radiation-Induced -- etiology KW - Aged KW - Combined Modality Therapy -- adverse effects KW - Dose-Response Relationship, Radiation KW - Radiotherapy -- adverse effects KW - Cyclophosphamide -- adverse effects KW - Risk KW - Radiotherapy Dosage KW - Leukemia, Myeloid, Acute -- etiology KW - Melphalan -- adverse effects KW - Case-Control Studies KW - Middle Aged KW - Alkylating Agents -- adverse effects KW - Myelodysplastic Syndromes -- etiology KW - Female KW - Breast Neoplasms -- drug therapy KW - Breast Neoplasms -- therapy KW - Leukemia -- etiology KW - Breast Neoplasms -- radiotherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72966855?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Physiology+%26+Behavior&rft.atitle=The+role+of+breakfast+and+a+mid-morning+snack+on+the+ability+of+children+to+concentrate+at+school&rft.au=Benton%2C+David%3BJarvis%2C+Megan&rft.aulast=Benton&rft.aufirst=David&rft.date=2007-02-01&rft.volume=90&rft.issue=2-3&rft.spage=382&rft.isbn=&rft.btitle=&rft.title=Physiology+%26+Behavior&rft.issn=00319384&rft_id=info:doi/10.1016%2Fj.physbeh.2006.09.029 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-26 N1 - Date created - 1992-06-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: N Engl J Med. 1992 Jun 25;326(26):1774-5 [1594020] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dolastatin 15, a potent antimitotic depsipeptide derived from Dolabella auricularia. Interaction with tubulin and effects of cellular microtubules. AN - 73070523; 1632820 AB - Dolastatin 15, a seven-subunit depsipeptide derived from Dolabella auricularia, is a potent antimitotic agent structurally related to the antitubulin agent dolastatin 10, a five-subunit peptide obtained from the same organism. We have compared dolastatin 15 with dolastatin 10 for its effects on cells grown in culture and on biochemical properties of tubulin. The IC50 values for cell growth were obtained for dolastatin 15 with L1210 murine leukemia cells, human Burkitt lymphoma cells, and Chinese hamster ovary (CHO) cells (3, 3, and 5 nM with the three cell lines, respectively). For dolastatin 10, IC50 values of 0.4 and 0.5 nM were obtained with the L1210 and CHO cells, respectively. At toxic concentrations dolastatin 15 caused the leukemia and lymphoma cells to arrest in mitosis. In the CHO cells both dolastatin 15 and dolastatin 10 caused moderate loss of microtubules at the IC50 values and complete disappearance of microtubules at concentrations 10-fold higher. Despite its potency and the loss of microtubules in treated cells, the interaction of dolastatin 15 with tubulin in vitro was weak. Its IC50 value for inhibition of glutamate-induced polymerization of tubulin was 23 microM, as compared to values of 1.2 microM for dolastatin 10 and 1.5 microM for vinblastine. Dolastatin 10 noncompetitively inhibits the binding of vincristine to tubulin, inhibits nucleotide exchange, stabilizes the colchicine binding activity of tubulin, and inhibits tubulin-dependent GTP hydrolysis (Bai et al., Biochem Pharmacol 39: 1941-1949, 1990; Bai et al. J Biol Chem 265: 17141-17149, 1990). Only the latter reaction was inhibited by dolastatin 15. Nevertheless, its structural similarity to dolastatin 10 indicates that dolastatin 15 may bind weakly in the "vinca domain" of tubulin (a region of the protein we postulate to be physically close to but not identical with the specific binding site of vinca alkaloids and maytansinoids), presumably in the same site as dolastatin 10 (the "peptide site"). JF - Biochemical pharmacology AU - Bai, R AU - Friedman, S J AU - Pettit, G R AU - Hamel, E AD - Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06/23/ PY - 1992 DA - 1992 Jun 23 SP - 2637 EP - 2645 VL - 43 IS - 12 SN - 0006-2952, 0006-2952 KW - Antineoplastic Agents KW - 0 KW - Depsipeptides KW - Glutamates KW - Microtubule-Associated Proteins KW - Oligopeptides KW - Tubulin KW - dolastatin 10 KW - 110417-88-4 KW - dolastatin 15 KW - 123884-00-4 KW - Vinblastine KW - 5V9KLZ54CY KW - Guanosine Triphosphate KW - 86-01-1 KW - Index Medicus KW - Vinblastine -- pharmacology KW - Cell Line -- ultrastructure KW - Animals KW - Mitotic Index -- drug effects KW - Microtubule-Associated Proteins -- pharmacology KW - Glutamates -- pharmacology KW - Cell Line -- drug effects KW - Molecular Sequence Data KW - Cell Line -- cytology KW - Amino Acid Sequence KW - Guanosine Triphosphate -- metabolism KW - Binding Sites KW - Tubulin -- chemistry KW - Mollusca -- chemistry KW - Antineoplastic Agents -- isolation & purification KW - Tubulin -- metabolism KW - Oligopeptides -- isolation & purification KW - Antineoplastic Agents -- chemical synthesis KW - Oligopeptides -- pharmacology KW - Microtubules -- drug effects KW - Oligopeptides -- chemical synthesis KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73070523?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+pharmacology&rft.atitle=Dolastatin+15%2C+a+potent+antimitotic+depsipeptide+derived+from+Dolabella+auricularia.+Interaction+with+tubulin+and+effects+of+cellular+microtubules.&rft.au=Bai%2C+R%3BFriedman%2C+S+J%3BPettit%2C+G+R%3BHamel%2C+E&rft.aulast=Bai&rft.aufirst=R&rft.date=1992-06-23&rft.volume=43&rft.issue=12&rft.spage=2637&rft.isbn=&rft.btitle=&rft.title=Biochemical+pharmacology&rft.issn=00062952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-14 N1 - Date created - 1992-08-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Frequent expression of the tumor antigen CAK1 in squamous-cell carcinomas. AN - 72977283; 1351045 AB - K1 is a murine monoclonal antibody (MAb) derived from a hybridoma generated by the fusion of splenocytes of BALB/c mice immunized with a human ovarian tumor cell line, OVCAR-3. This antibody reacts strongly with epithelial ovarian tumors and mesotheliomas. The antigen recognized by MAb K1, designated CAK1, has recently been characterized as a 40-kDa protein probably anchored to the cell surface by glycosyl-phosphatidylinositol. Using immunoperoxidase histochemical methods, we examined 37 squamous-cell carcinoma (SqCC) samples from cervix, lung, esophagus and other origins, and 12 normal squamous epithelia of the cervix and esophagus for their reactivity with MAb K1. Of the SqCC specimens, 81% showed K1 reactivity with variable intensity, but none of 12 normal tissue samples of squamous epithelia did so. Two patterns of CAK1 expression in tumor samples were found, i.e., a heterogeneous pattern with strong intensity, and a homogeneous pattern with weak intensity. Three carcinomas in situ of the larynx, vulva and esophagus were moderately positive with K1, suggesting that CAK1 antigen may occur in the early stage of carcinogenesis of SqCC. The expression of CAK1 was also compared with expression of CA125, HER-2/neu, p53 and P-glycoprotein, and MAb K1 was found to react most consistently with SqCC. Since K1 reacts with a majority of cervical and esophageal carcinomas but has no detectable reactivity in normal epithelia of the cervix uteri and esophagus, MAb K1 could be of value as a reagent to help distinguish between normal and neoplastic cells on sections as well as in cytological samples. JF - International journal of cancer AU - Chang, K AU - Pastan, I AU - Willingham, M C AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06/19/ PY - 1992 DA - 1992 Jun 19 SP - 548 EP - 554 VL - 51 IS - 4 SN - 0020-7136, 0020-7136 KW - Antigens, Neoplasm KW - 0 KW - Butanols KW - Membrane Glycoproteins KW - Oncogene Proteins, Viral KW - P-Glycoprotein KW - Tumor Suppressor Protein p53 KW - 1-Butanol KW - 8PJ61P6TS3 KW - Receptor, ErbB-2 KW - EC 2.7.10.1 KW - Phosphoric Diester Hydrolases KW - EC 3.1.4.- KW - Phosphoinositide Phospholipase C KW - EC 3.1.4.11 KW - Index Medicus KW - Tumor Suppressor Protein p53 -- analysis KW - Humans KW - Oncogene Proteins, Viral -- analysis KW - Membrane Glycoproteins -- analysis KW - Epithelium -- immunology KW - Female KW - Carcinoma, Squamous Cell -- immunology KW - Mouth Neoplasms -- immunology KW - Lung Neoplasms -- immunology KW - Antigens, Neoplasm -- analysis KW - Uterine Cervical Neoplasms -- immunology KW - Esophageal Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72977283?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=Frequent+expression+of+the+tumor+antigen+CAK1+in+squamous-cell+carcinomas.&rft.au=Chang%2C+K%3BPastan%2C+I%3BWillingham%2C+M+C&rft.aulast=Chang&rft.aufirst=K&rft.date=1992-06-19&rft.volume=51&rft.issue=4&rft.spage=548&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=00207136&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-13 N1 - Date created - 1992-07-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pilot study of interleukin-2 and lymphokine-activated killer cells combined with immunomodulatory doses of chemotherapy and sequenced with interferon alfa-2a in patients with metastatic melanoma and renal cell carcinoma. AN - 73052862; 1629914 AB - Experiments in animal tumor models suggest that the antitumor effects of interleukin-2 (IL-2) or IL-2 in combination with lymphokine-activated killer (LAK) cells can be enhanced by chemotherapy agents such as cyclophosphamide or doxorubicin or by the biologic agent interferon alpha. We determined the toxicity and clinical response rate of an IL-2-LAK cell regimen modified by the addition of moderate, immunomodulatory doses of chemotherapy and sequenced with interferon alfa-2a (IFN alpha-2a) in patients with metastatic melanoma and renal cell carcinoma. IL-2 (3-6 million units/m2 per day) was administered by continuous infusion on days 0-5 and days 11-16. LAK cells were infused on days 11 and 12 or on days 11, 12, and 14. Low doses of cyclophosphamide (300 mg/m2) and doxorubicin (25 mg/m2) were given on day 9 before the LAK cell infusions. Following the IL-2-LAK cell infusion, IFN alpha-2a (12 million units/m2) was administered for a total of nine doses to complete a cycle of treatment. A total of 89 patients were enrolled in the study. For each histology, there were eight partial responses in 40 assessable patients, for an overall response rate of 20% (90% confidence interval = 10%-33%). The median response duration was 5 months, although two patients with renal cell carcinoma and one patient with metastatic melanoma had almost complete disappearance of tumor and are still responding after 26+, 22+, and 26+ months, respectively. Toxic effects were severe in patients receiving the highest dose of IL-2 administered in this study and similar to those reported with other high-dose IL-2-LAK cell regimens. Although toxic effects were completely reversible in most patients, there were four treatment-related deaths. This regimen is active in patients with metastatic melanoma and renal cell carcinoma and produces meaningful responses in a small percentage of these patients; however, it is not clear whether cyclophosphamide, doxorubicin, and IFN alpha-2a as used in this protocol appreciably augmented the antitumor activity of the IL-2-LAK cell regimen. JF - Journal of the National Cancer Institute AU - Sznol, M AU - Clark, J W AU - Smith, J W AU - Steis, R G AU - Urba, W J AU - Rubinstein, L V AU - VanderMolen, L A AU - Janik, J AU - Sharfman, W H AU - Fenton, R G AD - Division of Cancer Treatment, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06/17/ PY - 1992 DA - 1992 Jun 17 SP - 929 EP - 937 VL - 84 IS - 12 SN - 0027-8874, 0027-8874 KW - Interferon-alpha KW - 0 KW - Interleukin-2 KW - Recombinant Proteins KW - interferon alfa-2a KW - 47RRR83SK7 KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Doxorubicin -- adverse effects KW - Drug Administration Schedule KW - Infusions, Intravenous KW - Humans KW - Immunotherapy KW - Aged KW - Heart -- drug effects KW - Pilot Projects KW - Doxorubicin -- administration & dosage KW - Cyclophosphamide -- adverse effects KW - Immune System -- drug effects KW - Adult KW - Lung -- drug effects KW - Middle Aged KW - Male KW - Female KW - Kidney Neoplasms -- therapy KW - Interleukin-2 -- adverse effects KW - Interferon-alpha -- therapeutic use KW - Interferon-alpha -- adverse effects KW - Carcinoma, Renal Cell -- therapy KW - Interleukin-2 -- therapeutic use KW - Melanoma -- therapy KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Killer Cells, Lymphokine-Activated -- transplantation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73052862?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Pilot+study+of+interleukin-2+and+lymphokine-activated+killer+cells+combined+with+immunomodulatory+doses+of+chemotherapy+and+sequenced+with+interferon+alfa-2a+in+patients+with+metastatic+melanoma+and+renal+cell+carcinoma.&rft.au=Sznol%2C+M%3BClark%2C+J+W%3BSmith%2C+J+W%3BSteis%2C+R+G%3BUrba%2C+W+J%3BRubinstein%2C+L+V%3BVanderMolen%2C+L+A%3BJanik%2C+J%3BSharfman%2C+W+H%3BFenton%2C+R+G&rft.aulast=Sznol&rft.aufirst=M&rft.date=1992-06-17&rft.volume=84&rft.issue=12&rft.spage=929&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-17 N1 - Date created - 1992-08-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A1 adenosine-receptor antagonists activate chloride efflux from cystic fibrosis cells. AN - 73015578; 1376923 AB - A1 adenosine-receptor-antagonist drugs such as 8-cyclopentyl-1,3-dipropylxanthine (CPX) and xanthine amine congener (XAC) are found to activate the efflux of 36Cl- from CFPAC cells. These cells are a pancreatic adenocarcinoma cell line derived from a cystic fibrosis (CF) patient homozygous for the common mutation, deletion of Phe-508. The active concentrations for these compounds are in the low nanomolar range, consistent with action on A1 adenosine receptors. In addition, drug action can be blocked by exogenous agonists such as 2-chloroadenosine and also can be antagonized by removal of endogenous agonists by treatment with adenosine deaminase. Cells lacking the CF genotype and phenotype, such as HT-29 and T84 colon carcinoma cell lines, appear to be resistant to activation of chloride efflux by either drug. CFPAC cells transfected with the CF transmembrane regulator gene, CFTR, are also resistant to activation by CPX. We conclude that, since these antagonists are of relatively low toxicity and appear to act somewhat selectively, they might be considered as promising therapeutic candidates for CF. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Eidelman, O AU - Guay-Broder, C AU - van Galen, P J AU - Jacobson, K A AU - Fox, C AU - Turner, R J AU - Cabantchik, Z I AU - Pollard, H B AD - Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 5562 EP - 5566 VL - 89 IS - 12 SN - 0027-8424, 0027-8424 KW - CFTR protein, human KW - 0 KW - Chlorides KW - Membrane Proteins KW - Purinergic Antagonists KW - Xanthines KW - Cystic Fibrosis Transmembrane Conductance Regulator KW - 126880-72-6 KW - 2-Chloroadenosine KW - 146-77-0 KW - 1,3-dipropyl-8-cyclopentylxanthine KW - 9PTP4FOI9E KW - Adenosine KW - K72T3FS567 KW - Index Medicus KW - Chromosome Deletion KW - Humans KW - Pancreatic Neoplasms KW - Membrane Proteins -- genetics KW - Phenotype KW - Genotype KW - Kinetics KW - 2-Chloroadenosine -- pharmacology KW - Adenocarcinoma KW - Colonic Neoplasms KW - Mutation KW - Cell Line KW - Adenosine -- pharmacology KW - Cystic Fibrosis -- genetics KW - Adenosine -- analogs & derivatives KW - Cystic Fibrosis -- physiopathology KW - Chlorides -- metabolism KW - Xanthines -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73015578?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=A1+adenosine-receptor+antagonists+activate+chloride+efflux+from+cystic+fibrosis+cells.&rft.au=Eidelman%2C+O%3BGuay-Broder%2C+C%3Bvan+Galen%2C+P+J%3BJacobson%2C+K+A%3BFox%2C+C%3BTurner%2C+R+J%3BCabantchik%2C+Z+I%3BPollard%2C+H+B&rft.aulast=Eidelman&rft.aufirst=O&rft.date=1992-06-15&rft.volume=89&rft.issue=12&rft.spage=5562&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-21 N1 - Date created - 1992-07-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Neurosci Lett. 1989 Apr 24;99(1-2):107-12 [2748004] Science. 1989 Sep 8;245(4922):1073-80 [2570460] J Clin Invest. 1986 Feb;77(2):348-54 [3003156] Proc Natl Acad Sci U S A. 1985 Sep;82(18):6167-71 [3862125] Am J Physiol. 1982 Feb;242(2):G116-23 [6121487] J Clin Invest. 1984 Sep;74(3):929-35 [6206092] Science. 1983 Sep 9;221(4615):1067-70 [6308769] Nature. 1983 Feb 3;301(5899):421-2 [6823316] N Engl J Med. 1983 May 19;308(20):1185-9 [6843595] Proc Natl Acad Sci U S A. 1990 May;87(10):4012-6 [1692630] Nature. 1991 Dec 19-26;354(6354):526-8 [1722027] J Med Chem. 1992 Feb 7;35(3):407-22 [1738138] J Biol Chem. 1991 Jun 5;266(16):10319-23 [2037584] FASEB J. 1990 Jul;4(10):2709-17 [2197151] Am J Physiol. 1989 Jun;256(6 Pt 1):C1111-9 [2472065] Naunyn Schmiedebergs Arch Pharmacol. 1989 Aug;340(2):204-9 [2554151] Br J Pharmacol. 1989 Nov;98(3):1066-74 [2590769] J Clin Invest. 1985 Nov;76(5):1837-42 [2997291] Biochem Pharmacol. 1988 Oct 1;37(19):3653-61 [3178879] Biochem J. 1971 Mar;122(1):115-20 [4330960] Proc Natl Acad Sci U S A. 1981 May;78(5):3260-4 [6265942] Am J Physiol. 1984 Oct;247(4 Pt 2):R646-9 [6496713] J Clin Invest. 1983 May;71(5):1410-7 [6853720] J Clin Invest. 1992 Mar;89(3):834-41 [1311718] Proc Natl Acad Sci U S A. 1992 Mar 1;89(5):1539-43 [1371876] J Recept Res. 1992;12(2):149-69 [1583620] J Pharm Pharmacol. 1991 Feb;43(2):138-9 [1672902] FASEB J. 1990 Jul;4(10):2718-25 [1695593] Cell. 1990 Sep 21;62(6):1227-33 [1698126] Science. 1991 Dec 20;254(5039):1797-9 [1722350] J Clin Invest. 1991 Dec;88(6):1933-9 [1752953] N Engl J Med. 1991 Aug 22;325(8):533-8 [1857389] N Engl J Med. 1990 Apr 26;322(17):1189-94 [2157983] Science. 1989 Jun 16;244(4910):1353-6 [2472006] Science. 1989 Sep 8;245(4922):1066-73 [2475911] Am J Physiol. 1989 Jan;256(1 Pt 1):C197-203 [2536228] Science. 1989 Sep 8;245(4922):1059-65 [2772657] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interlocus V-J recombination measures genomic instability in agriculture workers at risk for lymphoid malignancies. AN - 73012001; 1608939 AB - V(D)J [variable-(diversity)-joining] rearrangements occur between, as well as within, immune receptor loci, resulting in the generation of hybrid antigen-receptor genes and the formation of a variety of lymphocyte-specific chromosomal aberrations. Such hybrid genes occur at a low frequency in the peripheral blood lymphocytes (PBL) of normal individuals but show a markedly increased incidence in the PBL of individuals with the autosomal recessive disease ataxia-telangiectasia. In this manuscript we demonstrate that the frequency of hybrid antigen-receptor genes is 10- to 20-fold increased in the PBL of an occupational group, agriculture workers, with related environmental exposures. Both ataxia-telangiectasia patients and this population of agriculture workers are at increased risk for lymphoid malignancy. This result suggests that the measurement of hybrid antigen receptor-genes in PBL may be a sensitive assay for a type of lymphocyte-specific genomic instability. As a corollary, this assay may identify populations at risk of developing common types of lymphoid malignancy. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Lipkowitz, S AU - Garry, V F AU - Kirsch, I R AD - National Cancer Institute-Navy Medical Oncology Branch, Bethesda Naval Hospital, MD 20889-5105. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 5301 EP - 5305 VL - 89 IS - 12 SN - 0027-8424, 0027-8424 KW - Immunoglobulin Joining Region KW - 0 KW - Immunoglobulin Variable Region KW - Oligodeoxyribonucleotides KW - Receptors, Antigen, T-Cell KW - DNA KW - 9007-49-2 KW - Index Medicus KW - DNA -- isolation & purification KW - Base Sequence KW - Risk Factors KW - Humans KW - Polymerase Chain Reaction -- methods KW - DNA -- genetics KW - Molecular Sequence Data KW - Immunoglobulin Variable Region -- genetics KW - Lymphoma -- etiology KW - Agricultural Workers' Diseases -- immunology KW - Lymphoma -- genetics KW - Agricultural Workers' Diseases -- genetics KW - Recombination, Genetic KW - Gene Rearrangement KW - Lymphoma -- immunology KW - Receptors, Antigen, T-Cell -- genetics KW - Chromosomes, Human, Pair 7 KW - Immunoglobulin Joining Region -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73012001?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Interlocus+V-J+recombination+measures+genomic+instability+in+agriculture+workers+at+risk+for+lymphoid+malignancies.&rft.au=Lipkowitz%2C+S%3BGarry%2C+V+F%3BKirsch%2C+I+R&rft.aulast=Lipkowitz&rft.aufirst=S&rft.date=1992-06-15&rft.volume=89&rft.issue=12&rft.spage=5301&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-21 N1 - Date created - 1992-07-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: FASEB J. 1989 Oct;3(12):2344-59 [2676678] Cell. 1987 Jul 3;50(1):97-105 [3036367] Hum Genet. 1989 Nov;83(4):347-52 [2807275] Science. 1989 Oct 13;246(4927):251-5 [2799386] Cell. 1985 Dec;43(3 Pt 2):705-13 [3935328] Science. 1985 Sep 27;229(4720):1390-3 [3929382] Scand J Work Environ Health. 1985 Dec;11(6):397-407 [3912986] Proc Natl Acad Sci U S A. 1985 Dec;82(24):8624-8 [3866244] J Natl Cancer Inst. 1990 May 16;82(10):840-8 [2332902] J Exp Med. 1990 Aug 1;172(2):409-18 [1695665] Nature. 1983 Apr 14;302(5909):575-81 [6300689] Science. 1984 Jun 29;224(4656):1403-6 [6610211] Proc Natl Acad Sci U S A. 1983 Apr;80(7):1982-6 [6572957] J Genet Hum. 1981 Sep;29(3):235-47 [6950025] Mutat Res. 1980 Feb;69(2):369-74 [7360152] Nucleic Acids Res. 1976 Sep;3(9):2303-8 [987581] Cell. 1986 Apr 25;45(2):237-46 [2938743] Science. 1986 Oct 10;234(4773):197-200 [3092355] Annu Rev Immunol. 1986;4:339-68 [3085692] Adv Immunol. 1987;40:247-321 [3109221] Proc Natl Acad Sci U S A. 1989 Mar;86(6):2031-5 [2467296] Science. 1989 Sep 15;245(4923):1242-6 [2551037] Blood. 1989 Nov 1;74(6):2076-80 [2529926] Scand J Clin Lab Invest Suppl. 1968;97:77-89 [4179068] Nature. 1975 May 15;255(5505):241-5 [1143322] Epidemiology. 1990 Sep;1(5):349-56 [2078610] Science. 1990 Dec 7;250(4986):1426-9 [2255914] Cancer Res. 1990 Oct 15;50(20):6585-91 [2208120] Cancer Genet Cytogenet. 1987 May;26(1):95-104 [3470137] Annu Rev Immunol. 1987;5:253-77 [2885014] Cancer Genet Cytogenet. 1985 Sep;18(1):55-63 [3875398] Hum Genet. 1985;71(1):19-21 [4029952] JAMA. 1986 Sep 5;256(9):1141-7 [3801091] Nature. 1986 Apr 10-16;320(6062):549-51 [3008004] Blood. 1989 May 1;73(6):1402-15 [2653455] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reduced susceptibility to HIV-1 infection of ethyl-methanesulfonate-treated CEM subclones correlates with a blockade in their protein kinase C signaling pathway. AN - 73011014; 1351090 AB - We have described the isolation of chemically induced CEM subclones that express CD4 receptors and bind soluble gp120, yet show a markedly reduced susceptibility to infection with HIV-1. Two subclones were found to have an abnormal response to the protein kinase C (PKC) activator PMA. PMA treatment induced CD3 and CD25 (IL-2R) receptors on the parental line and on other ethyl-methanesulfonate-derived subclones, but not on these two mutants. Direct assays of PKC activity were conducted. Total cellular PKC enzymatic activity was found to be normal in these subclones. PMA-induced CD4 down-modulation occurred normally. In addition, activation of c-raf kinase was normal. Since HIV-1 long terminal repeat contains two functional nuclear factor kB (NF-kB) regulatory elements, we studied the ability of PMA to induce NF-kB binding activity by different assays. Chloramphenicol acetyl transferase (CAT) assays using the HIV-1 (-139)long terminal repeat-CAT construct showed no PMA induction of CAT activity in these subclones (unlike the parental line and other subclones). Okadaic acid, an inhibitor of phosphatases 1 and 2A, did not overcome the defect in these subclones. Gel retardation assays, using a 32P-probe containing the HIV-1 NF-kB probe and nuclear extracts from PMA-treated cells, showed significantly reduced induction of nuclear NF-kB binding proteins in these two subclones compared with wild type CEM and a control subclone. Deoxycholate treatment of cytoplasmic extracts from these subclones released much reduced NF-kB binding proteins from their cytoplasmic pools. Thus, reduced levels of PKC-induced nuclear NF-kB activity in two T cell subclones did not affect their normal cell growth, but correlated with a pronounced reduction in their susceptibility to HIV-1 infection. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Hillman, K AU - Qian, J AU - Siegel, J N AU - Roderiquez, G AU - Blackburn, R AU - Manischewitz, J AU - Norcross, M AU - Golding, H AD - Division of Virology, Food and Drug Administration, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 3991 EP - 3998 VL - 148 IS - 12 SN - 0022-1767, 0022-1767 KW - DNA-Binding Proteins KW - 0 KW - Ethers, Cyclic KW - NF-kappa B KW - Nuclear Proteins KW - Proto-Oncogene Proteins KW - Okadaic Acid KW - 1W21G5Q4N2 KW - Ethyl Methanesulfonate KW - 9H154DI0UP KW - Proto-Oncogene Proteins c-raf KW - EC 2.7.11.1 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Clone Cells KW - Humans KW - Proto-Oncogene Proteins -- metabolism KW - Gene Expression KW - Ethers, Cyclic -- pharmacology KW - HIV Long Terminal Repeat KW - Base Sequence KW - Ethyl Methanesulfonate -- pharmacology KW - Cells, Cultured KW - Cytoplasm -- metabolism KW - Cell Compartmentation KW - In Vitro Techniques KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Nuclear Proteins -- metabolism KW - Mutation KW - Signal Transduction KW - NF-kappa B -- metabolism KW - DNA-Binding Proteins -- metabolism KW - HIV Infections -- physiopathology KW - Protein Kinase C -- physiology KW - CD4-Positive T-Lymphocytes -- microbiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73011014?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Reduced+susceptibility+to+HIV-1+infection+of+ethyl-methanesulfonate-treated+CEM+subclones+correlates+with+a+blockade+in+their+protein+kinase+C+signaling+pathway.&rft.au=Hillman%2C+K%3BQian%2C+J%3BSiegel%2C+J+N%3BRoderiquez%2C+G%3BBlackburn%2C+R%3BManischewitz%2C+J%3BNorcross%2C+M%3BGolding%2C+H&rft.aulast=Hillman&rft.aufirst=K&rft.date=1992-06-15&rft.volume=148&rft.issue=12&rft.spage=3991&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-10 N1 - Date created - 1992-07-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The carboxylesterase family exhibits C-terminal sequence diversity reflecting the presence or absence of endoplasmic-reticulum-retention sequences. AN - 73007465; 1606962 AB - Resident proteins of the endoplasmic reticulum lumen are continuously retrieved from an early Golgi compartment by a receptor-mediated mechanism. The sorting or retention sequence on the endoplasmic reticulum proteins is located at the C-terminus and was initially shown to be the tetrapeptide KDEL in mammalian cells and HDEL in Saccharomyces cerevisiae. The carboxylesterases are a large family of enzymes primarily localized to the lumen of the endoplasmic reticulum. Retention sequences in these proteins have been difficult to identify due to atypical and heterogeneous C-terminal sequences. Utilizing the polymerase chain reaction with degenerate primers, we have identified and characterized the C-termini of four members of the carboxylesterase family from rat liver. Three of the carboxylesterases sequences contained C-terminal sequences (HVEL, HNEL or HTEL) resembling the yeast sorting signal which were reported to be non-functional in mammalian cells. A fourth carboxylesterase contained a distinct C-terminal sequence, TEHT. A full-length esterase cDNA clone, terminating in the sequence HVEL, was isolated and was used to assess the retention capabilities of the various esterase C-terminal sequences. This esterase was retained in COS-1 cells, but was secreted when its C-terminal tetrapeptide, HVEL, was deleted. Addition of C-terminal sequences containing HNEL and HTEL resulted in efficient retention. However, the C-terminal sequence containing TEHT was not a functional retention signal. Both HDEL, the authentic yeast retention signal, and KDEL were efficient retention sequences for the esterase. These studies show that some members of the rat liver carboxylesterase family contain novel C-terminal retention sequences that resemble the yeast signal. At least one member of the family does not contain a C-terminal retention signal and probably represents a secretory form. JF - European journal of biochemistry AU - Medda, S AU - Proia, R L AD - Genetics and Biochemistry Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda 20892. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 801 EP - 806 VL - 206 IS - 3 SN - 0014-2956, 0014-2956 KW - DNA KW - 9007-49-2 KW - Carboxylic Ester Hydrolases KW - EC 3.1.1.- KW - Carboxylesterase KW - EC 3.1.1.1 KW - Index Medicus KW - Endoplasmic Reticulum -- enzymology KW - Animals KW - Liver -- enzymology KW - Sequence Homology, Nucleic Acid KW - Gene Expression KW - Amino Acid Sequence KW - Mutagenesis KW - Cloning, Molecular KW - Rats, Inbred Strains KW - Rats KW - Polymerase Chain Reaction KW - Base Sequence KW - Transfection KW - DNA -- genetics KW - Molecular Sequence Data KW - DNA -- chemistry KW - Immunosorbent Techniques KW - Cell Line KW - Carboxylic Ester Hydrolases -- chemistry KW - Carboxylic Ester Hydrolases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73007465?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+biochemistry&rft.atitle=The+carboxylesterase+family+exhibits+C-terminal+sequence+diversity+reflecting+the+presence+or+absence+of+endoplasmic-reticulum-retention+sequences.&rft.au=Medda%2C+S%3BProia%2C+R+L&rft.aulast=Medda&rft.aufirst=S&rft.date=1992-06-15&rft.volume=206&rft.issue=3&rft.spage=801&rft.isbn=&rft.btitle=&rft.title=European+journal+of+biochemistry&rft.issn=00142956&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-23 N1 - Date created - 1992-07-23 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M85175; GENBANK; M85174; X65181; M85177; X65296; X65180; M85176; X65295; X65294; X65179 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cell surface and intracellular functions for ricin galactose binding. AN - 72992490; 1601861 AB - The role of the two galactose binding sites of ricin B chain in ricin toxicity was evaluated by studying a series of ricin point mutants. Wild-type (WT) ricin and three ricin B chain point mutants having mutations in either 1) the first galactose binding domain (site 1 mutant, Met in place of Lys-40 and Gly in place of Asn-46), 2) the second galactose binding domain (site 2 mutant, Gly in place of Asn-255), or 3) both galactose binding domains (double site mutant containing all three amino acid replacements formerly stated) were expressed in Xenopus oocytes and then reassociated with recombinant ricin A chain. The different ricin B chains were mannosylated to the same extent. Cytotoxicity of these toxins was evaluated when cell entry was mediated either by galactose-containing receptors or through an alternate receptor, the mannose receptor of macrophages. WT ricin and each of the single domain mutants was able to kill Vero cells following uptake by galactose containing receptors. Lactose blocked the toxicity of each of these ricins. Site 1 and 2 mutants were 20-40 times less potent than WT ricin, and the double site mutant had no detectable cytotoxicity. WT ricin, the site 1 mutant, and the site 2 mutant also inhibited protein synthesis of mannose receptor-containing cells. Ricin can enter these cells through either a cell-surface galactose-containing receptor or through the mannose receptor. By including lactose in the cell medium, galactose-containing receptor-mediated uptake is blocked and cytotoxicity occurs solely via the mannose receptor. WT ricin, site 1, and site 2 mutants were cytotoxic to macrophages in the presence of lactose with the relative potency, WT greater than site 2 mutant greater than site 1 mutant. The double site mutant lacked cytotoxicity either in the absence or presence of lactose. Thus, even for mannose receptor-mediated toxicity of ricin, at least one galactose binding site remains necessary for cytotoxicity and two galactose binding sites further increases potency. These results are consistent with the model that the ricin B chain galactose binding activity plays a role not only in cell surface binding but also intracellularly for ricin cytotoxicity. JF - The Journal of biological chemistry AU - Newton, D L AU - Wales, R AU - Richardson, P T AU - Walbridge, S AU - Saxena, S K AU - Ackerman, E J AU - Roberts, L M AU - Lord, J M AU - Youle, R J AD - Biochemistry Section, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 11917 EP - 11922 VL - 267 IS - 17 SN - 0021-9258, 0021-9258 KW - Lectins, C-Type KW - 0 KW - Mannose-Binding Lectins KW - Receptors, Cell Surface KW - Receptors, Immunologic KW - Receptors, Mitogen KW - Ricinus communis lectin receptor KW - mannose receptor KW - Ricin KW - 9009-86-3 KW - Mannose KW - PHA4727WTP KW - Galactose KW - X2RN3Q8DNE KW - Index Medicus KW - Bone Marrow Cells KW - Receptors, Immunologic -- drug effects KW - Animals KW - Peritoneal Cavity -- cytology KW - Cell Survival -- drug effects KW - Receptors, Immunologic -- metabolism KW - Vero Cells KW - Mannose -- metabolism KW - Macrophages -- drug effects KW - Mutation KW - Bone Marrow -- drug effects KW - Ricin -- genetics KW - Ricin -- toxicity KW - Ricin -- metabolism KW - Receptors, Mitogen -- metabolism KW - Galactose -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72992490?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Cell+surface+and+intracellular+functions+for+ricin+galactose+binding.&rft.au=Newton%2C+D+L%3BWales%2C+R%3BRichardson%2C+P+T%3BWalbridge%2C+S%3BSaxena%2C+S+K%3BAckerman%2C+E+J%3BRoberts%2C+L+M%3BLord%2C+J+M%3BYoule%2C+R+J&rft.aulast=Newton&rft.aufirst=D&rft.date=1992-06-15&rft.volume=267&rft.issue=17&rft.spage=11917&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-16 N1 - Date created - 1992-07-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Growth inhibition by cholera toxin of human lung carcinoma cell lines: correlation with GM1 ganglioside expression. AN - 72985515; 1375868 AB - The effect of cholera toxin (CT) on the growth of 12 small cell lung carcinoma (SCLC) and 15 non-small cell lung carcinoma (NSCLC) cell lines is presented. CT inhibited the growth of nine SCLC cell lines (concentration for 50% inhibition of growth, 27-700 ng/ml), all of which had abundant expression of GM1 ganglioside, the surface receptor for CT. CT-resistant SCLC all had greatly decreased GM1 expression. In contrast, CT inhibited the growth of only four of 15 NSCLC cell lines. Seven of the 11 CT-resistant NSCLC had levels of GM1 comparable to CT-sensitive NSCLC or SCLC. In a limited panel of cell lines, cyclic AMP (cAMP) agonists including forskolin, 8Br[cAMP], and dibutyryl[cAMP] did not consistently reproduce CT-mediated inhibition of cell growth, nor did these compounds overcome resistance of cells to the growth inhibitory effects of CT. Expression of the RI and RII regulatory subunits of cAMP-dependent protein kinase was similar in CT-resistant and CT-sensitive SCLC or NSCLC cell lines. In the presence of isobutylmethylxanthine, intracellular cAMP levels induced by CT in a CT-resistant, GM1(+) NSCLC cell line were comparable to those achieved in a CT-sensitive NSCLC cell line. We conclude that inhibition of lung carcinoma cell growth by CT in all cases requires expression of GM1, and in the case of SCLC cell lines the presence of GM1 is sufficient. In NSCLC cell lines, expression of GM1 is not sufficient for growth inhibition by CT. These findings imply refractoriness to growth inhibition by cAMP in GM1(+), CT-resistant NSCLC cell lines and the possibility of non-cAMP-related mechanisms for growth inhibition in CT-sensitive cell lines. JF - Cancer research AU - Kaur, G AU - Viallet, J AU - Laborda, J AU - Blair, O AU - Gazdar, A F AU - Minna, J D AU - Sausville, E A AD - Laboratory of Biological Chemistry, National Cancer Institute-Navy Medical Oncology Branch, Bethesda, Maryland 20892. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 3340 EP - 3346 VL - 52 IS - 12 SN - 0008-5472, 0008-5472 KW - G(M1) Ganglioside KW - 37758-47-7 KW - Cholera Toxin KW - 9012-63-9 KW - Cyclic AMP KW - E0399OZS9N KW - 1-Methyl-3-isobutylxanthine KW - TBT296U68M KW - Index Medicus KW - Drug Screening Assays, Antitumor KW - Cyclic AMP -- biosynthesis KW - Tumor Cells, Cultured KW - Humans KW - Cyclic AMP -- antagonists & inhibitors KW - Cell Division -- drug effects KW - 1-Methyl-3-isobutylxanthine -- pharmacology KW - Carcinoma, Small Cell -- pathology KW - G(M1) Ganglioside -- analysis KW - Carcinoma, Non-Small-Cell Lung -- metabolism KW - Lung Neoplasms -- chemistry KW - Carcinoma, Small Cell -- metabolism KW - Cholera Toxin -- pharmacology KW - Carcinoma, Non-Small-Cell Lung -- chemistry KW - Carcinoma, Small Cell -- chemistry KW - Lung Neoplasms -- pathology KW - Lung Neoplasms -- metabolism KW - Carcinoma, Non-Small-Cell Lung -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72985515?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Growth+inhibition+by+cholera+toxin+of+human+lung+carcinoma+cell+lines%3A+correlation+with+GM1+ganglioside+expression.&rft.au=Kaur%2C+G%3BViallet%2C+J%3BLaborda%2C+J%3BBlair%2C+O%3BGazdar%2C+A+F%3BMinna%2C+J+D%3BSausville%2C+E+A&rft.aulast=Kaur&rft.aufirst=G&rft.date=1992-06-15&rft.volume=52&rft.issue=12&rft.spage=3340&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-06 N1 - Date created - 1992-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential immunohistochemical detection of amphiregulin and cripto in human normal colon and colorectal tumors. AN - 72983620; 1596904 AB - Thirty-six primary human colorectal tumors, 43 noninvolved colon samples that were adjacent to either carcinomas of adenomas, 22 adenomas, and nine normal colon specimens were immunohistochemically examined for the presence and localization of two epidermal growth factor-related peptides, amphiregulin (AR) and cripto. Within the primary tumors, 18 (50%) showed moderate levels of AR expression. Approximately 60% of the tubular and tubulovillous adenomas were positive for AR expression, whereas only 15% of the adjacent, noninvolved colon mucosa expressed AR. A greater proportion of well-differentiated tumors (71%) were positive for AR expression than were poorly differentiated tumors (18%). All of the nine normal colon specimens were positive. Consequently, AR expression appeared to be associated with both normal and malignant epithelial cells that were more differentiated. The distribution of cripto expression was different. Seventy-nine % of the colon tumors expressed cripto with a frequency of expression that was approximately equivalent between well-differentiated and poorly differentiated tumors. Approximately 86% of the tubulovillous adenomas, but only 43% of the tubular adenomas, were positive for cripto expression. In contrast, whereas AR was expressed in normal colon specimens, none of these tissues expressed cripto, and only 12% of the noninvolved normal colon samples adjacent to tumors or adenomas were positive for cripto. Cripto expression therefore appeared related to neoplasia. These data suggest that AR and cripto may be functioning as potential autocrine and/or paracrine growth factors in the colon and that the differential expression of cripto may serve as a potential tumor marker for colonic carcinogenesis. JF - Cancer research AU - Saeki, T AU - Stromberg, K AU - Qi, C F AU - Gullick, W J AU - Tahara, E AU - Normanno, N AU - Ciardiello, F AU - Kenney, N AU - Johnson, G R AU - Salomon, D S AD - Laboratory of Tumor Immunology and Biology, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 3467 EP - 3473 VL - 52 IS - 12 SN - 0008-5472, 0008-5472 KW - AREG protein, human KW - 0 KW - Amphiregulin KW - Biomarkers, Tumor KW - EGF Family of Proteins KW - GPI-Linked Proteins KW - Glycoproteins KW - Growth Substances KW - Intercellular Signaling Peptides and Proteins KW - Membrane Glycoproteins KW - Neoplasm Proteins KW - RNA, Messenger KW - RNA, Neoplasm KW - TDGF1 protein, human KW - Epidermal Growth Factor KW - 62229-50-9 KW - Index Medicus KW - Phenotype KW - Adenoma -- chemistry KW - Tumor Cells, Cultured KW - Carcinoma -- chemistry KW - Humans KW - Colonic Polyps -- chemistry KW - Breast Neoplasms -- chemistry KW - Intestinal Mucosa -- chemistry KW - Immunoenzyme Techniques KW - Biomarkers, Tumor -- genetics KW - Growth Substances -- genetics KW - Glycoproteins -- analysis KW - RNA, Messenger -- analysis KW - RNA, Neoplasm -- analysis KW - Glycoproteins -- genetics KW - Colorectal Neoplasms -- chemistry KW - Neoplasm Proteins -- genetics KW - Biomarkers, Tumor -- analysis KW - Colon -- chemistry KW - Growth Substances -- analysis KW - Neoplasm Proteins -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72983620?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Canadian+Tax+Journal&rft.atitle=Provincial+Budget+Roundup%2C+2002&rft.au=Deborah+L.+Ort*+and+David+B.+Perry**&rft.aulast=Deborah+L.+Ort*+and+David+B.+Perry**&rft.aufirst=&rft.date=2002-05-01&rft.volume=50&rft.issue=3&rft.spage=933&rft.isbn=&rft.btitle=&rft.title=Canadian+Tax+Journal&rft.issn=00085111&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-06 N1 - Date created - 1992-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dose-response relationships for chronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin in a rat tumor promotion model: quantification and immunolocalization of CYP1A1 and CYP1A2 in the liver. AN - 72982082; 1596902 AB - The mechanisms responsible for the braod spectrum of effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) are not entirely clear but seem to involve an initial interaction with the Ah receptor. A major uncertainty in risk assessment for TCDD is the lack of adequate dose-response relationships following chronic exposure to TCDD. Induction of cytochrome P-450 enzymes (CYP1A1 and CYP1A2) is one of the most sensitive responses to TCDD and its structural analogues. We have used a two-stage model for hepatocarcinogenesis in female Sprague-Dawley rats to evaluate dose-response relationships for induction of CYP1A1 and CYP1A2 in diethylnitrosamine-initiated as well as in noninitiated rats. After initiation with a single dose of diethylnitrosamine, TCDD was administered biweekly by p.o. gavage at doses equivalent to 3.5, 10.7, 35.7, and 125 ng/kg/day for 30 weeks. CYP1A1 and CYP1A2 concentrations were quantified in hepatic microsomes by radioimmunoassay and localized in hepatic tissue slices by immunohistochemical techniques. Radioimmunoassay data revealed a maximum induction of 200-fold for CYP1A1 and 10-fold for CYP1A2 and there were no statistically significant differences between initiated and noninitiated rats. Induction at the lowest dose (3.5 ng/kg/day) was 20-fold for CYP1A1 and 3-fold for CYP1A2. Mathematical analysis indicates that the best fit of the induction data are inconsistent with a threshold for this response. There was a linear relationship between administered dose and TCDD liver concentration over the entire dose range of the study. This indicates that induction of CYP1A2 does not significantly alter the distribution of TCDD in our chronic dosing regimen. Immunolocalization of CYP1A1 and CYP1A2 revealed the same localization and induction pattern for both isozymes in the cytoplasm of hepatocytes. However, the hepatic distribution pattern was not uniform with the most intense staining observed around central veins. These studies help to clarify dose-response relationships for dioxin-mediated effects and demonstrate different sensitivity of hepatocytes to the effects of TCDD. JF - Cancer research AU - Tritscher, A M AU - Goldstein, J A AU - Portier, C J AU - McCoy, Z AU - Clark, G C AU - Lucier, G W AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 3436 EP - 3442 VL - 52 IS - 12 SN - 0008-5472, 0008-5472 KW - Isoenzymes KW - 0 KW - Polychlorinated Dibenzodioxins KW - Diethylnitrosamine KW - 3IQ78TTX1A KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Enzyme Induction -- drug effects KW - Dose-Response Relationship, Drug KW - Microsomes, Liver -- enzymology KW - Female KW - Cytochrome P-450 Enzyme System -- analysis KW - Isoenzymes -- analysis KW - Polychlorinated Dibenzodioxins -- analysis KW - Isoenzymes -- biosynthesis KW - Liver Neoplasms, Experimental -- enzymology KW - Liver Neoplasms, Experimental -- chemically induced KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Liver Neoplasms, Experimental -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72982082?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Dose-response+relationships+for+chronic+exposure+to+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin+in+a+rat+tumor+promotion+model%3A+quantification+and+immunolocalization+of+CYP1A1+and+CYP1A2+in+the+liver.&rft.au=Tritscher%2C+A+M%3BGoldstein%2C+J+A%3BPortier%2C+C+J%3BMcCoy%2C+Z%3BClark%2C+G+C%3BLucier%2C+G+W&rft.aulast=Tritscher&rft.aufirst=A&rft.date=1992-06-15&rft.volume=52&rft.issue=12&rft.spage=3436&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-06 N1 - Date created - 1992-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Combined use of cyclosporine and ketoconazole in the treatment of endogenous uveitis. AN - 72980754; 1598960 AB - Ten patients with endogenous uveitis were in clinical remission attributable to treatment with cyclosporine and prednisone. After the cyclosporine dose was reduced by two thirds, these patients were randomly assigned to treatment with or without ketoconazole, a potent inhibitor of cytochrome P-450, in a double-masked placebo-controlled study. The dose was reduced over three days. During a three-month follow-up, no patients treated with ketoconazole had a relapse of uveitis, while four of six (66%) control subjects had a flare-up. Toxicity in the ketoconazole-treated group was limited to a transient decrease in glomerular filtration rate (20% from baseline) at one month in two of six (33%) patients. Renal function was stabilized by further reduction of the cyclosporine dose. JF - American journal of ophthalmology AU - de Smet, M D AU - Rubin, B I AU - Whitcup, S M AU - Lopez, J S AU - Austin, H A AU - Nussenblatt, R B AD - Laboratory of Immunology, National Eye Institute, Bethesda, MD 20892. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 687 EP - 690 VL - 113 IS - 6 SN - 0002-9394, 0002-9394 KW - Cyclosporine KW - 83HN0GTJ6D KW - Ketoconazole KW - R9400W927I KW - Abridged Index Medicus KW - Index Medicus KW - Drug Therapy, Combination KW - Double-Blind Method KW - Humans KW - Glomerular Filtration Rate -- drug effects KW - Follow-Up Studies KW - Cyclosporine -- adverse effects KW - Ketoconazole -- therapeutic use KW - Cyclosporine -- therapeutic use KW - Autoimmune Diseases -- drug therapy KW - Ketoconazole -- adverse effects KW - Uveitis -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72980754?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+ophthalmology&rft.atitle=Combined+use+of+cyclosporine+and+ketoconazole+in+the+treatment+of+endogenous+uveitis.&rft.au=de+Smet%2C+M+D%3BRubin%2C+B+I%3BWhitcup%2C+S+M%3BLopez%2C+J+S%3BAustin%2C+H+A%3BNussenblatt%2C+R+B&rft.aulast=de+Smet&rft.aufirst=M&rft.date=1992-06-15&rft.volume=113&rft.issue=6&rft.spage=687&rft.isbn=&rft.btitle=&rft.title=American+journal+of+ophthalmology&rft.issn=00029394&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-06 N1 - Date created - 1992-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Neoplastic transformation of immortalized human keratinocytes by 2,3,7,8-tetrachlorodibenzo-p-dioxin. AN - 72978805; 1596905 AB - 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is the most powerful carcinogen ever tested in animals. Recent epidemiological studies have suggested its carcinogenic potential in humans. In the present study, nontumorigenic human epidermal keratinocytes immortalized by adenovirus 12-simian virus 40 (Ad12-SV40) were transformed by exposures of TCDD equal to or greater than 0.1 nM for 2 wk. These transformed cells showed morphological alterations and induced carcinomas when transplanted into nude mice, whereas no such transformation phenotypes were observed with exposures of less than 0.1 nM for 2 wk. Primary human epithelial keratinocytes exposed to various concentrations of TCDD failed to show any evidence of transformation. Induction of aryl hydrocarbon hydroxylase activity was dose dependent, as was transformation. Thus, the carcinogenicity of TCDD in this human cell system appears to be an Ah receptor-mediated process. The present study represents the first evidence of neoplastic conversion of human cells exposed to this environmentally important chemical. JF - Cancer research AU - Yang, J H AU - Thraves, P AU - Dritschilo, A AU - Rhim, J S AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 3478 EP - 3482 VL - 52 IS - 12 SN - 0008-5472, 0008-5472 KW - Polychlorinated Dibenzodioxins KW - 0 KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - Index Medicus KW - Carcinoma, Squamous Cell -- enzymology KW - Animals KW - Enzyme Induction -- drug effects KW - Carcinoma, Squamous Cell -- pathology KW - Humans KW - Carcinogenicity Tests KW - Carcinoma, Squamous Cell -- chemically induced KW - Mice, Nude KW - Mice KW - Tumor Stem Cell Assay KW - Aryl Hydrocarbon Hydroxylases -- biosynthesis KW - Skin Neoplasms -- enzymology KW - Cell Transformation, Neoplastic -- pathology KW - Keratinocytes -- enzymology KW - Skin Neoplasms -- chemically induced KW - Keratinocytes -- drug effects KW - Polychlorinated Dibenzodioxins -- toxicity KW - Cell Transformation, Neoplastic -- chemically induced KW - Skin Neoplasms -- pathology KW - Keratinocytes -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72978805?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Neoplastic+transformation+of+immortalized+human+keratinocytes+by+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin.&rft.au=Yang%2C+J+H%3BThraves%2C+P%3BDritschilo%2C+A%3BRhim%2C+J+S&rft.aulast=Yang&rft.aufirst=J&rft.date=1992-06-15&rft.volume=52&rft.issue=12&rft.spage=3478&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-06 N1 - Date created - 1992-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of a beta-hydroxyalkylnitrosamine to alkylating agents: evidence for the involvement of a sulfotransferase. AN - 72968243; 1596888 AB - N-Nitrosomethyl(2-hydroxyethyl)amine (NMHEA), when administered by gavage, is a strong liver carcinogen in F344 female rats, but a weak liver carcinogen in male rats. After repeated exposure to NMHEA, either in drinking water or by gavage, female rats accumulated higher levels of DNA-guanine adducts than did their male counterparts, suggesting a correlation with the observed disparity in carcinogenicity. NMHEA has been shown to alkylate rat liver DNA in vivo in a dose-dependent manner. Chemical investigations of NMHEA suggest that it becomes a strong electrophile when a good leaving group is substituted on the hydroxyl. We have proposed that NMHEA is activated to its ultimate carcinogenic form by conjugation with sulfate. The sulfate ester was postulated to undergo rapid cyclization to 3-methyl-1,2,3-oxadizolinium ion, which has previously been found to be a potent methylating agent in vitro. The effect of sulfotransferase inhibitors on the DNA alkylation in rats by NMHEA was studied in vivo. Dichloronitrophenol, a powerful inhibitor of phenol sulfotransferase, had little effect on the methylation and O6-hydroxyethylation of DNA guanine in female rats, while depressing the hydroxyethylation of the N-7 position of guanine. Dichloronitrophenol, however, dramatically enhanced the methylation of DNA in male rats. It also slightly inhibited the N-nitrosodimethylamine-induced methylation of DNA. On the other hand, propylene glycol, an alcohol sulfotransferase inhibitor, had a profound inhibitory effect on DNA methylation induced by NMHEA, very little effect on the formation of N7-(2-hydroxyethyl)guanine, but a very strong effect on the O6-hydroxyethylguanine lesions. NMHEA-induced alkylation was also studied in male and female brachymorphic mice, which are deficient in the ability to synthesize the sulfate donor 3'-phosphoadenosine 5'-phosphosulfate required for sulfotransferase activity, and their heterozygous siblings. No significant differences were seen between the heterozygous and brachymorphic mice in overall levels of alkylation, except in the case of 7-hydroxyethylation. In contrast to rats, male mice showed higher levels of formation of all DNA guanine adducts than did the females. However, propylene glycol was found to depress all the levels of alkylation in the brachymorphic mice, except for N7-(2-hydroxyethyl)guanine, as was observed in rats.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Cancer research AU - Kroeger-Koepke, M B AU - Koepke, S R AU - Hernandez, L AU - Michejda, C J AD - Molecular Aspects of Drug Design Section, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 3300 EP - 3305 VL - 52 IS - 12 SN - 0008-5472, 0008-5472 KW - Nitrophenols KW - 0 KW - Nitroso Compounds KW - methylethylnitrosamine KW - 10595-95-6 KW - 4-nitrosodimethylaniline KW - 138-89-6 KW - Guanine KW - 5Z93L87A1R KW - 2,6-dichloro-4-nitrophenol KW - 618-80-4 KW - DNA KW - 9007-49-2 KW - Sulfotransferases KW - EC 2.8.2.- KW - Dimethylnitrosamine KW - M43H21IO8R KW - Index Medicus KW - Rats KW - Animals KW - Sulfotransferases -- metabolism KW - Rats, Inbred F344 KW - Sex Factors KW - Biotransformation KW - Hydrolysis KW - Alkylation -- drug effects KW - Male KW - Guanine -- metabolism KW - Female KW - Dimethylnitrosamine -- pharmacokinetics KW - Nitrophenols -- pharmacology KW - DNA -- metabolism KW - Liver -- metabolism KW - Dimethylnitrosamine -- analogs & derivatives KW - Nitroso Compounds -- pharmacology KW - Dimethylnitrosamine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72968243?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Activation+of+a+beta-hydroxyalkylnitrosamine+to+alkylating+agents%3A+evidence+for+the+involvement+of+a+sulfotransferase.&rft.au=Kroeger-Koepke%2C+M+B%3BKoepke%2C+S+R%3BHernandez%2C+L%3BMichejda%2C+C+J&rft.aulast=Kroeger-Koepke&rft.aufirst=M&rft.date=1992-06-15&rft.volume=52&rft.issue=12&rft.spage=3300&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-06 N1 - Date created - 1992-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Regulation of P-glycoprotein gene expression in hepatocyte cultures and liver cell lines by a trans-acting transcriptional repressor. AN - 73034617; 1352042 AB - Previously we have demonstrated that expression of the multidrug resistance (mdr) genes in rat liver and primary rat hepatocyte cultures is induced by exposure to 2-acetylaminofluorene and 3-methylcholanthrene. The mdr expression induced by both of these compounds occurs primarily via increased gene transcription. To determine the nature of possible regulatory proteins involved in mdr gene regulation we inhibited protein synthesis using cycloheximide or emetine in primary rat hepatocyte cultures, mouse (HePa 1), human (Hep G2) and rat (H4-II-E) cell lines. Each cell type responded by strongly increasing its steady state mdr1 mRNA levels. In hepatocytes increased mdr expression was observed after greater than 50% inhibition of protein synthesis, and was first detected after 2h of protein synthesis inhibition with maximal induction occurring by 24h. Nuclear run-on analysis showed that the increased steady state mRNA level was due to increased gene transcription without alteration of the transcription start site. Combined these data indicate that one regulatory mechanism by which mdr gene expression is controlled is via a trans-acting transcriptional repressor. JF - Nucleic acids research AU - Gant, T W AU - Silverman, J A AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/06/11/ PY - 1992 DA - 1992 Jun 11 SP - 2841 EP - 2846 VL - 20 IS - 11 SN - 0305-1048, 0305-1048 KW - mdr1 KW - Membrane Glycoproteins KW - 0 KW - Oligodeoxyribonucleotides KW - P-Glycoprotein KW - Protein Synthesis Inhibitors KW - RNA, Messenger KW - Repressor Proteins KW - Cycloheximide KW - 98600C0908 KW - Emetine KW - X8D5EPO80M KW - Index Medicus KW - Animals KW - Blotting, Northern KW - Humans KW - Drug Resistance KW - Transcription, Genetic KW - Mice KW - RNA, Messenger -- genetics KW - Repressor Proteins -- genetics KW - Rats KW - Base Sequence KW - Protein Synthesis Inhibitors -- pharmacology KW - Cells, Cultured KW - Cycloheximide -- pharmacology KW - Oligodeoxyribonucleotides -- chemistry KW - Emetine -- pharmacology KW - Molecular Sequence Data KW - Gene Expression Regulation -- drug effects KW - Liver -- physiology KW - Membrane Glycoproteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73034617?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+acids+research&rft.atitle=Regulation+of+P-glycoprotein+gene+expression+in+hepatocyte+cultures+and+liver+cell+lines+by+a+trans-acting+transcriptional+repressor.&rft.au=Gant%2C+T+W%3BSilverman%2C+J+A%3BThorgeirsson%2C+S+S&rft.aulast=Gant&rft.aufirst=T&rft.date=1992-06-11&rft.volume=20&rft.issue=11&rft.spage=2841&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-29 N1 - Date created - 1992-07-29 N1 - Date revised - 2017-01-13 N1 - Gene symbol - mdr1 N1 - SuppNotes - Cited By: Anal Biochem. 1976 May 7;72:248-54 [942051] Dev Biol. 1973 Nov;35(1):83-96 [4362668] DNA Cell Biol. 1991 Nov;10(9):639-49 [1684503] J Biol Chem. 1990 Aug 5;265(22):13190-7 [1695903] Mol Cell Biol. 1990 Apr;10(4):1642-51 [1969609] Cell Growth Differ. 1990 Feb;1(2):57-62 [1982215] Mol Cell Biol. 1990 Nov;10(11):6036-40 [2248681] Proc Natl Acad Sci U S A. 1990 Mar;87(5):1753-7 [2308934] Science. 1986 May 9;232(4751):751-5 [2421411] Mol Cell Biol. 1986 May;6(5):1671-8 [2431283] J Biol Chem. 1989 Jul 15;264(20):12053-62 [2473069] J Biol Chem. 1989 Jul 15;264(20):11693-8 [2568355] J Natl Cancer Inst. 1989 Aug 2;81(15):1144-50 [2746668] J Natl Cancer Inst. 1988 Nov 2;80(17):1383-6 [2845109] Cancer Res. 1987 Nov 1;47(21):5577-83 [2889526] Proc Natl Acad Sci U S A. 1987 Nov;84(21):7701-5 [2890168] EMBO J. 1987 Nov;6(11):3325-31 [2892668] J Biol Chem. 1985 May 10;260(9):5648-53 [2985607] Nucleic Acids Res. 1985 Mar 11;13(5):1431-42 [2987824] Mol Cell Biol. 1988 Aug;8(8):3518-25 [3211150] Proc Natl Acad Sci U S A. 1988 May;85(10):3580-4 [3368466] Carcinogenesis. 1988 Aug;9(8):1475-9 [3402044] Mol Cell Biol. 1988 Jul;8(7):2770-8 [3405218] Science. 1986 May 2;232(4750):643-5 [3457471] Proc Natl Acad Sci U S A. 1987 May;84(10):3161-5 [3472202] Proc Natl Acad Sci U S A. 1987 May;84(9):3004-8 [3472246] Arch Biochem Biophys. 1986 Jan;244(1):261-72 [3753838] Fed Proc. 1973 Jun;32(6):1673-8 [4575885] Cancer Res. 1983 Sep;43(9):4413-9 [6135505] Anal Biochem. 1983 Jul 1;132(1):6-13 [6312838] Proc Natl Acad Sci U S A. 1984 Jul;81(13):3964-8 [6330726] Proc Natl Acad Sci U S A. 1984 Nov;81(22):7046-50 [6594679] Cell. 1983 Dec;35(3 Pt 2):603-10 [6606489] Proc Natl Acad Sci U S A. 1979 Jul;76(7):3256-60 [158758] Gene. 1991 Oct 15;106(2):229-36 [1682220] Mol Carcinog. 1991;4(6):499-509 [1686552] Mol Cell Biol. 1990 Jul;10(7):3596-606 [1972547] Br J Haematol. 1991 Jun;78(2):288-9 [2064972] Cell Growth Differ. 1990 Dec;1(12):607-15 [2288876] Mol Cell Biol. 1986 Apr;6(4):1050-7 [2431274] Cell. 1987 Oct 23;51(2):283-92 [2444342] Br J Haematol. 1989 May;72(1):40-4 [2736241] Blood. 1989 Sep;74(4):1388-95 [2765667] Nature. 1985 Aug 29-Sep 4;316(6031):817-9 [2863759] J Biol Chem. 1987 Dec 25;262(36):17432-6 [2891692] J Biol Chem. 1985 Feb 10;260(3):1676-81 [2981868] Chem Biol Interact. 1985 Aug-Sep;54(3):299-315 [2996791] Science. 1987 Jun 5;236(4806):1237-45 [3296191] Anal Biochem. 1988 Feb 15;169(1):49-70 [3369688] Mol Cell Biol. 1988 Jan;8(1):480-5 [3422100] Annu Rev Microbiol. 1971;25:487-562 [4949424] Anal Biochem. 1984 Feb;137(1):266-7 [6329026] Proc Natl Acad Sci U S A. 1984 Dec;81(23):7476-80 [6334309] Proc Natl Acad Sci U S A. 1986 Jun;83(12):4538-42 [3459187] Science. 1987 May 29;236(4805):1120-2 [3576227] J Biol Chem. 1991 Feb 5;266(4):2239-44 [1671222] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Vanilloid receptor loss in rat sensory ganglia associated with long term desensitization to resiniferatoxin. AN - 73236427; 1407700 AB - A dose-dependent loss of vanilloid receptors (specific [3H]resiniferatoxin binding sites) was found in sensory ganglia of rats 24 h after s.c. administration of resiniferatoxin (RTX), an ultrapotent capsaicin analog. This receptor loss displayed an ED50 of 30 micrograms/kg both in dorsal root and trigeminal ganglia; the ED50 was 6-fold higher than the ED50 for loss of the neurogenic inflammatory response and 30-60-fold higher than the ED50 for desensitization in the standard eye-wiping (chemogenic pain) response. The receptor loss appeared later (24 h) than the loss of the physiological responses (6 h) and showed modest recovery (to 20-30% of control levels) over the following 4 weeks. This vanilloid receptor loss may represent a novel, specific mechanism for vanilloid-induced chronic desensitization. JF - Neuroscience letters AU - Szallasi, A AU - Blumberg, P M AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/06/08/ PY - 1992 DA - 1992 Jun 08 SP - 51 EP - 54 VL - 140 IS - 1 SN - 0304-3940, 0304-3940 KW - Diterpenes KW - 0 KW - Receptors, Drug KW - resiniferatoxin KW - A5O6P1UL4I KW - Index Medicus KW - Rats KW - Animals KW - Trigeminal Ganglion -- metabolism KW - Trigeminal Ganglion -- drug effects KW - Dose-Response Relationship, Drug KW - Kinetics KW - Trigeminal Ganglion -- physiology KW - Rats, Wistar KW - Time Factors KW - Female KW - Inflammation KW - Binding Sites KW - Diterpenes -- pharmacology KW - Diterpenes -- toxicity KW - Receptors, Drug -- metabolism KW - Pain -- physiopathology KW - Receptors, Drug -- drug effects KW - Ganglia, Spinal -- physiology KW - Ganglia, Spinal -- metabolism KW - Ganglia, Spinal -- drug effects KW - Diterpenes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73236427?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+letters&rft.atitle=Vanilloid+receptor+loss+in+rat+sensory+ganglia+associated+with+long+term+desensitization+to+resiniferatoxin.&rft.au=Szallasi%2C+A%3BBlumberg%2C+P+M&rft.aulast=Szallasi&rft.aufirst=A&rft.date=1992-06-08&rft.volume=140&rft.issue=1&rft.spage=51&rft.isbn=&rft.btitle=&rft.title=Neuroscience+letters&rft.issn=03043940&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-26 N1 - Date created - 1992-10-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of c-fos mRNA in acute and kindled cocaine seizures in rats. AN - 73108787; 1498673 AB - In situ hybridization for c-fos mRNA was performed on brain sections (a) from rats after an acute cocaine-induced seizure or from saline-injected controls and (b) from rats after their first cocaine-kindled seizure, as well as from rats that had not yet developed cocaine-kindled seizures (but were exposed to the same amount of cocaine as those that did exhibit convulsions) and from saline-injected controls. Increased expression of c-fos mRNA was observed in animals demonstrating cocaine-induced seizures acutely or following pharmacological kindling. Rats that experienced acute seizures after cocaine (65 mg/kg) showed pronounced increase in expression of c-fos mRNA in the dentate gyrus of the hippocampus and olfactory bulb. Increases were also observed in several other limbic cortical regions, as well as the striatum and ventromedial hypothalamic nucleus (VMH). In rats that were injected daily with an initially subconvulsive dose of cocaine-HCl (40 mg/kg), the cocaine-kindled seizures induced elevations in c-fos mRNA in the same brain regions as with an acute cocaine-induced seizure with the single exception of the VMH. These findings not only suggest the involvement of limbic, cortical and striatal structures in the cocaine-induced seizure, but also raise the possibility that alterations in the proto-oncogene c-fos and its subsequent impact on gene expression could play a role in the changes in neural excitability associated with cocaine-induced kindling. JF - Brain research AU - Clark, M AU - Post, R M AU - Weiss, S R AU - Nakajima, T AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1992/06/05/ PY - 1992 DA - 1992 Jun 05 SP - 101 EP - 106 VL - 582 IS - 1 SN - 0006-8993, 0006-8993 KW - c-fos KW - RNA, Messenger KW - 0 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Reference Values KW - Kindling, Neurologic KW - Organ Specificity KW - Gene Expression Regulation -- drug effects KW - Male KW - Seizures -- chemically induced KW - Brain -- physiopathology KW - Seizures -- physiopathology KW - Brain -- drug effects KW - RNA, Messenger -- analysis KW - Genes, fos KW - Cocaine -- pharmacology KW - Brain -- physiology KW - RNA, Messenger -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73108787?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Expression+of+c-fos+mRNA+in+acute+and+kindled+cocaine+seizures+in+rats.&rft.au=Clark%2C+M%3BPost%2C+R+M%3BWeiss%2C+S+R%3BNakajima%2C+T&rft.aulast=Clark&rft.aufirst=M&rft.date=1992-06-05&rft.volume=582&rft.issue=1&rft.spage=101&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-14 N1 - Date created - 1992-09-14 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-fos N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Site-directed mutagenesis of the rat m1 muscarinic acetylcholine receptor. Role of conserved cysteines in receptor function. AN - 72989590; 1317867 AB - There are 9 cysteine residues in the rat m1 muscarinic acetylcholine receptor (mAChR) that are conserved among all five mammalian mAChR subtypes sequenced to date. To study the role of these cysteines in rat m1 mAChR function, site-directed mutagenesis was used to convert each Cys residue to Ser, and the mutant receptor genes were transfected into mAChR-deficient Chinese hamster ovary (CHO) cells. Substitution of Cys391 (extracellular loop III) or Cys421 and Cys435 (carboxyl terminus) produces receptors with wild type phenotype. Cells transfected with Ser98 or Ser178 (extracellular loops I and II, respectively) receptor genes display no carbachol-mediated hydrolysis of phosphoinositides (PI), and membranes prepared from these cells do not bind the muscarinic antagonist [3H] quinuclidinyl benzilate, even though the cells express transcripts of the m1 mAChR as determined by RNA hybridization analysis. Since biochemical evidence suggests that these cysteines form a disulfide bridge (Curtis, C. A. M., Wheatley, M., Bansal, S., Birdsall, N. J. M., Eveleigh, P., Pedder, E. K., Poyner, D., and Hulme, E. C. (1989) 264, 489-495), our findings imply that this disulfide linkage may be critical for formation of the ligand binding domain or for proper protein folding. The Ser394 mAChR (extracellular loop III) exhibits a 44% decrease in efficacy for carbachol-mediated stimulation of PI hydrolysis relative to the wild type receptor, but displays normal ligand binding affinities. The Ser407 m1 mAChR (transmembrane helix VII) displays a decreased efficacy for eliciting carbachol-mediated PI hydrolysis (39% that of CHO cells transfected with the wild type receptor) and a 4-fold shift to the right in the carbachol dose-response curve, which is consistent with the 4-fold decrease in carbachol affinity at the Ser407 m1 mAChR. In contrast, the Ser417 m1 mAChR (transmembrane helix VII) displays an increase in carbachol affinity and a shift to the left in the carbachol dose-response curve for PI hydrolysis. These findings suggest that cysteine residues in the seventh transmembrane helix of the m1 mAChR may influence agonist binding and the efficiency of receptor activation. JF - The Journal of biological chemistry AU - Savarese, T M AU - Wang, C D AU - Fraser, C M AD - Section on Molecular Neurobiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20852. Y1 - 1992/06/05/ PY - 1992 DA - 1992 Jun 05 SP - 11439 EP - 11448 VL - 267 IS - 16 SN - 0021-9258, 0021-9258 KW - Phosphatidylinositols KW - 0 KW - RNA, Messenger KW - Receptors, Muscarinic KW - Cysteine KW - K848JZ4886 KW - Index Medicus KW - Animals KW - Phosphatidylinositols -- metabolism KW - Blotting, Northern KW - Transcription, Genetic KW - Amino Acid Sequence KW - RNA, Messenger -- genetics KW - Hydrolysis KW - Cysteine -- physiology KW - Rats KW - Transfection KW - Molecular Sequence Data KW - CHO Cells KW - Substrate Specificity KW - Cricetinae KW - Mutagenesis, Site-Directed KW - Receptors, Muscarinic -- genetics KW - Receptors, Muscarinic -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72989590?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Site-directed+mutagenesis+of+the+rat+m1+muscarinic+acetylcholine+receptor.+Role+of+conserved+cysteines+in+receptor+function.&rft.au=Savarese%2C+T+M%3BWang%2C+C+D%3BFraser%2C+C+M&rft.aulast=Savarese&rft.aufirst=T&rft.date=1992-06-05&rft.volume=267&rft.issue=16&rft.spage=11439&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-06 N1 - Date created - 1992-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The epsilon-globin gene silencer. Characterization by in vitro transcription. AN - 72972177; 1597481 AB - K562 human erythroleukemia cells constitutively express epsilon- and gamma- but not beta-globin genes. We have previously shown that the differential expression of globin genes observed in intact K562 cells could be simulated in vitro as K562 nuclear extract (NE) actively transcribes the epsilon-globin (with 2 kilobases of 5'-flanking sequence) and gamma-globin gene DNA templates but not beta-globin gene templates. We have now used the K562 in vitro transcription system to examine a silencer transcriptional control element which has been reported to be localized between -177 and -392 base pairs (bp) 5' of the canonical cap site for the epsilon-globin gene. We find that K562 NE has markedly reduced synthesis of RNA in vitro from epsilon-globin gene DNA deletion templates which contain the silencer sequence, or part thereof, but not the adjacent 5'-positive regulatory region (-453 to -535 bp). Furthermore, those transcripts generated in vitro from DNA templates extending to -453 bp or less of the epsilon-globin gene were not correctly initiated at the canonical cap site. Separating the K562 NE by ion exchange chromatography, we isolated a fraction (F175) transcriptionally active for all tested globin genes including the epsilon-globin gene containing the silencer sequence and a fraction (F50) which contains the trans-acting factors associated with the silencer activity. F50 showed a strong dose-dependent inhibitory effect on correctly initiated epsilon-globin gene transcription directed by either unfractionated K562 NE or F175. This suppression by F50 was not observed on transcriptional activity of the permissive adenovirus 2 major late promoter. In electrophoretic mobility shift assays using the epsilon-globin gene silencer region as probe, F50 and F175 exhibited different DNA binding protein patterns; a specific protein band in F50 appears to be associated with the silencer activity. These studies suggest that this protein may be specifically responsible for the activity of the silencer element of the epsilon-globin gene. The expression and silencing of the epsilon-globin gene during development may be modulated by the interactions of this protein with the cis-acting DNA silencer. JF - The Journal of biological chemistry AU - Wada-Kiyama, Y AU - Peters, B AU - Noguchi, C T AD - Laboratory of Chemical Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/06/05/ PY - 1992 DA - 1992 Jun 05 SP - 11532 EP - 11538 VL - 267 IS - 16 SN - 0021-9258, 0021-9258 KW - Amanitins KW - 0 KW - DNA, Neoplasm KW - RNA, Neoplasm KW - Globins KW - 9004-22-2 KW - Index Medicus KW - Base Sequence KW - Tumor Cells, Cultured KW - Amanitins -- pharmacology KW - Humans KW - Molecular Sequence Data KW - Leukemia, Erythroblastic, Acute -- genetics KW - DNA, Neoplasm -- genetics KW - DNA Fingerprinting KW - Templates, Genetic KW - RNA, Neoplasm -- genetics KW - Transcription, Genetic -- drug effects KW - Globins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72972177?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=The+epsilon-globin+gene+silencer.+Characterization+by+in+vitro+transcription.&rft.au=Wada-Kiyama%2C+Y%3BPeters%2C+B%3BNoguchi%2C+C+T&rft.aulast=Wada-Kiyama&rft.aufirst=Y&rft.date=1992-06-05&rft.volume=267&rft.issue=16&rft.spage=11532&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-06 N1 - Date created - 1992-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of cysteines 640, 656, and 661 in steroid binding to rat glucocorticoid receptors. AN - 72970296; 1597467 AB - The involvement of a vicinally spaced dithiol group in steroid binding to the glucocorticoid receptor has been deduced from experiments with the thiol-specific reagent methyl methanethiolsulfonate and the vicinal dithiol-specific reagent sodium arsenite. The vicinally spaced dithiol appears to reside in the 16-kDa trypsin fragment of the receptor, which is thought to contain 3 cysteines (Cys-640, -656, and -661 of the rat receptor) and binds hormone with an approximately 23-fold lower affinity than does the intact 98-kDa receptor. We now report that the steroid binding specificity of preparations of this 16-kDa fragment and the intact receptor are virtually identical. This finding supports our designation of the 16-kDa fragment as a steroid-binding core domain and validates our continued use of this tryptic fragment in studies of steroid binding. To identify the cysteines which comprise the vicinally spaced dithiol group, and to examine further the role of cysteines in steroid binding, a total of five point mutant receptors were prepared: cysteine-to-serine for each suspected cysteine, cysteine-to-glycine for Cys-656, and the C656,661S double mutant. Unexpectedly, each receptor with a single point mutation still bound steroid. Even the double mutant (C656,661S) bound steroid with wild type affinity. These results suggest that none of these cysteines are directly required either for steroid binding to the glucocorticoid receptor or for heat shock protein 90 association with the receptor. However, the presence of Cys-656 was obligatory for covalent labeling of the receptor by [3H]dexamethasone 21-mesylate. Studies with preparations of the 98 and 16 kDa forms of these mutant receptors revealed both that Cys-656 and -661 comprise the vicinally spaced dithiols reacting with arsenite and that any two of the three thiols could form an intramolecular disulfide after treatment with low concentrations of methyl methanethiolsulfonate. These data, in conjunction with those from experiments on the effects of steric bulk on various receptor functions, support a model for the ligand binding cavity of the receptor that involves all three thiols in a flexible cleft but where thiol-steroid interactions are not essential for binding. JF - The Journal of biological chemistry AU - Chakraborti, P K AU - Garabedian, M J AU - Yamamoto, K R AU - Simons, S S AD - Steroid Hormones Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/06/05/ PY - 1992 DA - 1992 Jun 05 SP - 11366 EP - 11373 VL - 267 IS - 16 SN - 0021-9258, 0021-9258 KW - Affinity Labels KW - 0 KW - Arsenites KW - Heat-Shock Proteins KW - Peptide Fragments KW - Receptors, Glucocorticoid KW - Steroids KW - methyl methanethiosulfonate KW - 2949-92-0 KW - Dexamethasone KW - 7S5I7G3JQL KW - Methyl Methanesulfonate KW - AT5C31J09G KW - Cysteine KW - K848JZ4886 KW - arsenite KW - N5509X556J KW - Arsenic KW - N712M78A8G KW - dexamethasone 21-methanesulfonate KW - O9S11FMA79 KW - Index Medicus KW - Peptide Fragments -- metabolism KW - Heat-Shock Proteins -- metabolism KW - Animals KW - Electrophoresis, Polyacrylamide Gel KW - Arsenic -- pharmacology KW - Methyl Methanesulfonate -- analogs & derivatives KW - Methyl Methanesulfonate -- pharmacology KW - Rats KW - Dexamethasone -- analogs & derivatives KW - Base Sequence KW - Blotting, Western KW - Dexamethasone -- metabolism KW - Transfection KW - Molecular Sequence Data KW - Substrate Specificity KW - Mutation KW - Receptors, Glucocorticoid -- physiology KW - Receptors, Glucocorticoid -- genetics KW - Cysteine -- physiology KW - Steroids -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72970296?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Role+of+cysteines+640%2C+656%2C+and+661+in+steroid+binding+to+rat+glucocorticoid+receptors.&rft.au=Chakraborti%2C+P+K%3BGarabedian%2C+M+J%3BYamamoto%2C+K+R%3BSimons%2C+S+S&rft.aulast=Chakraborti&rft.aufirst=P&rft.date=1992-06-05&rft.volume=267&rft.issue=16&rft.spage=11366&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-06 N1 - Date created - 1992-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Letter-by-Letter Surface Alexia AN - 85553781; 9210099 AB - Letter-by-letter surface alexia is investigated in a description of a patient who developed letter-by-letter reading & the symptoms of surface alexia following a left hemisphere stroke. A case study is provided of this 62-year-old who suffered the stroke 2.5 years prior to this study. Experimental testing was conducted in the areas of oral reading, concreteness, part of speech, affixed words, pseudowords, spelling-to-sound regularity, & homophone usage. Tachistoscopic test results are given along with a measurement of S's ability to recognize orally spelled words. The differences between this case & those reported earlier by K. E. Patterson & J. Kay ("Letter-by-Letter Reading: Psychological Descriptions of a Neurological Syndrome," Quarterly Journal of Experimental Psychology, 1982, 34A, 411-441) are discussed. An additional theory presented here combines with two already suggested by Patterson & Kay to account for this combination of alexias. A model is presented that posits one shared orthographic lexicon. 3 Tables, 6 Figures, 33 References. Adapted from the source document JF - Cognitive Neuropsychology AU - Friedman, Rhonda B AU - Hadley, Jeffrey A AD - Medical Neurology Branch NIH/NINDS, Bethesda MD 20892 i3e@cu.nih.gov Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 185 EP - 208 VL - 9 IS - 3 SN - 0264-3294, 0264-3294 KW - alexia case study, letter-by-letter reading, shared orthographic lexicon model KW - tests KW - left-hemisphere stroke patient aged 62 KW - Oral Reading (61450) KW - Grapheme Phoneme Correspondence (29250) KW - Aphasia (03400) KW - Letter Recognition (46400) KW - Word Processing (98150) KW - article KW - 6410: language-pathological and normal; language-pathological and normal UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85553781?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Allba&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cognitive+Neuropsychology&rft.atitle=Letter-by-Letter+Surface+Alexia&rft.au=Friedman%2C+Rhonda+B%3BHadley%2C+Jeffrey+A&rft.aulast=Friedman&rft.aufirst=Rhonda&rft.date=1992-06-01&rft.volume=9&rft.issue=3&rft.spage=185&rft.isbn=&rft.btitle=&rft.title=Cognitive+Neuropsychology&rft.issn=02643294&rft_id=info:doi/ LA - English DB - Linguistics and Language Behavior Abstracts (LLBA) N1 - Date revised - 2003-10-01 N1 - Last updated - 2016-09-27 N1 - CODEN - COGNEP N1 - SubjectsTermNotLitGenreText - Aphasia (03400); Letter Recognition (46400); Oral Reading (61450); Grapheme Phoneme Correspondence (29250); Word Processing (98150) ER - TY - JOUR T1 - Age-related vulnerability. AN - 85214639; pmid-1608640 AB - This presentation considers the vulnerability of the upper alimentary and respiratory tracts to environmental insults during aging. A specific example, salivary gland secretion, is discussed. Available data suggest that while aging per se does not affect salivary performance adversely, it does appear to compromise the glands in such a way that older persons are more vulnerable to exogenous factors that can reduce secretory capacity and, consequently, diminish oropharyngeal health. JF - Otolaryngology--Head and Neck Surgery AU - Baum, B J AD - Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. PY - 1992 SP - 730 EP - 732 VL - 106 IS - 6 SN - 0194-5998, 0194-5998 KW - Salivation KW - Human KW - Aging KW - Aged KW - Salivary Glands UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85214639?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Otolaryngology--Head+and+Neck+Surgery&rft.atitle=Age-related+vulnerability.&rft.au=Baum%2C+B+J&rft.aulast=Baum&rft.aufirst=B&rft.date=1992-06-01&rft.volume=106&rft.issue=6&rft.spage=730&rft.isbn=&rft.btitle=&rft.title=Otolaryngology--Head+and+Neck+Surgery&rft.issn=01945998&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - The novel bilirubin/phenol UDP-glucuronosyltransferase UGT1 gene locus: implications for multiple nonhemolytic familial hyperbilirubinemia phenotypes. AN - 75520907; 1306114 AB - At least three types of congenital nonhemolytic unconjugated hyperbilirubinemias, including the rare Crigler-Najjar (CN) diseases (Types I or II) and Gilbert's syndrome (affecting 6% of the population) are associated with either absent or reduced hepatic UDP-glucuronosyltransferase (transferase) activity towards the potentially toxic endogenous acceptor, bilirubin. Here, we review the biochemical studies associated with these deficiencies. Accumulated evidence from studies with an animal model of CN Type I syndrome, the Gunn strain of hyperbilirubinemic rats, suggested that multiple isozymes are absent. These confounding observations have been clarified by a flurry of reports which have revealed the molecular basis for the complex disease phenotype in the Gunn rat and by the isolation and description of a novel human gene complex, UGT1, which encodes multiple and independently-regulated transferase isozymes that contain identical carboxyl terminal regions (246 amino acids). Finally, we discuss the implications of the gene organization and genetic defects determined for four different CN Type I individuals as a basis for a model which explains the inheritance pattern and genotypes of other familial unconjugated hyperbilirubinemias. JF - Pharmacogenetics AU - Owens, I S AU - Ritter, J K AD - Section of Genetic Disorders of Drug Metabolism, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 93 EP - 108 VL - 2 IS - 3 SN - 0960-314X, 0960-314X KW - UGT1 KW - DNA KW - 9007-49-2 KW - Glucuronosyltransferase KW - EC 2.4.1.17 KW - bilirubin glucuronoside glucuronosyltransferase KW - EC 2.4.1.95 KW - Index Medicus KW - Pedigree KW - Animals KW - Humans KW - Multigene Family KW - Rats, Gunn KW - Gilbert Disease -- enzymology KW - Gilbert Disease -- genetics KW - Cloning, Molecular KW - Rats KW - Phenotype KW - Crigler-Najjar Syndrome -- enzymology KW - DNA -- genetics KW - Crigler-Najjar Syndrome -- genetics KW - Female KW - Male KW - Glucuronosyltransferase -- genetics KW - Hyperbilirubinemia, Hereditary -- genetics KW - Hyperbilirubinemia, Hereditary -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75520907?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacogenetics&rft.atitle=The+novel+bilirubin%2Fphenol+UDP-glucuronosyltransferase+UGT1+gene+locus%3A+implications+for+multiple+nonhemolytic+familial+hyperbilirubinemia+phenotypes.&rft.au=Owens%2C+I+S%3BRitter%2C+J+K&rft.aulast=Owens&rft.aufirst=I&rft.date=1992-06-01&rft.volume=2&rft.issue=3&rft.spage=93&rft.isbn=&rft.btitle=&rft.title=Pharmacogenetics&rft.issn=0960314X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-30 N1 - Date created - 1993-07-30 N1 - Date revised - 2017-01-13 N1 - Gene symbol - UGT1 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Strychnine-insensitive glycine receptors in embryonic chick retina: characteristics and modulation of NMDA neurotoxicity. AN - 73528358; 1339019 AB - In the mammalian brain, the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor is coupled to a cation channel and a strychnine-insensitive glycine receptor. The present paper demonstrates the presence of NMDA receptor-coupled strychnine-insensitive glycine receptors in embryonic chick retina. Both glycine and 1-aminocyclopropanecarboxylic acid (ACPC) exhibited similar potencies (271 +/- 39 vs 247 +/- 39 nM, respectively) as inhibitors of strychnine-insensitive [3H]glycine binding to retinal membranes. Moreover, glycine and ACPC enhanced [3H]MK-801 binding to sites within the NMDA-coupled cation channel in retinal membranes with potencies comparable to those reported in rat brain. While the potency of ACPC was significantly higher than glycine (EC50 54 +/- 12 vs 256 +/- 57 nM, P < 0.02) in this measure, there were no significant differences in the maximum enhancement (efficacy) of [3H]MK-801 binding by these compounds. Since glycine appears to be required for the operation of NMDA-coupled cation channels, we examined the effects of glycine and ACPC on NMDA-induced acute excytotoxicity in the 14-day embryonic chick retina. Histological evaluation of retina revealed that either ACPC (10-100 microM) or glycine (200 microM) attenuated NMDA-induced (200 microM) retinal damage and a combination of these agents produced an enhanced protection against acute NMDA toxicity. ACPC (100 microM), but not MK-801 (1 microM) also afforded a modest protection against kainate-induced (25 microM) retinal damage. These findings demonstrate that while strychnine-insensitive glycine receptors are present in embryonic chick retina, occupation of these sites does not augment the cytotoxic actions of NMDA. Moreover, the ability of ACPC and glycine to attenuate NMDA-induced cytotoxicity does not appear to be mediated through occupation of these sites. JF - Neurochemistry international AU - Boje, K M AU - Skolnick, P AU - Raber, J AU - Fletcher, R T AU - Chader, G AD - Laboratory of Neuroscience, NIDDK, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 473 EP - 486 VL - 20 IS - 4 SN - 0197-0186, 0197-0186 KW - Amino Acids KW - 0 KW - Amino Acids, Cyclic KW - Neurotoxins KW - Receptors, Glycine KW - Receptors, Neurotransmitter KW - 1-aminocyclopropane-1-carboxylic acid KW - 3K9EJ633GL KW - gamma-Aminobutyric Acid KW - 56-12-2 KW - N-Methylaspartate KW - 6384-92-5 KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - Strychnine KW - H9Y79VD43J KW - Index Medicus KW - Animals KW - Chick Embryo KW - Drug Resistance KW - gamma-Aminobutyric Acid -- metabolism KW - Amino Acids -- pharmacology KW - Dizocilpine Maleate -- pharmacology KW - Retina -- metabolism KW - N-Methylaspartate -- toxicity KW - Strychnine -- pharmacology KW - Receptors, Neurotransmitter -- drug effects KW - Neurotoxins -- pharmacology KW - Retina -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73528358?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurochemistry+international&rft.atitle=Strychnine-insensitive+glycine+receptors+in+embryonic+chick+retina%3A+characteristics+and+modulation+of+NMDA+neurotoxicity.&rft.au=Boje%2C+K+M%3BSkolnick%2C+P%3BRaber%2C+J%3BFletcher%2C+R+T%3BChader%2C+G&rft.aulast=Boje&rft.aufirst=K&rft.date=1992-06-01&rft.volume=20&rft.issue=4&rft.spage=473&rft.isbn=&rft.btitle=&rft.title=Neurochemistry+international&rft.issn=01970186&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-15 N1 - Date created - 1993-07-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Renaturation of a single-chain immunotoxin facilitated by chaperones and protein disulfide isomerase. AN - 73279939; 1369490 AB - B3(Fv)-PE38KDEL, a recombinant immunotoxin, forms inclusion bodies when produced in Escherichia coli. In renaturation experiments, nonspecific aggregation of non-native polypeptide chains, and the formation of incorrect disulfide linkages lead to inactive molecules. To prevent these side reactions, we added molecular chaperones and protein disulfide isomerase (PDI) to the refolding buffer. Both DnaK and GroEL/S influenced the reactivation process. GroEL alone inhibited reactivation, but in the presence of ATP, GroEL and GroES significantly increased the yield of active protein. DnaK also increased the yield of properly folded protein and the stimulating effect of DnaK was also observed using immobilized DnaK, which can be used repeatedly without significant loss of activity. PDI, which catalyzes disulfide bridging of proteins, also stimulated reactivation of the immunotoxin. Under optimum conditions, reactivation yields in the presence of PDI were about twice that obtained with nonenzymatic disulfide bond formation. Furthermore, DnaK and PDI were additive when renaturation was performed in the presence of both proteins. JF - Bio/technology (Nature Publishing Company) AU - Buchner, J AU - Brinkmann, U AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 682 EP - 685 VL - 10 IS - 6 SN - 0733-222X, 0733-222X KW - Antibodies, Monoclonal KW - 0 KW - B3(Fv)-PE38KDEL recombinant immunotoxin KW - Bacterial Proteins KW - Chaperonin 10 KW - Chaperonin 60 KW - Escherichia coli Proteins KW - Exotoxins KW - HSP70 Heat-Shock Proteins KW - Heat-Shock Proteins KW - Immunotoxins KW - dnaK protein, E coli KW - EC 3.6.1.- KW - Isomerases KW - EC 5.- KW - Protein Disulfide-Isomerases KW - EC 5.3.4.1 KW - Biotechnology KW - Protein Conformation KW - Immunotoxins -- chemistry KW - Isomerases -- metabolism KW - Immunotoxins -- toxicity KW - Bacterial Proteins -- pharmacology KW - Immunotoxins -- immunology KW - Heat-Shock Proteins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73279939?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bio%2Ftechnology+%28Nature+Publishing+Company%29&rft.atitle=Renaturation+of+a+single-chain+immunotoxin+facilitated+by+chaperones+and+protein+disulfide+isomerase.&rft.au=Buchner%2C+J%3BBrinkmann%2C+U%3BPastan%2C+I&rft.aulast=Buchner&rft.aufirst=J&rft.date=1992-06-01&rft.volume=10&rft.issue=6&rft.spage=682&rft.isbn=&rft.btitle=&rft.title=Bio%2Ftechnology+%28Nature+Publishing+Company%29&rft.issn=0733222X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-02 N1 - Date created - 1992-12-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Astroglial membrane structure is affected by agents that raise cyclic AMP and by phosphatidylcholine phospholipase C. AN - 73260384; 1383432 AB - The role of signal transduction mechanisms in the production of the characteristic orthogonal arrays of particle assemblies in the astroglial plasma membrane was investigated in vitro by freeze-fracture electron microscopy. Agents which raise cellular cAMP levels and subsequently activate protein kinase A, such as forskolin (50 microM), isoproterenol (10 microM) and 8-bromo-cAMP (1 mM), increased the density, the number of assemblies per unit area of cleaved cell membrane, and the frequency of astrocytes with assemblies. Agents that lead to the activation of protein kinase C, such as phorbol 12,13-myristate acetate (at 50 nM) and choline-dependent phospholipase C (at 0.01-0.1 U ml-1), did not affect the assembly concentration. Thus, protein kinase A but not protein kinase C appears to be involved in the production of assemblies or their insertion into the astroglial plasma membrane. Although choline-dependent phospholipase C did not affect the astroglial assemblies, it caused the non-assembly, background particles to aggregate. A choline-dependent phospholipase C from a different source (B. cereus) was also active though at a higher concentration. Phospholipases of different specificities, such as phospholipase A2, phospholipase D or inositol-dependent phospholipase C were inactive over a wide range of concentrations. Two other astroglia derived cells, Müller cells and cells of the C6 glioma cell line, were also similarly affected by choline-dependent phospholipase C, while six other cells types including neurons, endothelial cells and fibroblasts were unaffected. It appears that phosphatidylcholine plays a significant role in determining the membrane structure of astrocytes. In a search for a means of isolating the assemblies, the binding of three lectins: ConA, WGA and PNA, conjugated to gold, was tested by label-fracture to ascertain whether the assemblies have an external oligosaccharide component. None of the lectins bound specifically to assemblies. JF - Journal of neurocytology AU - Tao-Cheng, J H AU - Bressler, J P AU - Brightman, M W AD - Laboratory of Neurobiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 458 EP - 467 VL - 21 IS - 6 SN - 0300-4864, 0300-4864 KW - Lectins KW - 0 KW - Phosphatidylcholines KW - Colforsin KW - 1F7A44V6OU KW - 8-Bromo Cyclic Adenosine Monophosphate KW - 23583-48-4 KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinases KW - EC 2.7.- KW - Protein Kinase C KW - EC 2.7.11.13 KW - Type C Phospholipases KW - EC 3.1.4.- KW - Phospholipase D KW - EC 3.1.4.4 KW - Isoproterenol KW - L628TT009W KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - 1-Methyl-3-isobutylxanthine KW - TBT296U68M KW - Index Medicus KW - Animals KW - Cell Membrane -- drug effects KW - Guinea Pigs KW - Cell Membrane -- ultrastructure KW - Phosphatidylcholines -- pharmacology KW - Stimulation, Chemical KW - Retina -- cytology KW - Rats KW - Protein Kinase C -- metabolism KW - Protein Kinases -- metabolism KW - Cattle KW - Glioma -- pathology KW - Freeze Fracturing KW - Tumor Cells, Cultured KW - Cells, Cultured KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Phospholipase D -- pharmacology KW - Immunohistochemistry KW - Lectins -- metabolism KW - Colforsin -- pharmacology KW - Astrocytes -- ultrastructure KW - Astrocytes -- drug effects KW - Second Messenger Systems -- drug effects KW - Cyclic AMP -- physiology KW - Type C Phospholipases -- pharmacology KW - 1-Methyl-3-isobutylxanthine -- pharmacology KW - 8-Bromo Cyclic Adenosine Monophosphate -- pharmacology KW - Isoproterenol -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73260384?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurocytology&rft.atitle=Astroglial+membrane+structure+is+affected+by+agents+that+raise+cyclic+AMP+and+by+phosphatidylcholine+phospholipase+C.&rft.au=Tao-Cheng%2C+J+H%3BBressler%2C+J+P%3BBrightman%2C+M+W&rft.aulast=Tao-Cheng&rft.aufirst=J&rft.date=1992-06-01&rft.volume=21&rft.issue=6&rft.spage=458&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurocytology&rft.issn=03004864&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-02 N1 - Date created - 1992-11-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Laterality of appendicular tardive dyskinesia in chronic schizophrenia. AN - 73198898; 1525274 AB - The notion that the neuropathology of schizophrenia is lateralized is supported, in part, by findings of asymmetries in tardive dyskinesia (TD). To verify the existence of asymmetric TD, this study used the AIMS examination to look for lateralization of limb movements in a sample of 58 patients with TD. Patients with schizophrenia were compared with patients with affective and schizoaffective disorders. Asymmetry was seen in the majority of patients, regardless of psychiatric diagnosis. There was no preference for one side over the other. In a subgroup of 16 patients rates repeatedly over 13 weeks, the presence and sidedness of asymmetry fluctuated. At least four ratings were needed to accurately predict the presence and sidedness of "persistent" asymmetry. This study does not support the notion that there is a consistent, lateralized asymmetry of TD in patients with schizophrenia. Moreover, it raises questions about the reliability of assessment of persistent laterality in TD using a single exam. JF - Biological psychiatry AU - Egan, M F AU - Hyde, T M AU - Tirschwell, D L AU - Kleinman, J E AU - Weinberger, D R AD - Intramural Research Program, National Institute of Mental Health, Washington, DC 20032. Y1 - 1992/06/01/ PY - 1992 DA - 1992 Jun 01 SP - 1098 EP - 1109 VL - 31 IS - 11 SN - 0006-3223, 0006-3223 KW - Index Medicus KW - Humans KW - Chi-Square Distribution KW - Adult KW - Retrospective Studies KW - Aged KW - Middle Aged KW - Male KW - Female KW - Dyskinesia, Drug-Induced -- physiopathology KW - Schizophrenia -- physiopathology KW - Functional Laterality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73198898?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biological+psychiatry&rft.atitle=Laterality+of+appendicular+tardive+dyskinesia+in+chronic+schizophrenia.&rft.au=Egan%2C+M+F%3BHyde%2C+T+M%3BTirschwell%2C+D+L%3BKleinman%2C+J+E%3BWeinberger%2C+D+R&rft.aulast=Egan&rft.aufirst=M&rft.date=1992-06-01&rft.volume=31&rft.issue=11&rft.spage=1098&rft.isbn=&rft.btitle=&rft.title=Biological+psychiatry&rft.issn=00063223&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A new class of alkaloids from a dendrobatid poison frog: a structure for alkaloid 251F. AN - 73194916; 1522417 AB - Alkaloids of a new class are present in skin extracts of the dendrobatid poison frog, Minyobates bombetes, of Colombia. The structure of the major alkaloid of this class, 251F, has been determined as a trimethylcyclopenta[b]quinolizidinemethanol 1 by nmr, gc-Ft-ir, and ms studies including ms-ms. At least nine congeners of 251F were detected in these extracts. JF - Journal of natural products AU - Spande, T F AU - Garraffo, H M AU - Yeh, H J AU - Pu, Q L AU - Pannell, L K AU - Daly, J W AD - Laboratory of Bioorganic Chemistry, National Institute of Diabetes, and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 707 EP - 722 VL - 55 IS - 6 SN - 0163-3864, 0163-3864 KW - Alkaloids KW - 0 KW - Index Medicus KW - Skin -- chemistry KW - Mass Spectrometry KW - Animals KW - Colombia KW - Alkaloids -- chemistry KW - Anura -- metabolism KW - Alkaloids -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73194916?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+natural+products&rft.atitle=A+new+class+of+alkaloids+from+a+dendrobatid+poison+frog%3A+a+structure+for+alkaloid+251F.&rft.au=Spande%2C+T+F%3BGarraffo%2C+H+M%3BYeh%2C+H+J%3BPu%2C+Q+L%3BPannell%2C+L+K%3BDaly%2C+J+W&rft.aulast=Spande&rft.aufirst=T&rft.date=1992-06-01&rft.volume=55&rft.issue=6&rft.spage=707&rft.isbn=&rft.btitle=&rft.title=Journal+of+natural+products&rft.issn=01633864&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-09 N1 - Date created - 1992-10-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Family history of alcoholism in the United States: prevalence and demographic characteristics. AN - 73190093; 1525535 AB - National estimates of the prevalence of family history for alcoholism in the USA were investigated using a general population sample of 43,809 respondents 18 years of age and older. Approximately 38% of the total sample reported a positive history for alcoholism. Positive reports were highest for Native Americans and lowest for Asian Americans. JF - British journal of addiction AU - Harford, T C AD - National Institute on Alcohol Abuse and Alcoholism, Division of Biometry and Epidemiology, Rockville, MD 20879. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 931 EP - 935 VL - 87 IS - 6 SN - 0952-0481, 0952-0481 KW - Index Medicus KW - Age Factors KW - Educational Status KW - Sex Factors KW - Humans KW - African Americans -- statistics & numerical data KW - Aged KW - Marriage KW - Inuits -- statistics & numerical data KW - Indians, North American -- statistics & numerical data KW - Income KW - Hispanic Americans -- statistics & numerical data KW - Adult KW - Middle Aged KW - Adolescent KW - United States -- epidemiology KW - Asian Americans -- statistics & numerical data KW - Male KW - Female KW - Prevalence KW - Alcoholism -- epidemiology KW - Family KW - Alcoholism -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73190093?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+addiction&rft.atitle=Family+history+of+alcoholism+in+the+United+States%3A+prevalence+and+demographic+characteristics.&rft.au=Harford%2C+T+C&rft.aulast=Harford&rft.aufirst=T&rft.date=1992-06-01&rft.volume=87&rft.issue=6&rft.spage=931&rft.isbn=&rft.btitle=&rft.title=British+journal+of+addiction&rft.issn=09520481&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hydrated clearance of gadolinium-DTPA as a measurement of glomerular filtration rate. AN - 73118528; 1501414 AB - Technetium (99mTc)-diethylene triamine pentaacetic acid (DTPA) hydrated clearance studies are accurate for determining GFR but require special facilities for handling and measuring samples. We investigated the potential of a non-radioactive paramagnetic analog, Gadolinium (Gd)-diethylene triamine pentaacetic acid (DTPA), an approved NMR contrast agent, as a glomerular filtration marker. Instead of relying on the radioactivity of technetium, this test is based on the fact that gadolinium induces alterations in the NMR T1 relaxation times in blood and urine samples. Ninety patients underwent simultaneous determinations of GFR using 1 mCi of Tc-DTPA and 0.05 mmol/kg Gd-DTPA (Berlex Labs) IV. The patients were hydrated with oral and intravenous fluid. Following a one hour equilibrium period, three or four consecutive urine collections were obtained; plasma samples were acquired at the beginning and end of each approximately 20-minute interval. 99mTc-DTPA radioactivity was determined with a scintillation counter. T1 relaxation times were measured on a 10 MHz NMR spectrometer. These were converted to Gd-DTPA concentration by comparison with standard solutions. The Gd-DTPA derived GFR closely approximated the 99mTc-DTPA derived GFR which ranged from 15 to 147 ml/min. The equation and correlation coefficient of the regression line is y = 1.04 x -2.2, r = 0.94. Thus, Gd-DTPA is a safe, non-radioactive indicator of GFR that may provide an alternative renal clearance method for clinical studies of progressive renal disease and nephrotoxicity. JF - Kidney international AU - Choyke, P L AU - Austin, H A AU - Frank, J A AU - Girton, M E AU - Diggs, R L AU - Dwyer, A J AU - Miller, L AU - Nussenblatt, R AU - McFarland, H AU - Simon, T AD - Department of Radiology and Nuclear Medicine, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 1595 EP - 1598 VL - 41 IS - 6 SN - 0085-2538, 0085-2538 KW - Contrast Media KW - 0 KW - Organometallic Compounds KW - Pentetic Acid KW - 7A314HQM0I KW - Gadolinium KW - AU0V1LM3JT KW - Gadolinium DTPA KW - K2I13DR72L KW - Technetium Tc 99m Pentetate KW - VW78417PU1 KW - Index Medicus KW - Evaluation Studies as Topic KW - Humans KW - Magnetic Resonance Spectroscopy KW - Kidney Function Tests -- methods KW - Glomerular Filtration Rate UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73118528?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Kidney+international&rft.atitle=Hydrated+clearance+of+gadolinium-DTPA+as+a+measurement+of+glomerular+filtration+rate.&rft.au=Choyke%2C+P+L%3BAustin%2C+H+A%3BFrank%2C+J+A%3BGirton%2C+M+E%3BDiggs%2C+R+L%3BDwyer%2C+A+J%3BMiller%2C+L%3BNussenblatt%2C+R%3BMcFarland%2C+H%3BSimon%2C+T&rft.aulast=Choyke&rft.aufirst=P&rft.date=1992-06-01&rft.volume=41&rft.issue=6&rft.spage=1595&rft.isbn=&rft.btitle=&rft.title=Kidney+international&rft.issn=00852538&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-15 N1 - Date created - 1992-09-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synthesis of a photoreactive, radiolabelled derivative of the oligosaccharide of GM1 ganglioside. AN - 73111895; 1498422 AB - A photoreactive, radioiodinatable derivative of the oligosaccharide (GM1OS) of ganglioside GM1 was synthesized as follows: GM1OS was generated from GM1 by ozonolysis and alkaline fragmentation, and reductively aminated to GM1OSNH2 (1-amino-1-deoxymonosialogangliotetraitol). The latter compound was then reacted with N-hydroxysuccinimidyl-4-azidosalicylic acid (NHS-ASA) to form GM1OSNH-ASA [1-(4-azidosalicoylamido)-1-deoxymonosialogangliotetraitol], which was radioiodinated and further purified. To test the [125I]GM1OSNH-IASA [1-(4-iodoazidosalicoylamido)-1-deoxymonosialogangliotetraitol+ ++] as a probe for ganglioside-binding proteins, the derivative was incubated with cholera toxin, which specifically binds GM1, followed by photolysis and sodium dodecyl sulphate-polyacrylamide gel electrophoresis. The probe only labelled the B or binding subunit of cholera toxin, but not the A or adenylyl cyclase activating subunit. Labelling was inhibited by excess GM1OS, but not by the oligosaccharides from gangliosides GD1a and GD1b. [125I]GM1OSNH-IASA and analogous oligosaccharide derivatives may be valuable probes for detecting ganglioside-binding proteins. JF - Glycobiology AU - Pacuszka, T AU - Fishman, P H AD - Membrane Biochemistry Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 251 EP - 255 VL - 2 IS - 3 SN - 0959-6658, 0959-6658 KW - Affinity Labels KW - 0 KW - Iodine Radioisotopes KW - Molecular Probes KW - Oligosaccharides KW - G(M1) Ganglioside KW - 37758-47-7 KW - Cholera Toxin KW - 9012-63-9 KW - Index Medicus KW - Molecular Probes -- chemistry KW - Molecular Probes -- chemical synthesis KW - Molecular Sequence Data KW - Carbohydrate Sequence KW - G(M1) Ganglioside -- chemistry KW - Oligosaccharides -- chemical synthesis KW - G(M1) Ganglioside -- chemical synthesis KW - Oligosaccharides -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73111895?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Glycobiology&rft.atitle=Synthesis+of+a+photoreactive%2C+radiolabelled+derivative+of+the+oligosaccharide+of+GM1+ganglioside.&rft.au=Pacuszka%2C+T%3BFishman%2C+P+H&rft.aulast=Pacuszka&rft.aufirst=T&rft.date=1992-06-01&rft.volume=2&rft.issue=3&rft.spage=251&rft.isbn=&rft.btitle=&rft.title=Glycobiology&rft.issn=09596658&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-15 N1 - Date created - 1992-09-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sample size determination for case-control studies and the comparison of stratified and unstratified analyses. AN - 73096966; 1637968 AB - Woolson, Bean, and Rojas (1986, Biometrics 42, 927-932) present a simple approximation of sample size for Cochran's (1954, Biometrics 10, 417-451) test for detecting association between exposure and disease. It is useful in the design of case-control studies. We derive a sample size formula for Cochran's statistic with continuity correction which guarantees that the actual Type I error rate of the test does not exceed the nominal level. The corrected sample size is necessarily larger than the uncorrected one given by Woolson et al. and the relative difference between the two sample sizes is considerable. Allocation of equal number of cases and controls within each stratum is asymptotically optimal when the costs per case and control are the same. When any effect of stratification is absent, Cochran's stratified test, although valid, is less efficient than the unstratified one except for the important case of a balanced design. JF - Biometrics AU - Nam, J AD - Mathematical Statistics and Applied Mathematics Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 389 EP - 395 VL - 48 IS - 2 SN - 0006-341X, 0006-341X KW - Chlorine KW - 4R7X1O2820 KW - Index Medicus KW - Humans KW - Male KW - Iowa -- epidemiology KW - Colonic Neoplasms -- etiology KW - Water Supply KW - Case-Control Studies KW - Mathematics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73096966?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biometrics&rft.atitle=Sample+size+determination+for+case-control+studies+and+the+comparison+of+stratified+and+unstratified+analyses.&rft.au=Nam%2C+J&rft.aulast=Nam&rft.aufirst=J&rft.date=1992-06-01&rft.volume=48&rft.issue=2&rft.spage=389&rft.isbn=&rft.btitle=&rft.title=Biometrics&rft.issn=0006341X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-01 N1 - Date created - 1992-09-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Brevetoxins bind to multiple classes of sites in rat brain synaptosomes. AN - 73096410; 1323018 AB - The brevetoxins (PbTx series), neurotoxins produced by the marine dinoflagellate Ptychodiscus brevis, cause dose-dependent activation of the voltage-sensitive sodium channel (VSSC). Saturation binding studies employing adult rat brain synaptosomes suggest the existence of a high affinity/low capacity (HA/LC) and a second, lower affinity/higher capacity (LA/HC) class of binding site. LIGAND analysis of saxitoxin and brevetoxin saturation binding data yields a statistically identical Bmax for the brevetoxin high affinity/low capacity (HA/LC) site (1.9 +/- 0.98 pmol/mg protein) and for saxitoxin (1.72 +/- 0.78 pmol/mg protein; P less than 0.001). The stoichiometry of HA/LC brevetoxin binding and saxitoxin binding approaches 1:1. Covalent modification of synaptosomes with a brevetoxin photoaffinity probe preferentially blocks the HA/LC binding site. Hill plots of saturation binding data yield a coefficient of 1.0 +/- 0.02, demonstrating a lack of cooperativity between brevetoxin binding site classes. Kd and Bmax for toxin binding are independent of membrane polarity, intimating that the observed low affinity/high capacity (LA/HC) binding characteristics are not due to modification of the HA/LC site, and strongly argue for the presence of multiple brevetoxin binding site classes. Half-maximal binding at the LA/HC site, and strongly argue for the presence of multiple brevetoxin binding site classes. Half-maximal binding at the LA/HC site occurs at concentration ranges for which the brevetoxins allosterically modulate binding of other natural toxins to their specific sites. JF - Brain research. Molecular brain research AU - Edwards, R A AU - Trainer, V L AU - Baden, D G AD - University of Miami, Rosenstiel School of Marine and Atmospheric Science, NIEHS Marine and Freshwater Biomedical Sciences Center, FL 33149. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 64 EP - 70 VL - 14 IS - 1-2 SN - 0169-328X, 0169-328X KW - Marine Toxins KW - 0 KW - Neurotoxins KW - Oxocins KW - Receptors, Cell Surface KW - Sodium Channels KW - brevetoxin receptor KW - Saxitoxin KW - 35523-89-8 KW - brevetoxin KW - 98225-48-0 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Molecular Structure KW - Animals KW - Binding, Competitive KW - Saxitoxin -- metabolism KW - Male KW - Receptors, Cell Surface -- metabolism KW - Neurotoxins -- metabolism KW - Brain -- metabolism KW - Marine Toxins -- metabolism KW - Synaptosomes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73096410?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research.+Molecular+brain+research&rft.atitle=Brevetoxins+bind+to+multiple+classes+of+sites+in+rat+brain+synaptosomes.&rft.au=Edwards%2C+R+A%3BTrainer%2C+V+L%3BBaden%2C+D+G&rft.aulast=Edwards&rft.aufirst=R&rft.date=1992-06-01&rft.volume=14&rft.issue=1-2&rft.spage=64&rft.isbn=&rft.btitle=&rft.title=Brain+research.+Molecular+brain+research&rft.issn=0169328X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-08 N1 - Date created - 1992-09-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Craving: consensus of status and agenda for future research. AN - 73083680; 1633752 AB - The term craving is used frequently in relationship to drug abuse and its treatment but there is disagreement over its definition and role. In February 1991, a meeting of experts from several disciplines, sponsored by the Addiction Research Center (ARC) of the National Institute on Drug Abuse, was convened with the goal of reaching consensus about the importance of craving and to suggest a future research program. The participants agreed that craving is a subjective state in humans that is associated with drug dependence but little is known about its determinants, relationship to drug taking, and measurement. To advance our knowledge, a substantial research program is required. The outcome of this research effort could have important consequences for increasing our understanding of the determinants of drug abuse. JF - Drug and alcohol dependence AU - Pickens, R W AU - Johanson, C E AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 127 EP - 131 VL - 30 IS - 2 SN - 0376-8716, 0376-8716 KW - Psychotropic Drugs KW - 0 KW - Street Drugs KW - Index Medicus KW - Humans KW - Motivation KW - Substance-Related Disorders -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73083680?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+and+alcohol+dependence&rft.atitle=Craving%3A+consensus+of+status+and+agenda+for+future+research.&rft.au=Pickens%2C+R+W%3BJohanson%2C+C+E&rft.aulast=Pickens&rft.aufirst=R&rft.date=1992-06-01&rft.volume=30&rft.issue=2&rft.spage=127&rft.isbn=&rft.btitle=&rft.title=Drug+and+alcohol+dependence&rft.issn=03768716&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-27 N1 - Date created - 1992-08-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effect of dietary intake of fruits and vegetables on the odds ratio of lung cancer among Yunnan tin miners. AN - 73073253; 1634303 AB - All newly diagnosed cases of lung cancer (N = 183) among male tin miners of Yunnan Province, China and age-sex matched occupational controls (N = 183 aged 45-79 years) were interviewed within 3 months following cancer diagnosis. The questionnaire included information about usual adult diet as well as employment and smoking histories. Over 95% of cases and controls were current smokers. The 27-item food frequency questionnaire included 11 fruits and vegetables rich in vitamin A and/or carotenoids. The effect of dietary intake of fruits and vegetables on risk of lung cancer was examined with adjustment for exposures to radon, arsenic, and smoking as previously documented risk factors for lung cancer. Tin miners with reduced intake of yellow and light green vegetables had statistically significant increased odds ratios (OR) of lung cancer (OR = 2.26 and OR = 2.39 for the lowest two quartiles of intake; P value for trend = 0.02) among cases compared with controls after multiple logistic regression adjustment for covariates; and this relationship was monotonic. Tin miners with reduced intake of tomatoes had statistically significant increased adjusted OR of lung cancer (OR = 2.64, OR = 3.09, OR = 2.36 for the three lowest quartiles of intake; P value for trend = 0.04). This is the first study to demonstrate a protective effect of vegetable intake versus the strong effects of smoking and occupational exposures on lung cancer risk. JF - International journal of epidemiology AU - Forman, M R AU - Yao, S X AU - Graubard, B I AU - Qiao, Y L AU - McAdams, M AU - Mao, B L AU - Taylor, P R AD - Cancer Prevention Studies Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 437 EP - 441 VL - 21 IS - 3 SN - 0300-5771, 0300-5771 KW - Tin KW - 7440-31-5 KW - Index Medicus KW - Odds Ratio KW - Risk Factors KW - Humans KW - China -- epidemiology KW - Case-Control Studies KW - Incidence KW - Aged KW - Middle Aged KW - Male KW - Vegetables KW - Lung Neoplasms -- prevention & control KW - Lung Neoplasms -- epidemiology KW - Occupational Diseases -- prevention & control KW - Occupational Diseases -- epidemiology KW - Nutritional Physiological Phenomena KW - Mining KW - Fruit UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73073253?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+epidemiology&rft.atitle=The+effect+of+dietary+intake+of+fruits+and+vegetables+on+the+odds+ratio+of+lung+cancer+among+Yunnan+tin+miners.&rft.au=Forman%2C+M+R%3BYao%2C+S+X%3BGraubard%2C+B+I%3BQiao%2C+Y+L%3BMcAdams%2C+M%3BMao%2C+B+L%3BTaylor%2C+P+R&rft.aulast=Forman&rft.aufirst=M&rft.date=1992-06-01&rft.volume=21&rft.issue=3&rft.spage=437&rft.isbn=&rft.btitle=&rft.title=International+journal+of+epidemiology&rft.issn=03005771&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-24 N1 - Date created - 1992-08-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ethanol induces marked changes in lymphocyte populations and natural killer cell activity in mice. AN - 73062583; 1626648 AB - Treatment of mice in vivo with 5% w/v ethanol given in a liquid diet causes marked changes in spleen, peripheral blood, and thymus lymphocytes. In both the thymus and spleen, there is an acute cellular depletion resulting in a significant decrease in gross tissue size and cell number. In spleen and peripheral blood, the percentage of T lymphocytes is increased relative to B lymphocytes, but the ratio of CD4+/CD8+ T cell sub-populations remains unchanged. Splenic natural killer (NK) cell activity is increased in ethanol-consuming mice, although the percentage of NK1.1+ cells is relatively unchanged. JF - Alcoholism, clinical and experimental research AU - Meadows, G G AU - Wallendal, M AU - Kosugi, A AU - Wunderlich, J AU - Singer, D S AD - Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 474 EP - 479 VL - 16 IS - 3 SN - 0145-6008, 0145-6008 KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Major Histocompatibility Complex -- immunology KW - Thymus Gland -- immunology KW - Mice, Inbred Strains KW - Leukocyte Count -- drug effects KW - Animals KW - Ethanol -- pharmacokinetics KW - Liver -- immunology KW - Spleen -- immunology KW - Mice KW - Cytotoxicity, Immunologic -- immunology KW - Lymphocyte Subsets -- immunology KW - Alcoholism -- immunology KW - Killer Cells, Natural -- immunology KW - Alcohol Drinking -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73062583?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%2C+clinical+and+experimental+research&rft.atitle=Ethanol+induces+marked+changes+in+lymphocyte+populations+and+natural+killer+cell+activity+in+mice.&rft.au=Meadows%2C+G+G%3BWallendal%2C+M%3BKosugi%2C+A%3BWunderlich%2C+J%3BSinger%2C+D+S&rft.aulast=Meadows&rft.aufirst=G&rft.date=1992-06-01&rft.volume=16&rft.issue=3&rft.spage=474&rft.isbn=&rft.btitle=&rft.title=Alcoholism%2C+clinical+and+experimental+research&rft.issn=01456008&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-12 N1 - Date created - 1992-08-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A double-blind, placebo controlled study of trazodone in patients with obsessive-compulsive disorder. AN - 73059662; 1629380 AB - Patients with obsessive-compulsive disorder (OCD) have been shown to be preferentially responsive to serotonin (5-HT) uptake-inhibiting antidepressants including clomipramine, fluoxetine, fluvoxamine, and sertraline. The nontricyclic antidepressant, trazodone, also possesses serotonin reuptake inhibiting properties and has been reported to be efficacious in OCD in several case reports and open trials. In order to investigate trazodone's potential antiobsessive efficacy in a controlled fashion, 21 patients with OCD were entered into a double-blind, parallel design comparison of trazodone and placebo. There were no significant differences in baseline rating scores of OCD or depressive symptoms between those who entered the trazodone phase (N = 13) versus those who entered the placebo phase (N = 8). As measured by standardized OCD and depression rating scales, there was no significant difference in OCD or depressive symptoms in the 17 patients who completed 10 weeks of trazodone (N = 11, mean daily dose, 235 +/- 10 mg) versus 10 weeks of placebo (N = 6) administration. In comparison to clomipramine and fluoxetine treatment which we have found to be associated with greater than 95% reduction in platelet 5-HT concentration, there was only a 26% mean reduction in platelet 5-HT concentration after 10 weeks of trazodone administration. These results indicate that trazodone lacks substantial antiobsessive effects and is associated with only modest reductions in platelet 5-HT concentrations. JF - Journal of clinical psychopharmacology AU - Pigott, T A AU - L'Heureux, F AU - Rubenstein, C S AU - Bernstein, S E AU - Hill, J L AU - Murphy, D L AD - Section on Clinical Neuropharmacology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 156 EP - 162 VL - 12 IS - 3 SN - 0271-0749, 0271-0749 KW - Piperazines KW - 0 KW - Serotonin KW - 333DO1RDJY KW - 1-(3-chlorophenyl)piperazine KW - REY0CNO998 KW - Trazodone KW - YBK48BXK30 KW - Index Medicus KW - Psychiatric Status Rating Scales KW - Double-Blind Method KW - Humans KW - Blood Platelets -- drug effects KW - Serotonin -- blood KW - Adult KW - Middle Aged KW - Blood Platelets -- metabolism KW - Adolescent KW - Piperazines -- blood KW - Male KW - Female KW - Trazodone -- therapeutic use KW - Trazodone -- adverse effects KW - Obsessive-Compulsive Disorder -- psychology KW - Obsessive-Compulsive Disorder -- drug therapy KW - Trazodone -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73059662?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+psychopharmacology&rft.atitle=A+double-blind%2C+placebo+controlled+study+of+trazodone+in+patients+with+obsessive-compulsive+disorder.&rft.au=Pigott%2C+T+A%3BL%27Heureux%2C+F%3BRubenstein%2C+C+S%3BBernstein%2C+S+E%3BHill%2C+J+L%3BMurphy%2C+D+L&rft.aulast=Pigott&rft.aufirst=T&rft.date=1992-06-01&rft.volume=12&rft.issue=3&rft.spage=156&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+psychopharmacology&rft.issn=02710749&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-20 N1 - Date created - 1992-08-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alcohol, nitric oxide, and neurotoxicity: is there a connection?--a review. AN - 73053845; 1320808 AB - A hypothesis is presented to explain the influence of alcohol on glutamate generated excitotoxicity. Chronic alcohol exposure is reported to increase glutamate-N-methyl-D-aspartate (NMDA) receptors and calcium ion channel activity, resulting in the neurotoxicity and seizure activity associated with alcohol withdrawal in certain persons. Recent information indicates that nitric oxide is responsible for the neurotoxicity associated with excessive glutamate stimulation of NMDA receptors. Thus, it is hypothesized that nitric oxide is involved in producing the neurotoxicity and cell disturbances associated with chronic alcohol exposure. JF - Alcoholism, clinical and experimental research AU - Lancaster, F E AD - Division of Basic Research, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 539 EP - 541 VL - 16 IS - 3 SN - 0145-6008, 0145-6008 KW - Calcium Channels KW - 0 KW - Receptors, Glutamate KW - Receptors, N-Methyl-D-Aspartate KW - Receptors, Neurotransmitter KW - Nitric Oxide KW - 31C4KY9ESH KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Nerve Degeneration -- drug effects KW - Animals KW - Cell Survival -- drug effects KW - Receptors, N-Methyl-D-Aspartate -- drug effects KW - Humans KW - Calcium Channels -- drug effects KW - Receptors, Neurotransmitter -- drug effects KW - Nitric Oxide -- toxicity KW - Brain -- drug effects KW - Ethanol -- toxicity KW - Brain Damage, Chronic -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73053845?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%2C+clinical+and+experimental+research&rft.atitle=Alcohol%2C+nitric+oxide%2C+and+neurotoxicity%3A+is+there+a+connection%3F--a+review.&rft.au=Lancaster%2C+F+E&rft.aulast=Lancaster&rft.aufirst=F&rft.date=1992-06-01&rft.volume=16&rft.issue=3&rft.spage=539&rft.isbn=&rft.btitle=&rft.title=Alcoholism%2C+clinical+and+experimental+research&rft.issn=01456008&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-12 N1 - Date created - 1992-08-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nosocomial human parvovirus B19 infection: lack of transmission from a chronically infected patient to hospital staff. AN - 73046953; 1619271 AB - To assess the potential for nosocomial spread of parvovirus B19 from a chronically infected patient. Employees exposed to the index case and control (unexposed) employees were evaluated by baseline and follow up parvovirus B19 serologies and hematologic assessments, and completed baseline and follow up epidemiologic questionnaires. A chronically infected patient was hospitalized on a hematology ward in a research referral hospital for 3.5 weeks prior to a diagnosis of parvovirus B19 infection and the institution of isolation precautions. Sera were screened for parvovirus B19 DNA (dot blot analysis), and IgG and IgM anti-B19 antibodies (capture immunoassay). Hematologic assessment included CBC, differential, and reticulocyte count. The index case had parvovirus B19 DNA at approximately 10(6) genome copies per ml of serum, elevated IgM and low levels of IgG B19 antibodies. Of the 21 exposed staff, 11 (52%) had IgG B19 antibodies and were immune; of the 8 unexposed staff, 6 (75%) had IgG B19 antibodies. No employees developed IgM B19 antibodies, B19 DNA, hematologic abnormalities, or clinical symptoms. In contrast to reports of documented nosocomial transmission of B19 parvovirus from patients in transient aplastic crisis, nosocomial transmission did not occur--even in the absence of isolation precautions--presumably from the lower level of B19 viremia in our chronically infected (rather than acutely infected) patient. JF - Infection control and hospital epidemiology AU - Koziol, D E AU - Kurtzman, G AU - Ayub, J AU - Young, N S AU - Henderson, D K AD - Hospital Epidemiology Service, Warren G. Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 343 EP - 348 VL - 13 IS - 6 SN - 0899-823X, 0899-823X KW - Antibodies, Viral KW - 0 KW - Index Medicus KW - Nursing KW - Antibodies, Viral -- blood KW - Immunoblotting KW - Parvovirus B19, Human -- immunology KW - Humans KW - Surveys and Questionnaires KW - Male KW - Female KW - Pregnancy KW - Personnel, Hospital KW - Cross Infection -- transmission KW - Occupational Diseases -- etiology KW - Erythema Infectiosum -- transmission UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73046953?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+control+and+hospital+epidemiology&rft.atitle=Nosocomial+human+parvovirus+B19+infection%3A+lack+of+transmission+from+a+chronically+infected+patient+to+hospital+staff.&rft.au=Koziol%2C+D+E%3BKurtzman%2C+G%3BAyub%2C+J%3BYoung%2C+N+S%3BHenderson%2C+D+K&rft.aulast=Koziol&rft.aufirst=D&rft.date=1992-06-01&rft.volume=13&rft.issue=6&rft.spage=343&rft.isbn=&rft.btitle=&rft.title=Infection+control+and+hospital+epidemiology&rft.issn=0899823X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-06 N1 - Date created - 1992-08-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Infect Control Hosp Epidemiol 1992 Sep;13(9):511 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Family history as a predictor of alcohol dependence. AN - 73043821; 1626658 AB - The effects of various levels of positive family history of alcoholism on the probability of past year alcohol dependence were investigated using a general population sample of 23,152 drinkers 18 years of age and older. Forty percent reported a positive family history. After adjustment for age, race, gender, and poverty and compared with persons with a negative family history, the odds of alcohol dependence were increased by 45% among persons with alcoholism in second or third degree relatives only, by 86% among those with alcoholism in first degree relatives only, and by 167% among those with alcoholism in first and second or third degree relatives. The effects of family history did not vary among population subgroups as defined by age, race, gender, and poverty. JF - Alcoholism, clinical and experimental research AU - Dawson, D A AU - Harford, T C AU - Grant, B F AD - National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 572 EP - 575 VL - 16 IS - 3 SN - 0145-6008, 0145-6008 KW - Index Medicus KW - Risk Factors KW - Humans KW - Adult KW - Models, Statistical KW - Adolescent KW - Male KW - Female KW - Child of Impaired Parents -- psychology KW - Alcohol Drinking -- psychology KW - Alcohol Drinking -- genetics KW - Alcoholism -- genetics KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73043821?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%2C+clinical+and+experimental+research&rft.atitle=Family+history+as+a+predictor+of+alcohol+dependence.&rft.au=Dawson%2C+D+A%3BHarford%2C+T+C%3BGrant%2C+B+F&rft.aulast=Dawson&rft.aufirst=D&rft.date=1992-06-01&rft.volume=16&rft.issue=3&rft.spage=572&rft.isbn=&rft.btitle=&rft.title=Alcoholism%2C+clinical+and+experimental+research&rft.issn=01456008&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-12 N1 - Date created - 1992-08-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Control of constitutively-expressed developmentally-activated rat hepatic cytochrome P450 genes. AN - 73032305; 1619850 AB - Cytochromes P450 (P450) collectively refer to a superfamily of heme-containing enzymes that use O2 and electrons from NADPH to insert a single atom of oxygen into any one of a large number of substrates. Two general classes of P450s exist; a relatively limited number of P450 forms, expressed in specialized tissues that are associated with pathways of steroidogenesis and a large number of forms responsible for metabolism of foreign compounds. Most of the latter P450s are expressed in liver, the primary site for metabolism of drugs, unusual dietary compounds and environmental pollutants. Numerous forms of P450 are expressed in liver of untreated animals and these are regulated quite differently. Both developmentally-programmed and sex-specific expressions have been observed. In this review, I will summarize recent findings on the mechanisms by which two P450 genes are regulated in livers of developing rats. The CYP2E1 gene is transcriptionally activated within a few hours after birth while the CYP2C6 gene is activated just prior to rats reaching puberty. These genes are under control of two transcription factors, HNF-1 alpha and DBP, respectively, that themselves are developmentally controlled. JF - The Keio journal of medicine AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 68 EP - 75 VL - 41 IS - 2 SN - 0022-9717, 0022-9717 KW - CYP2C6 KW - CYP2E1 KW - Albumins KW - 0 KW - Hormones KW - Transcription Factors KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Rats KW - Animals KW - Base Sequence KW - Hormones -- physiology KW - Albumins -- genetics KW - Molecular Sequence Data KW - Transcription Factors -- physiology KW - Liver -- enzymology KW - Liver -- growth & development KW - Cytochrome P-450 Enzyme System -- genetics KW - Gene Expression Regulation, Enzymologic -- physiology KW - Cytochrome P-450 Enzyme System -- chemistry KW - Cytochrome P-450 Enzyme System -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73032305?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Keio+journal+of+medicine&rft.atitle=Control+of+constitutively-expressed+developmentally-activated+rat+hepatic+cytochrome+P450+genes.&rft.au=Gonzalez%2C+F+J&rft.aulast=Gonzalez&rft.aufirst=F&rft.date=1992-06-01&rft.volume=41&rft.issue=2&rft.spage=68&rft.isbn=&rft.btitle=&rft.title=The+Keio+journal+of+medicine&rft.issn=00229717&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-03 N1 - Date created - 1992-08-03 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CYP2C6; CYP2E1 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Skin cancer and chromosomal aberrations induced by ultraviolet radiation. Evidence for lack of correlation in xeroderma pigmentosum variant and group E patients. AN - 73015574; 1606553 AB - Ultraviolet radiation (UV) in sunlight induces an abnormally high incidence of skin cancer in patients with xeroderma pigmentosum (XP), an autosomal recessive disease with defects in the repair of damaged DNA. We determined the frequency of UV-induced chromosomal aberrations in cultured lymphoblast lines from a patient with the variant form of XP, from a patient with the complementation group E form, and from two patients with the complementation group C form. In contrast to results with patients having other forms of XP, the group E and variant patients showed no abnormal increase in UV-induced chromosomal aberrations. Even in the presence of caffeine, which exacerbates the postreplication repair defect of UV-irradiated XP variant cells, there was still no abnormally elevated frequency of UV-induced chromosomal aberrations in the variant cells. These results, indicating that the level of UV-induced chromosomal aberrations is not correlated with these patients' marked susceptibility to skin cancer, suggests that some mechanism other than genetic transposition is causatively related to these XP patients' high incidence of sunlight-induced skin cancer. JF - Cancer genetics and cytogenetics AU - Seguin, L R AU - Ganges, M B AU - Tarone, R E AU - Robbins, J H AD - Dermatology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 111 EP - 116 VL - 60 IS - 2 SN - 0165-4608, 0165-4608 KW - Caffeine KW - 3G6A5W338E KW - Index Medicus KW - DNA Repair -- radiation effects KW - Humans KW - Caffeine -- pharmacology KW - Cell Line, Transformed KW - DNA Repair -- drug effects KW - Skin Neoplasms -- genetics KW - Ultraviolet Rays -- adverse effects KW - Chromosome Aberrations KW - Xeroderma Pigmentosum -- genetics KW - Neoplasms, Radiation-Induced -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73015574?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+genetics+and+cytogenetics&rft.atitle=Skin+cancer+and+chromosomal+aberrations+induced+by+ultraviolet+radiation.+Evidence+for+lack+of+correlation+in+xeroderma+pigmentosum+variant+and+group+E+patients.&rft.au=Seguin%2C+L+R%3BGanges%2C+M+B%3BTarone%2C+R+E%3BRobbins%2C+J+H&rft.aulast=Seguin&rft.aufirst=L&rft.date=1992-06-01&rft.volume=60&rft.issue=2&rft.spage=111&rft.isbn=&rft.btitle=&rft.title=Cancer+genetics+and+cytogenetics&rft.issn=01654608&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-23 N1 - Date created - 1992-07-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Does chemically induced hepatocyte proliferation predict liver carcinogenesis? AN - 73011500; 1612294 AB - Cell proliferation has long been recognized as having an important role in chemically induced carcinogenesis. Based on findings that certain nongenotoxic chemical carcinogens induced cell proliferation in the same organ that had an increased incidence of tumors, it has been hypothesized that a chemically induced response of enhanced DNA synthesis and cellular division causes cancer by increasing the rate of spontaneous mutations. It was further suggested that there would be no increased human risk of cancer by non-DNA-reactive compounds at doses that do not cause a proliferative response. An evaluation of the literature on the relationship between chemically induced cell proliferation and liver carcinogenesis reveals that very few systematic cell proliferation studies have been conducted over periods of extended exposure, and in many cases the exposure concentrations were not similar to those used in the cancer studies. The proliferative response resulting from exposure to many nongenotoxic carcinogens is not well sustained, whereas the carcinogenic response by these chemicals often requires prolonged exposure. The available literature leads to the conclusion that quantitative correspondences between cellular proliferation and carcinogenic responses have not been demonstrated and do not support the hypothesis that chemically induced cell proliferation is the primary mechanism by which nongenotoxic chemicals cause liver cancer. Studies of liver carcinogenesis in two-stage models point out the need to better understand chemical effects on cell loss as well as on cell replication, and demonstrate that measurements of cell proliferation alone are not sufficient to elucidate mechanisms of tumor development. JF - FASEB journal : official publication of the Federation of American Societies for Experimental Biology AU - Melnick, R L AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 2698 EP - 2706 VL - 6 IS - 9 SN - 0892-6638, 0892-6638 KW - Carcinogens KW - 0 KW - Mitogens KW - Index Medicus KW - Rats KW - Mitogens -- pharmacology KW - Causality KW - Carcinogens -- pharmacology KW - Animals KW - Liver -- drug effects KW - Cell Division -- drug effects KW - Mice KW - Male KW - Female KW - Liver Neoplasms -- chemically induced KW - Liver Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73011500?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FASEB+journal+%3A+official+publication+of+the+Federation+of+American+Societies+for+Experimental+Biology&rft.atitle=Does+chemically+induced+hepatocyte+proliferation+predict+liver+carcinogenesis%3F&rft.au=Melnick%2C+R+L&rft.aulast=Melnick&rft.aufirst=R&rft.date=1992-06-01&rft.volume=6&rft.issue=9&rft.spage=2698&rft.isbn=&rft.btitle=&rft.title=FASEB+journal+%3A+official+publication+of+the+Federation+of+American+Societies+for+Experimental+Biology&rft.issn=08926638&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-28 N1 - Date created - 1992-07-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Partial dopamine agonist therapy of levodopa-induced dyskinesias. AN - 72994593; 1351273 AB - We administered the partial dopamine agonist terguride under controlled conditions to patients with Parkinson's disease (PD), both as monotherapy and in conjunction with intravenous levodopa. Terguride produced a dose-dependent decrease in levodopa-induced dyskinesias (up to 53%) in seven patients without concomitant worsening of parkinsonism, and had no significant antiparkinsonian effect when administered alone. Partial dopamine agonists may hold some promise in the adjuvant therapy of patients with advanced PD. JF - Neurology AU - Baronti, F AU - Mouradian, M M AU - Conant, K E AU - Giuffra, M AU - Brughitta, G AU - Chase, T N AD - Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 1241 EP - 1243 VL - 42 IS - 6 SN - 0028-3878, 0028-3878 KW - Dopamine Agents KW - 0 KW - dironyl KW - 21OJT43Q88 KW - Levodopa KW - 46627O600J KW - Lisuride KW - E0QN3D755O KW - Abridged Index Medicus KW - Index Medicus KW - Dose-Response Relationship, Drug KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Movement KW - Dopamine Agents -- therapeutic use KW - Lisuride -- therapeutic use KW - Dyskinesia, Drug-Induced -- drug therapy KW - Lisuride -- analogs & derivatives KW - Dyskinesia, Drug-Induced -- physiopathology KW - Lisuride -- adverse effects KW - Levodopa -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72994593?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurology&rft.atitle=Partial+dopamine+agonist+therapy+of+levodopa-induced+dyskinesias.&rft.au=Baronti%2C+F%3BMouradian%2C+M+M%3BConant%2C+K+E%3BGiuffra%2C+M%3BBrughitta%2C+G%3BChase%2C+T+N&rft.aulast=Baronti&rft.aufirst=F&rft.date=1992-06-01&rft.volume=42&rft.issue=6&rft.spage=1241&rft.isbn=&rft.btitle=&rft.title=Neurology&rft.issn=00283878&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-13 N1 - Date created - 1992-07-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Neurology. 1993 Sep;43(9):1861 [8105426] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chemoprevention clinical trials. AN - 72991840; 1376431 AB - As part of a program to develop drugs which will delay or prevent cancer in humans, the Chemoprevention Branch, National Cancer Institute, National Institutes of Health, is sponsoring 12 Phase I and 22 Phase II and III clinical trials. Three agent classes are significantly advanced in the trials. These are the retinoids, including 13-cis-retinoic acid, retinol, and 4-hydroxyphenylretinamide (nine studies), beta-carotene (seven studies), and calcium compounds (three studies). In addition, six promising new compounds are in Phase I or Phase II trials. These are: piroxicam, ibuprofen, oltipraz (a dithiolthione), difluoromethylornithine, glycyrrhetinic acid, and N-acetylcysteine. Key concepts related to the development of cancer chemopreventive agents are (1) the need for long-term administration, (2) the need for oral route of administration, (3) the matching of toxic side effects to degree of cancer risk. JF - Mutation research AU - Kelloff, G J AU - Boone, C W AU - Malone, W F AU - Steele, V E AD - Chemoprevention Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 291 EP - 295 VL - 267 IS - 2 SN - 0027-5107, 0027-5107 KW - Anticarcinogenic Agents KW - 0 KW - Index Medicus KW - United States KW - Humans KW - National Institutes of Health (U.S.) KW - Female KW - Anticarcinogenic Agents -- therapeutic use KW - Clinical Trials as Topic KW - Neoplasms -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72991840?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+research&rft.atitle=Chemoprevention+clinical+trials.&rft.au=Kelloff%2C+G+J%3BBoone%2C+C+W%3BMalone%2C+W+F%3BSteele%2C+V+E&rft.aulast=Kelloff&rft.aufirst=G&rft.date=1992-06-01&rft.volume=267&rft.issue=2&rft.spage=291&rft.isbn=&rft.btitle=&rft.title=Mutation+research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-16 N1 - Date created - 1992-07-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - HIV encephalopathy and dementia. AN - 72989658; 1351284 AB - As of July 1991, 10 years after the onset of this modern pandemia, it is estimated that greater than 1 million persons worldwide have AIDS, 10 million people are HIV infected and by the end of the millenium, there will be 40 to 50 million persons infected. In the United States, 120,000 persons already have died of AIDS and 200,000 currently are infected. It has been calculated that by the year 2000, primary CNS lymphoma will be more common than meningiomas. Clearly, AIDS-related complications involving the CNS and manifested by behavioral and neurologic manifestations will remain one of the most common problems for physicians worldwide for years to come. JF - The Psychiatric clinics of North America AU - Pajeau, A K AU - Román, G C AD - Neuroepidemiology Branch, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 455 EP - 466 VL - 15 IS - 2 SN - 0193-953X, 0193-953X KW - Antipsychotic Agents KW - 0 KW - Zidovudine KW - 4B9XT59T7S KW - Index Medicus KW - AIDS/HIV KW - Zidovudine -- therapeutic use KW - Magnetic Resonance Imaging KW - Antipsychotic Agents -- administration & dosage KW - Humans KW - Brain -- pathology KW - Antipsychotic Agents -- therapeutic use KW - Tomography, X-Ray Computed KW - Neuropsychological Tests KW - Antipsychotic Agents -- adverse effects KW - Brain -- diagnostic imaging KW - Male KW - Female KW - AIDS Dementia Complex -- diagnostic imaging KW - AIDS Dementia Complex -- diagnosis KW - Dementia -- psychology KW - Dementia -- diagnosis KW - AIDS Dementia Complex -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72989658?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Psychiatric+clinics+of+North+America&rft.atitle=HIV+encephalopathy+and+dementia.&rft.au=Pajeau%2C+A+K%3BRom%C3%A1n%2C+G+C&rft.aulast=Pajeau&rft.aufirst=A&rft.date=1992-06-01&rft.volume=15&rft.issue=2&rft.spage=455&rft.isbn=&rft.btitle=&rft.title=The+Psychiatric+clinics+of+North+America&rft.issn=0193953X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-16 N1 - Date created - 1992-07-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - CONF T1 - NHLBI workshop summary. Environmental lung diseases. Relationship between acute inflammatory responses to air pollutants and chronic lung disease. AN - 72988609; 1596028 JF - The American review of respiratory disease AU - Crapo, J AU - Miller, F J AU - Mossman, B AU - Pryor, W A AU - Kiley, J P Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 1506 EP - 1512 VL - 145 IS - 6 KW - Air Pollutants KW - 0 KW - Asbestos KW - 1332-21-4 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Asbestos -- adverse effects KW - Chronic Disease KW - Lung -- pathology KW - Lung Diseases -- etiology KW - Lung Diseases -- pathology KW - Air Pollutants -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72988609?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=The+American+review+of+respiratory+disease&rft.atitle=NHLBI+workshop+summary.+Environmental+lung+diseases.+Relationship+between+acute+inflammatory+responses+to+air+pollutants+and+chronic+lung+disease.&rft.au=Crapo%2C+J%3BMiller%2C+F+J%3BMossman%2C+B%3BPryor%2C+W+A%3BKiley%2C+J+P&rft.aulast=Crapo&rft.aufirst=J&rft.date=1992-06-01&rft.volume=145&rft.issue=6&rft.spage=1506&rft.isbn=&rft.btitle=&rft.title=The+American+review+of+respiratory+disease&rft.issn=00030805&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-02 N1 - Date created - 1992-07-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Deposition, clearance, and translocation of chrysotile asbestos from peripheral and central regions of the rat lung. AN - 72982578; 1317793 AB - We investigated the pulmonary deposition, clearance, and translocation of chrysotile asbestos in the context of our previously developed model of asbestosis in the rat. Adult male rats were exposed for 3 hr to an aerosol of chrysotile asbestos. Subgroups were sacrificed up to 29 days postexposure and the lungs of the animals fixed. Peripheral and central regions of the left lung were resected, digested, and analyzed for fiber content by scanning electron microscopy. Pulmonary deposition did not differ between peripheral and central regions. There was no evidence of translocation of fibers from central to peripheral regions. The average diameter of retained fibers decreased over time, consistent with longitudinal splitting. The average length of retained fibers increased over time, consistent with slower clearance of longer fibers. We employed a novel counting scheme to ensure accurate fiber number measurements, allowing the calculation of clearance rates for fibers 0.5 to greater than or equal to 16 microns in length. Fibers of length greater than or equal to 16 microns were cleared slowly, if at all. These findings could have important implications for the pathogenesis of asbestos-related pleural disease. Many fibers are deposited in the peripheral region, and the longest (greater than or equal to 16 microns) will persist there for extended periods. JF - Environmental research AU - Coin, P G AU - Roggli, V L AU - Brody, A R AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 97 EP - 116 VL - 58 IS - 1 SN - 0013-9351, 0013-9351 KW - Aerosols KW - 0 KW - Asbestos, Serpentine KW - Asbestos KW - 1332-21-4 KW - Index Medicus KW - Specific Pathogen-Free Organisms KW - Rats, Inbred Strains KW - Rats KW - Regression Analysis KW - Animals KW - Half-Life KW - Disease Models, Animal KW - Male KW - Microscopy, Electron, Scanning KW - Asbestos -- pharmacokinetics KW - Asbestos -- administration & dosage KW - Lung -- chemistry KW - Lung -- ultrastructure KW - Lung -- metabolism KW - Asbestos -- toxicity KW - Asbestosis -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72982578?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+research&rft.atitle=Deposition%2C+clearance%2C+and+translocation+of+chrysotile+asbestos+from+peripheral+and+central+regions+of+the+rat+lung.&rft.au=Coin%2C+P+G%3BRoggli%2C+V+L%3BBrody%2C+A+R&rft.aulast=Coin&rft.aufirst=P&rft.date=1992-06-01&rft.volume=58&rft.issue=1&rft.spage=97&rft.isbn=&rft.btitle=&rft.title=Environmental+research&rft.issn=00139351&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-06 N1 - Date created - 1992-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Safety and pharmacokinetics of fluconazole in children with neoplastic diseases. AN - 72975586; 1593362 AB - To evaluate the safety, tolerance, and pharmacokinetics of fluconazole in children with neoplastic diseases, we studied fluconazole in 26 children, aged 5 to 15 years, with normal renal function who were receiving treatment for cancer. The patients received fluconazole, 2, 4, or 8 mg/kg per day for 7 days intravenously for a 2-hour period. Patients had no nausea or vomiting related to fluconazole; three patients had an asymptomatic rise in hepatic aminotransferase values after four to six doses (one patient at 2 mg/kg per day and two patients at 8 mg/kg per day), which returned to normal within 2 weeks after discontinuation of the drug. Fluconazole showed linear first-order kinetics over the dosage range tested and during multiple dosing. After the first dose, mean clearance was 22.8 +/- 2.3 ml/min, volume of distribution 0.87 +/- 0.06 L/kg, and terminal elimination half-life 16.8 +/- 1.1 hours. Similarly, after the last dose, clearance was 19.4 +/- 1.3 ml/min, volume of distribution 0.84 +/- 0.04 L/kg, and terminal elimination half-life 18.1 +/- 1.2 hours. Patients receiving their first fluconazole dose of 8 mg/kg achieved peak serum levels of 9.5 +/- 0.4 microgram/ml and trough levels of 2.7 +/- 0.5 microgram/ml 24 hours later, and an area under the serum concentration-time curve from time zero to infinity of 186 +/- 16 micrograms.hr per milliliter. Renal clearance of fluconazole was 65% +/- 5% of total clearance and demonstrated the predominantly renal excretion of this drug. We suggest that the shorter serum half-life and the higher frequency of aminotransferase elevations in comparison with those of adults warrant careful investigation of fluconazole in controlled clinical trials. JF - The Journal of pediatrics AU - Lee, J W AU - Seibel, N L AU - Amantea, M AU - Whitcomb, P AU - Pizzo, P A AU - Walsh, T J AD - Infectious Diseases Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 987 EP - 993 VL - 120 IS - 6 SN - 0022-3476, 0022-3476 KW - Fluconazole KW - 8VZV102JFY KW - Abridged Index Medicus KW - Index Medicus KW - Drug Evaluation KW - Kidney -- metabolism KW - Drug Administration Schedule KW - Humans KW - Liver -- metabolism KW - Child KW - Liver Function Tests KW - Male KW - Female KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- metabolism KW - Fluconazole -- toxicity KW - Leukemia, Myeloid, Acute -- metabolism KW - Fluconazole -- pharmacokinetics KW - Soft Tissue Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72975586?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pediatrics&rft.atitle=Safety+and+pharmacokinetics+of+fluconazole+in+children+with+neoplastic+diseases.&rft.au=Lee%2C+J+W%3BSeibel%2C+N+L%3BAmantea%2C+M%3BWhitcomb%2C+P%3BPizzo%2C+P+A%3BWalsh%2C+T+J&rft.aulast=Lee&rft.aufirst=J&rft.date=1992-06-01&rft.volume=120&rft.issue=6&rft.spage=987&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pediatrics&rft.issn=00223476&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-02 N1 - Date created - 1992-07-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Polyinosinic-polycytidylic acid complexed with poly-L-lysine and carboxymethylcellulose in combination with interleukin 2 in patients with cancer: clinical and immunological effects. AN - 72972505; 1591717 AB - We have performed a phase IB study of polyinosinic-polycytidylic acid complexed with poly-L-lysine and carboxymethylcellulose (poly-ICLC) in combination with interleukin 2 (IL-2) in 25 patients with a variety of cancers. Patients received weekly or biweekly poly-ICLC by i.m. injection, at doses ranging from 0.01 to 1.0 mg/m2, for 1 month. This was followed by 2 months of outpatient therapy with biweekly i.m. poly-ICLC in combination with IL-2 (3 x 10(6) units/m2) given i.v. by 24-h continuous infusion twice weekly, using a portable infusion pump. No objective tumor responses were observed. Toxicity was moderate at all poly-ICLC doses tested and increased only slightly following the addition of IL-2. No increases in peripheral blood natural killer (NK) activity were observed after treatment with poly-ICLC alone. However, high dose poly-ICLC (greater than or equal to 0.3 mg/m2) in combination with IL-2 resulted in NK activity greater than that seen using the same dose of IL-2 in combination with lower poly-ICLC doses. Increases in the number and percentage of CD56+ cells were evident only after initiation of IL-2 therapy and were unaffected by the poly-ICLC dose. In the majority of patients, these increases were preferentially associated with the subset of CD56+ cells coexpressing CD8, while the CD56+/CD16+ population was elevated to a lesser extent. Moderate increases in serum neopterin levels and 2',5'-oligoadenylate synthetase activity in peripheral blood mononuclear cells were noted at 72 h following initial treatment with 1.0 mg/m2 poly-ICLC. No induction of alpha or gamma interferon was detected. This study shows that the addition of poly-ICLC to a well tolerated IL-2 regimen can significantly enhance NK activity. Poly-ICLC can be used to enhance IL-2-induced NK lytic activity without increases in the dose and, therefore, the toxicity of IL-2 treatment. JF - Cancer research AU - Ewel, C H AU - Urba, W J AU - Kopp, W C AU - Smith, J W AU - Steis, R G AU - Rossio, J L AU - Longo, D L AU - Jones, M J AU - Alvord, W G AU - Pinsky, C M AD - Clinical Services Program, Program Resources, Inc./DynCorp, National Cancer Institute-Frederick Cancer Research Development Center, Maryland 21702. Y1 - 1992/06/01/ PY - 1992 DA - 1992 Jun 01 SP - 3005 EP - 3010 VL - 52 IS - 11 SN - 0008-5472, 0008-5472 KW - Antigens, CD KW - 0 KW - Interleukin-2 KW - Biopterin KW - 22150-76-1 KW - Poly I-C KW - 24939-03-5 KW - Polylysine KW - 25104-18-1 KW - poly ICLC KW - 59789-29-6 KW - Neopterin KW - 670-65-5 KW - Carboxymethylcellulose Sodium KW - K679OBS311 KW - Index Medicus KW - Biopterin -- analogs & derivatives KW - Drug Evaluation KW - Cytotoxicity, Immunologic KW - Antigens, CD -- analysis KW - Biopterin -- blood KW - Humans KW - Middle Aged KW - Male KW - Killer Cells, Natural -- immunology KW - Female KW - Poly I-C -- therapeutic use KW - Carboxymethylcellulose Sodium -- toxicity KW - Poly I-C -- toxicity KW - Interleukin-2 -- therapeutic use KW - Carboxymethylcellulose Sodium -- therapeutic use KW - Polylysine -- toxicity KW - Neoplasms -- therapy KW - Interleukin-2 -- toxicity KW - Polylysine -- therapeutic use KW - Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72972505?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Polyinosinic-polycytidylic+acid+complexed+with+poly-L-lysine+and+carboxymethylcellulose+in+combination+with+interleukin+2+in+patients+with+cancer%3A+clinical+and+immunological+effects.&rft.au=Ewel%2C+C+H%3BUrba%2C+W+J%3BKopp%2C+W+C%3BSmith%2C+J+W%3BSteis%2C+R+G%3BRossio%2C+J+L%3BLongo%2C+D+L%3BJones%2C+M+J%3BAlvord%2C+W+G%3BPinsky%2C+C+M&rft.aulast=Ewel&rft.aufirst=C&rft.date=1992-06-01&rft.volume=52&rft.issue=11&rft.spage=3005&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-30 N1 - Date created - 1992-06-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Development of an in vitro model to study carcinogen-induced neoplastic progression of initiated mouse epidermal cells. AN - 72965710; 1375535 AB - Initiation and promotion in mouse skin carcinogenesis produce multiple benign tumors, squamous papillomas, but only a few squamous cell carcinomas. The spontaneous conversion from the benign to the malignant phenotype occurs over many months and in stages, but induced malignant conversion can be accomplished more rapidly by exposure of papilloma-bearing mice to mutagens or by transfection of papilloma cell lines with specific oncogenes. The analysis of genetic targets responsible for carcinogen-induced neoplastic progression would be facilitated by the development of in vitro models where the process is rapid, focal, and quantitative. To this end, primary newborn mouse keratinocytes were initiated in vitro by the introduction of the v-rasHa oncogene via a defective retrovirus. Recipient cells produce squamous papillomas and have a high proliferation rate in culture medium with 0.05 mM Ca2+, but fail to grow in medium with 0.5 mM Ca2+ which is permissive for growth of malignant keratinocytes. When v-rasHa-keratinocytes were exposed to mutagens in vitro, proliferative foci emerged after culture in 0.5 mM Ca2+ for 4 weeks. These foci stained intensely red with rhodamine stain, could be easily quantitated, and readily incorporated bromodeoxyuridine. Dose-response studies with several mutagens indicated that the number of foci increased with concentration to the point where excessive cytotoxicity developed. Mutagens varied in potency for producing foci in the following order: cis-diamminedichloroplatinum greater than or equal to benzo(a)pyrene diolexpoxide I greater than N-methyl-N'-nitro-N-nitrosoguanidine greater than or equal to 4-nitroquinoline-N-oxide greater than N-acetoxy-acetyl- aminofluorene. The tumor promoter 12-O-tetradecanoylphorbol-13-acetate was inactive in the assay. A subset of cell lines derived from foci produced malignant tumors in vivo, while others were not tumorigenic. Analysis of DNA from cell lines and tumors revealed that most tumorigenic cell lines maintained the v-rasHa genome, whereas the viral sequences were deleted in nontumorigenic cell lines. Immunohistochemical analysis indicated that proliferative foci and quiescent v-rasHa keratinocytes expressed keratin 8, a marker of v-rasHa expression in cultured keratinocytes. Cells in foci, but not v-rasHa control cells, expressed keratin 13, a marker which is strongly associated with the malignant progression of skin tumors in vivo. This in vitro assay provides a quantitative model to study chemically induced focal neoplastic progression at the cellular level and to identify agents which may be selective for enhancing malignant conversion. JF - Cancer research AU - Morgan, D AU - Welty, D AU - Glick, A AU - Greenhalgh, D AU - Hennings, H AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/06/01/ PY - 1992 DA - 1992 Jun 01 SP - 3145 EP - 3156 VL - 52 IS - 11 SN - 0008-5472, 0008-5472 KW - v-ras KW - v-rasHa KW - Carcinogens KW - 0 KW - Oligodeoxyribonucleotides KW - Methylnitronitrosoguanidine KW - 12H3O2UGSF KW - Keratins KW - 68238-35-7 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Keratins -- genetics KW - Animals KW - Carcinoma, Squamous Cell -- chemically induced KW - Mice KW - Mice, Inbred BALB C KW - Animals, Newborn KW - Polymerase Chain Reaction KW - Base Sequence KW - Carcinoma, Squamous Cell -- pathology KW - Cells, Cultured KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Genes, ras KW - Carcinogens -- pharmacology KW - Epidermis -- drug effects KW - Papilloma -- pathology KW - Transfection KW - Skin Neoplasms -- chemically induced KW - Keratinocytes -- drug effects KW - Epidermis -- cytology KW - Methylnitronitrosoguanidine -- pharmacology KW - Skin Neoplasms -- pathology KW - Keratinocytes -- cytology KW - Papilloma -- chemically induced KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72965710?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Development+of+an+in+vitro+model+to+study+carcinogen-induced+neoplastic+progression+of+initiated+mouse+epidermal+cells.&rft.au=Morgan%2C+D%3BWelty%2C+D%3BGlick%2C+A%3BGreenhalgh%2C+D%3BHennings%2C+H%3BYuspa%2C+S+H&rft.aulast=Morgan&rft.aufirst=D&rft.date=1992-06-01&rft.volume=52&rft.issue=11&rft.spage=3145&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-30 N1 - Date created - 1992-06-30 N1 - Date revised - 2017-01-13 N1 - Gene symbol - v-ras; v-rasHa N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment of tardive dyskinesia with vitamin E. AN - 72965272; 1350428 AB - Vitamin E (alpha-tocopherol), a free-radical scavenger, has been reported to improve symptoms of tardive dyskinesia. The authors attempted to replicate this finding under more controlled conditions in a larger study group. Fifteen inpatients and six outpatients with tardive dyskinesia received up to 1600 IU/day of vitamin E for 6 weeks in a double-blind, placebo-controlled crossover study. Abnormal Involuntary Movement Scale (AIMS) examinations of these patients were videotaped and rated independently by two trained raters. Levels of neuroleptic medication and vitamin E were measured during both treatment periods. Eighteen patients who demonstrated high blood levels of vitamin E were included in the data analysis. Vitamin E levels were significantly higher while the patients were receiving vitamin E than while they were receiving placebo. For all 18 patients, there were no significant differences between AIMS scores after receiving vitamin E and AIMS scores after receiving placebo. In agreement with previous studies, however, the nine patients who had had tardive dyskinesia for 5 years or less had significantly lower AIMS scores after receiving vitamin E than after receiving placebo. There were no changes in neuroleptic levels during vitamin E treatment. Vitamin E had a minor beneficial effect on tardive dyskinesia ratings in a selected group of patients who had had tardive dyskinesia for 5 years or less. This effect was not due to an increase in blood levels of neuroleptic medications. JF - The American journal of psychiatry AU - Egan, M F AU - Hyde, T M AU - Albers, G W AU - Elkashef, A AU - Alexander, R C AU - Reeve, A AU - Blum, A AU - Saenz, R E AU - Wyatt, R J AD - Neuropsychiatry Branch, NIMH, Washington, D.C. 20032. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 773 EP - 777 VL - 149 IS - 6 SN - 0002-953X, 0002-953X KW - Antipsychotic Agents KW - 0 KW - Free Radical Scavengers KW - Placebos KW - Vitamin E KW - 1406-18-4 KW - Abridged Index Medicus KW - Index Medicus KW - Double-Blind Method KW - Mental Disorders -- drug therapy KW - Humans KW - Antipsychotic Agents -- therapeutic use KW - Adult KW - Aged KW - Middle Aged KW - Antipsychotic Agents -- adverse effects KW - Adolescent KW - Physical Examination KW - Dyskinesia, Drug-Induced -- drug therapy KW - Dyskinesia, Drug-Induced -- diagnosis KW - Vitamin E -- therapeutic use KW - Dyskinesia, Drug-Induced -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72965272?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+psychiatry&rft.atitle=Treatment+of+tardive+dyskinesia+with+vitamin+E.&rft.au=Egan%2C+M+F%3BHyde%2C+T+M%3BAlbers%2C+G+W%3BElkashef%2C+A%3BAlexander%2C+R+C%3BReeve%2C+A%3BBlum%2C+A%3BSaenz%2C+R+E%3BWyatt%2C+R+J&rft.aulast=Egan&rft.aufirst=M&rft.date=1992-06-01&rft.volume=149&rft.issue=6&rft.spage=773&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+psychiatry&rft.issn=0002953X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-25 N1 - Date created - 1992-06-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Am J Psychiatry. 1993 Jun;150(6):991-2; author reply 992-3 [8494096] Am J Psychiatry. 1993 Jun;150(6):991; author reply 992-3 [8494095] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vivo efficacy of a novel inhibitor of selected signal transduction pathways including calcium, arachidonate, and inositol phosphates. AN - 72965099; 1591730 AB - Aberrant signal transduction has been implicated in malignant transformation, growth, and progression. This has led to the proposal to use inhibitors of signal transduction pathways to treat cancer. One approach to circumventing potential toxicity and improving efficacy would be to target pathways upon which cancer cells selectively depend. Pathways associated with the malignant process involve calcium fluxes, the release of arachidonic acid, and the generation of phosphoinositides. In this report, CAI (L651582, NSC 609974), a substituted carboxyamido-imidazole and novel inhibitor of these selected signal transduction pathways, inhibits anchorage-dependent and -independent growth in a large series of human cancer cell lines. CAI pretreatment of HT-29 human colon cancer and 5R ras-transfected rat embryo fibroblast cells inhibits the formation and growth of experimental pulmonary metastases in nude mice. Oral administration of CAI in PEG-400 vehicle arrests growth and metastasis of transplanted human melanoma and ovarian cancer xenografts. No significant gross or histological toxicity was observed at CAI doses yielding blood levels in the concentration range demonstrated to inhibit select signal transduction pathways in vitro. These data indicate the feasibility and demonstrate a potential selectivity and sensitivity of using specific signal transduction inhibitors for the experimental treatment of cancer. JF - Cancer research AU - Kohn, E C AU - Sandeen, M A AU - Liotta, L A AD - Laboratory of Pathology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/06/01/ PY - 1992 DA - 1992 Jun 01 SP - 3208 EP - 3212 VL - 52 IS - 11 SN - 0008-5472, 0008-5472 KW - ras KW - Antineoplastic Agents KW - 0 KW - Arachidonic Acids KW - Inositol Phosphates KW - Triazoles KW - Aminoimidazole Carboxamide KW - 360-97-4 KW - carboxyamido-triazole KW - 99519-84-3 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Inositol Phosphates -- metabolism KW - Humans KW - Cell Division -- drug effects KW - Mice KW - Mice, Nude KW - Arachidonic Acids -- metabolism KW - Rats KW - Neoplasm Transplantation KW - Calcium -- metabolism KW - Genes, ras KW - Transfection KW - Transplantation, Heterologous KW - Cell Line KW - Cell Transformation, Neoplastic KW - Female KW - Melanoma -- pathology KW - Aminoimidazole Carboxamide -- therapeutic use KW - Ovarian Neoplasms -- pathology KW - Signal Transduction -- drug effects KW - Melanoma -- drug therapy KW - Colonic Neoplasms -- drug therapy KW - Aminoimidazole Carboxamide -- analogs & derivatives KW - Colonic Neoplasms -- pathology KW - Antineoplastic Agents -- therapeutic use KW - Ovarian Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72965099?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=In+vivo+efficacy+of+a+novel+inhibitor+of+selected+signal+transduction+pathways+including+calcium%2C+arachidonate%2C+and+inositol+phosphates.&rft.au=Kohn%2C+E+C%3BSandeen%2C+M+A%3BLiotta%2C+L+A&rft.aulast=Kohn&rft.aufirst=E&rft.date=1992-06-01&rft.volume=52&rft.issue=11&rft.spage=3208&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-30 N1 - Date created - 1992-06-30 N1 - Date revised - 2017-01-13 N1 - Gene symbol - ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antitumor effects of B3-PE and B3-LysPE40 in a nude mouse model of human breast cancer and the evaluation of B3-PE toxicity in monkeys. AN - 72965047; 1591729 AB - B3 is a tumor-reactive monoclonal antibody (mAb) that binds to a limited number of normal tissues. Immunotoxins made with B3 coupled to either Pseudomonas exotoxin (PE) or recombinant forms of PE with a deletion of the cell-binding domain (LysPE40) have been shown to cause complete tumor regression in nude mice bearing a rapidly growing A431 (L. H. Pai et al., Proc. Natl. Acad. Sci. USA, 88: 3358-3362, 1991) human epidermoid carcinoma. In this study we show that an immunotoxin composed of mAb B3 when chemically coupled to LysPE40 (B3-LysPE40) led to complete regression of a slowly growing breast cancer, MCF-7, in nude mice when given i.v. every other day for five doses. mAb B3 coupled to native PE also produced significant regression of the MCF-7 tumor. The reactivity of mAb B3 was evaluated using an immunohistochemical method on the two responsive tumors, MCF-7 and A431, and compared with a typical human colon carcinoma specimen that has B3 antigen on its surface. The results showed that both A431 and MCF-7 xenograft tumors have similar reactivity to B3 when compared with the human colon carcinoma specimen. To evaluate the toxicity of B3-PE in primates, Cynomolgus monkeys received escalating doses of B3-PE i.v. on Days 1, 3, and 5. Based on antibody localization studies using frozen sections of normal human and monkey tissue, gastric, trachea, and bladder mucosal injury could have occurred. However, no clinical signs of injury or histological damage to these organs were seen at the doses administered. Chemical hepatitis due to PE was transient and well tolerated at doses up to 50 micrograms/kg for three doses. The lethal dose was about 100 micrograms/kg, and the cause of death was liver necrosis, as shown by necropsy. We conclude that mAb B3, when coupled to PE40 or PE, can produce strong antitumor activity in vivo. The similar level of reactivity of the B3 antibody in our tumor models with a surgical specimen of a human colon carcinoma and the toxicity study in monkeys indicate that therapeutic doses of B3-PE and B3-LysPE40 can be delivered without causing toxicity to normal organs that express B3 antigen. Although both B3-PE and B3-LysPE40 have antitumor activity in nude mice bearing a human xenograft, B3-LysPE40 is better tolerated and should be further evaluated as a therapeutic agent for cancer patients. JF - Cancer research AU - Pai, L H AU - Batra, J K AU - FitzGerald, D J AU - Willingham, M C AU - Pastan, I AD - Laboratory of Molecular Biology, DCBDC, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/06/01/ PY - 1992 DA - 1992 Jun 01 SP - 3189 EP - 3193 VL - 52 IS - 11 SN - 0008-5472, 0008-5472 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Neoplasm KW - Bacterial Toxins KW - Exotoxins KW - Immunotoxins KW - Recombinant Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Animals KW - Chromosome Deletion KW - Pseudomonas aeruginosa -- genetics KW - Macaca fascicularis KW - Humans KW - Antigens, Neoplasm -- analysis KW - Mice, Nude KW - Amino Acid Sequence KW - Mice KW - Antibodies, Monoclonal -- therapeutic use KW - Recombinant Proteins -- toxicity KW - Neoplasm Transplantation KW - Recombinant Proteins -- isolation & purification KW - Base Sequence KW - Tumor Cells, Cultured KW - Antibodies, Monoclonal -- toxicity KW - Molecular Sequence Data KW - Transplantation, Heterologous KW - Recombinant Proteins -- therapeutic use KW - Cell Line KW - Female KW - Exotoxins -- genetics KW - Immunotoxins -- toxicity KW - Breast Neoplasms -- pathology KW - Immunotoxins -- therapeutic use KW - Exotoxins -- toxicity KW - Breast Neoplasms -- therapy KW - Exotoxins -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72965047?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Antitumor+effects+of+B3-PE+and+B3-LysPE40+in+a+nude+mouse+model+of+human+breast+cancer+and+the+evaluation+of+B3-PE+toxicity+in+monkeys.&rft.au=Pai%2C+L+H%3BBatra%2C+J+K%3BFitzGerald%2C+D+J%3BWillingham%2C+M+C%3BPastan%2C+I&rft.aulast=Pai&rft.aufirst=L&rft.date=1992-06-01&rft.volume=52&rft.issue=11&rft.spage=3189&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-30 N1 - Date created - 1992-06-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of the alveolar type II cell in the development and progression of pulmonary tumors induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in the A/J mouse. AN - 72965003; 1591728 AB - The role of the type II cell in the development of pulmonary tumors induced in the adult A/J mouse (6 weeks of age) by treatment with a single dose (100 mg/kg, i.p.) of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) was investigated. Twenty-four h following treatment with NNK, the concentration of O6-methylguanine was similar in Clara and type II cells. However, hyperplasias were detected only along the alveolar septa in lungs 14 weeks after carcinogen treatment. Examination of the ultrastructure of several hyperplasias revealed that the proliferating cells resembled type II pneumocytes. The proliferating cells were cuboidal in shape, with centrally localized ovoid nuclei characterized by minor indentations. Lamellar bodies, one of the major hallmarks of the type II cell, were present in the cytoplasm. The progression of pulmonary lesions was followed by sacrificing mice at 4-week intervals from 14 to 54 weeks after treatment with NNK. From 34 to 42 weeks after treatment, progression to neoplasia was demonstrated by a decline in the frequency of hyperplasias and an increase in the frequency of adenomas. Approximately 50% of the adenomas were observed arising within hyperplasias. Carcinomas appeared to increase in frequency 34 weeks after carcinogen treatment and comprised greater than 50% of the pulmonary lesions by 54 weeks. Approximately 30% of the carcinomas were observed arising within adenomas. The growth pattern of carcinomas began to change from solid to mixed (solid and papillary) 42 weeks after NNK. Moreover, electron micrographic analysis demonstrated that, within a hyperplasia, proliferating type II cells could change from cuboidal to columnar in shape and could also exhibit nuclear indentations, both characteristics displayed by the Clara cell. Thus, this divergence of the type II cell from its well characterized morphological features indicates that the selective growth advantage which these initiated cells possess can result in changes to the normal ultrastructure of this cell as it progresses toward malignancy. DNA was isolated from 20 hyperplasias and screened for the presence of an activated K-ras gene. This gene was activated in 17 of 20 lesions, with 85% of the mutations involving a GC to AT transition within codon 12 (GGT to GAT), a mutation consistent with base mispairing produced by the formation of the O6-methylguanine adduct. This specificity for activation of the K-ras gene was identical to that observed previously in adenocarcinomas induced by NNK.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Cancer research AU - Belinsky, S A AU - Devereux, T R AU - Foley, J F AU - Maronpot, R R AU - Anderson, M W AD - Laboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/06/01/ PY - 1992 DA - 1992 Jun 01 SP - 3164 EP - 3173 VL - 52 IS - 11 SN - 0008-5472, 0008-5472 KW - Carcinogens KW - 0 KW - Nitrosamines KW - 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone KW - 7S395EDO61 KW - Index Medicus KW - Mice, Inbred A KW - Animals KW - Hyperplasia KW - Microscopy, Electron KW - Mice KW - Time Factors KW - Female KW - Nitrosamines -- toxicity KW - Pulmonary Alveoli -- pathology KW - Carcinogens -- toxicity KW - Lung -- pathology KW - Carcinoma -- pathology KW - Adenoma -- chemically induced KW - Pulmonary Alveoli -- ultrastructure KW - Lung -- drug effects KW - Pulmonary Alveoli -- drug effects KW - Lung Neoplasms -- chemically induced KW - Adenoma -- pathology KW - Carcinoma -- chemically induced KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72965003?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Role+of+the+alveolar+type+II+cell+in+the+development+and+progression+of+pulmonary+tumors+induced+by+4-%28methylnitrosamino%29-1-%283-pyridyl%29-1-butanone+in+the+A%2FJ+mouse.&rft.au=Belinsky%2C+S+A%3BDevereux%2C+T+R%3BFoley%2C+J+F%3BMaronpot%2C+R+R%3BAnderson%2C+M+W&rft.aulast=Belinsky&rft.aufirst=S&rft.date=1992-06-01&rft.volume=52&rft.issue=11&rft.spage=3164&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-30 N1 - Date created - 1992-06-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A nonimmunogenic sarcoma transduced with the cDNA for interferon gamma elicits CD8+ T cells against the wild-type tumor: correlation with antigen presentation capability. AN - 72962887; 1588273 AB - To be recognized by CD8+ T lymphocytes, target cells must process and present peptide antigens in the context of major histocompatibility complex (MHC) class I molecules. The nonimmunogenic, low class I-expressing, methylcholanthrene (MCA)-induced murine sarcoma cell line, MCA 101, is a poor presenter of endogenously generated viral antigens to specific CD8+ T lymphocytes and cannot be used to generate tumor infiltrating lymphocytes (TIL). Since interferon gamma (IFN-gamma) has been shown to upregulate three sets of molecules important for antigen processing and presentation, we retrovirally transduced wild-type MCA 101 (101.WT) tumor with the mIFN-gamma cDNA to create the 101.NAT cell line. Unlike 101.WT, some clones of retrovirally transduced 101.NAT tumor expressed high levels of class I, and could be used to generate CD8+ TIL. More importantly, these TIL were therapeutic in vivo against established pulmonary metastases from the wild-type tumor. Although not uniformly cytotoxic amongst several separate cultures, these TIL did specifically release cytokines (IFN-gamma and tumor necrosis factor-alpha) in response to 101.WT targets. 101.WT's antigen presentation deficit was also reversed by gene modification with mIFN-gamma cDNA. 101.NAT had a greatly improved capacity to present viral antigens to CD8+ cytotoxic T lymphocytes. These findings show that a nonimmunogenic tumor, incapable of generating a CD8+ T cell immune response, could be gene-modified to generate a therapeutically useful immune response against the wild-type tumor. This strategy may be useful in developing treatments for tumor histologies not thought to be susceptible to T cell-based immunotherapy. JF - The Journal of experimental medicine AU - Restifo, N P AU - Spiess, P J AU - Karp, S E AU - Mulé, J J AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/06/01/ PY - 1992 DA - 1992 Jun 01 SP - 1423 EP - 1431 VL - 175 IS - 6 SN - 0022-1007, 0022-1007 KW - Antigens, CD8 KW - 0 KW - Tumor Necrosis Factor-alpha KW - Methylcholanthrene KW - 56-49-5 KW - Interferon-gamma KW - 82115-62-6 KW - Thymidine Kinase KW - EC 2.7.1.21 KW - Index Medicus KW - Animals KW - Lymphocytes, Tumor-Infiltrating -- immunology KW - Genetic Therapy KW - Mice KW - Tumor Necrosis Factor-alpha -- secretion KW - Promoter Regions, Genetic KW - Mice, Inbred C57BL KW - Flow Cytometry KW - Moloney murine leukemia virus -- genetics KW - Antigen-Presenting Cells -- immunology KW - Female KW - Thymidine Kinase -- genetics KW - Interferon-gamma -- secretion KW - Interferon-gamma -- genetics KW - Sarcoma, Experimental -- therapy KW - Sarcoma, Experimental -- chemically induced KW - Transfection KW - T-Lymphocyte Subsets -- immunology KW - Antigens, CD8 -- analysis KW - Interferon-gamma -- immunology KW - Sarcoma, Experimental -- immunology KW - Antigens, CD8 -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72962887?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+experimental+medicine&rft.atitle=A+nonimmunogenic+sarcoma+transduced+with+the+cDNA+for+interferon+gamma+elicits+CD8%2B+T+cells+against+the+wild-type+tumor%3A+correlation+with+antigen+presentation+capability.&rft.au=Restifo%2C+N+P%3BSpiess%2C+P+J%3BKarp%2C+S+E%3BMul%C3%A9%2C+J+J%3BRosenberg%2C+S+A&rft.aulast=Restifo&rft.aufirst=N&rft.date=1992-06-01&rft.volume=175&rft.issue=6&rft.spage=1423&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+experimental+medicine&rft.issn=00221007&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-23 N1 - Date created - 1992-06-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 1990 Dec 15;50(24):7820-5 [2123742] Nature. 1990 Dec 20-27;348(6303):738-41 [1979660] Nature. 1990 Dec 20-27;348(6303):741-4 [2259383] Mol Cell Biol. 1987 Jul;7(7):2625-30 [3475569] J Exp Med. 1989 Sep 1;170(3):1051-6 [2475569] Virology. 1987 Oct;160(2):336-45 [3310381] Proc Natl Acad Sci U S A. 1988 Nov;85(21):8181-5 [2973060] J Immunol. 1986 Jul 1;137(1):245-54 [3086451] J Immunol. 1987 Jul 1;139(1):285-94 [3108401] Annu Rev Immunol. 1988;6:465-83 [3289573] Cancer Res. 1989 Sep 1;49(17):4747-51 [2474372] Cell. 1986 Mar 28;44(6):959-68 [2420472] J Exp Med. 1985 May 1;161(5):1135-51 [2580935] Proc Natl Acad Sci U S A. 1989 Dec;86(23):9456-60 [2512580] Adv Cancer Res. 1989;53:181-245 [2678947] J Immunol. 1989 Dec 1;143(11):3792-7 [2685121] J Immunol. 1989 May 15;142(10):3714-25 [2785562] N Engl J Med. 1988 Dec 22;319(25):1676-80 [3264384] J Exp Med. 1988 Oct 1;168(4):1419-41 [3262710] J Exp Med. 1987 Dec 1;166(6):1716-33 [3500265] Science. 1986 Sep 19;233(4770):1318-21 [3489291] Nature. 1986 Feb 20-26;319(6055):675-8 [3951539] J Biol Response Mod. 1990 Apr;9(2):149-59 [1971302] Cell. 1990 Feb 9;60(3):397-403 [2137372] J Immunol. 1990 Feb 15;144(4):1531-7 [2303716] Interferon. 1983;5:23-42 [6202642] J Immunol. 1981 Jun;126(6):2100-3 [6453154] J Immunol. 1981 Jan;126(1):317-21 [6935293] Br J Cancer. 1976 Mar;33(3):241-59 [773395] Nature. 1991 Sep 26;353(6342):357-60 [1922342] Nature. 1991 Sep 26;353(6342):355-7 [1922341] Proc Natl Acad Sci U S A. 1991 Sep 1;88(17):7459-63 [1652751] Nature. 1990 Nov 15;348(6298):213-6 [1700303] J Exp Med. 1991 Aug 1;174(2):425-34 [1713253] Science. 1990 Dec 21;250(4988):1723-6 [2270487] J Immunol. 1991 Aug 15;147(4):1453-9 [1907999] Nature. 1990 Nov 15;348(6298):252-4 [1700304] Science. 1991 Dec 13;254(5038):1643-7 [1840703] Nature. 1991 Sep 26;353(6342):326-9 [1922338] Nature. 1991 Sep 26;353(6342):321-5 [1922337] J Exp Med. 1991 Mar 1;173(3):647-58 [1900079] Science. 1991 Sep 13;253(5025):1283-5 [1891717] Cancer Res. 1991 Sep 15;51(18 Suppl):5074s-5079s [1884383] Adv Immunol. 1991;49:281-355 [1853786] J Immunol. 1991 May 1;146(9):3227-34 [2016545] Nature. 1990 Dec 20-27;348(6303):744-7 [2259384] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - HeLa cell single-stranded DNA-binding protein increases the accuracy of DNA synthesis by DNA polymerase alpha in vitro. AN - 72961608; 1375330 AB - To determine whether cellular replication factors can influence the fidelity of DNA replication, the effect of HeLa cell single-stranded DNA-binding protein (SSB) on the accuracy of DNA replication by HeLa cell DNA polymerase alpha has been examined. An in vitro gap-filling assay, in which the single-stranded gap contains the supF target gene, was used to measure mutagenesis. Addition of SSB to the in vitro DNA synthesis reaction increased the accuracy of DNA polymerase alpha by 2- to 8-fold. Analysis of the products of DNA synthesis indicated that SSB reduces pausing by the polymerase at specific sites in the single-stranded supF template. Sequence analysis of the types of errors resulting from synthesis in the absence or presence of SSB reveals that, while the errors are primarily base substitutions under both conditions, SSB reduces the number of errors found at 3 hotspots in the supF gene. Thus, a cellular replication factor (SSB) can influence the fidelity of a mammalian DNA polymerase in vitro, suggesting that the high accuracy of cellular DNA replication may be determined in part by the interaction between replication factors, DNA polymerase and the DNA template in the replication complex. JF - Mutation research AU - Carty, M P AU - Levine, A S AU - Dixon, K AD - Section on Viruses and Cellular Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 29 EP - 43 VL - 274 IS - 1 SN - 0027-5107, 0027-5107 KW - supF KW - Bacterial Proteins KW - 0 KW - DNA, Single-Stranded KW - DNA-Binding Proteins KW - DNA KW - 9007-49-2 KW - DNA Polymerase II KW - EC 2.7.7.- KW - Index Medicus KW - DNA, Single-Stranded -- metabolism KW - Base Sequence KW - Bacterial Proteins -- genetics KW - HeLa Cells KW - Humans KW - Molecular Sequence Data KW - Escherichia coli -- genetics KW - Mutagenesis -- genetics KW - DNA Replication -- genetics KW - DNA Polymerase II -- metabolism KW - DNA -- biosynthesis KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72961608?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+research&rft.atitle=HeLa+cell+single-stranded+DNA-binding+protein+increases+the+accuracy+of+DNA+synthesis+by+DNA+polymerase+alpha+in+vitro.&rft.au=Carty%2C+M+P%3BLevine%2C+A+S%3BDixon%2C+K&rft.aulast=Carty&rft.aufirst=M&rft.date=1992-06-01&rft.volume=274&rft.issue=1&rft.spage=29&rft.isbn=&rft.btitle=&rft.title=Mutation+research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-23 N1 - Date created - 1992-06-23 N1 - Date revised - 2017-01-13 N1 - Gene symbol - supF N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of the liver-enriched transcription factor DBP in expression of the cytochrome P450 CYP2C6 gene. AN - 72958174; 1588973 AB - The CYP2C6 gene becomes maximally transcriptionally activated in livers of postpubertal rats. We examined the role of upstream DNA and liver-specific transcription factors in regulation of this promoter by use of transient transfection of heterologous chloramphenicol acetyltransferase gene constructs and vectors containing cDNAs encoding the liver-enriched transcription factors HNF-1 alpha, C/EBP, and DBP. Only DBP was able to activate the CYP2C6 promoter in HepG2 cells. Transactivation was not observed in one mouse and two human nonhepatic origin cell lines tested. Analysis of various constructs in which CYP2C6 upstream DNA was deleted revealed that DNA between -38 to -103 was involved in DBP-mediated activation. A partially purified preparation of DBP produced a footprint between -43 and -64 bp upstream of the transcription start site. A 32P-labeled double-stranded oligonucleotide, containing sequence information corresponding to -40 to -65, bound to both partially pure DBP and extracts from livers of rats as young as 1 week and as old as 25 weeks of age, as assessed by gel mobility shift analysis. This binding was eliminated by coincubation with excess unlabeled -40/-65 double-stranded oligonucleotide and by an oligonucleotide corresponding to the D site of the rat albumin gene. A gel mobility shift-Western immunoblot analysis revealed that the -40/-65 sequence bound to DBP only in liver nuclear extracts from rats older than 3 weeks; maximal binding was observed by 7 weeks of age, and no binding was detected from 1-week-old rat liver extracts. Interestingly, the DBP-binding regions of both CYP2C6 and albumin bind to C/EBP, but this factor is capable of transactivating only the latter gene. Although the DBP-binding regions in these two genes share no obvious sequence similarities, the CYP2C6 region contains consensus palindromic half sites for DBP-related binding proteins and affinity for recombinant DBP of 17-fold greater than that of the D site of albumin. This difference in affinity is probably responsible for the markedly lower amounts of DBP required for half-maximal activation of the CYP2C6 promoter, as compared with the albumin promoter, in transactivation transfection assays. These data indicate that the CYP2C6 gene may be regulated, at least in part, by DBP, a liver transcription factor produced when rats reach puberty that may also be involved in maintenance of albumin gene transcription. JF - Molecular and cellular biology AU - Yano, M AU - Falvey, E AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 2847 EP - 2854 VL - 12 IS - 6 SN - 0270-7306, 0270-7306 KW - CYP2C6 KW - DBP protein, human KW - 0 KW - DBP protein, rat KW - DNA-Binding Proteins KW - Dbp protein, mouse KW - RNA, Messenger KW - Transcription Factors KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Animals KW - Age Factors KW - DNA Mutational Analysis KW - Humans KW - Transcription, Genetic KW - Mice KW - RNA, Messenger -- genetics KW - Transcriptional Activation KW - Binding Sites KW - Rats KW - Regulatory Sequences, Nucleic Acid KW - Base Sequence KW - Molecular Sequence Data KW - Species Specificity KW - Promoter Regions, Genetic KW - Transcription Factors -- metabolism KW - Cytochrome P-450 Enzyme System -- genetics KW - DNA-Binding Proteins -- genetics KW - Gene Expression Regulation KW - Transcription Factors -- genetics KW - Liver -- physiology KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72958174?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+cellular+biology&rft.atitle=Role+of+the+liver-enriched+transcription+factor+DBP+in+expression+of+the+cytochrome+P450+CYP2C6+gene.&rft.au=Yano%2C+M%3BFalvey%2C+E%3BGonzalez%2C+F+J&rft.aulast=Yano&rft.aufirst=M&rft.date=1992-06-01&rft.volume=12&rft.issue=6&rft.spage=2847&rft.isbn=&rft.btitle=&rft.title=Molecular+and+cellular+biology&rft.issn=02707306&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-24 N1 - Date created - 1992-06-24 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CYP2C6 N1 - SuppNotes - Cited By: Genes Dev. 1991 Sep;5(9):1553-67 [1884998] Virology. 1973 Apr;52(2):456-67 [4705382] Genes Dev. 1990 Sep;4(9):1541-51 [2253878] DNA Cell Biol. 1991 Jan-Feb;10(1):1-14 [1991046] Genes Dev. 1991 Oct;5(10):1739-53 [1916262] Biochem J. 1992 Feb 1;281 ( Pt 3):577-92 [1536639] Cell. 1990 Dec 21;63(6):1257-66 [2261643] Genes Dev. 1988 Aug;2(8):957-74 [3169549] Science. 1989 Apr 21;244(4902):343-6 [2711183] Proc Natl Acad Sci U S A. 1987 Nov;84(21):7413-7 [2823261] Genes Dev. 1989 Sep;3(9):1314-22 [2558052] Trends Pharmacol Sci. 1989 Apr;10(4):149-53 [2665247] Int J Biochem. 1989;21(3):243-52 [2545475] Mol Cell Biol. 1987 Feb;7(2):725-37 [3821727] J Biol Chem. 1986 Dec 15;261(35):16689-97 [3782137] Pharmacol Rev. 1988 Dec;40(4):243-88 [3072575] Genes Dev. 1987 Apr;1(2):133-46 [2824279] J Biol Chem. 1989 May 15;264(14):8222-9 [2722778] J Biol Chem. 1988 Dec 5;263(34):17995-8002 [3192524] Nucleic Acids Res. 1988 Jul 11;16(13):6249 [3399405] Cell. 1987 Aug 14;50(4):627-38 [3607880] Biochemistry. 1986 Dec 2;25(24):7975-83 [3801454] Mol Cell Biol. 1986 Aug;6(8):2969-76 [3785219] Cell. 1986 Dec 5;47(5):767-76 [3779841] Mol Cell Biol. 1990 Sep;10(9):4495-505 [2388615] Cell. 1990 Apr 20;61(2):279-91 [2331750] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4 [388439] Cell Growth Differ. 1990 Jan;1(1):47-52 [2078499] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Suramin: a novel growth factor antagonist with activity in hormone-refractory metastatic prostate cancer. AN - 72956606; 1375283 AB - Suramin is known to inhibit the growth of malignant prostate carcinoma cells in vitro. This led us to evaluate the effectiveness of suramin in the treatment of 38 patients with prostate carcinoma refractory to hormone therapy. Suramin was administered by continuous infusion at a rate designed to reach a peak of 300 micrograms/mL at the end of 14 days. Patients were given 8 weeks to recover from any toxicity before beginning the second cycle. Subsequent cycles were administered in the same manner except the starting dose rate was 280 mg/m2. In 17 patients with measurable soft tissue disease, three had complete disappearance of soft tissue disease for 4, 5, and 11 months, whereas three patients had a greater than or equal to 50% decrease in the sum of the products of the diameters of all measurable disease for greater than or equal to 1 month. Of these 17 patients, pretreatment prostate-specific antigen (PSA) decreased by 75% or more in five (29%) and normalized in one (6%). The remaining 21 patients had disease limited to bone, and only one of these experienced resolution of more than 50% of all lesions on bone scan. Of these 21 patients, pretreatment PSA decreased by 75% or more in eight (38%) and normalized in five (25%). Median time to progression for all patients was 26.3 weeks, and median survival was 42.3 weeks. Patients with bone involvement alone exhibited a better survival than patients with soft tissue involvement (P2 = .02). Survival was strongly correlated (P2 = .0001) with a decline in the pretreatment PSA of greater than or equal to 75% by the eighth week on therapy, with nearly an 85% survival at 1 year compared with a 20% survival for those whose pretreatment PSA did not decline by that amount. We conclude that suramin is an active agent in hormone-refractory prostate carcinoma. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Myers, C AU - Cooper, M AU - Stein, C AU - LaRocca, R AU - Walther, M M AU - Weiss, G AU - Choyke, P AU - Dawson, N AU - Steinberg, S AU - Uhrich, M M AD - Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 881 EP - 889 VL - 10 IS - 6 SN - 0732-183X, 0732-183X KW - Antigens, Neoplasm KW - 0 KW - Biomarkers, Tumor KW - Growth Inhibitors KW - Suramin KW - 6032D45BEM KW - Prostate-Specific Antigen KW - EC 3.4.21.77 KW - Index Medicus KW - Aged, 80 and over KW - Humans KW - Bone Neoplasms -- drug therapy KW - Biomarkers, Tumor -- analysis KW - Antigens, Neoplasm -- analysis KW - Aged KW - Soft Tissue Neoplasms -- drug therapy KW - Middle Aged KW - Soft Tissue Neoplasms -- secondary KW - Male KW - Bone Neoplasms -- secondary KW - Prostatic Neoplasms -- pathology KW - Suramin -- adverse effects KW - Prostatic Neoplasms -- mortality KW - Growth Inhibitors -- adverse effects KW - Prostatic Neoplasms -- therapy KW - Growth Inhibitors -- therapeutic use KW - Suramin -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72956606?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Suramin%3A+a+novel+growth+factor+antagonist+with+activity+in+hormone-refractory+metastatic+prostate+cancer.&rft.au=Myers%2C+C%3BCooper%2C+M%3BStein%2C+C%3BLaRocca%2C+R%3BWalther%2C+M+M%3BWeiss%2C+G%3BChoyke%2C+P%3BDawson%2C+N%3BSteinberg%2C+S%3BUhrich%2C+M+M&rft.aulast=Myers&rft.aufirst=C&rft.date=1992-06-01&rft.volume=10&rft.issue=6&rft.spage=881&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=0732183X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-25 N1 - Date created - 1992-06-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Clin Oncol. 1992 Jun;10(6):875-7 [1588368] J Clin Oncol. 1992 Dec;10(12):1984-5; author reply 1985-6 [1453214] J Clin Oncol. 1992 Dec;10(12):1985-6 [1280675] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Low-grade angiosarcoma of the skin of the breast: a complication of lumpectomy and radiation therapy for breast carcinoma. AN - 72956196; 1317346 AB - A case of low-grade angiosarcoma arising in the skin of a breast previously irradiated for breast carcinoma is reported. Initially, an asymptomatic breast mass was detected. Excisional biopsy and axillary lymph node dissection revealed a 1.5-cm infiltrating ductal carcinoma with 21 negative lymph nodes. The neoplasm was staged as T1, N0, M0. The patient was entered in a research protocol and was treated with high-dose external beam (4,860 rad) and iridium implant (1,860 rad) irradiation. Seven years later the patient developed low-grade angiosarcoma of the breast skin. The lesion recurred following excision and eventually was treated by simple mastectomy. The patient never had evidence of lymphedema. Cutaneous angiosarcomas occurring as a complication of lumpectomy and radiation therapy for breast carcinoma are rare. In some reported cases the patients have had lymphedema, a known factor predisposing to angiosarcoma. Furthermore, almost all cases previously reported have been high grade. This case suggests that radiation therapy for breast carcinoma may also be complicated by low-grade angiosarcoma. JF - Human pathology AU - Moskaluk, C A AU - Merino, M J AU - Danforth, D N AU - Medeiros, L J AD - Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 710 EP - 714 VL - 23 IS - 6 SN - 0046-8177, 0046-8177 KW - Index Medicus KW - Carcinoma, Intraductal, Noninfiltrating -- radiotherapy KW - Carcinoma, Intraductal, Noninfiltrating -- surgery KW - Mastectomy, Segmental -- adverse effects KW - Humans KW - Breast KW - Middle Aged KW - Breast Neoplasms -- surgery KW - Breast Neoplasms -- radiotherapy KW - Female KW - Radiotherapy -- adverse effects KW - Neoplasms, Radiation-Induced -- pathology KW - Hemangiosarcoma -- pathology KW - Skin Neoplasms -- pathology KW - Neoplasms, Second Primary -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72956196?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+pathology&rft.atitle=Low-grade+angiosarcoma+of+the+skin+of+the+breast%3A+a+complication+of+lumpectomy+and+radiation+therapy+for+breast+carcinoma.&rft.au=Moskaluk%2C+C+A%3BMerino%2C+M+J%3BDanforth%2C+D+N%3BMedeiros%2C+L+J&rft.aulast=Moskaluk&rft.aufirst=C&rft.date=1992-06-01&rft.volume=23&rft.issue=6&rft.spage=710&rft.isbn=&rft.btitle=&rft.title=Human+pathology&rft.issn=00468177&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-01 N1 - Date created - 1992-07-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - IL-10 synergizes with IL-4 and transforming growth factor-beta to inhibit macrophage cytotoxic activity. AN - 72946598; 1588047 AB - After activation with IFN-gamma, thioglycollate-elicited murine peritoneal macrophages kill schistosomula of Schistosoma mansoni in vitro by an L-arginine-dependent mechanism which involves the production of reactive nitrogen oxides (NO). In the present study we demonstrate that the regulatory cytokines IL-10, IL-4, and transforming growth factor-beta (TGF-beta) are potent inhibitors of this extracellular killing function of activated macrophages. Each cytokine was found to suppress killing of schistosomula in a dose-dependent fashion. The activity of IL-10 was not permanent, because subsequent treatment with additional IFN-gamma 2 to 6 h later reversed the inhibition of macrophage larval killing. More importantly, the combination of suboptimal levels of any two of these three cytokines was found to give a potent synergistic suppression of schistosomulum killing by IFN-gamma-treated macrophages. Similarly, IL-10, IL-4, or TGF-beta alone blocked the production of NO, and when used in combination these cytokines exhibited an enhanced inhibitory effect on nitrite production. Macrophage-mediated killing of schistosomula through the generation of NO has been shown previously to be a major effector mechanism of schistosome immunity. The results presented here suggest that the suppression of this mechanism by induction of the regulatory cytokines IL-10, IL-4, and TGF-beta, which are known to be produced during schistosome infection, may be an important strategy used by the parasite to evade macrophage-mediated immune destruction. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Oswald, I P AU - Gazzinelli, R T AU - Sher, A AU - James, S L AD - Immunology and Cell Biology Section, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06/01/ PY - 1992 DA - 1992 Jun 01 SP - 3578 EP - 3582 VL - 148 IS - 11 SN - 0022-1767, 0022-1767 KW - Recombinant Proteins KW - 0 KW - Transforming Growth Factor beta KW - Interleukin-10 KW - 130068-27-8 KW - Interleukin-4 KW - 207137-56-2 KW - Nitric Oxide KW - 31C4KY9ESH KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Dose-Response Relationship, Drug KW - Macrophage Activation KW - Mice, Inbred C57BL KW - Nitric Oxide -- metabolism KW - Mice KW - Drug Synergism KW - Female KW - Transforming Growth Factor beta -- administration & dosage KW - Macrophages -- immunology KW - Interleukin-10 -- administration & dosage KW - Schistosoma mansoni -- immunology KW - Cytotoxicity, Immunologic -- drug effects KW - Interleukin-4 -- administration & dosage KW - Macrophages -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72946598?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=IL-10+synergizes+with+IL-4+and+transforming+growth+factor-beta+to+inhibit+macrophage+cytotoxic+activity.&rft.au=Oswald%2C+I+P%3BGazzinelli%2C+R+T%3BSher%2C+A%3BJames%2C+S+L&rft.aulast=Oswald&rft.aufirst=I&rft.date=1992-06-01&rft.volume=148&rft.issue=11&rft.spage=3578&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-25 N1 - Date created - 1992-06-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - HTLV-I Tax is a zinc-binding protein: role of zinc in Tax structure and function. AN - 72935707; 1585646 AB - We have examined the functional significance of the cysteine- and histidine-rich region (amino acids 22-53) of HTLV-I Tax. A modeling of this region suggests two possible overlapping zinc-finger-like motifs. Using a zinc blotting technique, we show that Tax binds zinc. An N-terminal deletion in Tax that removed this zinc-finger region abolished the ability to bind zinc. Site-directed mutagenesis was used to generate 10 separate mutations so as to discriminate between the two alternative zinc-binding structures. Each Tax mutant was studied for its ability to trans-activate the HTLV-I LTR. Five of the ten mutations inactivated trans-activation. Our results support that one of the two putative zinc fingers is an integral element of Tax structure. JF - Virology AU - Semmes, O J AU - Jeang, K T AD - Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 754 EP - 764 VL - 188 IS - 2 SN - 0042-6822, 0042-6822 KW - Gene Products, tax KW - 0 KW - Metalloproteins KW - Zinc KW - J41CSQ7QDS KW - Index Medicus KW - AIDS/HIV KW - Mutagenesis, Site-Directed KW - Peptide Mapping KW - Cell Nucleus -- metabolism KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Repetitive Sequences, Nucleic Acid KW - Structure-Activity Relationship KW - Protein Conformation KW - Metalloproteins -- chemistry KW - Gene Products, tax -- chemistry KW - Gene Products, tax -- metabolism KW - Human T-lymphotropic virus 1 -- chemistry KW - Zinc -- metabolism KW - Transcriptional Activation KW - Gene Products, tax -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72935707?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Virology&rft.atitle=HTLV-I+Tax+is+a+zinc-binding+protein%3A+role+of+zinc+in+Tax+structure+and+function.&rft.au=Semmes%2C+O+J%3BJeang%2C+K+T&rft.aulast=Semmes&rft.aufirst=O&rft.date=1992-06-01&rft.volume=188&rft.issue=2&rft.spage=754&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=00426822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-17 N1 - Date created - 1992-06-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Direct determination of the point mutation rate of a murine retrovirus. AN - 72935597; 1316475 AB - The point mutation rate of a murine leukemia virus (MuLV) genome (AKV) was determined under conditions in which the number of replicative cycles was carefully controlled and the point mutation rate was determined by direct examination of the RNA genomes of progeny viruses. A clonal cell line infected at a low multiplicity of infection (2 x 10(-3)) was derived to provide a source of virus with high genetic homogeneity. Virus stocks from this cell line were used to infect cells at a low multiplicity of infection, and the cells were seeded soon after infection to obtain secondary clonal cell lines. RNase T1-oligonucleotide fingerprinting analyses of virion RNAs from 93 secondary lines revealed only 3 base changes in nearly 130,000 bases analyzed. To obtain an independent assessment of the mutation rate, we directly sequenced virion RNAs by using a series of DNA oligonucleotide primers distributed across the genome. RNA sequencing detected no mutations in over 21,000 bases analyzed. The combined fingerprinting and sequencing analyses yielded a mutation rate for infectious progeny viruses of one base change per 50,000 (2 x 10(-5)) bases per replication cycle. Our results suggest that over 80% of infectious progeny MuLVs may be replicated with complete fidelity and that only a low percentage undergo more than one point mutation during a replication cycle. Previous estimates of retroviral mutation rates suggest that the majority of infectious progeny viruses have undergone one or more point mutations. Recent studies of the mutation rates of marker genes in spleen necrosis virus-based vectors estimate a base substitution rate lower than estimates for infectious avian retroviruses and nearly identical to our determinations with AKV. The differences between mutation rates observed in studies of retroviruses may reflect the imposition of different selective conditions. JF - Journal of virology AU - Monk, R J AU - Malik, F G AU - Stokesberry, D AU - Evans, L H AD - Laboratory of Persistent Viral Diseases, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 59840. Y1 - 1992/06// PY - 1992 DA - June 1992 SP - 3683 EP - 3689 VL - 66 IS - 6 SN - 0022-538X, 0022-538X KW - Oligonucleotides KW - 0 KW - RNA, Viral KW - Ribonuclease T1 KW - EC 3.1.27.3 KW - Index Medicus KW - Virus Replication KW - Muridae KW - Genetic Variation KW - Animals KW - Base Sequence KW - Ribonuclease T1 -- metabolism KW - Oligonucleotides -- analysis KW - Molecular Sequence Data KW - Mice KW - Genome, Viral KW - Nucleotide Mapping KW - Leukemia Virus, Murine -- genetics KW - RNA, Viral -- genetics KW - Mutagenesis -- genetics KW - RNA, Viral -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72935597?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Direct+determination+of+the+point+mutation+rate+of+a+murine+retrovirus.&rft.au=Monk%2C+R+J%3BMalik%2C+F+G%3BStokesberry%2C+D%3BEvans%2C+L+H&rft.aulast=Monk&rft.aufirst=R&rft.date=1992-06-01&rft.volume=66&rft.issue=6&rft.spage=3683&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-16 N1 - Date created - 1992-06-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Arch Gesamte Virusforsch. 1973;41(1):1-10 [4123810] Proc Natl Acad Sci U S A. 1982 Feb;79(4):1230-4 [6951170] Infect Immun. 1981 Jun;32(3):1045-50 [6166562] Virology. 1983 Oct 30;130(2):539-45 [6196911] Virology. 1984 Apr 15;134(1):196-207 [6200992] Proc Natl Acad Sci U S A. 1980 Aug;77(8):4454-8 [6254026] Ann N Y Acad Sci. 1980;354:410-25 [6261656] J Virol. 1990 Dec;64(12):6176-83 [1700832] J Virol. 1991 Apr;65(4):1779-88 [2002543] Proc Natl Acad Sci U S A. 1990 Aug;87(16):6024-8 [2166940] Cell. 1986 Jun 6;45(5):637-48 [2423250] J Virol. 1987 Dec;61(12):3783-9 [2446008] Cell. 1988 Jul 1;54(1):57-63 [2838179] J Virol. 1988 Sep;62(9):3084-91 [2841464] Proc Natl Acad Sci U S A. 1985 Jun;82(12):4198-201 [2987967] J Virol. 1984 Feb;49(2):471-8 [6319746] J Virol. 1984 Mar;49(3):772-81 [6422051] Infect Immun. 1983 Jul;41(1):67-73 [6862634] J Exp Med. 1976 Jan 1;143(1):73-84 [1244422] Proc Natl Acad Sci U S A. 1990 Aug;87(16):6019-23 [2201018] Proc Natl Acad Sci U S A. 1985 Oct;82(20):7086-90 [2996004] J Virol. 1986 Jan;57(1):71-80 [3001367] Science. 1986 Jun 20;232(4757):1548-53 [3012778] Science. 1986 Jul 11;233(4760):215-9 [3014648] J Virol. 1986 Aug;59(2):377-83 [3016304] J Virol. 1987 Jun;61(6):1882-92 [3033319] J Mol Evol. 1987;26(1-2):148-56 [3125332] Proc Natl Acad Sci U S A. 1988 Apr;85(8):2444-8 [3162770] Annu Rev Microbiol. 1987;41:409-33 [3318675] Mol Cell Biol. 1986 Dec;6(12):4387-95 [3796606] Methods Enzymol. 1987;152:556-62 [2443806] J Virol. 1988 Aug;62(8):2817-22 [2839703] Virology. 1985 Feb;141(1):110-8 [2983493] J Virol. 1986 Jan;57(1):219-28 [3001347] J Virol. 1986 Apr;58(1):67-74 [3005660] Cell. 1986 Jul 4;46(1):1-4 [3013415] Virology. 1986 Aug;153(1):122-36 [3016982] Science. 1986 Mar 21;231(4744):1393-8 [3082006] J Gen Virol. 1987 Nov;68 ( Pt 11):2729-40 [3316486] Mol Biol Evol. 1986 Jan;3(1):57-74 [3444396] Mol Biol Evol. 1985 Mar;2(2):150-74 [3916709] J Virol. 1984 Nov;52(2):695-8 [6092693] J Virol. 1983 Oct;48(1):52-60 [6193288] J Exp Med. 1980 Mar 1;151(3):542-52 [6244357] Virology. 1981 Jan 30;108(2):405-23 [6258294] J Gen Virol. 1982 Apr;59(Pt 2):345-56 [6281373] J Clin Invest. 1984 Mar;73(3):599-601 [6323522] Nucleic Acids Res. 1983 Oct 25;11(20):7191-203 [6634412] J Gen Virol. 1984 Aug;65 ( Pt 8):1395-9 [6086822] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A nonpromoting phorbol from the samoan medicinal plant Homalanthus nutans inhibits cell killing by HIV-1. AN - 72983932; 1597853 AB - Extracts of Homalanthus nutans, a plant used in Samoan herbal medicine, exhibited potent activity in an in vitro, tetrazolium-based assay which detects the inhibition of the cytopathic effects of human immunodeficiency virus (HIV-1). The active constituent was identified as prostratin, a relatively polar 12-deoxyphorbol ester. Noncytotoxic concentrations of prostratin from greater than or equal to 0.1 to greater than 25 microM protected T-lymphoblastoid CEM-SS and C-8166 cells from the killing effects of HIV-1. Cytoprotective concentrations of prostratin greater than or equal to 1 microM essentially stopped virus reproduction in these cell lines, as well as in the human monocytic cell line U937 and in freshly isolated human monocyte/macrophage cultures. Prostratin bound to and activated protein kinase C in vitro in CEM-SS cells and elicited other biochemical effects typical of phorbol esters in C3H10T1/2 cells; however, the compound does not appear to be a tumor promoter. In skin of CD-1 mice, high doses of prostratin induced ornithine decarboxylase only to 25-30% of the levels induced by typical phorbol esters at doses 1/30 or less than that used for prostratin, produced kinetics of edema formation characteristic of the nonpromoting 12-deoxyphorbol 13-phenylacetate, and failed to induce the acute or chronic hyperplasias typically caused by tumor-promoting phorbols at doses of 1/100 or less than that used for prostratin. JF - Journal of medicinal chemistry AU - Gustafson, K R AU - Cardellina, J H AU - McMahon, J B AU - Gulakowski, R J AU - Ishitoya, J AU - Szallasi, Z AU - Lewin, N E AU - Blumberg, P M AU - Weislow, O S AU - Beutler, J A AD - Laboratory of Drug Discovery Research and Development, National Cancer Institute (NCI), Frederick Cancer Research & Development Center (FCRDC), Maryland 21702-1201. Y1 - 1992/05/29/ PY - 1992 DA - 1992 May 29 SP - 1978 EP - 1986 VL - 35 IS - 11 SN - 0022-2623, 0022-2623 KW - Phorbol Esters KW - 0 KW - prostratin KW - 60857-08-1 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Ornithine Decarboxylase KW - EC 4.1.1.17 KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Skin -- enzymology KW - Humans KW - Skin -- pathology KW - Mice KW - Monocytes -- microbiology KW - Ornithine Decarboxylase -- biosynthesis KW - Magnetic Resonance Spectroscopy KW - Protein Kinase C -- metabolism KW - Edema -- chemically induced KW - Hyperplasia KW - Skin -- drug effects KW - Cell Survival -- drug effects KW - Virus Replication -- drug effects KW - T-Lymphocytes -- microbiology KW - Independent State of Samoa KW - Monocytes -- drug effects KW - T-Lymphocytes -- drug effects KW - Cell Line KW - Cytopathogenic Effect, Viral -- drug effects KW - Phorbol Esters -- pharmacology KW - Phorbol Esters -- isolation & purification KW - Phorbol Esters -- chemistry KW - HIV-1 -- drug effects KW - Plants, Medicinal -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72983932?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+medicinal+chemistry&rft.atitle=A+nonpromoting+phorbol+from+the+samoan+medicinal+plant+Homalanthus+nutans+inhibits+cell+killing+by+HIV-1.&rft.au=Gustafson%2C+K+R%3BCardellina%2C+J+H%3BMcMahon%2C+J+B%3BGulakowski%2C+R+J%3BIshitoya%2C+J%3BSzallasi%2C+Z%3BLewin%2C+N+E%3BBlumberg%2C+P+M%3BWeislow%2C+O+S%3BBeutler%2C+J+A&rft.aulast=Gustafson&rft.aufirst=K&rft.date=1992-05-29&rft.volume=35&rft.issue=11&rft.spage=1978&rft.isbn=&rft.btitle=&rft.title=Journal+of+medicinal+chemistry&rft.issn=00222623&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-08 N1 - Date created - 1992-07-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Monoclonal antibodies to rat liver microsomal cytochrome b5. AN - 72979167; 1599506 AB - Hybridomas obtained by the fusion of spleen cells from rat cytochrome b5-immunized mice with mouse myeloma cells produced five groups of monoclonal antibodies (MAbs) with three mouse immunoglobulin subtypes: IgG1, IgG2b and IgM. All of the MAbs bound strongly to rat cytochrome b5 as measured by radioimmunoassay (RIA). Four clones of MAbs were also strongly immunoreactive with cytochrome b5 when tested by Western blotting, but only one of the MAbs (1-39-2) weakly immunoprecipitated cytochrome b5 in an Ouchterlony double-immunodiffusion test. Two of the MAbs partially inhibited cytochrome b5-mediated NADH cytochrome c reduction catalyzed by liver microsomes (24-36%). Expression of immunodetectable cytochrome b5 was highest in the liver, next highest in the kidney, and quite low in the other tissues examined with MAb 1-17-1 by Western blotting. This MAb recognized homologous cytochrome b5 of human liver microsomes and in homogenates of TK- cells infected with recombinant vaccinia virus encoding human cytochrome b5. These MAbs to cytochrome b5 will be useful for the identification, quantification, and purification of cytochrome b5 from animal and human tissues, and for understanding its role in cytochrome P450 catalyzed drug metabolism and carcinogen activation with respect to tissue, organ and individual differences. JF - Biochemical pharmacology AU - Park, S S AU - Walker, W AU - Aoyama, T AU - Lapenson, D P AU - Waxman, D J AU - Gonzalez, F J AU - Gelboin, H V AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institute of Health, Bethesda, MD 20892. Y1 - 1992/05/28/ PY - 1992 DA - 1992 May 28 SP - 2201 EP - 2208 VL - 43 IS - 10 SN - 0006-2952, 0006-2952 KW - Antibodies, Monoclonal KW - 0 KW - Cytochromes b5 KW - 9035-39-6 KW - NADH Dehydrogenase KW - EC 1.6.99.3 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Age Factors KW - NADH Dehydrogenase -- immunology KW - Immunodiffusion KW - Kidney -- enzymology KW - Radioimmunoassay KW - Male KW - Female KW - Microsomes, Liver -- enzymology KW - Cytochromes b5 -- metabolism KW - Cytochromes b5 -- immunology KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72979167?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+pharmacology&rft.atitle=Monoclonal+antibodies+to+rat+liver+microsomal+cytochrome+b5.&rft.au=Park%2C+S+S%3BWalker%2C+W%3BAoyama%2C+T%3BLapenson%2C+D+P%3BWaxman%2C+D+J%3BGonzalez%2C+F+J%3BGelboin%2C+H+V&rft.aulast=Park&rft.aufirst=S&rft.date=1992-05-28&rft.volume=43&rft.issue=10&rft.spage=2201&rft.isbn=&rft.btitle=&rft.title=Biochemical+pharmacology&rft.issn=00062952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-08 N1 - Date created - 1992-07-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A controlled trial of buprenorphine treatment for opioid dependence. AN - 72923287; 1578593 AB - To assess the efficacy of buprenorphine for short-term maintenance/detoxification. A randomized, double-blind, parallel group study comparing buprenorphine, 8 mg/d, methadone, 60 mg/d, and methadone, 20 mg/d, in a 17-week maintenance phase followed by an 8-week detoxification phase. Outpatient facilities at the Addiction Research Center, Baltimore, Md. One hundred sixty-two volunteers seeking treatment for opioid dependence. In addition to the medication, counseling using a relapse prevention model was offered but not required. Retention time in treatment, urine samples negative for opioids, and failure to maintain abstinence. Throughout the maintenance phase, retention rates were significantly greater for buprenorphine (42%) than for methadone, 20 mg/d (20%, P less than .04); the percentage of urine samples negative for opioids was significantly greater for buprenorphine (53%, P less than .001) and methadone, 60 mg/d (44%, P less than .04), than for methadone, 20 mg/d (29%). Failure to maintain abstinence during the maintenance phase was significantly greater for methadone, 20 mg/d, than for buprenorphine (P less than .03). During the detoxification phase, no differences were observed between groups with respect to urine samples negative for opioids. For the entire 25 weeks, retention rates for buprenorphine (30%, P less than .01) and methadone, 60 mg/d (20%, P less than .05), were significantly greater than for methadone, 20 mg/d (6%). All treatments were well tolerated, with similar profiles of self-reported adverse effects. The percentages of patients who received counseling did not differ between groups. Buprenorphine was as effective as methadone, 60 mg/d, and both were superior to methadone, 20 mg/d, in reducing illicit opioid use and maintaining patients in treatment for 25 weeks. JF - JAMA AU - Johnson, R E AU - Jaffe, J H AU - Fudala, P J AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, Md. Y1 - 1992/05/27/ PY - 1992 DA - 1992 May 27 SP - 2750 EP - 2755 VL - 267 IS - 20 SN - 0098-7484, 0098-7484 KW - Narcotics KW - 0 KW - Buprenorphine KW - 40D3SCR4GZ KW - Heroin KW - 70D95007SX KW - Methadone KW - UC6VBE7V1Z KW - Abridged Index Medicus KW - Index Medicus KW - Methadone -- therapeutic use KW - Heroin Dependence -- urine KW - Double-Blind Method KW - Humans KW - Adult KW - Narcotics -- urine KW - Heroin Dependence -- rehabilitation KW - Middle Aged KW - Heroin -- urine KW - Male KW - Female KW - Proportional Hazards Models KW - Buprenorphine -- therapeutic use KW - Opioid-Related Disorders -- rehabilitation KW - Opioid-Related Disorders -- urine UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72923287?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=JAMA&rft.atitle=A+controlled+trial+of+buprenorphine+treatment+for+opioid+dependence.&rft.au=Johnson%2C+R+E%3BJaffe%2C+J+H%3BFudala%2C+P+J&rft.aulast=Johnson&rft.aufirst=R&rft.date=1992-05-27&rft.volume=267&rft.issue=20&rft.spage=2750&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-08 N1 - Date created - 1992-06-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: JAMA. 1992 Nov 4;268(17):2376-7 [1328697] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intoxication of cultured cells by cholera toxin: evidence for different pathways when bound to ganglioside GM1 or neoganglioproteins. AN - 72971070; 1317209 AB - We previously reported that when the oligosaccharide of ganglioside GM1 is covalently attached to cell surface proteins of GM1-deficient rat glioma C6 cells, the cells bind large amounts of cholera toxin (CT) but their cAMP response to CT is not enhanced [Pacuszka, T., & Fishman, P. H. (1990) J. Biol. Chem. 265, 7673-7668]. We now report that when such cells were exposed to CT in the presence of chloroquine, an acidotropic agent, they accumulated cAMP. This raised the possibility that CT bound to cell surface "neoganglioproteins" may be entering the cells through a different pathway from that of CT-bound GM1. To further explore this phenomenon, we covalently attached GM1 oligosaccharide to human transferrin (Tf). The modified protein (GM1OS-Tf) bound with high affinity to Tf receptors on HeLa cells and increased the binding of CT to the cells. The bound CT, however, was unable to activate adenylyl cyclase as measured by cyclic AMP accumulation. By contrast, treatment of HeLa cells with GM1 increased both CT binding and stimulation of cyclic AMP accumulation. Control cells and cells treated with either GM1 or GM1OS-Tf were exposed to CT in the presence of chloroquine. Whereas chloroquine had little or no effect on the response of control or GM1-treated cells to CT, it made the cells treated with GM1OS-Tf responsive to the toxin. Our results indicate that CT bound to its natural receptor GM1 enters the cells through a pathway different from that of toxin bound to neoganglioproteins. JF - Biochemistry AU - Pacuszka, T AU - Fishman, P H AD - Membrane Biochemistry Section, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892. Y1 - 1992/05/26/ PY - 1992 DA - 1992 May 26 SP - 4773 EP - 4778 VL - 31 IS - 20 SN - 0006-2960, 0006-2960 KW - Receptors, Transferrin KW - 0 KW - Transferrin KW - G(M1) Ganglioside KW - 37758-47-7 KW - Chloroquine KW - 886U3H6UFF KW - Cholera Toxin KW - 9012-63-9 KW - Cyclic AMP KW - E0399OZS9N KW - Index Medicus KW - Receptors, Transferrin -- analysis KW - Rats KW - Endocytosis KW - Animals KW - Tumor Cells, Cultured KW - Chloroquine -- pharmacology KW - Transferrin -- drug effects KW - Humans KW - Cyclic AMP -- metabolism KW - Transferrin -- chemistry KW - Receptors, Transferrin -- drug effects KW - HeLa Cells -- metabolism KW - HeLa Cells -- drug effects KW - G(M1) Ganglioside -- metabolism KW - Cholera Toxin -- toxicity KW - Glioma -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72971070?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=Intoxication+of+cultured+cells+by+cholera+toxin%3A+evidence+for+different+pathways+when+bound+to+ganglioside+GM1+or+neoganglioproteins.&rft.au=Pacuszka%2C+T%3BFishman%2C+P+H&rft.aulast=Pacuszka&rft.aufirst=T&rft.date=1992-05-26&rft.volume=31&rft.issue=20&rft.spage=4773&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-30 N1 - Date created - 1992-06-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Distinct regulation of vasoactive intestinal peptide (VIP) expression at mRNA and peptide levels in human neuroblastoma cells. AN - 73005900; 1319016 AB - Neuronal differentiation was induced in cultures of the human neuroblastoma cell line subclone SH-SY5Y by 14-day treatment with dibutyryl cAMP (dBcAMP), retinoic acid, and phorbol 12-myristate 13-acetate (PMA). An approximate 4-fold increase in vasoactive intestinal peptide (VIP) mRNA concentration was observed after differentiation with retinoic acid, whereas no change in VIP mRNA concentration was observed after differentiation with dBcAMP or PMA. A short-term treatment of cells with PMA did however result in a 5-fold transient increase in VIP mRNA; prior differentiation with retinoic acid or dBcAMP diminished this effect. Observed increases in VIP mRNA were in all cases accompanied by increases in VIP immunoreactivity. Remarkably, however, long-term treatment of cells with dBcAMP, which caused no change in mRNA levels, resulted in a six-fold increase in VIP immunoreactivity. Acute (36-h) treatment with carbachol also caused an increase in VIP immunoreactivity (about 2-fold, and blocked by atropine) without an increase in VIP mRNA level. Thus, a quantitative change in gene transcription or mRNA stability appears not to be a prerequisite for increased VIP expression, indicating that regulation can occur at translational or post-translational steps. JF - Neuroscience letters AU - Agoston, D V AU - Colburn, S AU - Krajniak, K G AU - Waschek, J A AD - Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1992/05/25/ PY - 1992 DA - 1992 May 25 SP - 213 EP - 216 VL - 139 IS - 2 SN - 0304-3940, 0304-3940 KW - RNA, Messenger KW - 0 KW - Vasoactive Intestinal Peptide KW - 37221-79-7 KW - Tretinoin KW - 5688UTC01R KW - Bucladesine KW - 63X7MBT2LQ KW - Carbachol KW - 8Y164V895Y KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Tretinoin -- pharmacology KW - Tumor Cells, Cultured -- metabolism KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Bucladesine -- pharmacology KW - Radioimmunoassay KW - Carbachol -- pharmacology KW - Vasoactive Intestinal Peptide -- biosynthesis KW - Peptide Biosynthesis KW - Neuroblastoma -- metabolism KW - RNA, Messenger -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73005900?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+letters&rft.atitle=Distinct+regulation+of+vasoactive+intestinal+peptide+%28VIP%29+expression+at+mRNA+and+peptide+levels+in+human+neuroblastoma+cells.&rft.au=Agoston%2C+D+V%3BColburn%2C+S%3BKrajniak%2C+K+G%3BWaschek%2C+J+A&rft.aulast=Agoston&rft.aufirst=D&rft.date=1992-05-25&rft.volume=139&rft.issue=2&rft.spage=213&rft.isbn=&rft.btitle=&rft.title=Neuroscience+letters&rft.issn=03043940&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-20 N1 - Date created - 1992-07-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of myogenesis by okadaic acid, an inhibitor of protein phosphatases, 1 and 2A, correlates with the induction of AP1. AN - 72951910; 1316910 AB - Recently, we demonstrated that okadaic acid, an inhibitor of protein phosphatases 1 and 2A, inhibits myogenesis by extinguishing the expression of MyoD1 and inducing the expression of Id. Since it has been reported that transformation by c-fos also inhibits myogenesis through inhibition of MyoD1 expression, we examined the effects of okadaic acid on the activation of the c-fos and jun family of proto-oncogenes in an attempt to understand the mechanism by which okadaic acid inhibits the myogenic differentiation. Treatment of C2C12 cells in growth medium with okadaic acid increased expression of the mRNAs for the c-fos family continuously and for the jun family to a lesser extent. In contrast, in differentiation medium, the induction of c-fos, c-jun, and fos B mRNAs by okadaic acid was transient, whereas fra-1, jun D, and jun B mRNAs were induced continuously, suggesting that okadaic acid regulates the expression of the c-fos and jun family through complex regulatory mechanisms depending on the state of differentiation of the cells. Transfection of c-jun and c-fos promoter-chloramphenicol acetyltransferase constructs demonstrated that the effects of okadaic acid on the induction of c-fos and c-jun are mediated through the activation of promoter elements. These results suggest that some of the targets of protein phosphatases 1 and 2A may include transcription factors capable of forming AP1 complexes and that these factors may play an important role during myogenic differentiation. JF - The Journal of biological chemistry AU - Park, K AU - Chung, M AU - Kim, S J AD - Laboratory of Chemoprevention, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/05/25/ PY - 1992 DA - 1992 May 25 SP - 10810 EP - 10815 VL - 267 IS - 15 SN - 0021-9258, 0021-9258 KW - DNA-Binding Proteins KW - 0 KW - Ethers, Cyclic KW - Isoenzymes KW - Muscle Proteins KW - MyoD Protein KW - Proto-Oncogene Proteins c-jun KW - RNA, Messenger KW - Okadaic Acid KW - 1W21G5Q4N2 KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Phosphoprotein Phosphatases KW - EC 3.1.3.16 KW - Index Medicus KW - Muscle Proteins -- metabolism KW - Transcription, Genetic KW - RNA, Messenger -- genetics KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Base Sequence KW - Promoter Regions, Genetic KW - Chimera KW - Transfection KW - Molecular Sequence Data KW - Genes, fos KW - Cell Line KW - DNA-Binding Proteins -- metabolism KW - Genes, jun KW - Phosphoprotein Phosphatases -- antagonists & inhibitors KW - Isoenzymes -- antagonists & inhibitors KW - Muscles -- cytology KW - Proto-Oncogene Proteins c-jun -- biosynthesis KW - Ethers, Cyclic -- pharmacology KW - Muscles -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72951910?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Inhibition+of+myogenesis+by+okadaic+acid%2C+an+inhibitor+of+protein+phosphatases%2C+1+and+2A%2C+correlates+with+the+induction+of+AP1.&rft.au=Park%2C+K%3BChung%2C+M%3BKim%2C+S+J&rft.aulast=Park&rft.aufirst=K&rft.date=1992-05-25&rft.volume=267&rft.issue=15&rft.spage=10810&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-25 N1 - Date created - 1992-06-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Failure of a protein synthesis inhibitor to modify glutamate receptor-mediated neurotoxicity in vivo. AN - 73096973; 1379868 AB - The delayed neuronal death (DND) resulting from brief forebrain ischemia has recently been reported to be markedly attenuated by parenteral administration of the reversible protein synthesis inhibitor, anisomycin. Previous work suggests that ischemia-induced DND is mediated by glutamate acting at one or more glutamate receptors, since glutamate receptor antagonists have been reported to reduce ischemia-induced DND. Consequently, we tested whether anisomycin could modify DND induced by direct intracerebral administration of the excitotoxins, N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methylisoxasole (AMPA) or kainic acid. Anisomycin, administered parenterally, in multiple doses did not alter DND induced by any of these excitotoxins, nor did combined parenteral and direct intracerebral injection of anisomycin protect against DND induced by AMPA. Thus, neurotoxicity induced by direct intracerebral administration of NMDA, AMPA or kainic acid does not appear to require de novo protein synthesis, and, therefore, is not likely to be mediated by the expression of a programmed cell death cascade. JF - Brain research AU - Leppin, C AU - Finiels-Marlier, F AU - Crawley, J N AU - Montpied, P AU - Paul, S M AD - Clinical Neuroscience Branch, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1992/05/22/ PY - 1992 DA - 1992 May 22 SP - 168 EP - 170 VL - 581 IS - 1 SN - 0006-8993, 0006-8993 KW - Glutamates KW - 0 KW - Receptors, Glutamate KW - Receptors, Neurotransmitter KW - Ibotenic Acid KW - 2552-55-8 KW - N-Methylaspartate KW - 6384-92-5 KW - Anisomycin KW - 6C74YM2NGI KW - alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid KW - 77521-29-0 KW - Glutamate Decarboxylase KW - EC 4.1.1.15 KW - Kainic Acid KW - SIV03811UC KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Glutamate Decarboxylase -- drug effects KW - Animals KW - Kainic Acid -- pharmacology KW - N-Methylaspartate -- pharmacology KW - Ibotenic Acid -- analogs & derivatives KW - Cell Death -- drug effects KW - Male KW - Ibotenic Acid -- pharmacology KW - Protein Biosynthesis KW - Neurons -- drug effects KW - Receptors, Neurotransmitter -- drug effects KW - Anisomycin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73096973?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Failure+of+a+protein+synthesis+inhibitor+to+modify+glutamate+receptor-mediated+neurotoxicity+in+vivo.&rft.au=Leppin%2C+C%3BFiniels-Marlier%2C+F%3BCrawley%2C+J+N%3BMontpied%2C+P%3BPaul%2C+S+M&rft.aulast=Leppin&rft.aufirst=C&rft.date=1992-05-22&rft.volume=581&rft.issue=1&rft.spage=168&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-15 N1 - Date created - 1992-09-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Controlled trial of plasma exchange and leukapheresis in polymyositis and dermatomyositis. AN - 72905394; 1472183 AB - The therapeutic options for patients with polymyositis or dermatomyositis that is resistant to corticosteroids are limited, unproved, and often toxic. Uncontrolled trials concluded that both plasma exchange and leukapheresis are beneficial, but despite the considerable use of these approaches, proof of their efficacy is lacking. Thirty-nine patients with definite polymyositis or dermatomyositis were randomly assigned to receive plasma exchange (replacement of one volume of plasma with 5 percent albumin in saline), leukapheresis (removal of 5 x 10(9) to 10 x 10(9) lymphocytes), or sham apheresis in a double-blind manner, with 12 treatments given over a one-month period. Muscle strength, functional capacity, and serum levels of muscle-associated enzymes were measured before and after the 12 procedures. In each group 3 of 13 patients had improvements in strength and functional capacity. The condition of 3 patients treated with leukapheresis and 1 treated with plasma exchange deteriorated, and it was unchanged in the other 26 patients. Adverse effects of apheresis included the need for a central venous catheter (9 patients), major vasovagal episodes (3 patients), and severe citrate reactions (2 patients). Despite the occurrence of significant reductions in the serum levels of muscle enzymes with plasma exchange (P less than 0.001) and significant decreases in lymphocyte counts with leukapheresis (P = 0.002), there were no significant differences among the three treatment groups in the final muscle strength or functional capacity of the patients. As treatments for corticosteroid-resistant polymyositis or dermatomyositis, leukapheresis and plasma exchange are no more effective than sham apheresis. JF - The New England journal of medicine AU - Miller, F W AU - Leitman, S F AU - Cronin, M E AU - Hicks, J E AU - Leff, R L AU - Wesley, R AU - Fraser, D D AU - Dalakas, M AU - Plotz, P H AD - National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, MD 20892. Y1 - 1992/05/21/ PY - 1992 DA - 1992 May 21 SP - 1380 EP - 1384 VL - 326 IS - 21 SN - 0028-4793, 0028-4793 KW - Creatine Kinase KW - EC 2.7.3.2 KW - Abridged Index Medicus KW - Index Medicus KW - Creatine Kinase -- blood KW - Double-Blind Method KW - Humans KW - Adult KW - Drug Resistance KW - Activities of Daily Living KW - Male KW - Leukocyte Count KW - Female KW - Leukapheresis KW - Myositis -- enzymology KW - Plasma Exchange KW - Myositis -- therapy KW - Dermatomyositis -- therapy KW - Myositis -- physiopathology KW - Dermatomyositis -- enzymology KW - Dermatomyositis -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72905394?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+New+England+journal+of+medicine&rft.atitle=Controlled+trial+of+plasma+exchange+and+leukapheresis+in+polymyositis+and+dermatomyositis.&rft.au=Miller%2C+F+W%3BLeitman%2C+S+F%3BCronin%2C+M+E%3BHicks%2C+J+E%3BLeff%2C+R+L%3BWesley%2C+R%3BFraser%2C+D+D%3BDalakas%2C+M%3BPlotz%2C+P+H&rft.aulast=Miller&rft.aufirst=F&rft.date=1992-05-21&rft.volume=326&rft.issue=21&rft.spage=1380&rft.isbn=&rft.btitle=&rft.title=The+New+England+journal+of+medicine&rft.issn=00284793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-26 N1 - Date created - 1992-05-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: N Engl J Med. 1992 Oct 1;327(14):1030-1 [1518542] N Engl J Med. 1992 May 21;326(21):1425-7 [1569977] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of mutation frequencies obtained using transgenes and specific-locus mutation systems in male mouse germ cells. AN - 72954251; 1375340 JF - Mutation research AU - Malling, H V AU - Burkhart, J G AD - Laboratory of Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/05/16/ PY - 1992 DA - 1992 May 16 SP - 149 EP - 151 VL - 279 IS - 2 SN - 0027-5107, 0027-5107 KW - Index Medicus KW - Animals KW - Mutagenicity Tests KW - Mice KW - Male KW - Spermatozoa KW - Mutation KW - Mice, Transgenic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72954251?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+research&rft.atitle=Comparison+of+mutation+frequencies+obtained+using+transgenes+and+specific-locus+mutation+systems+in+male+mouse+germ+cells.&rft.au=Malling%2C+H+V%3BBurkhart%2C+J+G&rft.aulast=Malling&rft.aufirst=H&rft.date=1992-05-16&rft.volume=279&rft.issue=2&rft.spage=149&rft.isbn=&rft.btitle=&rft.title=Mutation+research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-25 N1 - Date created - 1992-06-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Mutat Res. 1992 Dec;298(2):145-7 [1282212] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reduced density of NMDA receptors and increased sensitivity to dizocilpine-induced learning impairment in aged rats. AN - 73133255; 1387035 AB - About 20 min prior to training in a shock-motivated 14-unit T-maze, young (3-4 months) and aged (24-25 months) male Fischer-344 rats were given s.c. injections of either saline or dizocilpine (MK-801, 0.02 or 0.04 mg/kg), a non-competitive antagonist of the N-methyl-D-aspartate (NMDA) receptor. The aged rats showed a dose-dependent impairment in maze performance. Deficiencies were manifested as increases in errors, in runtime from start to goal, and in the number and duration of shocks received. In contrast, young rats exhibited no detrimental effects of dizocilpine on maze performance. Analysis of [3H]glutamate binding in these rats revealed a marked age-related decline in NMDA receptor binding in hippocampus. A significant correlation was observed between errors in the maze and hippocampal [3H]-glutamate binding, but the correlation was positive, i.e., rats that made the most errors had the highest level of NMDA receptor binding. Thus, compared to young rats, aged rats were more sensitive to the behavioral effects of NMDA receptor antagonism and they showed a hippocampal loss of [3H]glutamate in binding, which may be related to the increased sensitivity to dizocilpine. The positive correlation between poor maze performance and NMDA receptor binding suggests that the behaviors assessed involve complex interactions between NMDA receptors and other neuronal systems in the hippocampus. JF - Brain research AU - Ingram, D K AU - Garofalo, P AU - Spangler, E L AU - Mantione, C R AU - Odano, I AU - London, E D AD - Molecular Physiology and Genetics Section, Nathan W. Shock Laboratories, National Institute on Aging, Baltimore, MD 21224. Y1 - 1992/05/15/ PY - 1992 DA - 1992 May 15 SP - 273 EP - 280 VL - 580 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Receptors, N-Methyl-D-Aspartate KW - 0 KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Male KW - Aging -- metabolism KW - Aging -- drug effects KW - Hippocampus -- metabolism KW - Receptors, N-Methyl-D-Aspartate -- antagonists & inhibitors KW - Receptors, N-Methyl-D-Aspartate -- metabolism KW - Learning Disorders -- chemically induced KW - Hippocampus -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73133255?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Reduced+density+of+NMDA+receptors+and+increased+sensitivity+to+dizocilpine-induced+learning+impairment+in+aged+rats.&rft.au=Ingram%2C+D+K%3BGarofalo%2C+P%3BSpangler%2C+E+L%3BMantione%2C+C+R%3BOdano%2C+I%3BLondon%2C+E+D&rft.aulast=Ingram&rft.aufirst=D&rft.date=1992-05-15&rft.volume=580&rft.issue=1-2&rft.spage=273&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-23 N1 - Date created - 1992-09-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Extracellular matrix receptors and mouse skin carcinogenesis: altered expression linked to appearance of early markers of tumor progression. AN - 72949223; 1533815 AB - Interaction of cells with the basement membrane is important for cell proliferation and differentiation. Disruption of the basement membrane is an early event during progression of benign tumors to cancer. Using the techniques of immunohistochemistry and immunofluorescence, we show that cell-matrix interactions via the cell surface integrin receptors alpha 3 beta 1, alpha 5 beta 1, alpha 6 beta 4, the Mr 67,000 laminin receptor (67LR) laminin-binding protein, and the secreted matrix protein laminin are strictly regulated during differentiation of mouse epidermis. While alpha 6 beta 4 and alpha 5 beta 1 are polarized to the basal surface of basal cells in contact with the basement membrane, alpha 3 beta 1 and the non-integrin 67LR are primarily detected in the cell periphery of suprabasal cells, where cell to cell contacts are found. Sequential changes in expression of matrix receptors occur following multistage carcinogenesis of mouse skin. In an analysis of benign and malignant skin tumors induced by chemical carcinogens or oncogene transduction, we found that alpha 3 beta 1 and alpha 5 beta 1 as well as the non-integrin 67LR are sequentially down-regulated in the progression from benign to malignant, while alpha 6 beta 4 is the predominant receptor expressed in the carcinomas. Tumor expression of alpha 6 beta 4 is not polarized and is dissociated from its colocalized normal partner bullous pemphigoid antigen, which remains restricted to the basement membrane. The changes in matrix receptors are linked to appearance of keratin 13 in suprabasal regions, but always in alpha 6 beta 4 negative cells. The predominance of alpha 6 beta 4 in the proliferating cells during progression is associated with decreased expression of keratin 13 in carcinomas. These results suggest that matrix interactions with its receptors are important determinants of ordered differentiation in normal skin and show characteristic alterations during carcinogenesis that parallel changes in differentiation of the tumors. JF - Cancer research AU - Tennenbaum, T AU - Yuspa, S H AU - Grover, A AU - Castronovo, V AU - Sobel, M E AU - Yamada, Y AU - De Luca, L M AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/05/15/ PY - 1992 DA - 1992 May 15 SP - 2966 EP - 2976 VL - 52 IS - 10 SN - 0008-5472, 0008-5472 KW - v-fos KW - v-rasHa KW - Biomarkers, Tumor KW - 0 KW - Laminin KW - Receptors, Cytoadhesin KW - Receptors, Immunologic KW - Receptors, Laminin KW - Index Medicus KW - Keratinocytes -- physiology KW - Basement Membrane -- ultrastructure KW - Animals KW - Oncogenes -- genetics KW - Cells, Cultured KW - Cell Transformation, Viral -- genetics KW - Laminin -- analysis KW - Mice, Nude KW - Mice KW - Mice, Inbred BALB C KW - Immunohistochemistry KW - Skin Neoplasms -- genetics KW - Skin -- ultrastructure KW - Papilloma -- etiology KW - Skin Neoplasms -- ultrastructure KW - Skin Neoplasms -- etiology KW - Papilloma -- ultrastructure KW - Biomarkers, Tumor -- analysis KW - Receptors, Cytoadhesin -- analysis KW - Receptors, Immunologic -- analysis KW - Extracellular Matrix -- ultrastructure KW - Papilloma -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72949223?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Extracellular+matrix+receptors+and+mouse+skin+carcinogenesis%3A+altered+expression+linked+to+appearance+of+early+markers+of+tumor+progression.&rft.au=Tennenbaum%2C+T%3BYuspa%2C+S+H%3BGrover%2C+A%3BCastronovo%2C+V%3BSobel%2C+M+E%3BYamada%2C+Y%3BDe+Luca%2C+L+M&rft.aulast=Tennenbaum&rft.aufirst=T&rft.date=1992-05-15&rft.volume=52&rft.issue=10&rft.spage=2966&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-12 N1 - Date created - 1992-06-12 N1 - Date revised - 2017-01-13 N1 - Gene symbol - v-fos; v-rasHa N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Coupling of dual signaling pathways: epidermal growth factor action involves the estrogen receptor. AN - 72941355; 1584801 AB - Epidermal growth factor (EGF) reproduces many of the effects of estrogen on the murine female reproductive tract and may partially mediate estrogen-induced growth and differentiation. This study was performed to investigate the mechanism by which EGF elicits estrogen-like actions in the whole animal. EGF was administered to adult ovariectomized mice by slow release pellets implanted under the kidney capsule. The induction of uterine DNA synthesis and phosphatidylinositol lipid turnover by EGF or administration of diethylstilbestrol (5 micrograms/kg), a potent estrogen, was attenuated by the estrogen receptor antagonist ICI 164,384. Furthermore, EGF mimicked the effects of estrogen on enhanced nuclear localization of the estrogen receptor and the formation of a unique form of the estrogen receptor found exclusively in the nucleus. These results suggest that EGF may induce effects similar to those of estrogen in the mouse uterus by an interaction between the EGF signaling pathway and the classical estrogen receptor. The demonstration of cross-talk between polypeptide growth factors and steroid hormone receptors may be of importance to our understanding of the regulation of normal growth and differentiation as well as the mechanisms of transmission of extracellular mitogen signals to the nucleus. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Ignar-Trowbridge, D M AU - Nelson, K G AU - Bidwell, M C AU - Curtis, S W AU - Washburn, T F AU - McLachlan, J A AU - Korach, K S AD - Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709. Y1 - 1992/05/15/ PY - 1992 DA - 1992 May 15 SP - 4658 EP - 4662 VL - 89 IS - 10 SN - 0027-8424, 0027-8424 KW - Delayed-Action Preparations KW - 0 KW - Estrogen Antagonists KW - Inositol Phosphates KW - Phosphatidylinositols KW - Polyunsaturated Alkamides KW - Receptors, Estrogen KW - Estradiol KW - 4TI98Z838E KW - Epidermal Growth Factor KW - 62229-50-9 KW - Diethylstilbestrol KW - 731DCA35BT KW - ICI 164384 KW - 84LT43726C KW - Index Medicus KW - Phosphatidylinositols -- metabolism KW - Animals KW - Cell Nucleus -- metabolism KW - Inositol Phosphates -- metabolism KW - Estradiol -- pharmacology KW - Mice KW - Estradiol -- metabolism KW - Estradiol -- analogs & derivatives KW - Mice, Inbred Strains KW - Estrogen Antagonists -- pharmacology KW - Diethylstilbestrol -- pharmacology KW - Ovariectomy KW - Female KW - Receptors, Estrogen -- drug effects KW - Uterus -- physiology KW - Signal Transduction -- drug effects KW - Receptors, Estrogen -- metabolism KW - Epidermal Growth Factor -- pharmacology KW - Receptors, Estrogen -- physiology KW - Uterus -- drug effects KW - DNA Replication -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72941355?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Coupling+of+dual+signaling+pathways%3A+epidermal+growth+factor+action+involves+the+estrogen+receptor.&rft.au=Ignar-Trowbridge%2C+D+M%3BNelson%2C+K+G%3BBidwell%2C+M+C%3BCurtis%2C+S+W%3BWashburn%2C+T+F%3BMcLachlan%2C+J+A%3BKorach%2C+K+S&rft.aulast=Ignar-Trowbridge&rft.aufirst=D&rft.date=1992-05-15&rft.volume=89&rft.issue=10&rft.spage=4658&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-16 N1 - Date created - 1992-06-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Endocrinology. 1991 Oct;129(4):2000-10 [1915080] Endocrinology. 1991 Nov;129(5):2423-30 [1935776] Science. 1990 Dec 21;250(4988):1740-3 [2176746] Proc Natl Acad Sci U S A. 1988 Jan;85(1):69-73 [3422428] J Steroid Biochem. 1989 Mar;32(3):339-43 [2784840] Cell. 1989 Jun 30;57(7):1101-7 [2472218] Proc Natl Acad Sci U S A. 1989 Sep;86(18):6940-3 [2550926] Endocrinology. 1988 Jun;122(6):2355-63 [3286224] Mol Endocrinol. 1988 Mar;2(3):230-5 [3398852] J Biol Chem. 1985 Aug 15;260(17):9820-4 [2991264] Endocrinology. 1988 Nov;123(5):2540-8 [2844515] Science. 1988 May 13;240(4854):889-95 [3283939] Biochem Biophys Res Commun. 1987 Aug 14;146(3):1502-8 [3304294] Endocr Rev. 1987 Feb;8(1):29-43 [3549276] J Steroid Biochem. 1987;27(1-3):235-43 [3695483] Endocrinology. 1987 Dec;121(6):2099-111 [3678140] Endocrinology. 1987 Sep;121(3):1083-8 [3622377] Mol Endocrinol. 1990 Mar;4(3):510-23 [2342484] Endocrinology. 1990 Feb;126(2):891-8 [2404751] Ann N Y Acad Sci. 1990;595:348-56 [2375612] Mol Endocrinol. 1990 Feb;4(2):276-86 [2330006] Endocrinology. 1979 May;104(5):1324-32 [436778] Mol Cell Biol. 1991 Feb;11(2):913-9 [1990291] Proc Natl Acad Sci U S A. 1991 Jan 1;88(1):21-5 [1986369] Science. 1990 Nov 30;250(4985):1253-6 [1700866] Science. 1991 Dec 13;254(5038):1636-9 [1749936] Science. 1991 Jun 14;252(5012):1546-8 [2047861] Mol Endocrinol. 1991 Feb;5(2):235-42 [2038345] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transcriptional and posttranscriptional modulation of human neutrophil elastase gene expression. AN - 72940483; 1586720 AB - Human neutrophil elastase (NE), a 29-Kd potent serine protease stored in azurophilic granules of mature neutrophils, is coded for by the NE gene, a single copy gene with 5 exons spanning a 6-kb segment of chromosome 11 at q14. With the knowledge that the NE gene expression is limited to early myeloid cell differentiation, mechanisms modulating expression of the NE gene were evaluated in the HL-60 promyelocytic leukemia cell line, a model of early bone marrow precursor cells. Consistent with the presence of NE messenger RNA (mRNA) transcripts in undifferentiated HL-60 cells, nuclear transcription run-on analyses showed that HL-60 cells actively transcribed the NE gene. However, the transcription rate of the NE gene was relatively low, only 40% of the myeloperoxidase gene, a gene expressed in parallel with NE. When induced toward the mononuclear phagocytic lineage with phorbol 12-myristate 13-acetate (PMA), HL-60 cells exhibited marked suppression of NE gene transcription, declining to 17% of the resting rate within 2 days. Induction toward mononuclear phagocytic lineage differentiation caused no change in NE mRNA transcript half-life (T1/2), but mRNA levels decreased markedly over time, with levels undetectable 1.5 days after PMA stimulation. In contrast, when induced toward the myelocytic lineage with dimethyl sulfoxide, the rate of NE gene transcription increased 1.9-fold within 5 days. Interestingly, the mRNA transcript levels increased 2.5-fold by 5 days despite the fact that induction toward myelocytic lineage differentiation was accompanied by a marked reduction of NE mRNA transcript T1/2. Together, these observations suggest that the NE gene expression during bone marrow differentiation is modulated mainly at the transcriptional level, with some posttranscriptional modulation contributing, particularly during myelocytic lineage differentiation. JF - Blood AU - Yoshimura, K AU - Crystal, R G AD - Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/05/15/ PY - 1992 DA - 1992 May 15 SP - 2733 EP - 2740 VL - 79 IS - 10 SN - 0006-4971, 0006-4971 KW - RNA, Messenger KW - 0 KW - Pancreatic Elastase KW - EC 3.4.21.36 KW - Leukocyte Elastase KW - EC 3.4.21.37 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Dimethyl Sulfoxide KW - YOW8V9698H KW - Abridged Index Medicus KW - Index Medicus KW - Dimethyl Sulfoxide -- pharmacology KW - Blotting, Northern KW - Exons KW - HeLa Cells KW - Humans KW - RNA, Messenger -- genetics KW - Chromosomes, Human, Pair 11 KW - Genes KW - RNA, Messenger -- metabolism KW - Kinetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Monocytes KW - Cell Differentiation -- drug effects KW - Time Factors KW - Cell Line KW - T-Lymphocytes KW - Transcription, Genetic -- drug effects KW - Gene Expression Regulation, Enzymologic KW - Pancreatic Elastase -- genetics KW - RNA Processing, Post-Transcriptional -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72940483?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Blood&rft.atitle=Transcriptional+and+posttranscriptional+modulation+of+human+neutrophil+elastase+gene+expression.&rft.au=Yoshimura%2C+K%3BCrystal%2C+R+G&rft.aulast=Yoshimura&rft.aufirst=K&rft.date=1992-05-15&rft.volume=79&rft.issue=10&rft.spage=2733&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-19 N1 - Date created - 1992-06-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evaluation of metastatic human tumor burden and response to therapy in a nude mouse xenograft model using a molecular probe for repetitive human DNA sequences. AN - 72938986; 1581891 AB - A sensitive DNA dot-blot assay for repetitive human DNA sequences was developed and applied to the quantitative determination of spontaneous metastases of a human melanoma in various tissues of nude mice. The assay was useful for defining the time course and pattern of tissue distribution of metastatic cells as well as for assessing response to therapy. The methodology is relatively simple, can be performed using nonradioactive DNA probes, and should be broadly applicable to studies of metastasis of human tumors in nude mice. JF - Cancer research AU - Shoemaker, R H AU - Smythe, A M AU - Wu, L AU - Balaschak, M S AU - Boyd, M R AD - Laboratory of Drug Discovery Research and Development, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1992/05/15/ PY - 1992 DA - 1992 May 15 SP - 2791 EP - 2796 VL - 52 IS - 10 SN - 0008-5472, 0008-5472 KW - DNA Probes KW - 0 KW - DNA, Neoplasm KW - Cyclophosphamide KW - 8N3DW7272P KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Immunoblotting KW - Humans KW - Lung Neoplasms -- secondary KW - Lung Neoplasms -- drug therapy KW - Disease Models, Animal KW - Mice, Nude KW - Mice KW - Neoplasm Transplantation KW - Evaluation Studies as Topic KW - Tumor Cells, Cultured KW - DNA -- genetics KW - Transplantation, Heterologous KW - Middle Aged KW - Female KW - Male KW - Cyclophosphamide -- pharmacology KW - Neoplasm Metastasis -- genetics KW - Melanoma, Experimental -- drug therapy KW - DNA, Neoplasm -- genetics KW - Neoplasm Metastasis -- pathology KW - Repetitive Sequences, Nucleic Acid -- genetics KW - Melanoma, Experimental -- pathology KW - Melanoma, Experimental -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72938986?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Evaluation+of+metastatic+human+tumor+burden+and+response+to+therapy+in+a+nude+mouse+xenograft+model+using+a+molecular+probe+for+repetitive+human+DNA+sequences.&rft.au=Shoemaker%2C+R+H%3BSmythe%2C+A+M%3BWu%2C+L%3BBalaschak%2C+M+S%3BBoyd%2C+M+R&rft.aulast=Shoemaker&rft.aufirst=R&rft.date=1992-05-15&rft.volume=52&rft.issue=10&rft.spage=2791&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-12 N1 - Date created - 1992-06-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Cancer Res 1992 Nov 1;52(21):6137 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Analysis of the glycosylation and phosphorylation of the alpha-subunit of the lysosomal enzyme, beta-hexosaminidase A, by site-directed mutagenesis. AN - 72926758; 1533633 AB - The glycosylation and subsequent phosphorylation of mannose residues is a pivotal modification during the biosynthesis of lysosomal enzymes. We have identified the sites of N-linked glycosylation and oligosaccharide phosphorylation on the alpha-subunit of beta-hexosaminidase and have determined the influence of the oligosaccharides on the folding and transport of the enzyme. The potential glycosylation sequences, either singly or in combination, were eliminated through site-directed mutagenesis of the cDNA. By expression of the mutant cDNAs in COS-1 cells, each of the three glycosylation sites on the alpha-subunit was found to be modified by an oligosaccharide. One of the three oligosaccharides was the preferred site of phosphorylation. The absence of any individual oligosaccharide did not diminish the expression of the catalytic activity associated with the alpha-chain, implying proper folding and assembly of subunits. A profound effect was observed, however, when all three oligosaccharides were absent. The unglycosylated alpha-subunit, resulting from genetic alteration of all three glycosylation sites or synthesis of the wild-type protein in the presence of tunicamycin, was catalytically inactive. It was found to be improperly folded into an insoluble aggregate, linked through inappropriate disulfide bonds. The unglycosylated protein was trapped in the lumen of the endoplasmic reticulum and was found in a complex with the Ig heavy chain-binding protein, BiP. The properties of the nonglycosylated, misfolded alpha-subunit were similar to some mutant alpha-subunits in Tay-Sachs disease patients. The results indicate that the oligosaccharides are essential, although not in a site-specific manner, for proper folding and cellular transport of the alpha-subunit. JF - The Journal of biological chemistry AU - Weitz, G AU - Proia, R L AD - Genetics and Biochemistry Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/05/15/ PY - 1992 DA - 1992 May 15 SP - 10039 EP - 10044 VL - 267 IS - 14 SN - 0021-9258, 0021-9258 KW - Antibodies KW - 0 KW - Codon KW - Macromolecular Substances KW - Oligodeoxyribonucleotides KW - Oligopeptides KW - beta-N-Acetylhexosaminidases KW - EC 3.2.1.52 KW - Index Medicus KW - Animals KW - Sequence Homology, Nucleic Acid KW - Oligopeptides -- immunology KW - Amino Acid Sequence KW - Glycosylation KW - Oligopeptides -- chemical synthesis KW - Base Sequence KW - Phosphorylation KW - Transfection KW - Molecular Sequence Data KW - Immunohistochemistry KW - Cell Line KW - Mutagenesis, Site-Directed KW - beta-N-Acetylhexosaminidases -- metabolism KW - Protein Processing, Post-Translational KW - beta-N-Acetylhexosaminidases -- analysis KW - Lysosomes -- enzymology KW - beta-N-Acetylhexosaminidases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72926758?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Analysis+of+the+glycosylation+and+phosphorylation+of+the+alpha-subunit+of+the+lysosomal+enzyme%2C+beta-hexosaminidase+A%2C+by+site-directed+mutagenesis.&rft.au=Weitz%2C+G%3BProia%2C+R+L&rft.aulast=Weitz&rft.aufirst=G&rft.date=1992-05-15&rft.volume=267&rft.issue=14&rft.spage=10039&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-09 N1 - Date created - 1992-06-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Direct evidence for inhibition of free radical formation from Cu(I) and hydrogen peroxide by glutathione and other potential ligands using the EPR spin-trapping technique. AN - 72921458; 1315504 AB - Copper-induced oxidative damage is generally attributed to the formation of the highly reactive hydroxyl radical by a mechanism analogous to the Haber-Weiss cycle for Fe(II) and H2O2. In the present work, the reaction between the Cu(I) ion and H2O2 is studied using the EPR spin-trapping technique. The hydroxyl radical adduct was observed when Cu(I), dissolved in acetonitrile under N2, was added to pH 7.4 phosphate buffer containing 100 mM 5,5-dimethyl-1-pyrroline N-oxide (DMPO). Formation of the hydroxyl radical was dependent on the presence of O2 and subsequent formation of H2O2. The kscav/kDMPO ratios obtained were below those expected for a mechanism involving free hydroxyl radical and reflect the interference of nucleophilic addition of H2O to DMPO to form the DMPO/.OH adduct in the presence of nonchelated copper ion. Addition of ethanol or dimethyl sulfoxide to the reaction suggests that a high-valent metal intermediate, possibly Cu(III), was also formed. Spin trapping of hydroxyl radical was almost completely inhibited upon addition of Cu(I) to a solution of either nitrilotriacetate or histidine, even though the copper was fully oxidized to Cu(II) and H2O2 was formed. Bathocuproinedisulfonate, thiourea, and reduced glutathione all stabilized the Cu(I) ion toward oxidation by O2. Upon addition of H2O2, the Cu(I) in all three complexes was oxidized to varying degrees; however, only the thiourea complex was fully oxidized within 2 min of reaction and produced detectable hydroxyl radicals. No radicals were detected from the bathocuproinedisulfonate or glutathione complexes. Overall, these results suggest that the deleterious effects of copper ions in vivo are diminished by biochemical chelators, especially glutathione, which probably has a major role in moderating the toxicological effects of copper. JF - Archives of biochemistry and biophysics AU - Hanna, P M AU - Mason, R P AD - National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1992/05/15/ PY - 1992 DA - 1992 May 15 SP - 205 EP - 213 VL - 295 IS - 1 SN - 0003-9861, 0003-9861 KW - Free Radical Scavengers KW - 0 KW - Free Radicals KW - Ligands KW - Phenanthrolines KW - bathocuproine sulfonate KW - 73348-75-1 KW - Copper KW - 789U1901C5 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Glutathione KW - GAN16C9B8O KW - Index Medicus KW - Phenanthrolines -- chemistry KW - Oxygen Consumption KW - Electron Spin Resonance Spectroscopy KW - Free Radicals -- chemistry KW - Glutathione -- chemistry KW - Copper -- chemistry KW - Hydrogen Peroxide -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72921458?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+biochemistry+and+biophysics&rft.atitle=Direct+evidence+for+inhibition+of+free+radical+formation+from+Cu%28I%29+and+hydrogen+peroxide+by+glutathione+and+other+potential+ligands+using+the+EPR+spin-trapping+technique.&rft.au=Hanna%2C+P+M%3BMason%2C+R+P&rft.aulast=Hanna&rft.aufirst=P&rft.date=1992-05-15&rft.volume=295&rft.issue=1&rft.spage=205&rft.isbn=&rft.btitle=&rft.title=Archives+of+biochemistry+and+biophysics&rft.issn=00039861&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-02 N1 - Date created - 1992-06-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Features of the dopaminergic neurotoxin MPTP. AN - 73082979; 1637076 JF - Annals of the New York Academy of Sciences AU - Kopin, I J AD - National Institutes of Health, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892. Y1 - 1992/05/11/ PY - 1992 DA - 1992 May 11 SP - 96 EP - 104 VL - 648 SN - 0077-8923, 0077-8923 KW - Free Radicals KW - 0 KW - Neurotoxins KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Calcium KW - SY7Q814VUP KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Calcium -- metabolism KW - Animals KW - 1-Methyl-4-phenylpyridinium -- toxicity KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- metabolism KW - Humans KW - Neurons -- metabolism KW - Neurons -- drug effects KW - MPTP Poisoning KW - Brain -- pathology KW - Brain -- drug effects KW - Astrocytes -- drug effects KW - Dopamine -- metabolism KW - Brain -- metabolism KW - Astrocytes -- pathology KW - Neurons -- pathology KW - Astrocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73082979?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=Features+of+the+dopaminergic+neurotoxin+MPTP.&rft.au=Kopin%2C+I+J&rft.aulast=Kopin&rft.aufirst=I&rft.date=1992-05-11&rft.volume=648&rft.issue=&rft.spage=96&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-21 N1 - Date created - 1992-08-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Binding of [3H]bryostatin 4 to protein kinase C. AN - 72975813; 1596288 AB - The bryostatins represent a unique class of activators of protein kinase C (PKC) which induce only a subset of the responses typical of the phorbol esters and block those responses to the phorbol esters which they themselves do not induce. To better understand the interaction of the bryostatins with PKC, we have synthesized [26-3H]bryostatin 4 and characterized its binding to PKC. [3H]Bryostatin 4 and [3H]phorbol 12,13-dibutyrate ([3H]PDBu) differed markedly in their binding to PKC reconstituted with phosphatidylserine (PS). The binding affinity of [3H]bryostatin 4 under these conditions was too high to measure and the rate of release of bound bryostatin was much slower than that of the phorbol esters, with a half-time of several hours. These properties caused bryostatin 1 to appear to inhibit [3H]PDBu binding under these conditions in a non-competitive fashion. Both the high potency and the slow rate of release of the bryostatins may contribute to their unique pattern of biological activity. By reconstituting PKC in a mixture of 1.5% Triton X-100:0.3% PS, we were able to establish reversible conditions for [3H]bryostatin 4 binding. Under these latter conditions, binding of [3H]bryostatin 4 was competitively inhibited by PDBu, consistent with both the bryostatin and phorbol esters binding to PKC in a qualitatively similar fashion. Binding affinities to PKC isozymes alpha, beta, and gamma were compared and little difference was found, suggesting that differential recognition by these isozymes does not account for the unique biological activity of the bryostatins. JF - Biochemical pharmacology AU - Lewin, N E AU - Dell'Aquila, M L AU - Pettit, G R AU - Blumberg, P M AU - Warren, B S AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/05/08/ PY - 1992 DA - 1992 May 08 SP - 2007 EP - 2014 VL - 43 IS - 9 SN - 0006-2952, 0006-2952 KW - Bryostatins KW - 0 KW - Lactones KW - Macrolides KW - Phosphatidylserines KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - bryostatin 4 KW - 91523-82-9 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Index Medicus KW - Rats KW - Brain -- enzymology KW - Animals KW - Phorbol 12,13-Dibutyrate -- metabolism KW - Enzyme Activation KW - Kinetics KW - Binding, Competitive KW - Cell Line -- enzymology KW - Protein Kinase C -- metabolism KW - Protein Kinase C -- isolation & purification KW - Lactones -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72975813?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+pharmacology&rft.atitle=Binding+of+%5B3H%5Dbryostatin+4+to+protein+kinase+C.&rft.au=Lewin%2C+N+E%3BDell%27Aquila%2C+M+L%3BPettit%2C+G+R%3BBlumberg%2C+P+M%3BWarren%2C+B+S&rft.aulast=Lewin&rft.aufirst=N&rft.date=1992-05-08&rft.volume=43&rft.issue=9&rft.spage=2007&rft.isbn=&rft.btitle=&rft.title=Biochemical+pharmacology&rft.issn=00062952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-26 N1 - Date created - 1992-06-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of desipramine, amitriptyline, and fluoxetine on pain in diabetic neuropathy. AN - 72882611; 1560801 AB - Amitriptyline reduces the pain caused by peripheral-nerve disease, but treatment is often limited by side effects related to the drug's many pharmacologic actions. Selective agents might be safer and more effective. We carried out two randomized, double-blind, crossover studies in patients with painful diabetic neuropathy, comparing amitriptyline with the relatively selective blocker of norepinephrine reuptake desipramine in 38 patients, and comparing the selective blocker of serotonin reuptake fluoxetine with placebo in 46 patients. Fifty-seven patients were randomly assigned to a study as well as to the order of treatment, permitting comparison among all three drugs and placebo as the first treatment. The patients rated the degree of pain present each day using verbal descriptors, and they also assessed the extent of pain relief globally at the end of each treatment period. After individual dose titration, the mean daily doses of the drugs were as follows: amitriptyline, 105 mg; desipramine, 111 mg; and fluoxetine, 40 mg. There was moderate or greater relief of pain in 28 of the 38 patients (74 percent) who received amitriptyline, 23 of the 38 patients (61 percent) who received desipramine, 22 of the 46 patients (48 percent) who received fluoxetine, and 19 of the 46 patients (41 percent) who received placebo. The differences in responses between amitriptyline and desipramine and between fluoxetine and placebo were not statistically significant, but both amitriptyline and desipramine were superior to placebo. Amitriptyline and desipramine were as effective in patients who were not depressed as in depressed patients, but fluoxetine was effective only in depressed patients. Desipramine relieves pain caused by diabetic neuropathy with efficacy similar to that of amitriptyline, offering an alternative for patients unable to tolerate the latter. Blockade of norepinephrine reuptake is likely to mediate the analgesic effect of these antidepressant drugs in diabetic neuropathy. Fluoxetine, which blocks serotonin uptake, is no more effective than placebo for the relief of pain. JF - The New England journal of medicine AU - Max, M B AU - Lynch, S A AU - Muir, J AU - Shoaf, S E AU - Smoller, B AU - Dubner, R AD - Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/05/07/ PY - 1992 DA - 1992 May 07 SP - 1250 EP - 1256 VL - 326 IS - 19 SN - 0028-4793, 0028-4793 KW - Analgesics KW - 0 KW - Fluoxetine KW - 01K63SUP8D KW - Amitriptyline KW - 1806D8D52K KW - Desipramine KW - TG537D343B KW - Abridged Index Medicus KW - Index Medicus KW - Pain -- drug therapy KW - Double-Blind Method KW - Aged, 80 and over KW - Humans KW - Depression -- complications KW - Adult KW - Infant, Newborn KW - Aged KW - Middle Aged KW - Male KW - Female KW - Fluoxetine -- adverse effects KW - Amitriptyline -- administration & dosage KW - Amitriptyline -- adverse effects KW - Desipramine -- therapeutic use KW - Desipramine -- adverse effects KW - Fluoxetine -- administration & dosage KW - Desipramine -- administration & dosage KW - Amitriptyline -- therapeutic use KW - Fluoxetine -- therapeutic use KW - Diabetic Neuropathies -- drug therapy KW - Analgesics -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72882611?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+New+England+journal+of+medicine&rft.atitle=Effects+of+desipramine%2C+amitriptyline%2C+and+fluoxetine+on+pain+in+diabetic+neuropathy.&rft.au=Max%2C+M+B%3BLynch%2C+S+A%3BMuir%2C+J%3BShoaf%2C+S+E%3BSmoller%2C+B%3BDubner%2C+R&rft.aulast=Max&rft.aufirst=M&rft.date=1992-05-07&rft.volume=326&rft.issue=19&rft.spage=1250&rft.isbn=&rft.btitle=&rft.title=The+New+England+journal+of+medicine&rft.issn=00284793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-08 N1 - Date created - 1992-05-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: N Engl J Med. 1992 May 7;326(19):1287-8 [1560806] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of the human gene encoding ADP-ribosylation factor 1, a guanine nucleotide-binding activator of cholera toxin. AN - 72936454; 1577740 AB - Mammalian ADP-ribosylation factors (ARFs), approximately 20-kDa guanine nucleotide-binding proteins that stimulate cholera toxin ADP-ribosyltransferase activity, were grouped into three classes based on deduced amino acid sequence. Human ARF 1, a class I ARF, is identical with its bovine counterpart, has a distinctive pattern of tissue and developmental expression, and is encoded by a approximately 1.9-kilobase mRNA. ARF 1 cDNAs were isolated from a human fibroblast cDNA library; one arose via an alternative polyadenylation signal (AA-TACA) 84 nucleotides 5' to the polyadenylation signal (AATAAA) used in the 1815-base pair cDNA. The polyadenylation signals, their respective locations, and the surrounding nucleotide sequences are conserved in human and rat. The human ARF 1 gene, with four introns, spans approximately 16.5 kilobases. Exon 1 (46 base pairs) contains only untranslated sequence. Translation initiates in exon 2, which encodes the sequence GXXXXGK involved in phosphate binding (GTP hydrolysis). The sequence DVGG is encoded in exon 3, and NKQD, which is involved in the interaction with the guanine ring, is interrupted following the codon for Q by intron 4. The carboxyl-terminal 53 amino acids and greater than 1110 base pairs of 3'-untranslated region are encoded in exon 5. Primer extension and mung bean and S1 nuclease mapping indicated multiple transcription initiation sites and were consistent with Northern analyses. The 5'-flanking region has a high GC content but no TATA or CAAT box, as found in housekeeping genes. In addition, the two human class I ARF genes, ARF 1 and ARF 3, have similar exon/intron organizations and use GC-rich promoters. JF - The Journal of biological chemistry AU - Lee, C M AU - Haun, R S AU - Tsai, S C AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/05/05/ PY - 1992 DA - 1992 May 05 SP - 9028 EP - 9034 VL - 267 IS - 13 SN - 0021-9258, 0021-9258 KW - ARF 1 KW - ARF 3 KW - hARF 1 KW - DNA Probes KW - 0 KW - RNA, Messenger KW - DNA KW - 9007-49-2 KW - Cholera Toxin KW - 9012-63-9 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - ADP-Ribosylation Factors KW - EC 3.6.5.2 KW - Index Medicus KW - Animals KW - Blotting, Northern KW - Sequence Homology, Nucleic Acid KW - Humans KW - Transcription, Genetic KW - Amino Acid Sequence KW - Nucleic Acid Hybridization KW - RNA, Messenger -- genetics KW - Rats KW - Polymerase Chain Reaction KW - Base Sequence KW - DNA -- genetics KW - Molecular Sequence Data KW - GTP-Binding Proteins -- metabolism KW - GTP-Binding Proteins -- genetics KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72936454?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Characterization+of+the+human+gene+encoding+ADP-ribosylation+factor+1%2C+a+guanine+nucleotide-binding+activator+of+cholera+toxin.&rft.au=Lee%2C+C+M%3BHaun%2C+R+S%3BTsai%2C+S+C%3BMoss%2C+J%3BVaughan%2C+M&rft.aulast=Lee&rft.aufirst=C&rft.date=1992-05-05&rft.volume=267&rft.issue=13&rft.spage=9028&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-05 N1 - Date created - 1992-06-05 N1 - Date revised - 2017-01-13 N1 - Gene symbol - ARF 1; ARF 3; hARF 1 N1 - Genetic sequence - M84326; GENBANK; M84327; M84332; M74320; M74321; M74322; M74323; M74324; M74318; M74319 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Automated detection of the tongue surface in sequences of ultrasound images. AN - 85149638; pmid-1629491 AB - An image processing system has been developed for a Macintosh II personal computer. It is designed to process sequences of sagittal tongue sections that are digitized in real time and stored in standard tagged image file format (TIFF). The successive processing steps are: (a) a low-pass filter for noise reduction, (b) a resampling of the sector of interest in polar coordinates, (c) a matched filter (vertical differentiator) for the enhancement of the tissue/air interface in the surface region of the tongue, and (d) an extraction of border points by searching for an optimal radial path along the angular dimension. This latter task is achieved by dynamic programming, which has the following advantages. First, due to the use of a global criterion to guide the detection, it is very robust. Second, as a result of certain restrictions of the allowable transitions, the extracted contours are smooth. Finally, the method permits the specification of particular predefined contour points. This system was implemented in a program that can handle image sequences in a fully automatic mode. Results obtained using ultrasound data are presented. JF - The Journal of the Acoustical Society of America AU - Unser, M AU - Stone, M AD - Biomedical Engineering and Instrumentation Program, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 3001 EP - 3007 VL - 91 IS - 5 SN - 0001-4966, 0001-4966 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85149638?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+the+Acoustical+Society+of+America&rft.atitle=Automated+detection+of+the+tongue+surface+in+sequences+of+ultrasound+images.&rft.au=Unser%2C+M%3BStone%2C+M&rft.aulast=Unser&rft.aufirst=M&rft.date=1992-05-01&rft.volume=91&rft.issue=5&rft.spage=3001&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+the+Acoustical+Society+of+America&rft.issn=00014966&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Patients' perceptions on participation in a cancer chemoprevention trial. AN - 73539437; 1303133 AB - The perceptions of patients regarding the benefits, disadvantages, and importance of their participation in a long-term cancer chemoprevention trial, the Isotretinoin-Basal Cell Carcinoma Prevention Trial, were assessed through a questionnaire mailed at the conclusion of the 3-year treatment period of the trial. Responses were evaluated overall, as well as within subgroups defined by sex, age, education level, treatment group, presence of side effects, and the number of skin biopsies performed during the 3-year intervention phase. Overall, "careful medical follow-up received" (43%) and "being part of a research effort" (24%) were the most frequently cited important benefits, while the "amount of time taken to attend clinic" (32%) and "side effects" (20%) were the most frequently cited unpleasant aspects of trial participation. Most surveyed patients viewed the study as "very or extremely important" to their general health (62%) and their skin cancer condition (88%) and, as a result of participation, felt "much or somewhat better" physically (52%). The majority indicated that they would "definitely or probably" be willing to take part in another research study (79%) and take the study medication, if it were shown to be effective in the trial (78%). Overall and subgroup data provide important insights into patient motivations and attitudes regarding cancer chemoprevention trial participation, adherence, and satisfaction. JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology AU - Tangrea, J A AU - Adrianza, M E AU - Helsel, W E AD - Cancer Prevention Studies Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892. PY - 1992 SP - 325 EP - 330 VL - 1 IS - 4 SN - 1055-9965, 1055-9965 KW - Placebos KW - 0 KW - Isotretinoin KW - EH28UP18IF KW - Index Medicus KW - Age Factors KW - Educational Status KW - Sex Factors KW - Double-Blind Method KW - Patient Satisfaction KW - Humans KW - Aged KW - Attitude KW - Adult KW - Incidence KW - Middle Aged KW - Time Factors KW - Female KW - Male KW - Isotretinoin -- administration & dosage KW - Carcinoma, Basal Cell -- prevention & control KW - Attitude to Health KW - Isotretinoin -- adverse effects KW - Skin Neoplasms -- prevention & control KW - Neoplasm Recurrence, Local -- prevention & control KW - Isotretinoin -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73539437?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.atitle=Patients%27+perceptions+on+participation+in+a+cancer+chemoprevention+trial.&rft.au=Tangrea%2C+J+A%3BAdrianza%2C+M+E%3BHelsel%2C+W+E&rft.aulast=Tangrea&rft.aufirst=J&rft.date=1992-05-01&rft.volume=1&rft.issue=4&rft.spage=325&rft.isbn=&rft.btitle=&rft.title=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.issn=10559965&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-24 N1 - Date created - 1993-06-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reproductive toxicity of triethylene glycol and its diacetate and dimethyl ether derivatives in a continuous breeding protocol in Swiss CD-1 mice. AN - 73194190; 1526373 AB - Triethylene glycol and two of its derivatives were evaluated for reproductive toxicity in a continuous breeding protocol with Swiss CD-1 mice. Triethylene glycol (TEG: 0, 0.3, 1.5, and 3%), triethylene glycol diacetate (TGD: 0, 0.75, 1.5, and 3%), and triethylene glycol dimethyl ether (TGDME: 0, 0.25, 0.5, and 1%) were administered in drinking water to breeding pairs (20 pairs per treatment group, 40 control pairs) during a 98-day cohabitation period. Reproductive function was assessed by the number of litters per pair, live pups per litter, proportion of pups born alive, and pup weight. There were no apparent effects on reproductive function in the animals receiving TEG or TGD at doses up to 3% in the drinking water (representing 6.78 or 5.45 g/kg, respectively). However, some developmental toxicity was demonstrated for both TEG and TGD. Continuous exposure of dams to 1.5 or 3% TEG significantly reduced live pup weight at birth compared to control and 0.3% TEG, while exposure to 3% TGD during lactation significantly (but reversibly) reduced pup body weights on Postnatal Days 14 and 21. In contrast, TGDME was toxic to the reproductive system as evidenced by decreases at the highest dose (1% TGDME; 1.47 g/kg) in the proportion of pairs that produced at least one litter, live pups per litter, and proportion of pups born alive, with dose-related trends seen in the latter two parameters. A crossover mating trial showed that TGDME was more toxic to the female than the male reproductive system. These data indicate that TGDME (1.47 g/kg) is a reproductive toxicant in Swiss mice while reproductive toxicity was not demonstrated in mice receiving TEG or TGD (at doses up to 6.78 or 5.45 g/kg, respectively). JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Bossert, N L AU - Reel, J R AU - Lawton, A D AU - George, J D AU - Lamb, J C AD - Developmental and Reproductive Toxicology Group, National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 602 EP - 608 VL - 18 IS - 4 SN - 0272-0590, 0272-0590 KW - Ethylene Glycols KW - 0 KW - Polyethylene Glycols KW - 30IQX730WE KW - triglyme KW - 32YXG88KK0 KW - triethylene glycol KW - 3P5SU53360 KW - triethylene glycol diacetate KW - A559792B4Q KW - Index Medicus KW - Genitalia -- drug effects KW - Mice, Inbred Strains KW - Autopsy KW - Animals KW - Liver -- drug effects KW - Brain -- drug effects KW - Mice KW - Male KW - Female KW - Organ Size -- drug effects KW - Ethylene Glycols -- toxicity KW - Reproduction -- drug effects KW - Polyethylene Glycols -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73194190?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=Reproductive+toxicity+of+triethylene+glycol+and+its+diacetate+and+dimethyl+ether+derivatives+in+a+continuous+breeding+protocol+in+Swiss+CD-1+mice.&rft.au=Bossert%2C+N+L%3BReel%2C+J+R%3BLawton%2C+A+D%3BGeorge%2C+J+D%3BLamb%2C+J+C&rft.aulast=Bossert&rft.aufirst=N&rft.date=1992-05-01&rft.volume=18&rft.issue=4&rft.spage=602&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-19 N1 - Date created - 1992-10-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytotoxic quassinoids from Cedronia granatensis. AN - 73155920; 1517739 AB - The NCI in vitro primary disease-oriented antitumor screen has been used to select and guide the fractionation of the organic and aqueous extracts of Cedronia granatensis. Two quassinoids, sergiolide [1] and isobrucein B [2], to which the screening panel cell lines exhibited up to a 1000-fold range of differential sensitivity, were isolated. At concentrations of 10(-5)-10(-8) M, the compounds typically produced LC50-level responses against a majority of the melanoma lines and several of the colon, lung, and other solid tumor lines. These and related quassinoids may, therefore, be of interest for in vivo evaluation in appropriate xenograft tumor models. JF - Journal of natural products AU - Tischler, M AU - Cardellina, J H AU - Boyd, M R AU - Cragg, G M AD - Laboratory of Drug Discovery Research and Development, National Cancer Institute, Frederick, Maryland 21702-1201. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 667 EP - 671 VL - 55 IS - 5 SN - 0163-3864, 0163-3864 KW - Antineoplastic Agents, Phytogenic KW - 0 KW - Quassins KW - isobrucein B KW - 53663-03-9 KW - sergeolide KW - 82290-17-3 KW - Glaucarubin KW - EH6H7VS52J KW - Index Medicus KW - Molecular Structure KW - Drug Screening Assays, Antitumor KW - Tumor Cells, Cultured KW - Humans KW - Glaucarubin -- chemistry KW - Antineoplastic Agents, Phytogenic -- isolation & purification KW - Glaucarubin -- isolation & purification KW - Antineoplastic Agents, Phytogenic -- chemistry KW - Glaucarubin -- pharmacology KW - Antineoplastic Agents, Phytogenic -- pharmacology KW - Glaucarubin -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73155920?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+natural+products&rft.atitle=Cytotoxic+quassinoids+from+Cedronia+granatensis.&rft.au=Tischler%2C+M%3BCardellina%2C+J+H%3BBoyd%2C+M+R%3BCragg%2C+G+M&rft.aulast=Tischler&rft.aufirst=M&rft.date=1992-05-01&rft.volume=55&rft.issue=5&rft.spage=667&rft.isbn=&rft.btitle=&rft.title=Journal+of+natural+products&rft.issn=01633864&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-06 N1 - Date created - 1992-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vitro inhibition of human immunodeficiency virus (HIV) type 1 replication by C2 symmetry-based HIV protease inhibitors as single agents or in combinations. AN - 73154715; 1510415 AB - C2 symmetry-based human immunodeficiency virus (HIV) protease inhibitors were examined in vitro as single agents or in combination with 3'-azido-2',3'-dideoxythymidine (AZT) or 2',3'-dideoxyinosine for activity against HIV type 1 (HIV-1). Ten C2 symmetry-based or pseudo-C2 symmetry-based HIV protease inhibitors were active against a laboratory strain (HIV-1IIIB) in the HIV-1 cytopathic effect inhibition assay. Three inhibitors, A75925, A76928, and A77003, selected to represent a range of aqueous solubility and antiviral activity, were active against four different HIV-1 strains tested. These three inhibitors exhibited a significant inhibition of the cytopathic effect of HIV-1 against the CD4+ ATH8 cell line, with 90% inhibitory concentrations ranging from 0.1 to 4 microM. Cellular toxicity was negligible at up to 20 microM. Furthermore, they completely inhibited the replication of monocytotropic strain HIV-1Ba-L in purified monocytes and macrophages at 0.75 to 2 microM. Potent inhibitory activity against a primary HIV-1 isolate and an AZT-resistant HIV-1 variant was also observed for all three inhibitors in phytohemagglutinin-activated peripheral blood mononuclear cells. When these three HIV protease inhibitors and AZT or 2',3'-dideoxyinosine were used in combinations against a primary HIV isolate in phytohemagglutinin-activated peripheral blood mononuclear cells and the results were analyzed with the COMBO program package, their antiviral activities were identified to be synergistic in some cases and additive in others. The present data warrant further investigations of these compounds as potential antiviral agents for the therapy of HIV infections. JF - Antimicrobial agents and chemotherapy AU - Kageyama, S AU - Weinstein, J N AU - Shirasaka, T AU - Kempf, D J AU - Norbeck, D W AU - Plattner, J J AU - Erickson, J AU - Mitsuya, H AD - Experimental Retrovirology Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 926 EP - 933 VL - 36 IS - 5 SN - 0066-4804, 0066-4804 KW - HIV Protease Inhibitors KW - 0 KW - Zidovudine KW - 4B9XT59T7S KW - Didanosine KW - K3GDH6OH08 KW - Index Medicus KW - AIDS/HIV KW - Drug Therapy, Combination KW - Drug Interactions KW - Humans KW - Zidovudine -- pharmacology KW - Didanosine -- pharmacology KW - Virus Replication -- drug effects KW - HIV-1 -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73154715?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+agents+and+chemotherapy&rft.atitle=In+vitro+inhibition+of+human+immunodeficiency+virus+%28HIV%29+type+1+replication+by+C2+symmetry-based+HIV+protease+inhibitors+as+single+agents+or+in+combinations.&rft.au=Kageyama%2C+S%3BWeinstein%2C+J+N%3BShirasaka%2C+T%3BKempf%2C+D+J%3BNorbeck%2C+D+W%3BPlattner%2C+J+J%3BErickson%2C+J%3BMitsuya%2C+H&rft.aulast=Kageyama&rft.aufirst=S&rft.date=1992-05-01&rft.volume=36&rft.issue=5&rft.spage=926&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+agents+and+chemotherapy&rft.issn=00664804&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-22 N1 - Date created - 1992-09-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1990 Dec;87(23):9426-30 [2251284] Proc Natl Acad Sci U S A. 1986 Mar;83(6):1911-5 [3006077] Science. 1986 Mar 28;231(4745):1580-4 [2420008] Science. 1989 Jul 28;245(4916):412-5 [2502840] AIDS. 1989 Jul;3(7):411-5 [2504243] Lancet. 1988 Jan 16;1(8577):76-81 [2891981] Science. 1986 Jul 11;233(4760):215-9 [3014648] Science. 1984 May 4;224(4648):497-500 [6200935] Science. 1990 Sep 28;249(4976):1533-44 [1699273] Proc Natl Acad Sci U S A. 1990 Nov;87(22):8889-93 [1701055] Antimicrob Agents Chemother. 1991 Nov;35(11):2209-14 [1803993] J Med Chem. 1991 Mar;34(3):1225-8 [2002465] N Engl J Med. 1990 May 10;322(19):1333-40 [2139173] N Engl J Med. 1990 May 10;322(19):1340-5 [2139174] Science. 1990 Aug 3;249(4968):527-33 [2200122] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7472-6 [2217178] Proc Natl Acad Sci U S A. 1988 Jul;85(13):4686-90 [3290901] Nature. 1990 Jan 4;343(6253):90-2 [1688646] FASEB J. 1991 Jul;5(10):2369-81 [1712326] N Engl J Med. 1990 Oct 11;323(15):1009-14 [1977079] Ann N Y Acad Sci. 1990;616:367-84 [2078029] J Acquir Immune Defic Syndr. 1990;3 Suppl 2:S99-103 [2172507] J Med Chem. 1990 Oct;33(10):2687-9 [2213822] Proc Natl Acad Sci U S A. 1990 Sep;87(17):6574-8 [2395859] Proc Natl Acad Sci U S A. 1985 Oct;82(20):7096-100 [2413459] Science. 1989 Mar 31;243(4899):1731-4 [2467383] Ann Intern Med. 1989 Feb 1;110(3):189-94 [2536257] Science. 1990 Jan 26;247(4941):454-6 [2405486] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutagenic activation of benzidine requires prior bacterial acetylation and subsequent conversion by prostaglandin H synthase to 4-nitro-4'-(acetylamino)biphenyl. AN - 73137595; 1504268 AB - We have used the Ames test in combination with prostaglandin H synthase (PHS) to study the bioactivation of benzidine as well as other aromatic amines. Previous investigations established that the formation of benzidine mutagens by PHS is dramatically enhanced in Salmonella typhimurium strains with high levels of acetyl CoA-dependent arylamine N-acetyltransferase/arylhydroxylamine O-acetyltransferase activity despite the fact that acetylation of aromatic amines decreases their susceptibility to oxidation by peroxidases. In this study, we used a new strain (YG1012) that has very high acetylation capability to investigate the metabolism and mutagenicity of benzidine and N-acetylbenzidine catalyzed by PHS (from ram seminal vesicle microsomes) and horseradish peroxidase (HRP). YG1012 bacteria rapidly acetylated benzidine to N-acetylbenzidine and N,N'-diacetylbenzidine. Preincubation of the bacteria with benzidine before addition of PHS increased the mutagenicity. Under conditions identical to those used to assess mutagenicity, PHS metabolized benzidine rapidly, but the substrate was not totally consumed, with about 40% of the original concentration remaining intact. These data suggest that conversion to N-acetylbenzidine may be the initial step in the bioactivation of benzidine in the PHS-mediated Ames assay. N-Acetylbenzidine is a cosubstrate for PHS peroxidase activity as measured by 5-phenyl-4-pentenyl hydroperoxide reduction, spectral changes, and formation of protein adducts. N-Acetylbenzidine was converted to mutagens by PHS but not HRP, with enhanced mutagenicity observed in bacteria with high acetylation activity. We used reverse- phase HPLC to characterize the metabolites of N-acetylbenzidine formed by PHS and HRP.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Chemical research in toxicology AU - Smith, B J AU - DeBruin, L AU - Josephy, P D AU - Eling, T E AD - Eicosanoid Biochemistry Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. PY - 1992 SP - 431 EP - 439 VL - 5 IS - 3 SN - 0893-228X, 0893-228X KW - Acetamides KW - 0 KW - Benzidines KW - Biphenyl Compounds KW - Mutagens KW - 4-nitro-4'-(acetylamino)biphenyl KW - 28533-02-0 KW - benzidine KW - 2X02101HVF KW - Horseradish Peroxidase KW - EC 1.11.1.- KW - Peroxidases KW - Prostaglandin-Endoperoxide Synthases KW - EC 1.14.99.1 KW - Index Medicus KW - Animals KW - Acetylation KW - Mutagenicity Tests KW - Biotransformation KW - Sheep KW - In Vitro Techniques KW - Salmonella typhimurium -- drug effects KW - Salmonella typhimurium -- genetics KW - Female KW - Chromatography, High Pressure Liquid KW - Peroxidases -- metabolism KW - Benzidines -- metabolism KW - Bacteria -- metabolism KW - Prostaglandin-Endoperoxide Synthases -- metabolism KW - Mutagens -- metabolism KW - Acetamides -- metabolism KW - Benzidines -- toxicity KW - Biphenyl Compounds -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73137595?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=Mutagenic+activation+of+benzidine+requires+prior+bacterial+acetylation+and+subsequent+conversion+by+prostaglandin+H+synthase+to+4-nitro-4%27-%28acetylamino%29biphenyl.&rft.au=Smith%2C+B+J%3BDeBruin%2C+L%3BJosephy%2C+P+D%3BEling%2C+T+E&rft.aulast=Smith&rft.aufirst=B&rft.date=1992-05-01&rft.volume=5&rft.issue=3&rft.spage=431&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-21 N1 - Date created - 1992-09-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The oxidation of 4-aminobiphenyl by horseradish peroxidase. AN - 73128446; 1504256 AB - The oxidation of the carcinogen 4-aminobiphenyl (4-ABP) catalyzed by the model peroxidase enzyme horseradish peroxidase (HRP) was investigated. 4-ABP served as a reducing cosubstrate for HRP during the enzyme-catalyzed reduction of the synthetic hydroperoxide, 5-phenyl-4-penten-1-yl hydroperoxide, to its corresponding alcohol. Spectral analysis during the incubation of HRP, 4-ABP, and H2O2 showed an increase in absorbance at 230 and 325 nm and decrease at 270 nm, suggesting metabolite formation. Oxygen consumption was not detected in incubations of HRP, 4-ABP, and H2O2. However, oxygen uptake was observed after the addition of glutathione, which indicated that a free radical metabolite of 4-ABP was formed by the peroxidase. The 4-ABP free radical reacted with glutathione forming a glutathionyl radical which, in turn, reacted with and consumed oxygen. HPLC analysis of organic extracts of incubations with HRP, [3H]-4-ABP, and H2O2 showed the formation of one major peak identified by mass spectroscopy as 4,4'-azobis(biphenyl). The addition of glutathione to the incubations decreased the formation of 4-ABP metabolites, suggesting a reduction of the 4-ABP free radical and/or the formation of glutathione conjugates. Subsequent HPLC analysis of incubations including [35S]glutathione indicated formation of several unidentified 4-ABP-glutathione conjugates as well as recovery of parent compound. These studies suggest that HRP metabolizes 4-ABP by a one-electron oxidation mechanism, resulting in formation of a free radical. This radical can either react with a second radical to form azobis(biphenyl), be reduced by glutathione back to parent, or react with glutathione to form glutathione conjugates. JF - Chemical research in toxicology AU - Hughes, M F AU - Smith, B J AU - Eling, T E AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. PY - 1992 SP - 340 EP - 345 VL - 5 IS - 3 SN - 0893-228X, 0893-228X KW - Aminobiphenyl Compounds KW - 0 KW - Free Radicals KW - 4-biphenylamine KW - 16054949HJ KW - Horseradish Peroxidase KW - EC 1.11.1.- KW - Glutathione KW - GAN16C9B8O KW - Index Medicus KW - Oxidation-Reduction KW - Oxygen Consumption KW - Spectrophotometry, Ultraviolet KW - Glutathione -- chemistry KW - Aminobiphenyl Compounds -- chemistry KW - Horseradish Peroxidase -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73128446?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=The+oxidation+of+4-aminobiphenyl+by+horseradish+peroxidase.&rft.au=Hughes%2C+M+F%3BSmith%2C+B+J%3BEling%2C+T+E&rft.aulast=Hughes&rft.aufirst=M&rft.date=1992-05-01&rft.volume=5&rft.issue=3&rft.spage=340&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-21 N1 - Date created - 1992-09-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Biological asymmetries and the fidelity of eukaryotic DNA replication. AN - 73091701; 1637361 AB - A diploid human genome contains approximately six billion nucleotides. This enormous amount of genetic information can be replicated with great accuracy in only a few hours. However, because DNA strands are oriented antiparallel while DNA polymerization only occurs in the 5'----3' direction, semi-conservative replication of double-stranded DNA is an asymmetric process, i.e., there is a leading and a lagging strand. This provides a considerable opportunity for non-random error rates, because the architecture of the two strands as well as the DNA polymerases that replicate them may be different. In addition, the proteins that start or finish chains may well be different from those that perform the bulk of chain elongation. Furthermore, while replication fidelity depends on the absolute and relative concentrations of the four deoxyribonucleotide precursors, these are not equal in vivo, not constant throughout the cell cycle, and not necessarily equivalent in all cell types. Finally, the fidelity of DNA synthesis is sequence-dependent and the eukaryotic nuclear genome is a heterogeneous substrate. It contains repetitive and non-repetitive sequences and can actually be considered as two subgenomes that differ in nucleotide composition and gene content and that replicate at different times. The effects that each of these asymmetries may have on error rates during replication of the eukaryotic genome are discussed. JF - BioEssays : news and reviews in molecular, cellular and developmental biology AU - Kunkel, T A AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 303 EP - 308 VL - 14 IS - 5 SN - 0265-9247, 0265-9247 KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - Index Medicus KW - Mutagenesis KW - Eukaryotic Cells KW - DNA Replication UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73091701?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BioEssays+%3A+news+and+reviews+in+molecular%2C+cellular+and+developmental+biology&rft.atitle=Biological+asymmetries+and+the+fidelity+of+eukaryotic+DNA+replication.&rft.au=Kunkel%2C+T+A&rft.aulast=Kunkel&rft.aufirst=T&rft.date=1992-05-01&rft.volume=14&rft.issue=5&rft.spage=303&rft.isbn=&rft.btitle=&rft.title=BioEssays+%3A+news+and+reviews+in+molecular%2C+cellular+and+developmental+biology&rft.issn=02659247&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-24 N1 - Date created - 1992-08-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pharmacogenetic assessment of the effects of carbamazepine on cocaine-kindled and cocaine-induced seizures. AN - 73055663; 1623406 AB - The effects of chronic carbamazepine (CBZ) on the development and expression of cocaine-kindled seizures and seizures produced by an acute injection of cocaine were evaluated in BALB/cByJ, C57Bl/6J and SJL/J mice. The repeated administration of a subconvulsant dose of cocaine initially resulted in the development of an increased sensitivity to the convulsant effects of cocaine in the three strains. Chronic, dietary carbamazepine attenuated this initial sensitization to cocaine-induced seizures. While the continued administration of cocaine resulted in a relatively permanent sensitization to cocaine-induced seizures among SJL mice, tolerance to cocaine-induced seizures ultimately developed among C57 mice and to a lesser degree among BALB mice. Genetic factors were found to mediate the effects of chronic CBZ on the development of sensitization and/or tolerance to the convulsant effects of cocaine. Among BALB mice, chronic CBZ appears to have eliminated the development of tolerance to cocaine-induced seizures and allowed an underlying sensitization to be manifest. Among SJL mice, however, the sensitization observed following repeated cocaine injections was reduced, but not eliminated. Genetic factors were also found to be associated with the effects of CBZ on seizures induced by the acute administration of cocaine. BALB and C57 mice, but not SJL mice, chronically treated with dietary CBZ were less susceptible to a consulvant dose of cocaine than their corresponding dietary controls for at least 72 h after stopping CBZ administration. In addition, there were genotype-specific lethal effects associated with the concurrent administration of CBZ and cocaine. JF - Brain research AU - Marley, R J AU - Goldberg, S R AD - National Institute on Drug Abuse, Addiction Research Center, Baltimore, MD 21224. Y1 - 1992/05/01/ PY - 1992 DA - 1992 May 01 SP - 43 EP - 49 VL - 579 IS - 1 SN - 0006-8993, 0006-8993 KW - Anticonvulsants KW - 0 KW - Carbamazepine KW - 33CM23913M KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Genotype KW - Mice, Inbred Strains KW - Animals KW - Mice, Inbred C57BL KW - Mice KW - Mice, Inbred BALB C KW - Male KW - Seizures -- chemically induced KW - Anticonvulsants -- pharmacology KW - Kindling, Neurologic -- drug effects KW - Seizures -- genetics KW - Carbamazepine -- pharmacology KW - Seizures -- drug therapy KW - Cocaine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73055663?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Pharmacogenetic+assessment+of+the+effects+of+carbamazepine+on+cocaine-kindled+and+cocaine-induced+seizures.&rft.au=Marley%2C+R+J%3BGoldberg%2C+S+R&rft.aulast=Marley&rft.aufirst=R&rft.date=1992-05-01&rft.volume=579&rft.issue=1&rft.spage=43&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-10 N1 - Date created - 1992-08-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dioxin induces expression of c-fos and c-jun proto-oncogenes and a large increase in transcription factor AP-1. AN - 73016531; 1605850 AB - Among environmental pollutants, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; dioxin) is one of the most potent tumor promoters and teratogens known. The molecular mechanisms responsible for the biological activity of TCDD, however, remain largely unknown. In this report, we show that the first observable effects of TCDD in cultured murine hepatoma cells are a rapid, transient increase in Ca2+ influx and a minor but significant elevation of activated, membrane-bound protein kinase C. These changes are then followed by induction of the immediate early proto-oncogenes c-fos, jun-B, c-jun, and jun-D, and by large increases in AP-1 transcription factor activity. Induction of these changes by TCDD is delayed compared with that by phorbol esters, although the magnitude of the effects caused by both treatments is similar, and both induction processes can be blocked by staurosporine, a protein kinase C inhibitor. In cultured cells, proto-oncogene induction by TCDD appears to be independent of the presence of a functional aryl hydrocarbon (Ah) receptor or nuclear translocation protein. These results reveal early events that may lead to the elucidation of the molecular basis of TCDD-induced tumor promotion. JF - DNA and cell biology AU - Puga, A AU - Nebert, D W AU - Carrier, F AD - Laboratory of Developmental Pharmacology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 269 EP - 281 VL - 11 IS - 4 SN - 1044-5498, 1044-5498 KW - Cyp1a-1 KW - c-fos KW - c-jun KW - jun-B KW - jun-D KW - Alkaloids KW - 0 KW - DNA Probes KW - Polychlorinated Dibenzodioxins KW - Proto-Oncogene Proteins c-jun KW - Protein Kinase C KW - EC 2.7.11.13 KW - Staurosporine KW - H88EPA0A3N KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Protein Kinase C -- metabolism KW - Calcium -- metabolism KW - Animals KW - DNA Probes -- genetics KW - Base Sequence KW - Tumor Cells, Cultured KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Alkaloids -- pharmacology KW - Mice KW - Polychlorinated Dibenzodioxins -- pharmacology KW - Proto-Oncogene Proteins c-jun -- metabolism KW - Genes, fos -- genetics KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Genes, jun -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73016531?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=DNA+and+cell+biology&rft.atitle=Dioxin+induces+expression+of+c-fos+and+c-jun+proto-oncogenes+and+a+large+increase+in+transcription+factor+AP-1.&rft.au=Puga%2C+A%3BNebert%2C+D+W%3BCarrier%2C+F&rft.aulast=Puga&rft.aufirst=A&rft.date=1992-05-01&rft.volume=11&rft.issue=4&rft.spage=269&rft.isbn=&rft.btitle=&rft.title=DNA+and+cell+biology&rft.issn=10445498&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-20 N1 - Date created - 1992-07-20 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Cyp1a-1; c-fos; c-jun; jun-B; jun-D N1 - Genetic sequence - J00370; GENBANK; V00727; X57154; X57155; X57156; M12345 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Diazepam- and chlordiazepoxide-mediated increases in erythrocyte aldehyde dehydrogenase activity and its possible implications. AN - 73007937; 1605886 AB - Erythrocyte ALDH activity was assayed in alcoholic (n = 70) and nonalcoholic (n = 40) subjects. In general, alcoholics without any prior medications (n = 57) were found to have a decreased ALDH activity (mean +/- SD: 3.38 +/- 1.7 mU; p less than 0.001) as compared to control group (5.10 +/- 1.57 mU). However, a group of alcoholics who were detoxified with benzodiazepines (n = 13) prior to blood collection for enzyme assay were found to have higher ALDH activity (4.92 +/- 2.46 mU; p less than 0.05) as compared to alcoholics who were not detoxified. In vitro experiments demonstrated that both diazepam (DZM) and chlordiazepoxide (CDP) could activate the ALDH. The magnitude of enzyme activation by DZM and CDP appear to correlate with their relative potency of tranquilizing effect. Further, the observed ability of DZM to reverse the inhibition of ALDH mediated by disulfiram may explain the biochemical basis of the reported ability of benzodiazepines (BDZ) to reduce the intensity of disulfiram ethanol reaction (DER). JF - Alcohol (Fayetteville, N.Y.) AU - Murthy, P AU - Guru, S C AU - Shetty, K T AU - Ray, R AU - Channabasavanna, S M AD - Department of Neurochemistry, National Institute of Mental Health and Neuro Sciences, Bangalore, India. PY - 1992 SP - 199 EP - 202 VL - 9 IS - 3 SN - 0741-8329, 0741-8329 KW - Benzodiazepines KW - 12794-10-4 KW - Chlordiazepoxide KW - 6RZ6XEZ3CR KW - Aldehyde Dehydrogenase KW - EC 1.2.1.3 KW - Diazepam KW - Q3JTX2Q7TU KW - Index Medicus KW - Osmolar Concentration KW - Benzodiazepines -- therapeutic use KW - Reference Values KW - Dose-Response Relationship, Drug KW - Humans KW - Adult KW - Middle Aged KW - Alcoholism -- drug therapy KW - Alcoholism -- blood KW - Aldehyde Dehydrogenase -- blood KW - Erythrocytes -- enzymology KW - Chlordiazepoxide -- pharmacology KW - Diazepam -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73007937?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcohol+%28Fayetteville%2C+N.Y.%29&rft.atitle=Diazepam-+and+chlordiazepoxide-mediated+increases+in+erythrocyte+aldehyde+dehydrogenase+activity+and+its+possible+implications.&rft.au=Murthy%2C+P%3BGuru%2C+S+C%3BShetty%2C+K+T%3BRay%2C+R%3BChannabasavanna%2C+S+M&rft.aulast=Murthy&rft.aufirst=P&rft.date=1992-05-01&rft.volume=9&rft.issue=3&rft.spage=199&rft.isbn=&rft.btitle=&rft.title=Alcohol+%28Fayetteville%2C+N.Y.%29&rft.issn=07418329&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-23 N1 - Date created - 1992-07-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prophylaxis for Pneumocystis carinii pneumonia in patients infected with human immunodeficiency virus. AN - 73001631; 1350925 AB - Following the initial observation by Dr. Margaret Fischl that trimethoprim-sulfamethoxazole can prevent Pneumocystis carinii infection in patients with Kaposi's sarcoma, initiating prophylaxis for pneumocystic infection in all patients with less than 200 CD4+ cells/mm3 has become accepted practice. This prophylactic intervention has been found not only to reduce the development of pneumonia due to P. carinii but also to prolong life. Drs. Henry Masur and Joseph A. Kovacs first reviewed prophylaxis for P. carinii pneumonia in patients infected with the human immunodeficiency virus for the AIDS Commentary 3 years ago. They have updated that initial review for this AIDS Commentary, placing currently available information into concise clinical perspective and detailing a rational plan for the clinician to follow based on results of recent studies. JF - Clinical infectious diseases : an official publication of the Infectious Diseases Society of America AU - Kovacs, J A AU - Masur, H AD - Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 1005 EP - 1009 VL - 14 IS - 5 SN - 1058-4838, 1058-4838 KW - Aerosols KW - 0 KW - Zidovudine KW - 4B9XT59T7S KW - Pentamidine KW - 673LC5J4LQ KW - Trimethoprim, Sulfamethoxazole Drug Combination KW - 8064-90-2 KW - Index Medicus KW - AIDS/HIV KW - Zidovudine -- therapeutic use KW - Risk Factors KW - Humans KW - Administration, Inhalation KW - Leukocyte Count KW - CD4-Positive T-Lymphocytes KW - Pneumonia, Pneumocystis -- prevention & control KW - Pentamidine -- administration & dosage KW - HIV Infections -- complications KW - Opportunistic Infections -- prevention & control KW - Trimethoprim, Sulfamethoxazole Drug Combination -- therapeutic use KW - Pentamidine -- adverse effects KW - Trimethoprim, Sulfamethoxazole Drug Combination -- adverse effects KW - Pentamidine -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73001631?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+infectious+diseases+%3A+an+official+publication+of+the+Infectious+Diseases+Society+of+America&rft.atitle=Prophylaxis+for+Pneumocystis+carinii+pneumonia+in+patients+infected+with+human+immunodeficiency+virus.&rft.au=Kovacs%2C+J+A%3BMasur%2C+H&rft.aulast=Kovacs&rft.aufirst=J&rft.date=1992-05-01&rft.volume=14&rft.issue=5&rft.spage=1005&rft.isbn=&rft.btitle=&rft.title=Clinical+infectious+diseases+%3A+an+official+publication+of+the+Infectious+Diseases+Society+of+America&rft.issn=10584838&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-10 N1 - Date created - 1992-07-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of tumor necrosis factor in oxygen toxicity. AN - 72983241; 1601798 AB - mRNA from lungs of mice exposed to high-dose oxygen (greater than 95%) for 3 days demonstrated increased expression of the genes for tumor necrosis factor (TNF), interleukin-1, and interleukin-6 compared with mRNA from lungs of mice exposed to room air. Daily treatment of mice exposed to high-dose oxygen with an antibody to TNF improved survival compared with mice receiving a similar dose of control immunoglobulin G. Pretreatment of mice with repetitive sublethal intraperitoneal doses of recombinant human TNF for 3 days or a single intravenous dose followed by exposure to high-dose oxygen afforded a significant survival advantage compared with high-dose oxygen-exposed mice pretreated with vehicle or interleukin-1. The repetitive intraperitoneal TNF pretreatment reduced the development of interstitial pneumonitis, pulmonary edema, and lung weight gain associated with oxygen toxicity and enhanced expression of the gene for the free radical protective enzyme manganous superoxide dismutase in lung tissue, a gene that is augmented as mice are exposed to high-dose oxygen. Furthermore a single intravenous dose of TNF 24 h after oxygen exposure was still protective. The results suggest that the toxicity of oxygen therapy can be partially ameliorated by either treatment with anti-TNF antibody or pretreatment and early treatment with TNF. These findings are consistent with the hypothesis that oxygen exposure induces TNF, which causes part of the toxicity of high-dose oxygen, and that pretreatment or early treatment with TNF induces the gene for an enzyme that recently has been shown to be very effective in protecting mice from the toxicity of oxygen. JF - Journal of applied physiology (Bethesda, Md. : 1985) AU - Jensen, J C AU - Pogrebniak, H W AU - Pass, H I AU - Buresh, C AU - Merino, M J AU - Kauffman, D AU - Venzon, D AU - Langstein, H N AU - Norton, J A AD - Surgical Metabolism and Thoracic Oncology Sections, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 1902 EP - 1907 VL - 72 IS - 5 SN - 8750-7587, 8750-7587 KW - Interleukin-1 KW - 0 KW - Interleukin-6 KW - RNA, Messenger KW - Tumor Necrosis Factor-alpha KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Oxygen KW - S88TT14065 KW - Index Medicus KW - Animals KW - RNA, Messenger -- metabolism KW - Interleukin-6 -- genetics KW - Mice, Inbred C57BL KW - Lung -- drug effects KW - Gene Expression KW - Superoxide Dismutase -- genetics KW - Mice KW - Interleukin-1 -- genetics KW - RNA, Messenger -- genetics KW - Lung -- physiopathology KW - Female KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Lung Injury KW - Tumor Necrosis Factor-alpha -- physiology KW - Tumor Necrosis Factor-alpha -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72983241?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+applied+physiology+%28Bethesda%2C+Md.+%3A+1985%29&rft.atitle=Role+of+tumor+necrosis+factor+in+oxygen+toxicity.&rft.au=Jensen%2C+J+C%3BPogrebniak%2C+H+W%3BPass%2C+H+I%3BBuresh%2C+C%3BMerino%2C+M+J%3BKauffman%2C+D%3BVenzon%2C+D%3BLangstein%2C+H+N%3BNorton%2C+J+A&rft.aulast=Jensen&rft.aufirst=J&rft.date=1992-05-01&rft.volume=72&rft.issue=5&rft.spage=1902&rft.isbn=&rft.btitle=&rft.title=Journal+of+applied+physiology+%28Bethesda%2C+Md.+%3A+1985%29&rft.issn=87507587&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-13 N1 - Date created - 1992-07-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of murine cell lines from diethylstilbestrol-induced uterine endometrial adenocarcinomas. AN - 72977252; 1597405 AB - Neonatal treatment with estrogens is associated with development of uterine adenocarcinomas in CD-1 mice. Treatment with the synthetic estrogen diethylstilbestrol (DES) on Days 1 to 5 after birth results in 90% incidence of these hormone-dependent lesions in 18-mo.-old mice. Three cell lines were established from these DES-associated tumors. Each of these cell lines exhibited morphologic and ultrastructural characteristics of transformed epithelial cells, including an increased nuclear:cytoplasmic ratio, enlarged and irregular nuclei with multiple nucleoli and areas of chromatin condensation, positive staining for cytokeratin, desmosomes, and microvilli. After subcutaneous injection into nude mice, all three cell lines formed solid tumors within 4 wk. Although the primary uterine tumors and tumor transplants in nude mice had been shown to be estrogen-dependent and estrogen-receptor positive, neither the monolayer growth nor the tumorigenicity of any of the three cell lines in this study was enhanced by or dependent on estrogen. Estrogen receptor levels were low in early and intermediate passage cells. Allele-specific oligonucleotide hybridization analysis of PCR-amplified cell line DNA revealed no point mutations in the 12th, 13th, or 61st codons of the K-ras or H-ras protooncogenes. Southern analysis revealed no changes in genomic organization of the putative tumor suppressor gene DCC, but demonstrated a three- to four-fold amplification of the c-myc gene in one cell line. Expression of c-myc RNA was concomitantly increased in the same cell line. These three transformed cell lines represent the end point in the process of hormone-associated tumorigenesis and as such should prove useful in investigating the molecular changes and the mechanisms involved in hormonal carcinogenesis. JF - In vitro cellular & developmental biology : journal of the Tissue Culture Association AU - Hébert, C D AU - Endo, S AU - Korach, K S AU - Boyd, J AU - Barrett, J C AU - McLachlan, J A AU - Newbold, R R AD - Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 327 EP - 336 VL - 28A IS - 5 SN - 0883-8364, 0883-8364 KW - DCC KW - H-ras KW - K-ras KW - c-myc KW - Chromatin KW - 0 KW - DNA, Neoplasm KW - Receptors, Estrogen KW - Diethylstilbestrol KW - 731DCA35BT KW - Index Medicus KW - Animals KW - Cell Nucleus -- pathology KW - Genes, Tumor Suppressor KW - Genes, myc KW - Mice, Nude KW - DNA, Neoplasm -- analysis KW - Mice KW - Receptors, Estrogen -- metabolism KW - Cytoplasm -- pathology KW - Neoplasm Transplantation KW - Genes, ras KW - Tumor Cells, Cultured KW - Blotting, Southern KW - Chromatin -- pathology KW - Cell Nucleolus -- pathology KW - Microscopy, Electron KW - Mutation KW - Female KW - Uterine Neoplasms -- genetics KW - Adenocarcinoma -- chemically induced KW - Uterine Neoplasms -- chemically induced KW - Adenocarcinoma -- genetics KW - Uterine Neoplasms -- pathology KW - Adenocarcinoma -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72977252?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=In+vitro+cellular+%26+developmental+biology+%3A+journal+of+the+Tissue+Culture+Association&rft.atitle=Characterization+of+murine+cell+lines+from+diethylstilbestrol-induced+uterine+endometrial+adenocarcinomas.&rft.au=H%C3%A9bert%2C+C+D%3BEndo%2C+S%3BKorach%2C+K+S%3BBoyd%2C+J%3BBarrett%2C+J+C%3BMcLachlan%2C+J+A%3BNewbold%2C+R+R&rft.aulast=H%C3%A9bert&rft.aufirst=C&rft.date=1992-05-01&rft.volume=28A&rft.issue=5&rft.spage=327&rft.isbn=&rft.btitle=&rft.title=In+vitro+cellular+%26+developmental+biology+%3A+journal+of+the+Tissue+Culture+Association&rft.issn=08838364&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-09 N1 - Date created - 1992-07-09 N1 - Date revised - 2017-01-13 N1 - Gene symbol - DCC; H-ras; K-ras; c-myc N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selection of controls in case-control studies. I. Principles. AN - 72974299; 1595688 AB - A synthesis of classical and recent thinking on the issues involved in selecting controls for case-control studies is presented in this and two companion papers (S. Wacholder et al. Am J Epidemiol 1992;135:1029-50). In this paper, a theoretical framework for selecting controls in case-control studies is developed. Three principles of comparability are described: 1) study base, that all comparisons be made within the study base; 2) deconfounding, that comparisons of the effects of the levels of exposure on disease risk not be distorted by the effects of other factors; and 3) comparable accuracy, that any errors in measurement of exposure be nondifferential between cases and controls. These principles, if adhered to in a study, can reduce selection, confounding, and information bias, respectively. The principles, however, are constrained by an additional efficiency principle regarding resources and time. Most problems and controversies in control selection reflect trade-offs among these four principles. JF - American journal of epidemiology AU - Wacholder, S AU - McLaughlin, J K AU - Silverman, D T AU - Mandel, J S AD - Biostatistics Branch, National Cancer Institute, Bethesda, MD. Y1 - 1992/05/01/ PY - 1992 DA - 1992 May 01 SP - 1019 EP - 1028 VL - 135 IS - 9 SN - 0002-9262, 0002-9262 KW - Index Medicus KW - Efficiency KW - Reproducibility of Results KW - Random Allocation KW - Humans KW - Confounding Factors (Epidemiology) KW - Sampling Studies KW - Environmental Exposure KW - Effect Modifier, Epidemiologic KW - Case-Control Studies KW - Research Design -- standards KW - Selection Bias UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72974299?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+epidemiology&rft.atitle=Selection+of+controls+in+case-control+studies.+I.+Principles.&rft.au=Wacholder%2C+S%3BMcLaughlin%2C+J+K%3BSilverman%2C+D+T%3BMandel%2C+J+S&rft.aulast=Wacholder&rft.aufirst=S&rft.date=1992-05-01&rft.volume=135&rft.issue=9&rft.spage=1019&rft.isbn=&rft.btitle=&rft.title=American+journal+of+epidemiology&rft.issn=00029262&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-02 N1 - Date created - 1992-07-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mortality among laboratory workers employed at the U.S. Department of Agriculture. AN - 72969096; 1591326 AB - We evaluated the mortality of 835 white male and 36 female laboratory workers employed by the U.S. Department of Agriculture who died between January 1, 1970, and December 31, 1979. For males, the mortality odds ratio for all cancers was 1.0 (95% confidence interval = 0.8-1.2). Colon cancer, lymphosarcoma and reticulosarcoma, nonmalignant diseases of the blood and blood-forming organs, and suicide showed elevated mortality odds ratios. Only colon cancer showed an association with duration of employment as a laboratory worker. In an accompanying case-control study, the risk of colon cancer rose to 3.2 among those who had 20 or more years of employment as a laboratory worker. Among females, breast cancer was elevated (mortality odds ratio = 5.3; 95% confidence interval = 2.8-10.1). JF - Epidemiology (Cambridge, Mass.) AU - Dosemeci, M AU - Alavanja, M AU - Vetter, R AU - Eaton, B AU - Blair, A AD - Epidemiology and Biostatistics Program, National Cancer Institute, Rockville, MD 20892. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 258 EP - 262 VL - 3 IS - 3 SN - 1044-3983, 1044-3983 KW - Index Medicus KW - Odds Ratio KW - Random Allocation KW - Risk Factors KW - Humans KW - United States Department of Agriculture KW - United States -- epidemiology KW - Male KW - Female KW - Medical Laboratory Personnel KW - Occupational Diseases -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72969096?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epidemiology+%28Cambridge%2C+Mass.%29&rft.atitle=Mortality+among+laboratory+workers+employed+at+the+U.S.+Department+of+Agriculture.&rft.au=Dosemeci%2C+M%3BAlavanja%2C+M%3BVetter%2C+R%3BEaton%2C+B%3BBlair%2C+A&rft.aulast=Dosemeci&rft.aufirst=M&rft.date=1992-05-01&rft.volume=3&rft.issue=3&rft.spage=258&rft.isbn=&rft.btitle=&rft.title=Epidemiology+%28Cambridge%2C+Mass.%29&rft.issn=10443983&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-02 N1 - Date created - 1992-07-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Persistent effects of a single dose of Aroclor 1254 on cytochromes P450IA1 and IIB1 in mouse lung. AN - 72965475; 1585368 AB - The polychlorinated biphenyl mixture Aroclor 1254 has been shown to elicit prolonged biochemical responses in several rodent species, particularly induction of mixed function oxygenases in hepatic tissue. Lung is also of interest since a single dose of Aroclor 1254 has been demonstrated to have a tumor promoting effect, increasing the numbers of lung tumors in Swiss mice initiated with N-nitrosodimethylamine. To investigate the enzyme induction response in lung, male Swiss mice were given a single 100 or 500 mg/kg dose of Aroclor 1254 and euthanized at time intervals ranging from 48 hr to 30 weeks. Both cytochromes P450IA1 and IIB1 were followed by use of specific enzyme activities and Western immunoblotting. The IA1 isoform, as quantified by ethoxyresorufin-O-deethylase activity and immunoblotting with monoclonal antibody 1-7-1, was significantly elevated for 30 weeks after both doses. In contrast, benzyloxy-resorufin-O-dealkylase activity (P450IIB1 specific), which is constitutively expressed in rodent lung, was unaffected by Aroclor treatment at the lower dose at early time points, but induced twofold at 30 weeks. At the higher dose, however, enzymatic activity was decreased to 50% of control values, an effect which persisted for 4 weeks postexposure. These changes were confirmed by Western immunoblotting utilizing monoclonal antibody 2-66-3. Concomitantly, content of individual PCB congeners in lungs and carcass was quantified by gas chromatography with electron capture detection. One congener, 2,3,3',4,4'-pentachlorobiphenyl, was selectively retained in lung compared to carcass. Lack of correlation between changes in lung content of PCBs and levels of the P450 isoforms suggested interactions between congeners in control of P450 induction and repression. These data confirm a prolonged P450 induction response in nonhepatic tissue following Aroclor exposure, and further suggest a bidirectional role for certain PCB congeners in the regulation of P450IA1 and P450IIB1 expression in lung tissue. JF - Toxicology and applied pharmacology AU - Beebe, L AU - Fox, S D AU - Riggs, C W AU - Park, S S AU - Gelboin, H V AU - Issaq, H J AU - Anderson, L M AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, Maryland 21702. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 16 EP - 24 VL - 114 IS - 1 SN - 0041-008X, 0041-008X KW - Aroclors KW - 0 KW - Chlorodiphenyl (54% Chlorine) KW - 11097-69-1 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Oxidoreductases KW - EC 1.- KW - Cytochrome P-450 CYP2B1 KW - EC 1.14.14.1 KW - Index Medicus KW - Animals KW - Enzyme Induction -- drug effects KW - Mice KW - Male KW - Organ Size -- drug effects KW - Aroclors -- pharmacology KW - Lung -- drug effects KW - Aroclors -- pharmacokinetics KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Lung -- enzymology KW - Oxidoreductases -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72965475?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Persistent+effects+of+a+single+dose+of+Aroclor+1254+on+cytochromes+P450IA1+and+IIB1+in+mouse+lung.&rft.au=Beebe%2C+L%3BFox%2C+S+D%3BRiggs%2C+C+W%3BPark%2C+S+S%3BGelboin%2C+H+V%3BIssaq%2C+H+J%3BAnderson%2C+L+M&rft.aulast=Beebe&rft.aufirst=L&rft.date=1992-05-01&rft.volume=114&rft.issue=1&rft.spage=16&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=0041008X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-18 N1 - Date created - 1992-06-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Application of the EPR spin-trapping technique to the detection of radicals produced in vivo during inhalation exposure of rats to ozone. AN - 72964398; 1316646 AB - Ozone is known to induce lipid peroxidation of lung tissue, although no direct evidence of free radical formation has been reported. We have used the electron paramagnetic resonance (EPR) spin-trapping technique to search for free radicals produced in vivo by ozone exposure. The spin trap alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone (4-POBN) was administered ip to male Sprague-Dawley rats. The rats were then exposed for 2 hr to either 0, 0.5, 1.0, 1.5, or 2.0 ppm ozone with 8% CO2 to increase their respiratory rate. A six-line 4-POBN/radical spin adduct signal (aN = 15.02 G and a beta H = 3.27 G) was detected by EPR spectroscopy in lipid extracts from lungs of rats treated with 4-POBN and then exposed to ozone. Only a weak signal was observed in the corresponding solution from rats exposed to 0 ppm ozone (air with CO2 only). The concentration of the radical adduct increased as a function of ozone concentration. After administration of 4-POBN, rats were exposed for either 0.5, 1.0, 2.0, or 4.0 hr to either 0 or 2.0 ppm ozone (with CO2). The radical adduct concentration of the ozone-exposed groups at exposure times of 2.0 and 4.0 hr was significantly different from that of the corresponding air control groups. A correlation was observed between the radical adduct concentration and the lung weight/body weight ratio. These results demonstrate that ozone induces the production of free radicals in rat lungs during inhalation exposure and that radical production may be involved in the induction of pulmonary toxicity by ozone. This is the first direct evidence for ozone-induced free radical production in vivo. JF - Toxicology and applied pharmacology AU - Kennedy, C H AU - Hatch, G E AU - Slade, R AU - Mason, R P AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 41 EP - 46 VL - 114 IS - 1 SN - 0041-008X, 0041-008X KW - Free Radicals KW - 0 KW - Nitrogen Oxides KW - Pyridines KW - Spin Labels KW - Tissue Extracts KW - alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone KW - Ozone KW - 66H7ZZK23N KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Free Radicals -- analysis KW - Animals KW - Electron Spin Resonance Spectroscopy KW - Body Weight -- drug effects KW - Tissue Extracts -- analysis KW - Administration, Inhalation KW - Male KW - Organ Size -- drug effects KW - Ozone -- pharmacology KW - Lung -- drug effects KW - Lung -- metabolism KW - Ozone -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72964398?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Application+of+the+EPR+spin-trapping+technique+to+the+detection+of+radicals+produced+in+vivo+during+inhalation+exposure+of+rats+to+ozone.&rft.au=Kennedy%2C+C+H%3BHatch%2C+G+E%3BSlade%2C+R%3BMason%2C+R+P&rft.aulast=Kennedy&rft.aufirst=C&rft.date=1992-05-01&rft.volume=114&rft.issue=1&rft.spage=41&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=0041008X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-18 N1 - Date created - 1992-06-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Results of the National Institute of Allergy and Infectious Diseases Collaborative Clinical Trial to test the predictive value of skin testing with major and minor penicillin derivatives in hospitalized adults. AN - 72951644; 1580706 AB - A history (or lack thereof) of penicillin allergy is known to be unreliable in predicting reactions on subsequent administration of the drug. This study tests the usefulness of four penicillin allergen skin tests in the prediction of IgE-mediated reactions subsequent to administration of penicillin. Eight centers cooperated in the National Institute of Allergy and Infectious Diseases trial of the predictive value of skin testing with major and minor penicillin derivatives. Hospitalized adults were tested with a major determinant (octa-benzylpenicilloyl-ocytalysine) and a minor determinant mixture and its components (potassium benzylpenicillin, benzylpenicilloate, and benzylpenicilloyl-N-propylamine). Patients then received a therapeutic course of penicillin and were observed, for 48 hours, for adverse reactions compatible with an IgE-mediated immediate or accelerated allergy. Among 726 history-positive patients, 566 with negative skin tests received penicillin and only seven (1.2%) had possibly IgE-mediated reactions. Among 600 history-negative patients, 568 with negative skin tests received penicillin and none had a reaction. Only nine of the 167 positive skin test reactors received a penicillin agent and then usually by cautious incremental dosing. Two (22%) of these nine patients had reactions compatible with IgE-mediated immediate or accelerated penicillin allergy; both were positive to the two determinants. These data corroborate previous data about the negative predictive value of negative skin tests to these materials. The reaction rate in skin test-positive patients was significantly higher than in those with negative skin tests, demonstrating the positive predictive value of positive tests to both major and minor determinants. The number of patients positive only to the major determinant or only to the minor determinant mix was too small to draw conclusions about the positive predictive value of either reagent alone. JF - Archives of internal medicine AU - Sogn, D D AU - Evans, R AU - Shepherd, G M AU - Casale, T B AU - Condemi, J AU - Greenberger, P A AU - Kohler, P F AU - Saxon, A AU - Summers, R J AU - VanArsdel, P P AD - National Institute of Allergy and Infectious Diseases, Bethesda, MD. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 1025 EP - 1032 VL - 152 IS - 5 SN - 0003-9926, 0003-9926 KW - Benzeneacetamides KW - 0 KW - Indicators and Reagents KW - Penicillins KW - benzylpenicilloyl G KW - 2642-55-9 KW - Penicillin G KW - Q42T66VG0C KW - Abridged Index Medicus KW - Index Medicus KW - Penicillin G -- analogs & derivatives KW - Humans KW - Adult KW - Predictive Value of Tests KW - Inpatients KW - Male KW - Female KW - Drug Hypersensitivity -- epidemiology KW - Skin Tests KW - Penicillins -- adverse effects KW - Drug Hypersensitivity -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72951644?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+internal+medicine&rft.atitle=Results+of+the+National+Institute+of+Allergy+and+Infectious+Diseases+Collaborative+Clinical+Trial+to+test+the+predictive+value+of+skin+testing+with+major+and+minor+penicillin+derivatives+in+hospitalized+adults.&rft.au=Sogn%2C+D+D%3BEvans%2C+R%3BShepherd%2C+G+M%3BCasale%2C+T+B%3BCondemi%2C+J%3BGreenberger%2C+P+A%3BKohler%2C+P+F%3BSaxon%2C+A%3BSummers%2C+R+J%3BVanArsdel%2C+P+P&rft.aulast=Sogn&rft.aufirst=D&rft.date=1992-05-01&rft.volume=152&rft.issue=5&rft.spage=1025&rft.isbn=&rft.btitle=&rft.title=Archives+of+internal+medicine&rft.issn=00039926&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-08 N1 - Date created - 1992-06-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The cerebral radioprotective effect of alternative barbiturates to pentobarbital. AN - 72945831; 1584384 AB - The potential for normal brain tissue injury is one of the limiting factors in the use of radiotherapy for brain tumors. As attempts to enhance brain tumor radiation sensitivity have been unsuccessful, the use of cerebral radioprotectants provides an attractive alternative. Pentobarbital has recently been shown to be a cerebral radioprotectant in the rodent and primate models of single fraction radiation injury. Because daily high doses of pentobarbital bring certain significant risks, the potential usefulness of alternative barbiturates was explored. Seven groups of rats received 70 Gy of whole-brain-only irradiation in the single fraction. Group 1 was treated while awake. Groups 2, 3, and 4 received pentobarbital, thiopental, and methohexital, respectively. Groups 5, 6, and 7 received increasing doses of phenobarbital. Mean group survival at 30 days after treatment was determined and compared with the survival of animals treated while awake. Thiopental enhanced survival, similar to pentobarbital. Methohexital and phenobarbital were of no radioprotective value. The differences in the hypnotic effects of these barbiturates is based on dissimilar effects on the kinetics of chloride ion channel patency. We propose that these differences also influence their radioprotective properties. Thiopental is a shorter acting alternative to pentobarbital for cerebral radioprotection. Use of it should permit safer and easier investigation of this radioprotective effect in human trials. JF - Neurosurgery AU - Olson, J J AU - Shelley, C AU - Orr, K AU - DeLaney, T AU - Oldfield, E H AD - Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 720 EP - 723 VL - 30 IS - 5 SN - 0148-396X, 0148-396X KW - Barbiturates KW - 0 KW - Radiation-Protective Agents KW - Thiopental KW - 76-75-5 KW - Methohexital KW - E5B8ND5IPE KW - Pentobarbital KW - I4744080IR KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Survival Rate KW - Male KW - Radiation Injuries, Experimental -- mortality KW - Brain Neoplasms -- radiotherapy KW - Radiation Injuries, Experimental -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72945831?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurosurgery&rft.atitle=The+cerebral+radioprotective+effect+of+alternative+barbiturates+to+pentobarbital.&rft.au=Olson%2C+J+J%3BShelley%2C+C%3BOrr%2C+K%3BDeLaney%2C+T%3BOldfield%2C+E+H&rft.aulast=Olson&rft.aufirst=J&rft.date=1992-05-01&rft.volume=30&rft.issue=5&rft.spage=720&rft.isbn=&rft.btitle=&rft.title=Neurosurgery&rft.issn=0148396X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-18 N1 - Date created - 1992-06-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Neonatal capsaicin treatment attenuates spinal Fos activation and dynorphin gene expression following peripheral tissue inflammation and hyperalgesia. AN - 72932608; 1374461 AB - An animal model of nociception involving unilateral hindpaw inflammation has been used to examine behavioral, molecular, and biochemical aspects of well-characterized spinal cord neural circuits involved in pain transmission. The neurotoxin capsaicin administered neonatally was used to modify this neuronal system by producing a selective destruction of most small, unmyelinated primary afferent axons. Capsaicin had minimal effects on the behavioral hyperalgesia and edema associated with the hindpaw inflammation and on the constitutive expression of preprodynorphin (PPD) mRNA and preproenkephalin mRNA in the spinal cord. However, the inflammation-induced increases in Fos-like immunoreactivity (Fos-LI) and in PPD mRNA were greatly attenuated by neonatal capsaicin treatment. The data indicate that input from small-diameter unmyelinated primary afferents is important for the stimulus-induced increase in Fos-LI and PPD mRNA. Our finding that neonatal capsaicin reduces the levels of Fos-LI and PPD mRNA in a related fashion in the spinal dorsal horn provides further evidence for a relationship between the protein product of the c-fos protooncogene and regulation of dynorphin gene transcription. JF - The Journal of neuroscience : the official journal of the Society for Neuroscience AU - Hylden, J L AU - Noguchi, K AU - Ruda, M A AD - Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 1716 EP - 1725 VL - 12 IS - 5 SN - 0270-6474, 0270-6474 KW - Enkephalins KW - 0 KW - Protein Precursors KW - Proto-Oncogene Proteins c-fos KW - pre-prodynorphin KW - Substance P KW - 33507-63-0 KW - Dynorphins KW - 74913-18-1 KW - preproenkephalin KW - 93443-35-7 KW - Capsaicin KW - S07O44R1ZM KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals, Newborn KW - Animals KW - Protein Precursors -- metabolism KW - Substance P -- metabolism KW - Foot Diseases -- metabolism KW - Enkephalins -- metabolism KW - Inflammation -- metabolism KW - Male KW - Female KW - Gene Expression -- drug effects KW - Spinal Cord -- metabolism KW - Hyperalgesia -- metabolism KW - Proto-Oncogene Proteins c-fos -- physiology KW - Dynorphins -- metabolism KW - Dynorphins -- genetics KW - Capsaicin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72932608?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+neuroscience+%3A+the+official+journal+of+the+Society+for+Neuroscience&rft.atitle=Neonatal+capsaicin+treatment+attenuates+spinal+Fos+activation+and+dynorphin+gene+expression+following+peripheral+tissue+inflammation+and+hyperalgesia.&rft.au=Hylden%2C+J+L%3BNoguchi%2C+K%3BRuda%2C+M+A&rft.aulast=Hylden&rft.aufirst=J&rft.date=1992-05-01&rft.volume=12&rft.issue=5&rft.spage=1716&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+neuroscience+%3A+the+official+journal+of+the+Society+for+Neuroscience&rft.issn=02706474&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-05 N1 - Date created - 1992-06-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pesticides and other agricultural risk factors for non-Hodgkin's lymphoma among men in Iowa and Minnesota. AN - 72917170; 1568215 AB - Data from an in-person interview study of 622 white men with newly diagnosed non-Hodgkin's lymphoma and 1245 population-based controls in Iowa and Minnesota were used to measure the risk associated with farming occupation and specific agricultural exposures. Men who ever farmed were at slightly elevated risk of non-Hodgkin's lymphoma (odds ratio = 1.2, 95% confidence interval = 1.0-1.5) that was not linked to specific crops or particular animals. Elevated risks were found, with odds ratio generally 1.5-fold or greater, for personal handling, mixing, or application of several pesticide groups and for individual insecticides, including carbaryl, chlordane, dichlorodiphenyltrichloroethane, diazinon, dichlorvos, lindane, malathion, nicotine, and toxaphene. Associations were generally stronger for first use prior to 1965 than more recently, and when protective clothing or equipment was not used. Small risks were associated with the use of the phenoxyacetic acid herbicide 2,4-dichlorophenoxyacetic acid, but the risks did not increase with latency or failure to use protective equipment. Exposure to numerous pesticides poses problems of interpreting risk associated with a particular chemical, and multiple comparisons increase the chances of false-positive findings. In contrast, nondifferential exposure misclassification due to inaccurate recall can bias risk estimates toward the null and mask positive associations. In the face of these methodological and statistical issues, the consistency of several findings, both within this study and with observations of others, suggests an important role for several insecticides in the etiology of non-Hodgkin's lymphoma among farmers. JF - Cancer research AU - Cantor, K P AU - Blair, A AU - Everett, G AU - Gibson, R AU - Burmeister, L F AU - Brown, L M AU - Schuman, L AU - Dick, F R AD - Environmental Epidemiology Branch, Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/05/01/ PY - 1992 DA - 1992 May 01 SP - 2447 EP - 2455 VL - 52 IS - 9 SN - 0008-5472, 0008-5472 KW - Pesticides KW - 0 KW - Index Medicus KW - Risk Factors KW - Humans KW - Adult KW - Case-Control Studies KW - Interviews as Topic KW - Aged KW - Middle Aged KW - Minnesota -- epidemiology KW - Male KW - Iowa -- epidemiology KW - Lymphoma, Non-Hodgkin -- epidemiology KW - Agricultural Workers' Diseases -- epidemiology KW - Pesticides -- classification KW - Agricultural Workers' Diseases -- chemically induced KW - Lymphoma, Non-Hodgkin -- chemically induced KW - Pesticides -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72917170?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Pesticides+and+other+agricultural+risk+factors+for+non-Hodgkin%27s+lymphoma+among+men+in+Iowa+and+Minnesota.&rft.au=Cantor%2C+K+P%3BBlair%2C+A%3BEverett%2C+G%3BGibson%2C+R%3BBurmeister%2C+L+F%3BBrown%2C+L+M%3BSchuman%2C+L%3BDick%2C+F+R&rft.aulast=Cantor&rft.aufirst=K&rft.date=1992-05-01&rft.volume=52&rft.issue=9&rft.spage=2447&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-26 N1 - Date created - 1992-05-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Cancer Res. 1993 May 15;53(10 Suppl):2421 [8329071] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dose-intensive induction therapy with cyclophosphamide, cisplatin, and consolidative abdominal radiation in advanced-stage epithelial ovarian cancer. AN - 72917058; 1569445 AB - The primary goal of this trial was to evaluate the clinical activity of a high-dose cisplatin-based induction regimen for women with advanced-stage ovarian cancer. A secondary goal was to assess the use of whole-abdominal radiation as consolidative therapy in the subset of women left with less than 5 mm residual disease after completion of chemotherapy. Fifty consecutive patients with newly diagnosed, advanced-stage ovarian cancer received cisplatin 40 mg/m2/d and cyclophosphamide 200 mg/m2/d intravenously (IV) for 5 days, every 4 to 6 weeks. After three to four cycles of chemotherapy, patients who still had residual disease less than 5 mm in greatest diameter at second-look surgery were given whole-abdominal radiotherapy. The overall response rate in 49 patients assessable for response was 61.3% (24.5% pathologic complete responses [pCRs], 32.7% pathologic partial responses [pPRs], and 4.1% clinical partial responses [cPRs]). Median survival for all patients was 23.4 months, and actuarial 4-year survival was 33.7% (95% confidence interval [CI], 21.8% to 48.1%). Multivariate analysis showed stage III and serous histology as independent favorable prognostic factors for survival. Median survival for stage III patients was 36.5 months, with an actuarial 4-year survival of 41.6% (95% CI, 25.5% to 59.6%). Median survival for stage IV patients was 12.0 months, with actuarial 4-year survival of 22.9% (95% CI, 9.5% to 45.5%). The major acute toxicities encountered were myelosuppression and peripheral neuropathy. Patients who received consolidative radiotherapy were at increased risk of developing late-onset enteropathy. This regimen is active against advanced-stage ovarian cancer, but the associated toxicity is severe. Consolidative whole-abdominal radiation did not appear to prolong survival in the subset of women left with less than 5 mm residual disease after chemotherapy. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Rothenberg, M L AU - Ozols, R F AU - Glatstein, E AU - Steinberg, S M AU - Reed, E AU - Young, R C AD - Medicine Branch, National Cancer Institute, Bethesda, MD. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 727 EP - 734 VL - 10 IS - 5 SN - 0732-183X, 0732-183X KW - Cyclophosphamide KW - 8N3DW7272P KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Neoplasm Staging KW - Combined Modality Therapy KW - Humans KW - Aged KW - Cisplatin -- administration & dosage KW - Multivariate Analysis KW - Adult KW - Middle Aged KW - Adolescent KW - Female KW - Survival Analysis KW - Remission Induction KW - Ovarian Neoplasms -- radiotherapy KW - Carcinoma -- pathology KW - Ovarian Neoplasms -- pathology KW - Carcinoma -- radiotherapy KW - Carcinoma -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Ovarian Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72917058?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Dose-intensive+induction+therapy+with+cyclophosphamide%2C+cisplatin%2C+and+consolidative+abdominal+radiation+in+advanced-stage+epithelial+ovarian+cancer.&rft.au=Rothenberg%2C+M+L%3BOzols%2C+R+F%3BGlatstein%2C+E%3BSteinberg%2C+S+M%3BReed%2C+E%3BYoung%2C+R+C&rft.aulast=Rothenberg&rft.aufirst=M&rft.date=1992-05-01&rft.volume=10&rft.issue=5&rft.spage=727&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=0732183X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-28 N1 - Date created - 1992-05-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Clin Oncol. 1992 May;10(5):683-5 [1569441] J Clin Oncol. 1992 Nov;10(11):1820-1 [1403064] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Recognition and management of benzodiazepine dependence. AN - 72916546; 1575121 AB - Primary care physicians prescribe the majority of benzodiazepines and thus may see most patients who are dependent on these drugs. The diagnosis of benzodiazepine misuse is based on the history, the physical examination and drug use patterns. The treatment of benzodiazepine misuse can be a challenging process that requires the physician's patience, caution and sound clinical judgment. Patients who misuse benzodiazepines may have coexisting psychiatric problems that require treatment, such as depression or panic disorder. Family physicians can manage these patients but should be prepared to refer them for hospitalization when habituation and withdrawal reactions are complicated by medical instability, noncompliance or clinical deterioration. JF - American family physician AU - Gonzales, J J AU - Stern, T A AU - Emmerich, A D AU - Rauch, S L AD - National Institute of Mental Health, Rockville, Maryland. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 2269 EP - 2276 VL - 45 IS - 5 SN - 0002-838X, 0002-838X KW - Benzodiazepines KW - 12794-10-4 KW - Abridged Index Medicus KW - Index Medicus KW - Diagnosis, Differential KW - Humans KW - Ambulatory Care KW - Substance-Related Disorders -- therapy KW - Substance-Related Disorders -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72916546?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+family+physician&rft.atitle=Recognition+and+management+of+benzodiazepine+dependence.&rft.au=Gonzales%2C+J+J%3BStern%2C+T+A%3BEmmerich%2C+A+D%3BRauch%2C+S+L&rft.aulast=Gonzales&rft.aufirst=J&rft.date=1992-05-01&rft.volume=45&rft.issue=5&rft.spage=2269&rft.isbn=&rft.btitle=&rft.title=American+family+physician&rft.issn=0002838X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-29 N1 - Date created - 1992-05-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prostaglandin E2 and other cyclic AMP-elevating agents modulate IL-2 and IL-2R alpha gene expression at multiple levels. AN - 72913205; 1374102 AB - cAMP is an intracellular second messenger that conveys inhibitory signals for T cell activation and clonal proliferation. cAMP also inhibits the production of IL-2 and IL-2R alpha-chain expression. To determine the mechanisms of this inhibition, human peripheral blood T lymphocytes were stimulated with anti-CD3 mAb, PHA, PMA, or ionomycin, alone or in combination. cAMP elevation by PGE2, cholera toxin, or the cell-permeable analogue 8-bromo-cAMP inhibited the tyrosine phosphorylation of a protein of 100 kDa. This inhibition was associated with decreased IL-2 production and IL-2R alpha expression at both the protein product and the mRNA levels. Nuclear run-off assays showed that the inhibitory effect of cAMP on IL-2 and IL-2R alpha gene expression is mediated at the transcriptional level. H-8, an inhibitor of protein kinase A, reversed the inhibitory effect of cAMP on nuclear transcription of the IL-2 gene, suggesting that this is mediated through activation of protein kinase A. Post-transcriptionally, cAMP elevation decreased the t1/2 of IL-2 mRNA by more than 50%. These data indicate that cAMP inhibits cell membrane, cytoplasmic, and nuclear events associated with T cell activation and highlight the complexities of its action of lymphocyte function. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Anastassiou, E D AU - Paliogianni, F AU - Balow, J P AU - Yamada, H AU - Boumpas, D T AD - Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/05/01/ PY - 1992 DA - 1992 May 01 SP - 2845 EP - 2852 VL - 148 IS - 9 SN - 0022-1767, 0022-1767 KW - Interleukin-2 KW - 0 KW - Isoquinolines KW - Phytohemagglutinins KW - Receptors, Antigen, T-Cell KW - Receptors, Interleukin-2 KW - 8-Bromo Cyclic Adenosine Monophosphate KW - 23583-48-4 KW - RNA KW - 63231-63-0 KW - N-(2-(methylamino)ethyl)-5-isoquinolinesulfonamide KW - 84478-11-5 KW - Cholera Toxin KW - 9012-63-9 KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinase C KW - EC 2.7.11.13 KW - Dinoprostone KW - K7Q1JQR04M KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Transcription, Genetic -- drug effects KW - Blotting, Northern KW - Humans KW - Cholera Toxin -- pharmacology KW - RNA -- analysis KW - 8-Bromo Cyclic Adenosine Monophosphate -- pharmacology KW - RNA Processing, Post-Transcriptional KW - Receptors, Antigen, T-Cell -- physiology KW - Phosphorylation -- drug effects KW - Isoquinolines -- pharmacology KW - Protein Kinase C -- antagonists & inhibitors KW - Lymphocyte Activation -- physiology KW - Gene Expression -- drug effects KW - Dinoprostone -- pharmacology KW - Receptors, Interleukin-2 -- biosynthesis KW - Interleukin-2 -- biosynthesis KW - Cyclic AMP -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72913205?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Prostaglandin+E2+and+other+cyclic+AMP-elevating+agents+modulate+IL-2+and+IL-2R+alpha+gene+expression+at+multiple+levels.&rft.au=Anastassiou%2C+E+D%3BPaliogianni%2C+F%3BBalow%2C+J+P%3BYamada%2C+H%3BBoumpas%2C+D+T&rft.aulast=Anastassiou&rft.aufirst=E&rft.date=1992-05-01&rft.volume=148&rft.issue=9&rft.spage=2845&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-02 N1 - Date created - 1992-06-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Infection with human T lymphotropic virus types I and II in sexually transmitted disease clinics in Baltimore and New Orleans. AN - 72908544; 1569344 AB - Patients attending sexually transmitted disease (STD) clinics in Baltimore (n = 4880) and New Orleans (n = 1054) were surveyed in 1987 to estimate the prevalence of human T lymphotropic virus (HTLV)-I/II infection. In Baltimore, 0.4% (95% confidence interval [CI], 0.2-1.1) were HTLV-I/II-seropositive and 4.9% were human immunodeficiency virus (HIV-1)-positive. In New Orleans, 1.8% (CI, 1.2-2.9) of sera were HTLV-I/II-seropositive and 5.1% were HIV-1-seropositive. In both cities, HTLV-I/II prevalence increased significantly with age, and the New Orleans age- and sex-adjusted HTLV-I/II prevalence was significantly higher than that of Baltimore (P less than .001). In Baltimore, almost all HTLV-I/II seropositivity was associated with a history of parenteral drug use or sexual contact with partners who were drug users or male homosexuals. In addition, individuals in both cities who were seropositive for HIV-1 or syphilis were significantly more likely to be HTLV-I/II-seropositive. JF - The Journal of infectious diseases AU - Wiktor, S Z AU - Cannon, R O AU - Atkinson, W L AU - Lutz, B AU - Hook, E W AU - Blattner, W A AU - Quinn, T C AD - Viral Epidemiology Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 920 EP - 924 VL - 165 IS - 5 SN - 0022-1899, 0022-1899 KW - HIV Antibodies KW - 0 KW - HTLV-I Antibodies KW - HTLV-II Antibodies KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Age Factors KW - Humans KW - Baltimore -- epidemiology KW - HTLV-I Antibodies -- blood KW - HIV Antibodies -- blood KW - Risk Factors KW - Adult KW - HTLV-II Antibodies -- blood KW - Substance Abuse, Intravenous -- complications KW - Adolescent KW - Female KW - Male KW - Louisiana -- epidemiology KW - Prevalence KW - HIV-1 -- immunology KW - HTLV-I Infections -- epidemiology KW - HTLV-II Infections -- epidemiology KW - HIV Infections -- epidemiology KW - Sexually Transmitted Diseases -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72908544?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+infectious+diseases&rft.atitle=Infection+with+human+T+lymphotropic+virus+types+I+and+II+in+sexually+transmitted+disease+clinics+in+Baltimore+and+New+Orleans.&rft.au=Wiktor%2C+S+Z%3BCannon%2C+R+O%3BAtkinson%2C+W+L%3BLutz%2C+B%3BHook%2C+E+W%3BBlattner%2C+W+A%3BQuinn%2C+T+C&rft.aulast=Wiktor&rft.aufirst=S&rft.date=1992-05-01&rft.volume=165&rft.issue=5&rft.spage=920&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=00221899&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-28 N1 - Date created - 1992-05-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Estrogens modulate the responsiveness of osteoblast-like cells (ROS 17/2.8) stably transfected with estrogen receptor. AN - 72906210; 1572285 AB - Recent studies have demonstrated the presence of estrogen receptor (ER) in both normal human osteoblast-like and osteoblast-like osteosarcoma cells. The number of ER in cultured osteoblastic cells is very low (200-500 sites/cell). This has complicated characterization of the biological role of estrogens in bone cells. To study the responsiveness of bone cells to estrogens, we established osteoblast-like cell lines expressing higher ER levels. ROS 17/2.8, an osteoblastic cell line, was stably transfected with the cDNA encoding for the mouse ER. After a selection period, positive clones were isolated and evaluated for the presence of ER by both Northern blot analysis and ligand binding assays. Using these techniques, we detected a significant increase in the level of both ER transcript and binding compared to that in wild-type cells. The levels of expressed ER protein were similar to those reported in normal human osteoblast-like cells in primary culture (approximately 2000 sites/cell). To test whether the exogenously inserted ER was responsive, both wild-type and ER stably transfected cells were transiently transfected with a reporter construct containing an estrogen-responsive element linked to a truncated thymidine kinase promoter and a chloramphenicol acetyltransferase (CAT) reporter gene. Exposure of the cells to increased concentrations of estradiol induced a slight increase in CAT activity in wild-type cells (approximately 1.5-fold) at maximal stimulation; however, it provoked a clear concentration-dependent increase in CAT activity in the ER stably transfected cells, with a maximal stimulation of approximately 10-fold. This event was receptor mediated, since ICI 164,384, an ER antagonist, blocked the enhancement of estradiol-induced CAT activity, and it was specific, since other steroid hormones did not stimulate CAT activity. Finally, we evaluated the ability of ER to modulate an endogenous estrogen-responsive gene by measuring the activity of the enzyme alkaline phosphatase. In addition, diethylstilbestrol, a synthetic estrogen agonist, increased the activity of both the CAT reporter gene and the endogenous alkaline phosphatase enzyme. In summary, we have established osteoblast-like cells expressing high levels of an exogenously inserted ER, which has characteristics similar to those of the endogenous ER in terms of its Kd. Finally, the exogenous ER regulates both exogenously inserted construct (VITERECAT) and endogenous properties of the cells (enzymatic activity and proliferation). JF - Endocrinology AU - Migliaccio, S AU - Davis, V L AU - Gibson, M K AU - Gray, T K AU - Korach, K S AD - Receptor Biology Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 2617 EP - 2624 VL - 130 IS - 5 SN - 0013-7227, 0013-7227 KW - Oligodeoxyribonucleotides KW - 0 KW - Receptors, Estrogen KW - Progesterone KW - 4G7DS2Q64Y KW - Estradiol KW - 4TI98Z838E KW - Diethylstilbestrol KW - 731DCA35BT KW - Dexamethasone KW - 7S5I7G3JQL KW - Globins KW - 9004-22-2 KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Alkaline Phosphatase KW - EC 3.1.3.1 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Analysis of Variance KW - Blotting, Northern KW - Dose-Response Relationship, Drug KW - Progesterone -- pharmacology KW - Dexamethasone -- pharmacology KW - Globins -- genetics KW - Osteosarcoma KW - Alkaline Phosphatase -- metabolism KW - Chloramphenicol O-Acetyltransferase -- metabolism KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Base Sequence KW - Kinetics KW - Genetic Vectors KW - Restriction Mapping KW - Molecular Sequence Data KW - Diethylstilbestrol -- pharmacology KW - Cell Line KW - Osteoblasts -- drug effects KW - Osteoblasts -- physiology KW - Receptors, Estrogen -- genetics KW - Receptors, Estrogen -- drug effects KW - Transfection KW - Estradiol -- pharmacology KW - Receptors, Estrogen -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72906210?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrinology&rft.atitle=Estrogens+modulate+the+responsiveness+of+osteoblast-like+cells+%28ROS+17%2F2.8%29+stably+transfected+with+estrogen+receptor.&rft.au=Migliaccio%2C+S%3BDavis%2C+V+L%3BGibson%2C+M+K%3BGray%2C+T+K%3BKorach%2C+K+S&rft.aulast=Migliaccio&rft.aufirst=S&rft.date=1992-05-01&rft.volume=130&rft.issue=5&rft.spage=2617&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-03 N1 - Date created - 1992-06-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Detection of frequent allelic loss on proximal chromosome 17q in sporadic breast carcinoma using microsatellite length polymorphisms. AN - 72904660; 1568230 AB - Analyses of losses of heterozygosity and linkage studies have implicated a gene(s) on chromosome 17q in the genesis of sporadic and early-onset familial breast carcinomas, respectively. To define the critical region of 17q, we examined DNAs from a series of 20 sporadic breast carcinomas and corresponding blood samples for allelic losses of chromosome 17q using microsatellite length polymorphisms. With these highly informative markers (average heterozygosity, 0.73), we observed frequent deletions of 17q at several loci. We found that D17S250 was deleted in 50% (7 of 14), THRA1 in 79% (11 of 14), D17S579 in 59% (11 of 19), NME1 in 29% (5 of 17), MPO in 36% (4 of 11), and GH in 25% (4 of 16) in the tumor set examined. A common region of deletion was found that was flanked by D17S250 to D15S579. These markers have recently been localized to a 6-cM interval of proximal chromosome 17q in bands 17q11.2-q21 and map within the region of the early-onset familial breast cancer locus, implying that the same gene or genes may be involved in both sporadic and familial breast tumors. Thyroid hormone receptor alpha and retinoic acid receptor alpha are two potential candidate genes in this region. JF - Cancer research AU - Futreal, P A AU - Söderkvist, P AU - Marks, J R AU - Iglehart, J D AU - Cochran, C AU - Barrett, J C AU - Wiseman, R W AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, NIH, Research Triangle Park 27709. Y1 - 1992/05/01/ PY - 1992 DA - 1992 May 01 SP - 2624 EP - 2627 VL - 52 IS - 9 SN - 0008-5472, 0008-5472 KW - ERBB2 KW - p53 KW - DNA, Neoplasm KW - 0 KW - DNA, Satellite KW - Genetic Markers KW - Index Medicus KW - Genetic Markers -- genetics KW - Base Sequence KW - Nucleic Acid Amplification Techniques KW - Humans KW - Polymerase Chain Reaction -- methods KW - Molecular Sequence Data KW - Chromosome Mapping KW - Female KW - DNA, Neoplasm -- chemistry KW - Breast Neoplasms -- genetics KW - DNA, Satellite -- chemistry KW - Chromosomes, Human, Pair 17 KW - Chromosome Deletion KW - Heterozygote UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72904660?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Detection+of+frequent+allelic+loss+on+proximal+chromosome+17q+in+sporadic+breast+carcinoma+using+microsatellite+length+polymorphisms.&rft.au=Futreal%2C+P+A%3BS%C3%B6derkvist%2C+P%3BMarks%2C+J+R%3BIglehart%2C+J+D%3BCochran%2C+C%3BBarrett%2C+J+C%3BWiseman%2C+R+W&rft.aulast=Futreal&rft.aufirst=P&rft.date=1992-05-01&rft.volume=52&rft.issue=9&rft.spage=2624&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-26 N1 - Date created - 1992-05-26 N1 - Date revised - 2017-01-13 N1 - Gene symbol - ERBB2; p53 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Anti-CD3 monoclonal antibody treatment of patients with CD3-negative tumors: a phase IA/B study. AN - 72903883; 1533172 AB - Anti-CD3 monoclonal antibodies induce the proliferation of human T-cells in vitro and activate specific and nonspecific cytolysis by human T-cell clones and human peripheral blood lymphocytes. In vivo administration of anti-CD3 prevents tumor growth of a UV-induced mouse fibrosarcoma. We conducted a phase I trial to determine the toxicity and immunomodulatory properties of low doses of anti-CD3 in 36 patients with cancer. In 23 patients, anti-CD3 was given i.v. over 3 h at 1, 10, 30, and 100 mcg/patient. Five other patients received anti-CD3 at 30 mcg by i.v. bolus. Patients were treated every 3 days for a total of four doses. An additional eight patients received anti-CD3 daily for 14 days at 3 mcg by i.v. bolus, 3-h infusion, or 24-h infusion. Dose-limiting toxicity was headache. Headache was often accompanied by signs and symptoms of meningeal irritation leading to performance of a lumbar puncture in nine patients. The opening pressure was usually elevated, and six patients had a cerebrospinal fluid lymphocytosis with an elevated protein. Increased levels of interleukin 6 were identified in the cerebrospinal fluid. The maximum tolerated dose by 3-h infusion was 30 mcg. There were no objective tumor responses. There was a dose-related increase in the number of peripheral blood lymphocytes expressing the T-cell activation antigen CD69 (Leu 23), but no changes were seen in CD25 (interleukin 2 receptor) expression, and no changes were observed in the serum levels of the soluble interleukin 2 receptor. Even at these low doses of anti-CD3, 8 of 16 patients tested developed human anti-mouse antibodies. JF - Cancer research AU - Urba, W J AU - Ewel, C AU - Kopp, W AU - Smith, J W AU - Steis, R G AU - Ashwell, J D AU - Creekmore, S P AU - Rossio, J AU - Sznol, M AU - Sharfman, W AD - Clinical Services Program, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1992/05/01/ PY - 1992 DA - 1992 May 01 SP - 2394 EP - 2401 VL - 52 IS - 9 SN - 0008-5472, 0008-5472 KW - Antigens, CD3 KW - 0 KW - Antigens, Differentiation, T-Lymphocyte KW - Cytokines KW - Muromonab-CD3 KW - Receptors, Antigen, T-Cell KW - Index Medicus KW - Drug Administration Schedule KW - Dose-Response Relationship, Drug KW - Humans KW - Aged KW - Cytokines -- metabolism KW - Leukocyte Count KW - Lymphocyte Activation KW - Drug Evaluation KW - Adult KW - Middle Aged KW - Female KW - Male KW - Spinal Puncture KW - Muromonab-CD3 -- metabolism KW - Muromonab-CD3 -- therapeutic use KW - Neoplasms -- blood KW - Receptors, Antigen, T-Cell -- immunology KW - Headache -- etiology KW - Antigens, Differentiation, T-Lymphocyte -- immunology KW - Neoplasms -- therapy KW - Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72903883?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Anti-CD3+monoclonal+antibody+treatment+of+patients+with+CD3-negative+tumors%3A+a+phase+IA%2FB+study.&rft.au=Urba%2C+W+J%3BEwel%2C+C%3BKopp%2C+W%3BSmith%2C+J+W%3BSteis%2C+R+G%3BAshwell%2C+J+D%3BCreekmore%2C+S+P%3BRossio%2C+J%3BSznol%2C+M%3BSharfman%2C+W&rft.aulast=Urba&rft.aufirst=W&rft.date=1992-05-01&rft.volume=52&rft.issue=9&rft.spage=2394&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-26 N1 - Date created - 1992-05-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenic potency of alkylating agents in rodents and humans. AN - 72903258; 1568217 AB - Alkylating agents are known to produce second tumors in cancer patients treated for their primary cancer. Since therapeutic doses are high and the pharmacokinetics of the drugs are thoroughly studied, these agents provide a unique opportunity to compare intrinsic carcinogenic potency between experimental animals and humans. We have examined the carcinogenicity of melphalan, chlorambucil, and cyclophosphamide in causing leukemia in patients treated for cancer or polycythemia vera and lymphosarcoma in rats and mice. A good correlation among species is observed when the carcinogenic potency is based on the total lifetime exposure to active species derived from these drugs. JF - Cancer research AU - Dedrick, R L AU - Morrison, P F AD - Biomedical Engineering and Instrumentation Program, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/05/01/ PY - 1992 DA - 1992 May 01 SP - 2464 EP - 2467 VL - 52 IS - 9 SN - 0008-5472, 0008-5472 KW - Chlorambucil KW - 18D0SL7309 KW - Cyclophosphamide KW - 8N3DW7272P KW - Melphalan KW - Q41OR9510P KW - Index Medicus KW - Rats KW - Animals KW - Humans KW - Carcinogenicity Tests KW - Mice KW - Cyclophosphamide -- administration & dosage KW - Chlorambucil -- administration & dosage KW - Melphalan -- administration & dosage KW - Melphalan -- adverse effects KW - Chlorambucil -- adverse effects KW - Chlorambucil -- pharmacokinetics KW - Cyclophosphamide -- pharmacokinetics KW - Melphalan -- pharmacokinetics KW - Neoplasms, Second Primary -- chemically induced KW - Cyclophosphamide -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72903258?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Carcinogenic+potency+of+alkylating+agents+in+rodents+and+humans.&rft.au=Dedrick%2C+R+L%3BMorrison%2C+P+F&rft.aulast=Dedrick&rft.aufirst=R&rft.date=1992-05-01&rft.volume=52&rft.issue=9&rft.spage=2464&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-26 N1 - Date created - 1992-05-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - p53 and Kirsten-ras mutations in human mesothelioma cell lines. AN - 72903195; 1568228 AB - Twenty cell lines from 17 individuals with malignant mesothelioma have been examined for p53 alterations by direct sequencing of genomic DNA, by evaluation of mRNA expression levels, and by immunocytochemical analysis of p53 protein expression in comparison with normal human pleural mesothelial cells. The results of this study show p53 abnormalities in cell lines from 3 individuals. These include 2 point mutations and one null cell line. Interestingly, while both cell lines with point mutations exhibit high levels of p53 protein, normal mesothelial cells as well as 12 of the mesotheliomas evaluated express low but significant levels. In addition, sequencing of K-ras at codons 12, 13, and 61 reveals wild-type sequence in all 20 mesothelioma cell lines. The capacity to induce tumors in athymic nude mice did not correlate with the presence of a p53 mutation or elevated p53 protein levels. These data suggest that neither p53 alteration nor K-ras activation constitutes a critical step in the development of human mesothelioma. JF - Cancer research AU - Metcalf, R A AU - Welsh, J A AU - Bennett, W P AU - Seddon, M B AU - Lehman, T A AU - Pelin, K AU - Linnainmaa, K AU - Tammilehto, L AU - Mattson, K AU - Gerwin, B I AD - Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/05/01/ PY - 1992 DA - 1992 May 01 SP - 2610 EP - 2615 VL - 52 IS - 9 SN - 0008-5472, 0008-5472 KW - p53 KW - ras KW - Codon KW - 0 KW - RNA, Messenger KW - Tumor Suppressor Protein p53 KW - Index Medicus KW - Animals KW - Tumor Suppressor Protein p53 -- analysis KW - Tumor Cells, Cultured KW - Humans KW - DNA Mutational Analysis KW - RNA, Messenger -- analysis KW - Mice, Nude KW - Mice KW - Genes, ras -- genetics KW - Codon -- genetics KW - Codon -- chemistry KW - Genes, p53 -- genetics KW - Mesothelioma -- genetics KW - Mutation -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72903195?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=p53+and+Kirsten-ras+mutations+in+human+mesothelioma+cell+lines.&rft.au=Metcalf%2C+R+A%3BWelsh%2C+J+A%3BBennett%2C+W+P%3BSeddon%2C+M+B%3BLehman%2C+T+A%3BPelin%2C+K%3BLinnainmaa%2C+K%3BTammilehto%2C+L%3BMattson%2C+K%3BGerwin%2C+B+I&rft.aulast=Metcalf&rft.aufirst=R&rft.date=1992-05-01&rft.volume=52&rft.issue=9&rft.spage=2610&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-26 N1 - Date created - 1992-05-26 N1 - Date revised - 2017-01-13 N1 - Gene symbol - p53; ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The correct dose: pharmacologically guided end point for anti-growth factor therapy. AN - 72885221; 1314137 AB - Strategies to block the effects of tumor growth factors, such as estrogen, and to recruit other regulatory elements, such as with retinoids, have focused interest on the possibility of successful tumor intervention approaches. Approaches that neutralize the effects of critical molecules that drive tumor promotion are attractive targets for evaluation as new intervention agents. Clinical intervention trials with early stage patients or with subjects from "high risk" populations impose stricter types of constraints than conventional chemotherapy approaches in advanced stage patients. The potential for short-term toxicity has to be considered, as it may affect subject accrual or compliance. The longer expected survival of intervention subjects mandates closer attention to the possibilities of unexpected long-term toxicities with chronic administration of an intervention agent. As part of a Phase I clinical trial evaluating the utility of a monoclonal antibody directed against the autocrine growth factor, gastrin-releasing peptide to block the growth of small cell lung cancer, we developed a mathematical model to predict the requisite amount of antibody to neutralize growth factor effect. This model requires knowledge of the equilibrium concentration of the secreted growth factor, specific receptor, and bioavailability of the antibody in the tumor interstitium. A range of possible target doses of antibody can be developed to address the potential for heterogeneity frequently encountered in such systems, including a range of levels for peptide production and specific receptor expression. This approach could be applied to rationally derive treatment or intervention in which specific information regarding the relevant binding parameters is available. Through refinement of this modeling approach more context-specific dosing of agonist/antagonists could be determined which may decrease side effects associated with the drug administration. JF - Cancer research AU - Mulshine, J L AU - Shuke, N AU - Daghighian, F AU - Carrasquillo, J AU - Ghosh, B AU - Walsh, T AU - Avis, I AU - Reynolds, J C AU - Cuttitta, F AU - Larson, S M AD - Biomarkers and Prevention Research Branch, National Cancer Institute, Kensington, Maryland 20895. Y1 - 1992/05/01/ PY - 1992 DA - 1992 May 01 SP - 2743s EP - 2746s VL - 52 IS - 9 Suppl SN - 0008-5472, 0008-5472 KW - Antibodies, Monoclonal KW - 0 KW - Peptides KW - Gastrin-Releasing Peptide KW - 80043-53-4 KW - Index Medicus KW - Dose-Response Relationship, Drug KW - Humans KW - Cell Division -- drug effects KW - Models, Biological KW - Carcinoma, Small Cell -- pathology KW - Lung Neoplasms -- drug therapy KW - Peptides -- immunology KW - Carcinoma, Small Cell -- drug therapy KW - Antibodies, Monoclonal -- administration & dosage KW - Peptides -- antagonists & inhibitors KW - Lung Neoplasms -- pathology KW - Antibodies, Monoclonal -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72885221?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=The+correct+dose%3A+pharmacologically+guided+end+point+for+anti-growth+factor+therapy.&rft.au=Mulshine%2C+J+L%3BShuke%2C+N%3BDaghighian%2C+F%3BCarrasquillo%2C+J%3BGhosh%2C+B%3BWalsh%2C+T%3BAvis%2C+I%3BReynolds%2C+J+C%3BCuttitta%2C+F%3BLarson%2C+S+M&rft.aulast=Mulshine&rft.aufirst=J&rft.date=1992-05-01&rft.volume=52&rft.issue=9+Suppl&rft.spage=2743s&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-21 N1 - Date created - 1992-05-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Long-term activation of protein kinase C by nicotine in bovine adrenal chromaffin cells. AN - 72879950; 1560224 AB - Previous results from our laboratory suggest that long-term treatment of primary cultured bovine adrenal medullary (BAM) chromaffin cells with nicotine or phorbol 12-myristate 13-acetate, either of which directly activates protein kinase C (PKC), increases the mRNA levels encoding catecholamine-synthesizing enzymes and proenkephalin. In the present study, we have examined the effects of nicotine on BAM cell PKC activity with special emphasis on long-term effects. Nicotine increased particulate PKC activity in a concentration-dependent manner when measured using in vitro enzyme assay with histone as the substrate. This effect is mediated through nicotinic cholinergic receptors, because 1,1-dimethylphenylpiperazinium, a nicotinic agonist, had a similar effect. In addition, chlorisondamine, a specific nicotine-receptor blocking drug, antagonized the effect of nicotine. Nicotine also increased specific [3H]phorbol 12,13-dibutyrate ([3H]PdBu) binding within 1 min, the effect of which was maximal between 3 and 12 min. This effect was reversed by chlorisondamine similarly after 12 min and after 18 h of nicotine treatment, indicating that continual nicotinic-receptor occupancy is required for persistent PKC activation. Compared to PKC activation, the onset of nicotine-stimulated diacylglycerol production was slow, and it was observed after 12 min of incubation with nicotine. The diacylglycerol levels, specific [3H]PdBu binding, and PKC activity remained significantly elevated for at least 18 h with continuous nicotine incubation. Furthermore, nicotine increased the PKC immunoreactivity of a particulate protein with a molecular mass of 82 kDa in the western blot. These results suggest that nicotinic-receptor activation increases PKC activity and immunoreactivity in BAM cells.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Journal of neurochemistry AU - Tuominen, R K AU - McMillian, M K AU - Ye, H AU - Stachowiak, M K AU - Hudson, P M AU - Hong, J S AD - Neuropharmacology Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1992/05// PY - 1992 DA - May 1992 SP - 1652 EP - 1658 VL - 58 IS - 5 SN - 0022-3042, 0022-3042 KW - Diglycerides KW - 0 KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Dimethylphenylpiperazinium Iodide KW - 54-77-3 KW - Nicotine KW - 6M3C89ZY6R KW - Atropine KW - 7C0697DR9I KW - Protein Kinase C KW - EC 2.7.11.13 KW - Chlorisondamine KW - JD3M24F66I KW - Index Medicus KW - Chlorisondamine -- pharmacology KW - Immunoblotting KW - Animals KW - Cattle KW - Dimethylphenylpiperazinium Iodide -- pharmacology KW - Cells, Cultured KW - Enzyme Activation -- drug effects KW - Atropine -- pharmacology KW - Time Factors KW - Phorbol 12,13-Dibutyrate -- pharmacology KW - Diglycerides -- metabolism KW - Protein Kinase C -- metabolism KW - Chromaffin System -- enzymology KW - Adrenal Glands -- metabolism KW - Nicotine -- pharmacology KW - Adrenal Glands -- cytology KW - Adrenal Glands -- enzymology KW - Chromaffin System -- metabolism KW - Chromaffin System -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72879950?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=Long-term+activation+of+protein+kinase+C+by+nicotine+in+bovine+adrenal+chromaffin+cells.&rft.au=Tuominen%2C+R+K%3BMcMillian%2C+M+K%3BYe%2C+H%3BStachowiak%2C+M+K%3BHudson%2C+P+M%3BHong%2C+J+S&rft.aulast=Tuominen&rft.aufirst=R&rft.date=1992-05-01&rft.volume=58&rft.issue=5&rft.spage=1652&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-11 N1 - Date created - 1992-05-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selenocysteyl-tRNAs recognize UGA in Beta vulgaris, a higher plant, and in Gliocladium virens, a filamentous fungus. AN - 72899441; 1567433 AB - Selenocysteyl-tRNAs that decode UGA were previously identified in representatives of three of the five life kingdoms which were the monera, animal and protist kingdoms. In the present study, we show that these tRNAs also occur in representatives of the two remaining kingdoms, plants and fungi; i.e., selenocysteyl-tRNAs which code for UGA occur in Beta vulgaris, a higher plant, and in Gliocladium virens, a filamentous fungus. The fact that selenocysteyl-tRNAs are present in all five life kingdoms strongly suggests that UGA, in addition to dictating the cessation of protein synthesis, also codes for selenocysteine in the universal genetic code. JF - Biochemical and biophysical research communications AU - Hatfield, D AU - Choi, I S AU - Mischke, S AU - Owens, L D AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/04/15/ PY - 1992 DA - 1992 Apr 15 SP - 254 EP - 259 VL - 184 IS - 1 SN - 0006-291X, 0006-291X KW - Codon KW - 0 KW - RNA, Transfer, Amino Acid-Specific KW - Selenium Radioisotopes KW - tRNA, selenocysteine- KW - Selenium KW - H6241UJ22B KW - Index Medicus KW - Selenium -- metabolism KW - Base Sequence KW - Plants -- metabolism KW - Codon -- genetics KW - RNA, Transfer, Amino Acid-Specific -- genetics KW - Plants -- genetics KW - RNA, Transfer, Amino Acid-Specific -- metabolism KW - Mitosporic Fungi -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72899441?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+biophysical+research+communications&rft.atitle=Selenocysteyl-tRNAs+recognize+UGA+in+Beta+vulgaris%2C+a+higher+plant%2C+and+in+Gliocladium+virens%2C+a+filamentous+fungus.&rft.au=Hatfield%2C+D%3BChoi%2C+I+S%3BMischke%2C+S%3BOwens%2C+L+D&rft.aulast=Hatfield&rft.aufirst=D&rft.date=1992-04-15&rft.volume=184&rft.issue=1&rft.spage=254&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+biophysical+research+communications&rft.issn=0006291X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-20 N1 - Date created - 1992-05-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenesis and mutagenesis by N-nitroso compounds having a basic center. AN - 72896393; 1562986 AB - Two N-nitroso compounds that are derivatives of N,N-dimethylethylenediamine and are therefore strongly basic, were tested for carcinogenic activity. They were methylnitrosamino-N,N-dimethylethylamine (MNDMEA) and N,N-dimethylaminoethylnitrosoethylurea (DMENEU). Each was administered orally to male and female F344 rats by gavage. MNDMEA was also given by gavage to Syrian hamsters and to rats as a solution in drinking water. The response of rats treated with MNDMEA was almost the same by the two modes of treatment and all developed tumors of the esophagus and died in less than 40 weeks; many also had tumors of the nasal mucosa. Hamsters were less susceptible to the nitrosamine than rats, since they survived longer following a larger dose and the tumor incidence was small; several hamsters had tumors of the nasal mucosa, some males also had tumors of the liver and lung and one male and two females had a tumor of the colon. Although it is a strong directly acting mutagen, dimethylaminoethylnitrosoethylurea was weakly carcinogenic in rats, giving rise to tumors of the uterus and mammary gland in females, but having no particular target organ in male rats. The presence of a basic center in these N-nitroso compounds does not prevent their absorption nor their entry into cells, which they can transform to tumors. JF - Cancer letters AU - Lijinsky, W AU - Kovatch, R M AU - Saavedra, J E AD - ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, Frederick, MD 21702. Y1 - 1992/04/15/ PY - 1992 DA - 1992 Apr 15 SP - 101 EP - 107 VL - 63 IS - 2 SN - 0304-3835, 0304-3835 KW - Carcinogens KW - 0 KW - Ethylamines KW - Indicators and Reagents KW - Methylamines KW - Mutagens KW - Nitroso Compounds KW - Nitrosourea Compounds KW - N,N-dimethylaminoethylnitrosoethylurea KW - 142713-74-4 KW - methylnitrosamino-N,N-dimethylethylamine KW - 23834-30-2 KW - Index Medicus KW - Administration, Oral KW - Molecular Structure KW - Animals KW - Salmonella typhimurium -- drug effects KW - Structure-Activity Relationship KW - Rats, Inbred Strains KW - Rats KW - Mutagenicity Tests KW - Rats, Inbred F344 KW - Carcinogenicity Tests KW - Mesocricetus KW - Female KW - Male KW - Cricetinae KW - Esophageal Neoplasms -- chemically induced KW - Ethylamines -- chemical synthesis KW - Carcinogens -- pharmacology KW - Nitrosourea Compounds -- pharmacology KW - Ethylamines -- pharmacology KW - Ethylamines -- toxicity KW - Nitrosourea Compounds -- chemical synthesis KW - Methylamines -- chemical synthesis KW - Carcinogens -- toxicity KW - Nitrosourea Compounds -- toxicity KW - Mutagens -- toxicity KW - Methylamines -- toxicity KW - Nitroso Compounds -- chemical synthesis KW - Mutagens -- chemical synthesis KW - Neoplasms, Experimental -- pathology KW - Mutagens -- pharmacology KW - Carcinogens -- chemical synthesis KW - Esophageal Neoplasms -- pathology KW - Neoplasms, Experimental -- chemically induced KW - Nitroso Compounds -- toxicity KW - Nitroso Compounds -- pharmacology KW - Methylamines -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72896393?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+letters&rft.atitle=Carcinogenesis+and+mutagenesis+by+N-nitroso+compounds+having+a+basic+center.&rft.au=Lijinsky%2C+W%3BKovatch%2C+R+M%3BSaavedra%2C+J+E&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1992-04-15&rft.volume=63&rft.issue=2&rft.spage=101&rft.isbn=&rft.btitle=&rft.title=Cancer+letters&rft.issn=03043835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-20 N1 - Date created - 1992-05-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Humanization of immunotoxins. AN - 72890198; 1565609 AB - The construction and expression of a chimeric gene encoding a mouse/human antibody to the human transferrin receptor fused to the gene for angiogenin, a human homolog of pancreatic RNase, are described. F(ab')2-like antibody-enzyme fusions were prepared by linking the gene for human angiogenin to a chimeric anti-transferrin receptor heavy chain gene. The antibody-enzyme fusion gene was introduced into a transfectoma that secretes the chimeric light chain of the same antibody, and cell lines were cloned that synthesize and secrete the antibody-enzyme fusion protein of the expected size at a concentration of 1-5 ng/ml. Culture supernatants from clones secreting the fusion protein caused inhibition of growth and protein synthesis of K562 cells that express the human transferrin receptor but not toward a non-human-derived cell line that lacks this receptor. Whereas excess antibody to the same receptor did not itself inhibit protein synthesis, it was able to completely prevent the protein synthesis inhibition caused by the fusion protein. These results indicate that the cytotoxicity is due to a transferrin receptor-mediated mechanism involving the angiogenin portion of the fusion protein and demonstrate the feasibility of constructing recombinant antibody-RNase molecules capable of killing tumor cells bearing the transferrin receptor. The significance of the acquired cytotoxicity of a mouse/human chimeric antibody linked to a human protein may bear importantly in human therapeutic strategies that use mouse antibodies linked to toxins from plants or bacteria to target tumor cells. It is expected that the humanization of immunotoxins will lead to less toxicity and immunogenicity than currently available reagents. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Rybak, S M AU - Hoogenboom, H R AU - Meade, H M AU - Raus, J C AU - Schwartz, D AU - Youle, R J AD - Biochemistry Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20896. Y1 - 1992/04/15/ PY - 1992 DA - 1992 Apr 15 SP - 3165 EP - 3169 VL - 89 IS - 8 SN - 0027-8424, 0027-8424 KW - Antibodies KW - 0 KW - Immunotoxins KW - Neoplasm Proteins KW - Proteins KW - Receptors, Transferrin KW - Recombinant Fusion Proteins KW - angiogenin KW - EC 3.1.27.- KW - Ribonuclease, Pancreatic KW - EC 3.1.27.5 KW - Index Medicus KW - Neoplasm Proteins -- biosynthesis KW - Animals KW - Transfection KW - Kinetics KW - Humans KW - Restriction Mapping KW - Leukemia, Myelogenous, Chronic, BCR-ABL Positive KW - Cell Division -- drug effects KW - Recombinant Fusion Proteins -- pharmacology KW - Mice KW - Plasmids KW - Cell Line KW - Immunotoxins -- toxicity KW - Receptors, Transferrin -- genetics KW - Receptors, Transferrin -- immunology KW - Proteins -- genetics KW - Proteins -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72890198?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Humanization+of+immunotoxins.&rft.au=Rybak%2C+S+M%3BHoogenboom%2C+H+R%3BMeade%2C+H+M%3BRaus%2C+J+C%3BSchwartz%2C+D%3BYoule%2C+R+J&rft.aulast=Rybak&rft.aufirst=S&rft.date=1992-04-15&rft.volume=89&rft.issue=8&rft.spage=3165&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-15 N1 - Date created - 1992-05-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1986 May;83(10):3146-50 [3458170] Biochemistry. 1985 Sep 24;24(20):5494-9 [2866795] J Immunol. 1986 Nov 1;137(9):2913-7 [3760576] Nucleic Acids Symp Ser. 1981;(10):203-9 [7312642] Cell. 1991 Mar 8;64(5):1017-23 [1900455] J Biol Chem. 1991 Nov 5;266(31):21202-7 [1939162] J Biol Chem. 1991 Nov 5;266(31):21208-14 [1939163] Proc Natl Acad Sci U S A. 1990 Mar;87(6):2047-51 [2315301] Biochemistry. 1986 Jun 17;25(12):3527-32 [2424496] Science. 1987 Jul 17;237(4812):280-2 [2440105] Biochemistry. 1985 Sep 24;24(20):5486-94 [2866794] Biochemistry. 1988 Apr 5;27(7):2288-94 [3289612] Proc Natl Acad Sci U S A. 1987 Dec;84(23):8330-4 [3479795] Biochem Biophys Res Commun. 1987 Aug 14;146(3):1240-8 [3619929] Gene. 1986;43(3):319-24 [3744051] Biochemistry. 1985 Sep 24;24(20):5480-6 [4074709] Nature. 1984 Dec 13-19;312(5995):604-8 [6095112] EMBO J. 1983;2(8):1373-8 [10872333] Biochem Biophys Res Commun. 1975 Nov 3;67(1):110-8 [1008] Mol Immunol. 1991 Sep;28(9):1027-37 [1922108] Biochim Biophys Acta. 1991 Jun 5;1096(4):345-54 [2065106] J Immunol. 1990 Apr 15;144(8):3211-7 [2324499] Biochem Biophys Res Commun. 1989 May 30;161(1):121-6 [2730651] Biochemistry. 1987 Aug 11;26(16):5141-6 [3663649] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Threonine 183 and adjacent flexible loop residues in the tryptophan synthase alpha subunit have critical roles in modulating the enzymatic activities of the beta subunit in the alpha 2 beta 2 complex. AN - 72878911; 1559990 AB - This study investigates the catalytic and allosteric roles of a flexible loop in the tryptophan synthase alpha 2 beta 2 complex. This loop connects helix 6 and strand 6 in the alpha subunit, an 8-fold alpha/beta barrel polypeptide. We have engineered three mutations in this disordered loop: a deletion of residues 185-187 and the replacement of threonine 183 by serine (T183S) or by alanine (T183A). Position 183 is a site of an inactivating mutation identified by Yanofsky's group (Yanofsky, C., Drapeau, G. R., Guest, J. R., and Carlton, B. C. (1967) Proc. Natl. Acad. Sci. U.S.A. 57, 296-298). The three engineered alpha subunits form stable, stoichiometric alpha 2 beta 2 complexes with the beta subunit which bind alpha and beta subunit ligands. Although changing threonine 183 to serine has little effect on the enzymatic properties, changing threonine 183 to alanine or deleting residues 185-187 results in a 50-fold reduction in the intrinsic activity of the alpha subunit alone and in the alpha site activity of the alpha 2 beta 2 complex. The latter two mutations profoundly alter the way in which the alpha subunit modulates the spectral properties and the activities of the wild-type beta subunit. These mutations also eliminate the effects of alpha subunit ligands on the beta subunit. Although the beta subunit ligand, L-serine, greatly stabilizes the wild-type alpha 2 beta 2 complex to dissociation and to proteolysis, L-serine stabilizes the T183A alpha 2 beta 2 complex weakly or not at all. Our findings suggest that the hydroxyl residue at position 183 and the adjacent residues in the alpha subunit loop play critical roles in the reciprocal communication between the alpha and beta subunits in the alpha 2 beta 2 complex. The results also help to explain how the wild-type alpha subunit or ammonium ion modulates the activities of the beta subunit. JF - The Journal of biological chemistry AU - Yang, X J AU - Miles, E W AD - Laboratory of Biochemical Pharmacology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/04/15/ PY - 1992 DA - 1992 Apr 15 SP - 7520 EP - 7528 VL - 267 IS - 11 SN - 0021-9258, 0021-9258 KW - Glycerophosphates KW - 0 KW - Indoles KW - Threonine KW - 2ZD004190S KW - indoleglycerol phosphate KW - 4220-97-7 KW - Serine KW - 452VLY9402 KW - Tryptophan Synthase KW - EC 4.2.1.20 KW - Index Medicus KW - Fluorescence KW - Electrophoresis, Polyacrylamide Gel KW - Amino Acid Sequence KW - Glycerophosphates -- metabolism KW - Hydrolysis KW - Serine -- metabolism KW - Salmonella typhimurium -- enzymology KW - Mutagenesis, Site-Directed KW - Kinetics KW - Molecular Sequence Data KW - Indoles -- metabolism KW - Mutation KW - Catalysis KW - Protein Conformation KW - Tryptophan Synthase -- metabolism KW - Threonine -- metabolism KW - Tryptophan Synthase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72878911?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Threonine+183+and+adjacent+flexible+loop+residues+in+the+tryptophan+synthase+alpha+subunit+have+critical+roles+in+modulating+the+enzymatic+activities+of+the+beta+subunit+in+the+alpha+2+beta+2+complex.&rft.au=Yang%2C+X+J%3BMiles%2C+E+W&rft.aulast=Yang&rft.aufirst=X&rft.date=1992-04-15&rft.volume=267&rft.issue=11&rft.spage=7520&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-12 N1 - Date created - 1992-05-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Rapid high-affinity transport of a chemotherapeutic amino acid across the blood-brain barrier. AN - 72878033; 1559223 AB - The therapeutic efficacy of many anticancer drugs against intracerebral tumors is limited by poor uptake into the central nervous system. One way to enhance brain delivery is to design agents that are transported into the brain by the saturable nutrient carriers of the blood-brain barrier. In this paper, we describe a nitrogen mustard amino acid, DL-2-amino-7-bis[(2-chloroethyl)amino/bd-1,2,3,4-tetrahydro-2-napthoi c acid, that is taken up into brain with high affinity by the large neutral amino acid carrier of the blood-brain barrier. Brain transport of DL-2-amino-7-bis[(2-chloroethyl)aminol-1,2,3,4-tetrahydro-2-naphth oic acid in the rat was found to be rapid (cerebrovascular permeability-surface area product approximately 2 x 10(-2) ml/s/g), saturable and inhibitable by large neutral amino acids. Maximal influx rate (Vmax) and half-saturation (Km) constants equaled 0.26 nmol/min/g and 0.19 microM, respectively, in the parietal cortex. Regional brain uptake of acid exceeded that of the clinical analogue, melphalan, by greater than 20-fold. The results demonstrate that drug modification to produce high-affinity ligands for the cerebrovascular nutrient carriers is a viable means to enhance drug delivery to brain for the treatment of brain tumors and other central nervous system disorders. JF - Cancer research AU - Takada, Y AU - Vistica, D T AU - Greig, N H AU - Purdon, D AU - Rapoport, S I AU - Smith, Q R AD - Laboratory of Neurosciences, National Institute on Aging, NIH, Bethesda, Maryland 20892. Y1 - 1992/04/15/ PY - 1992 DA - 1992 Apr 15 SP - 2191 EP - 2196 VL - 52 IS - 8 SN - 0008-5472, 0008-5472 KW - Nitrogen Mustard Compounds KW - 0 KW - 2-amino-7-(bis(2-chloroethyl)amino)-1,2,3,4-tetrahydro-2-naphthoic acid KW - 106094-83-1 KW - Phenylalanine KW - 47E5O17Y3R KW - 2-Naphthylamine KW - CKR7XL41N4 KW - Melphalan KW - Q41OR9510P KW - Index Medicus KW - Rats KW - Animals KW - Phenylalanine -- pharmacokinetics KW - Melphalan -- pharmacokinetics KW - Male KW - 2-Naphthylamine -- pharmacokinetics KW - Blood-Brain Barrier -- physiology KW - Brain -- metabolism KW - Nitrogen Mustard Compounds -- pharmacokinetics KW - 2-Naphthylamine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72878033?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Rapid+high-affinity+transport+of+a+chemotherapeutic+amino+acid+across+the+blood-brain+barrier.&rft.au=Takada%2C+Y%3BVistica%2C+D+T%3BGreig%2C+N+H%3BPurdon%2C+D%3BRapoport%2C+S+I%3BSmith%2C+Q+R&rft.aulast=Takada&rft.aufirst=Y&rft.date=1992-04-15&rft.volume=52&rft.issue=8&rft.spage=2191&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-08 N1 - Date created - 1992-05-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cellular mechanisms of the antitumor activity of recombinant IL-6 in mice. AN - 72877883; 1348521 AB - The systemic administration of human rIL-6 to mice resulted in the regression of established, 3-day pulmonary micrometastases from two weakly immunogenic tumors, but not from a nonimmunogenic tumor, in the absence of observable toxicity. Although IL-6 alone failed to have a significant therapeutic impact on advanced, 10-day pulmonary macrometastases from weakly immunogenic tumors, substantial cure rates of mice could be achieved when this cytokine was combined with cyclophosphamide. Histologic analysis of the lungs of mice receiving IL-6 revealed infiltration with lymphoid cells during the regression of pulmonary nodules from a weakly immunogenic tumor. IL-6-mediated tumor regression could be abrogated after selective in vivo depletion of either CD4 or CD8 T cell subsets by the systemic administration of specific mAb. In vivo generation of tumor-specific CTL, but not of lymphokine-activated killer cells, was detected in the lungs of IL-6-treated mice during regression of pulmonary metastases. Collectively, these findings demonstrate a role for IL-6 in the treatment of established solid tumors that have the capacity to elicit T cell responses in the host. Differences in host cellular mechanisms involved in tumor regression mediated by immunotherapy using IL-6 vs IL-2 are discussed. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Mulé, J J AU - Custer, M C AU - Travis, W D AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/04/15/ PY - 1992 DA - 1992 Apr 15 SP - 2622 EP - 2629 VL - 148 IS - 8 SN - 0022-1767, 0022-1767 KW - Antineoplastic Agents KW - 0 KW - Interleukin-6 KW - Recombinant Proteins KW - Cyclophosphamide KW - 8N3DW7272P KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Recombinant Proteins -- pharmacology KW - Cyclophosphamide -- therapeutic use KW - Lung Neoplasms -- secondary KW - Lymphocyte Depletion KW - Mice, Inbred C57BL KW - CD4-Positive T-Lymphocytes -- physiology KW - T-Lymphocytes, Cytotoxic -- immunology KW - Mice KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Recombinant Proteins -- therapeutic use KW - Female KW - Interleukin-6 -- therapeutic use KW - Interleukin-6 -- pharmacology KW - Neoplasms, Experimental -- drug therapy KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72877883?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Cellular+mechanisms+of+the+antitumor+activity+of+recombinant+IL-6+in+mice.&rft.au=Mul%C3%A9%2C+J+J%3BCuster%2C+M+C%3BTravis%2C+W+D%3BRosenberg%2C+S+A&rft.aulast=Mul%C3%A9&rft.aufirst=J&rft.date=1992-04-15&rft.volume=148&rft.issue=8&rft.spage=2622&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-13 N1 - Date created - 1992-05-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interleukin-7 mediates the generation and expansion of murine allosensitized and antitumor CTL. AN - 72876834; 1555257 AB - Interleukin-7 (IL-7) is a 25-kDa cytokine that was initially described as a pre-B cell growth factor and more recently has been shown to cause T cell proliferation. We have investigated the in vitro effects of IL-7 on mature T cells to include the generation and further expansion of allospecific and antitumor CTL. B6 anti-DBA allospecific CTL were generated in the presence of IL-7, IL-2, the combination IL-7 plus IL-2, or no cytokine. IL-7 alone or when combined with IL-2 enhanced the generation of allospecific CTL. To evaluate the proliferative effects of IL-7, 4-day B6 anti-DBA cultures were cultured in IL-7, IL-2, or no cytokine. Cell proliferation and duration of growth of cells cultured in IL-7 were significantly greater than cells cultured in IL-2 or in the absence of cytokine. Allospecific cytolytic activity was maintained during proliferation in IL-7 to a maximum of 60 days. In contrast with the ability of IL-2 to generate LAK cells, murine splenocytes cultured at varying doses of IL-7 (1 to 10,000 ng/ml), resulted in minimal LAK cell activity. The effect of IL-7 in the generation of CTL with antitumor activity was also studied. Seven days after footpad injection of MCA 203 or 205 sarcoma, draining lymph nodes (DLN) were harvested and restimulated in vitro with MCA 203 or 205, respectively, and maintained in culture with either IL-7, IL-2, the combination of IL-7 plus IL-2, or no cytokine. After 10 days in culture, cells generated in IL-7 or IL-2 exhibited similar cytotoxicity against the syngeneic autologous MCA tumor. IL-7 generated cells, however, showed specificity when tested by 51Cr release which was not seen with IL-2-generated cells. Cells generated in IL-7 plus IL-2 were more cytolytic than cells cultured with either cytokine alone. To further define the mechanism of action of IL-7 in antitumor CTL cultures, a monoclonal antibody, S4B6.1, capable of blocking murine-specific IL-2 was employed. The partial inhibition by this mAb of the generation of antitumor CTL demonstrated that IL-7 acted, in part, by an IL-2-dependent mechanism. Finally, IL-7 cultures restimulated at Day 11 with autologous MCA 203 showed greater proliferation than IL-2 cultures and remained lytic at Day 21 of culture.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Cellular immunology AU - Jicha, D L AU - Schwarz, S AU - Mulé, J J AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/04/15/ PY - 1992 DA - 1992 Apr 15 SP - 71 EP - 83 VL - 141 IS - 1 SN - 0008-8749, 0008-8749 KW - Interleukin-2 KW - 0 KW - Interleukin-7 KW - Recombinant Proteins KW - Index Medicus KW - Lymphocyte Activation KW - Animals KW - Recombinant Proteins -- pharmacology KW - Tumor Cells, Cultured KW - Killer Cells, Lymphokine-Activated -- immunology KW - Killer Cells, Lymphokine-Activated -- drug effects KW - Mice, Inbred C57BL KW - Cell Division -- drug effects KW - Mice KW - Drug Synergism KW - Female KW - Mice, Inbred DBA KW - Interleukin-2 -- pharmacology KW - Interleukin-7 -- immunology KW - T-Lymphocytes, Cytotoxic -- immunology KW - Interleukin-2 -- immunology KW - Interleukin-7 -- pharmacology KW - T-Lymphocytes, Cytotoxic -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72876834?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cellular+immunology&rft.atitle=Interleukin-7+mediates+the+generation+and+expansion+of+murine+allosensitized+and+antitumor+CTL.&rft.au=Jicha%2C+D+L%3BSchwarz%2C+S%3BMul%C3%A9%2C+J+J%3BRosenberg%2C+S+A&rft.aulast=Jicha&rft.aufirst=D&rft.date=1992-04-15&rft.volume=141&rft.issue=1&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=Cellular+immunology&rft.issn=00088749&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-06 N1 - Date created - 1992-05-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - NIH conference. Membranous nephropathy. AN - 72848112; 1546869 AB - Membranous nephropathy is a worldwide problem that accounts for about 20% of the cases of the adult-onset nephrotic syndrome. This disease places many patients at risk for both end-stage renal failure and the complications of hyperlipidemia. Immune-mediated injury to the glomerular capillary wall in patients with membranous nephropathy is characterized by subepithelial immune complex formation and generation of the membrane attack complex of complement. Glomerular capillary hypertension, hyperlipidemia, and possibly cytokines could contribute to the glomerular sclerosis seen in the advanced stages of the disorder. In some cases, production of pathogenic antibody can be suppressed by treating the underlying condition. The mechanisms of action of immunosuppressive agents are being investigated and treatments are being tested in clinical trials to optimize the balance of efficacy and toxicity. Alternate-day treatment with corticosteroids is often recommended for nephrotic patients with idiopathic membranous nephropathy, but this approach has not been proved beneficial. Ongoing studies are evaluating whether cytotoxic drugs or cyclosporin A combined with prednisone is more effective than treatment with corticosteroids alone. Lipid-lowering drug therapy is warranted in cases of the persistent nephrotic syndrome to avert the cardiovascular sequelae of hyperlipidemia. JF - Annals of internal medicine AU - Austin, H A AU - Antonovych, T T AU - MacKay, K AU - Boumpas, D T AU - Balow, J E AD - National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/04/15/ PY - 1992 DA - 1992 Apr 15 SP - 672 EP - 682 VL - 116 IS - 8 SN - 0003-4819, 0003-4819 KW - Immunosuppressive Agents KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Cardiovascular Diseases -- etiology KW - Humans KW - Disease Models, Animal KW - Immunosuppressive Agents -- therapeutic use KW - Cardiovascular Diseases -- prevention & control KW - Glomerulonephritis, Membranous -- pathology KW - Glomerulonephritis, Membranous -- drug therapy KW - Glomerulonephritis, Membranous -- immunology KW - Glomerulonephritis, Membranous -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72848112?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+internal+medicine&rft.atitle=NIH+conference.+Membranous+nephropathy.&rft.au=Austin%2C+H+A%3BAntonovych%2C+T+T%3BMacKay%2C+K%3BBoumpas%2C+D+T%3BBalow%2C+J+E&rft.aulast=Austin&rft.aufirst=H&rft.date=1992-04-15&rft.volume=116&rft.issue=8&rft.spage=672&rft.isbn=&rft.btitle=&rft.title=Annals+of+internal+medicine&rft.issn=00034819&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-14 N1 - Date created - 1992-04-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Translocation mediated by domain II of Pseudomonas exotoxin A: transport of barnase into the cytosol. AN - 72906279; 1567815 AB - Pseudomonas exotoxin A (PE) is a protein toxin composed of three structural domains. Functional analysis of PE has revealed that domain I is the cell-binding domain and that domain III functions in ADP ribosylation. Domain II was originally designated as the translocation domain, mediating the transfer of domain III to the cytosol, because mutations in this domain result in toxin molecules with normal cell-binding and ADP-ribosylation activities but which are not cytotoxic. However, the results do not rule out the possibility that regions of PE outside of domain II also participate in the translocation process. To investigate this problem, we have now constructed a toxin in which domain III of PE is replaced with barnase, the extracellular ribonuclease of Bacillus amyloliquefaciens. This chimeric toxin, termed PE1-412-Bar, is cytotoxic to a murine fibroblast cell line and to a murine hybridoma resistant to the ADP-ribosylation activity of PE. A mutant form of PE1-412-Bar with an inactivating mutation in domain II at position 276 was significantly less toxic. Because the cytotoxic effect of PE1-412-Bar was due to the ribonuclease-activity of barnase molecules which had been translocated to the cytosol, we conclude that domain II of PE is not only essential but also probably sufficient to carry out the translocation process. JF - Biochemistry AU - Prior, T I AU - FitzGerald, D J AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/04/14/ PY - 1992 DA - 1992 Apr 14 SP - 3555 EP - 3559 VL - 31 IS - 14 SN - 0006-2960, 0006-2960 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Recombinant Fusion Proteins KW - Virulence Factors KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Ribonucleases KW - EC 3.1.- KW - Bacillus amyloliquefaciens ribonuclease KW - EC 3.1.4.- KW - Thymidine KW - VC2W18DGKR KW - Index Medicus KW - Animals KW - Fibroblasts -- drug effects KW - Electrophoresis, Polyacrylamide Gel KW - Biological Transport KW - Mice KW - Adenosine Diphosphate Ribose -- metabolism KW - Plasmids KW - DNA Replication -- drug effects KW - Thymidine -- metabolism KW - Recombinant Fusion Proteins -- metabolism KW - Recombinant Fusion Proteins -- genetics KW - Recombinant Fusion Proteins -- pharmacology KW - Cell Line KW - Exotoxins -- genetics KW - Cytosol -- metabolism KW - Exotoxins -- pharmacology KW - Ribonucleases -- genetics KW - Exotoxins -- metabolism KW - Ribonucleases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72906279?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=Translocation+mediated+by+domain+II+of+Pseudomonas+exotoxin+A%3A+transport+of+barnase+into+the+cytosol.&rft.au=Prior%2C+T+I%3BFitzGerald%2C+D+J%3BPastan%2C+I&rft.aulast=Prior&rft.aufirst=T&rft.date=1992-04-14&rft.volume=31&rft.issue=14&rft.spage=3555&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-26 N1 - Date created - 1992-05-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Site-directed mutagenesis of cytochrome P450s CYP2A1 and CYP2A2: influence of the distal helix on the kinetics of testosterone hydroxylation. AN - 72874156; 1554718 AB - Cytochrome P450s CYP2A1 and CYP2A2 exhibit 88% sequence similarity, yet CYP2A1 metabolizes testosterone almost exclusively (90%) at the 7 alpha-position, whereas CYP2A2 forms several metabolites, with 15 alpha-hydroxytestosterone as a major metabolite. One of the regions with relatively low sequence homology corresponds by sequence alignment to the I and J helices of P450cam. Since this region is known to be part of the active site for P450cam, 26 single point and two double point mutants were prepared where the amino acid for one form was substituted with that of the other. Mutant and wild-type enzymes were expressed in Hep G2 cells using the vaccinia virus vector. Analysis of testosterone regioselectivity revealed that 25 of the mutants show the same regioselectivity as the parent wild-type enzymes and three are inactive, suggesting that no single amino acid in this region is totally responsible for the different selectivities of CYP2A1 and CYP2A2. Kinetic analysis of the CYP2A1 mutants showed that four of the mutants with changes near the conserved oxygen-binding region had Km values with much higher and Vmax values much lower than those of the wild-type enzyme and one mutant had a Vmax value twice as high as that of the wild-type enzyme. Deuterium isotope effects on 7 alpha-hydroxxylation were used to determine changes in the rate of reduction and estimate the relative amount of excess water formation. Changes in reduction rates and the amount of water produced are not sufficient to account for the differences in Vmax values, suggesting that the amount of hydrogen peroxide released is a primary determinant for changes in Vmax. JF - Biochemistry AU - Hanioka, N AU - Gonzalez, F J AU - Lindberg, N A AU - Liu, G AU - Gelboin, H V AU - Korzekwa, K R AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/04/07/ PY - 1992 DA - 1992 Apr 07 SP - 3364 EP - 3370 VL - 31 IS - 13 SN - 0006-2960, 0006-2960 KW - CYP2A1 KW - CYP2A2 KW - Recombinant Proteins KW - 0 KW - Testosterone KW - 3XMK78S47O KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Steroid Hydroxylases KW - EC 1.14.- KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - steroid hormone 7-alpha-hydroxylase KW - Index Medicus KW - Vaccinia virus -- genetics KW - Sequence Homology, Nucleic Acid KW - Amino Acid Sequence KW - Recombinant Proteins -- genetics KW - Structure-Activity Relationship KW - Binding Sites KW - Hydroxylation KW - Oxidation-Reduction KW - Base Sequence KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Molecular Sequence Data KW - Recombinant Proteins -- chemistry KW - Protein Conformation KW - Mutagenesis, Site-Directed KW - Testosterone -- metabolism KW - Cytochrome P-450 Enzyme System -- genetics KW - Cytochrome P-450 Enzyme System -- chemistry KW - Steroid Hydroxylases -- metabolism KW - Steroid Hydroxylases -- chemistry KW - Cytochrome P-450 Enzyme System -- metabolism KW - Steroid Hydroxylases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72874156?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=Site-directed+mutagenesis+of+cytochrome+P450s+CYP2A1+and+CYP2A2%3A+influence+of+the+distal+helix+on+the+kinetics+of+testosterone+hydroxylation.&rft.au=Hanioka%2C+N%3BGonzalez%2C+F+J%3BLindberg%2C+N+A%3BLiu%2C+G%3BGelboin%2C+H+V%3BKorzekwa%2C+K+R&rft.aulast=Hanioka&rft.aufirst=N&rft.date=1992-04-07&rft.volume=31&rft.issue=13&rft.spage=3364&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-06 N1 - Date created - 1992-05-06 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CYP2A1; CYP2A2 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dinucleotide repeat polymorphism in the THRA1 gene. AN - 73534088; 1301142 JF - Human molecular genetics AU - Futreal, P A AU - Barrett, J C AU - Wiseman, R W AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 66 VL - 1 IS - 1 SN - 0964-6906, 0964-6906 KW - THRA1 KW - Genetic Markers KW - 0 KW - Oligodeoxyribonucleotides KW - Index Medicus KW - Breast Neoplasms -- genetics KW - Base Sequence KW - Exons KW - Humans KW - Polymerase Chain Reaction -- methods KW - Molecular Sequence Data KW - Chromosome Mapping KW - Female KW - Chromosomes, Human, Pair 17 KW - Genes, Dominant KW - Polymorphism, Genetic KW - Repetitive Sequences, Nucleic Acid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73534088?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+molecular+genetics&rft.atitle=Dinucleotide+repeat+polymorphism+in+the+THRA1+gene.&rft.au=Futreal%2C+P+A%3BBarrett%2C+J+C%3BWiseman%2C+R+W&rft.aulast=Futreal&rft.aufirst=P&rft.date=1992-04-01&rft.volume=1&rft.issue=1&rft.spage=66&rft.isbn=&rft.btitle=&rft.title=Human+molecular+genetics&rft.issn=09646906&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-28 N1 - Date created - 1993-05-28 N1 - Date revised - 2017-01-13 N1 - Gene symbol - THRA1 N1 - Genetic sequence - M88637; GENBANK; M88636; X68230; M88633; M88632; X65457; M88635; M88634; X55068; X64599 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effects of two different inhibitors of PNMT and their interactions with ethanol. AN - 73152690; 1515594 AB - The effects of two structurally different inhibitors of phenylethanolamine-N-methyltransferase, LY 134046 and CGS 19281A were investigated in a holeboard test of directed exploration and locomotor activity. Both compounds dose-dependently reduced exploratory head-dipping without affecting locomotor activity. The interaction of each drug with ethanol was also studied by testing the ataxia. Administration of these compounds had differential effects in a test of ethanol-induced ataxia. LY 134046 significantly attenuated ethanol-induced ataxia whereas CGS 19281A was without effect or (at 50 mg kg-1) potentiated ethanol's effect. These results suggest that the ethanol attenuating properties of LY 134046 may not solely be due the inhibition of PNMT and that its alpha 2-adrenoceptor blocking properties may be playing a role. JF - Neuroreport AU - Durcan, M J AU - Lister, R G AU - Linnoila, M AD - Laboratory of Clinical Studies, DICBR, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 349 EP - 352 VL - 3 IS - 4 SN - 0959-4965, 0959-4965 KW - Benzazepines KW - 0 KW - Carbolines KW - 4,9-dihydro-7-methoxy-3H-pyrido(3,4b)indole KW - 31652-37-6 KW - Ethanol KW - 3K9958V90M KW - LY 134046 KW - 71274-97-0 KW - Phenylethanolamine N-Methyltransferase KW - EC 2.1.1.28 KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Reference Values KW - Drug Interactions KW - Analysis of Variance KW - Dose-Response Relationship, Drug KW - Mice KW - Male KW - Benzazepines -- pharmacology KW - Ethanol -- pharmacology KW - Exploratory Behavior -- drug effects KW - Motor Activity -- drug effects KW - Carbolines -- pharmacology KW - Phenylethanolamine N-Methyltransferase -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73152690?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroreport&rft.atitle=The+effects+of+two+different+inhibitors+of+PNMT+and+their+interactions+with+ethanol.&rft.au=Durcan%2C+M+J%3BLister%2C+R+G%3BLinnoila%2C+M&rft.aulast=Durcan&rft.aufirst=M&rft.date=1992-04-01&rft.volume=3&rft.issue=4&rft.spage=349&rft.isbn=&rft.btitle=&rft.title=Neuroreport&rft.issn=09594965&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-07 N1 - Date created - 1992-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The expanding use of immunosuppression in the treatment of non-infectious ocular disease. AN - 73137691; 1503617 AB - Cyclosporin has been used for an increasing number of ocular indications. This review attempts to put into perspective the present scope of cyclosporin use in the treatment of ophthalmic disorders. This includes a review of randomized masked trials performed to date and work done to minimize and characterize cyclosporin induced renal toxicity. In addition, the ocular surface is an ideal target for topical cyclosporin therapy, and the status of this therapeutic approach is reviewed. JF - Journal of autoimmunity AU - Nussenblatt, R AD - Laboratory of Immunology, National Eye Institute, NIH, Bethesda, MD 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 247 EP - 257 VL - 5 Suppl A SN - 0896-8411, 0896-8411 KW - Bromocriptine KW - 3A64E3G5ZO KW - Cyclosporine KW - 83HN0GTJ6D KW - Prednisone KW - VB0R961HZT KW - Index Medicus KW - Drug Therapy, Combination KW - Prednisone -- therapeutic use KW - Humans KW - Keratoconjunctivitis -- drug therapy KW - Bromocriptine -- therapeutic use KW - Endophthalmitis -- drug therapy KW - Uveitis -- drug therapy KW - Immunosuppression KW - Corneal Transplantation KW - Eye Diseases -- drug therapy KW - Cyclosporine -- adverse effects KW - Cyclosporine -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73137691?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+autoimmunity&rft.atitle=The+expanding+use+of+immunosuppression+in+the+treatment+of+non-infectious+ocular+disease.&rft.au=Nussenblatt%2C+R&rft.aulast=Nussenblatt&rft.aufirst=R&rft.date=1992-04-01&rft.volume=5+Suppl+A&rft.issue=&rft.spage=247&rft.isbn=&rft.btitle=&rft.title=Journal+of+autoimmunity&rft.issn=08968411&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-18 N1 - Date created - 1992-09-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hyperthermic antiblastic perfusion for the treatment of soft tissue limb sarcoma. AN - 73054831; 1622873 AB - Eighty patients with locally advanced, high grade soft tissue sarcoma of the extremities were studied prospectively in order to determine the efficacy of hyperthermic antiblastic perfusion (H.A.P.) as the first step of a combined multimodality therapy. All of the patients have been evaluated in terms of functional results, loco-regional control and survival according to the different treatment schedules adopted. The first clinical trial employed H.A.P., followed by surgery alone. Because the results obtained were unsatisfactory, the protocol was modified to include a continuous intra-arterial (i.a.) infusion of doxorubicin (dx) or radiotherapy before surgery. The best results have been obtained with the radiotherapy-including protocol showing a conservative surgery rate of 100% and a 94% rate of loco-regional control. The disease-free, distant disease-free and overall survival rates were 68%, 75% and 70%, respectively. The importance of the treatment protocol has been confirmed in a multivariate analysis which demonstrated that the treatment protocol adopted is one of the prognostic factors with an independent value (p = 0.06). JF - Annals of oncology : official journal of the European Society for Medical Oncology AU - Di Filippo, F AU - Giannarelli, D AU - Botti, C AU - Carlini, S AU - Cavaliere, F AU - Garinei, R AU - Schiratti, M AU - Casaldi, V AU - Tedesco, M AU - Cavaliere, R AD - Department of Surgical Oncology, Regina Elena National Cancer Institute, Rome, Italy. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - S71 EP - S74 VL - 3 Suppl 2 SN - 0923-7534, 0923-7534 KW - Index Medicus KW - Extremities KW - Prospective Studies KW - Survival Rate KW - Combined Modality Therapy KW - Humans KW - Soft Tissue Neoplasms -- mortality KW - Sarcoma -- mortality KW - Hyperthermia, Induced -- adverse effects KW - Soft Tissue Neoplasms -- therapy KW - Chemotherapy, Cancer, Regional Perfusion -- methods KW - Chemotherapy, Cancer, Regional Perfusion -- adverse effects KW - Hyperthermia, Induced -- methods KW - Sarcoma -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73054831?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+oncology+%3A+official+journal+of+the+European+Society+for+Medical+Oncology&rft.atitle=Hyperthermic+antiblastic+perfusion+for+the+treatment+of+soft+tissue+limb+sarcoma.&rft.au=Di+Filippo%2C+F%3BGiannarelli%2C+D%3BBotti%2C+C%3BCarlini%2C+S%3BCavaliere%2C+F%3BGarinei%2C+R%3BSchiratti%2C+M%3BCasaldi%2C+V%3BTedesco%2C+M%3BCavaliere%2C+R&rft.aulast=Di+Filippo&rft.aufirst=F&rft.date=1992-04-01&rft.volume=3+Suppl+2&rft.issue=&rft.spage=S71&rft.isbn=&rft.btitle=&rft.title=Annals+of+oncology+%3A+official+journal+of+the+European+Society+for+Medical+Oncology&rft.issn=09237534&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-11 N1 - Date created - 1992-08-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Targeting growth factor receptors with fusion toxins. AN - 73049760; 1319965 AB - Recombinant toxins which bind to growth factor receptors have been prepared and used to kill cells responsible for malignant or autoimmune disease. Our strategy has been to genetically fuse ligands to different forms of Pseudomonas exotoxin which due to mutations or deletions do not bind to normal cells. The resulting recombinant chimeric toxins, in concentrations often less than 1 ng/ml, selectively kill cells expressing the appropriate growth factor receptor. The ligand may be a growth factor, such as transforming growth factor alpha (TGF alpha), interleukin 6 (IL6) or interleukin 2 (IL2), or single chain antigen binding proteins, such as the variable heavy and light regions of the monoclonal antibody anti-Tac. These chimeric toxins kill not only established cell lines but also fresh tumor cells from patients and display anti-tumor activity toward human malignant tumors in nude mice. While clinical trials are beginning with some of these agents, work continues to improve the effectiveness of recombinant chimeric toxins, and to widen the scope of disorders which might be treated by this approach. JF - International journal of immunopharmacology AU - Kreitman, R J AU - FitzGerald, D AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 465 EP - 472 VL - 14 IS - 3 SN - 0192-0561, 0192-0561 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Immunotoxins KW - Interleukin-2 KW - Interleukin-6 KW - Interleukins KW - Receptors, Cell Surface KW - Recombinant Fusion Proteins KW - Transforming Growth Factor alpha KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Interleukin-2 -- pharmacology KW - Neoplasms -- drug therapy KW - Interleukin-2 -- metabolism KW - Interleukin-6 -- therapeutic use KW - Humans KW - Interleukin-6 -- metabolism KW - Interleukin-6 -- pharmacology KW - Pseudomonas KW - Recombinant Fusion Proteins -- metabolism KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - Interleukin-2 -- therapeutic use KW - Recombinant Fusion Proteins -- pharmacology KW - Recombinant Fusion Proteins -- therapeutic use KW - Exotoxins -- pharmacology KW - Transforming Growth Factor alpha -- therapeutic use KW - Interleukins -- metabolism KW - Transforming Growth Factor alpha -- metabolism KW - Receptors, Cell Surface -- metabolism KW - Interleukins -- pharmacology KW - Interleukins -- therapeutic use KW - Transforming Growth Factor alpha -- pharmacology KW - Exotoxins -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73049760?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+immunopharmacology&rft.atitle=Targeting+growth+factor+receptors+with+fusion+toxins.&rft.au=Kreitman%2C+R+J%3BFitzGerald%2C+D%3BPastan%2C+I&rft.aulast=Kreitman&rft.aufirst=R&rft.date=1992-04-01&rft.volume=14&rft.issue=3&rft.spage=465&rft.isbn=&rft.btitle=&rft.title=International+journal+of+immunopharmacology&rft.issn=01920561&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-03 N1 - Date created - 1992-08-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA binding, multimerization, and transcription stimulation by the Xenopus Y box proteins in vitro. AN - 73047971; 1622930 AB - The Y box factors bind to a specific DNA sequence (the Y box, containing a reverse CCAAT element) and have been implicated in the regulation of transcription. We have used deletion mutagenesis to define the protein domains of two Xenopus Y box factors, FRG Y1 and FRG Y2, that are essential for DNA binding, multimerization, and transcription. A domain of the Y box factors homologous to an Escherichia coli cold shock protein is required for DNA binding. Both the E. coli protein and the Y box factors recognize DNA sequences with similar selectivity. The conserved region between these proteins does not contain any previously defined DNA-binding motifs. The hydrophilic C-terminal tail of the proteins contributes to the assembly of nucleoprotein complexes. This region contains an unusual pattern of basic and acidic amino acids and represents a new type of domain mediating protein-protein interactions in transcription factors. Both the DNA-binding and the multimerization domains are important for stimulating transcription from the Xenopus hsp70 promoter in vitro. JF - The New biologist AU - Tafuri, S R AU - Wolffe, A P AD - Laboratory of Molecular Embryology, NICHD, NIH, Bethesda, MD 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 349 EP - 359 VL - 4 IS - 4 SN - 1043-4674, 1043-4674 KW - DNA-Binding Proteins KW - 0 KW - Heat-Shock Proteins KW - Nucleoproteins KW - Transcription Factors KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Nucleoproteins -- genetics KW - Nucleoproteins -- metabolism KW - Transcription, Genetic KW - Amino Acid Sequence KW - Binding Sites KW - Base Sequence KW - Promoter Regions, Genetic KW - In Vitro Techniques KW - Genetic Complementation Test KW - Molecular Sequence Data KW - Xenopus KW - Mutation KW - Heat-Shock Proteins -- genetics KW - Protein Conformation KW - Transcription Factors -- metabolism KW - DNA -- metabolism KW - DNA -- genetics KW - DNA-Binding Proteins -- genetics KW - Transcription Factors -- genetics KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73047971?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+New+biologist&rft.atitle=DNA+binding%2C+multimerization%2C+and+transcription+stimulation+by+the+Xenopus+Y+box+proteins+in+vitro.&rft.au=Tafuri%2C+S+R%3BWolffe%2C+A+P&rft.aulast=Tafuri&rft.aufirst=S&rft.date=1992-04-01&rft.volume=4&rft.issue=4&rft.spage=349&rft.isbn=&rft.btitle=&rft.title=The+New+biologist&rft.issn=10434674&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-07 N1 - Date created - 1992-08-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Readthrough suppression in the mammalian type C retroviruses and what it has taught us. AN - 73047925; 1320396 AB - Mammalian type C retroviruses use translational suppression to synthesize the enzymes which function in virus replication. The UAG termination codon at the end of the coding region for the viral core proteins is translated as glutamine at a frequency of approximately 5%, allowing synthesis of the enzymes as part of a large fusion protein. This unusual mechanism has several benefits for the virus: first, it modulates the relative levels of synthesis of the core proteins and the enzymes. This is essential for the proper assembly of the virus particle, since the fusion protein alone is apparently unable to assemble into particles. Second, the presence of the core protein moiety in the fusion protein probably provides a mechanism for targeting the enzymes to the virus particle. The mechanism of the suppression phenomenon is now under investigation. Recent studies have revealed that suppression in the viral context is dependent upon a complex cis-acting signal in the viral mRNA, including a pseudoknot beginning 9 nucleotides 3' of the termination codon. In addition, studies with viral mutants have shown that UAA and UGA, like UAG, are efficiently suppressed in the presence of this signal, and have identified the amino acids used in the suppression of these termination codons in reticulocyte lysates. In several cases, this analysis revealed the existence of previously unknown suppressor tRNAs. One important question which has not been answered is whether the suppression mechanism used by the virus has a parallel in the synthesis of host proteins. JF - The New biologist AU - Rein, A AU - Levin, J G AD - Laboratory of Molecular Virology and Carcinogenesis, ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, Frederick, MD 21702. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 283 EP - 289 VL - 4 IS - 4 SN - 1043-4674, 1043-4674 KW - Codon KW - 0 KW - Fusion Proteins, gag-pol KW - RNA, Viral KW - Index Medicus KW - Fusion Proteins, gag-pol -- biosynthesis KW - Protein Biosynthesis KW - Virus Replication -- genetics KW - Base Sequence KW - Codon -- genetics KW - Molecular Sequence Data KW - Fusion Proteins, gag-pol -- genetics KW - RNA, Viral -- genetics KW - Retroviridae -- physiology KW - Suppression, Genetic KW - Retroviridae -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73047925?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+New+biologist&rft.atitle=Readthrough+suppression+in+the+mammalian+type+C+retroviruses+and+what+it+has+taught+us.&rft.au=Rein%2C+A%3BLevin%2C+J+G&rft.aulast=Rein&rft.aufirst=A&rft.date=1992-04-01&rft.volume=4&rft.issue=4&rft.spage=283&rft.isbn=&rft.btitle=&rft.title=The+New+biologist&rft.issn=10434674&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-07 N1 - Date created - 1992-08-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular model for DNA recognition by the family of basic-helix-loop-helix-zipper proteins. AN - 73038657; 1622934 AB - The basic-helix-loop-helix-zipper (bHLH-Zip) motif is a conserved region of approximately 70 amino acids that mediates both sequence-specific DNA binding and protein dimerization. This motif is found in protein sequences from many eukaryotic organisms and is contained in the protein sequence of the oncogene myc and its partner max, and a shortened version of the motif (bHLH) is found in the muscle determination factor myoD and its partner E12. An evaluation of the conserved amino acids that define the motif coupled with the published mutagenic studies of this region has led to our formulation of a molecular model for the binding of this motif as a dimer to specific sequences of DNA. This model has the dimeric protein interacting with an abutted, dyad-symmetric DNA sequence. Helix 2 of each monomer is modeled as a coiled-coil extension of the C-terminal "leucine zipper." Helix 1 does not interact with helix 1 from its partner in the dimer but with the hydrophobic surface created when the helix 2 regions of the dimer interact with each other as a coiled-coil. Sequence-specific interactions are proposed between the basic region and the invariant cis elements that all bHLH-Zip proteins bind. JF - The New biologist AU - Vinson, C R AU - Garcia, K C AD - Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 396 EP - 403 VL - 4 IS - 4 SN - 1043-4674, 1043-4674 KW - DNA-Binding Proteins KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Leucine Zippers -- genetics KW - Sequence Homology, Nucleic Acid KW - Humans KW - DNA -- metabolism KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Protein Conformation KW - Binding Sites KW - DNA-Binding Proteins -- chemistry KW - Models, Molecular KW - DNA-Binding Proteins -- genetics KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73038657?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+New+biologist&rft.atitle=Molecular+model+for+DNA+recognition+by+the+family+of+basic-helix-loop-helix-zipper+proteins.&rft.au=Vinson%2C+C+R%3BGarcia%2C+K+C&rft.aulast=Vinson&rft.aufirst=C&rft.date=1992-04-01&rft.volume=4&rft.issue=4&rft.spage=396&rft.isbn=&rft.btitle=&rft.title=The+New+biologist&rft.issn=10434674&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-07 N1 - Date created - 1992-08-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of hepatic CYP1A activity as a biomarker for environmental exposure to Aroclor 1254 in feral rodents. AN - 73030639; 1616319 AB - Specimens of the feral mouse species Reithrodontomys fulvescens trapped from a polychlorinated biphenyl (PCB)-contaminated field location had hepatic ethoxyresorufin (ETR) O-dealkylase activities and immunoreactive CYP1A protein contents which were two- to threefold higher than those measured in animals of the same species and sex collected from non PCB-contaminated reference sites. Specimens with hepatic ETR O-dealkylase activities differing by as little as 50% could readily be assigned as originating from the PCB or reference sites by the use of a specific chemical inhibitor of cytochrome P450IA (CYP1A). The relative levels of ETR O-dealkylase activity in R. fulvescens significantly correlated with hepatic PCB burdens (r = 0.819, P less than 0.01). When the magnitudes of the induced ETR O-dealkylase activities corresponding to given hepatic PCB burdens were compared between the feral animals, F344/NCr rats (Rattus norvegicus) or B6C3F1 mice (Mus musculus) exposed in the laboratory to dietary Aroclor 1254, the order of sensitivity to the inducing effects of PCBs were F344/NCr rat greater than B6C3F1 mouse greater than R. fulvescens. JF - Archives of environmental contamination and toxicology AU - Lubet, R A AU - Nims, R W AU - Beebe, L E AU - Fox, S D AU - Issaq, H J AU - McBee, K AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, PRI-DynCorp, Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 339 EP - 344 VL - 22 IS - 3 SN - 0090-4341, 0090-4341 KW - Aroclors KW - 0 KW - Biomarkers KW - Carcinogens KW - Chlorodiphenyl (54% Chlorine) KW - 11097-69-1 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Polychlorinated Biphenyls KW - DFC2HB4I0K KW - Oxidoreductases KW - EC 1.- KW - Cytochrome P-450 CYP1A1 KW - EC 1.14.14.1 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Body Burden KW - Environmental Exposure KW - Polychlorinated Biphenyls -- metabolism KW - Mice KW - Species Specificity KW - Male KW - Female KW - Liver -- enzymology KW - Liver -- drug effects KW - Carcinogens -- toxicity KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Aroclors -- toxicity KW - Oxidoreductases -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73030639?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+environmental+contamination+and+toxicology&rft.atitle=Induction+of+hepatic+CYP1A+activity+as+a+biomarker+for+environmental+exposure+to+Aroclor+1254+in+feral+rodents.&rft.au=Lubet%2C+R+A%3BNims%2C+R+W%3BBeebe%2C+L+E%3BFox%2C+S+D%3BIssaq%2C+H+J%3BMcBee%2C+K&rft.aulast=Lubet&rft.aufirst=R&rft.date=1992-04-01&rft.volume=22&rft.issue=3&rft.spage=339&rft.isbn=&rft.btitle=&rft.title=Archives+of+environmental+contamination+and+toxicology&rft.issn=00904341&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-27 N1 - Date created - 1992-07-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Analyzing the fusion process of influenza hemagglutinin by mutagenesis and molecular modeling. AN - 72996687; 1600107 JF - Biophysical journal AU - Guy, H R AU - Durell, S R AU - Schoch, C AU - Blumenthal, R AD - Lab of Mathematical Biology, DCBDC, NCI, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 95 EP - 97 VL - 62 IS - 1 SN - 0006-3495, 0006-3495 KW - Hemagglutinin Glycoproteins, Influenza Virus KW - 0 KW - Hemagglutinins, Viral KW - Viral Envelope Proteins KW - Viral Fusion Proteins KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - Viral Envelope Proteins -- chemistry KW - Viral Fusion Proteins -- chemistry KW - Models, Molecular KW - In Vitro Techniques KW - Viral Fusion Proteins -- genetics KW - Biophysical Phenomena KW - Viral Envelope Proteins -- genetics KW - Protein Conformation KW - Biophysics KW - Membrane Fusion -- physiology KW - Membrane Fusion -- genetics KW - Hemagglutinins, Viral -- chemistry KW - Hemagglutinins, Viral -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72996687?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biophysical+journal&rft.atitle=Analyzing+the+fusion+process+of+influenza+hemagglutinin+by+mutagenesis+and+molecular+modeling.&rft.au=Guy%2C+H+R%3BDurell%2C+S+R%3BSchoch%2C+C%3BBlumenthal%2C+R&rft.aulast=Guy&rft.aufirst=H&rft.date=1992-04-01&rft.volume=62&rft.issue=1&rft.spage=95&rft.isbn=&rft.btitle=&rft.title=Biophysical+journal&rft.issn=00063495&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-16 N1 - Date created - 1992-07-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Mol Biol. 1985 Aug 20;184(4):667-76 [4046029] Nature. 1989 Nov 30;342(6249):555-8 [2586627] J Cell Biol. 1989 Jul;109(1):113-22 [2745545] Annu Rev Physiol. 1990;52:675-97 [2184772] J Biol Chem. 1989 Mar 5;264(7):3972-8 [2917985] EMBO J. 1990 Dec;9(13):4231-41 [2265606] J Virol. 1986 Dec;60(3):833-9 [3783818] J Cell Biol. 1986 Jan;102(1):11-23 [3753607] Nature. 1981 Jan 29;289(5796):366-73 [7464906] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Atomic scale structure and functional models of voltage-gated potassium channels. AN - 72983800; 1600096 AB - Recent mutagenesis experiments have confirmed our hypothesis that a segment between S5 and S6 forms the ion selective portion of voltage-gated ion channels. Based on these and other new data, we have revised previous models of the general folding pattern of voltage-gated channel proteins and have developed atomic scale models of the entire transmembrane region of the Shaker A K+ channel. In these models, the ion selective region is a beta-barrel that spans the outer half of the membrane. The inner half of the pore is larger. The voltage-dependent conformational changes of activation gating are modeled to occur by the "helical screw" mechanism, in which the four S4 segments move along and rotate about their axes. These changes are followed by a voltage-independent conformational change, in which the segments linking S4 to S5 move from blocking the intracellular entrance of the pore to forming part of the lining of the large inner portion of the pore. The NH2-terminal of the protein was modeled as an alpha-helix that plugs the intracellular half of the pore to inactivate the channel. JF - Biophysical journal AU - Durell, S R AU - Guy, H R AD - Laboratory of Mathematical Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 238 EP - 47; discussion 247-50 VL - 62 IS - 1 SN - 0006-3495, 0006-3495 KW - Potassium Channels KW - 0 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Ion Channel Gating -- physiology KW - Animals KW - Models, Molecular KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Biophysical Phenomena KW - Protein Conformation KW - Biophysics KW - Potassium Channels -- chemistry KW - Potassium Channels -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72983800?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biophysical+journal&rft.atitle=Atomic+scale+structure+and+functional+models+of+voltage-gated+potassium+channels.&rft.au=Durell%2C+S+R%3BGuy%2C+H+R&rft.aulast=Durell&rft.aufirst=S&rft.date=1992-04-01&rft.volume=62&rft.issue=1&rft.spage=238&rft.isbn=&rft.btitle=&rft.title=Biophysical+journal&rft.issn=00063495&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-16 N1 - Date created - 1992-07-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Pflugers Arch. 1991 May;418(4):423-9 [1876487] Int J Pept Protein Res. 1980 Mar;15(3):211-24 [7380605] Science. 1991 Feb 22;251(4996):939-42 [2000494] Nature. 1991 Feb 21;349(6311):700-4 [1899917] Science. 1990 Oct 12;250(4978):276-9 [2218530] Proteins. 1990;8(1):14-22 [2217160] Nature. 1991 Feb 21;349(6311):657-8 [1705014] Nature. 1991 Mar 21;350(6315):232-5 [1706481] Eur Biophys J. 1991;20(3):127-33 [1660394] Nature. 1991 Jan 24;349(6307):305-10 [1846229] Nature. 1991 Sep 5;353(6339):86-90 [1881453] Science. 1991 Aug 2;253(5019):551-5 [1857984] Proc Natl Acad Sci U S A. 1991 Apr 1;88(7):2931-5 [2011602] Proc Natl Acad Sci U S A. 1991 Jan 15;88(2):561-4 [1988953] Eur Biophys J. 1990;18(6):327-33 [2170103] Science. 1990 Oct 26;250(4980):568-71 [2122520] Science. 1990 Dec 14;250(4987):1558-60 [2274786] Science. 1988 Oct 7;242(4875):50-61 [2459775] Science. 1987 Aug 14;237(4816):770-5 [2441471] Proc Natl Acad Sci U S A. 1986 Jan;83(2):508-12 [2417247] FEBS Lett. 1989 Dec 18;259(1):213-6 [2557243] Nature. 1989 Jun 22;339(6226):597-603 [2543931] Science. 1989 Aug 4;245(4917):510-3 [2667138] Biophys J. 1985 Jan;47(1):61-70 [3978191] Trends Neurosci. 1990 Jun;13(6):201-6 [1694324] J Membr Biol. 1990 Jun;116(2):117-28 [2166163] Biophys J. 1990 May;57(5):1049-64 [2340341] J Gen Physiol. 1990 Jan;95(1):29-60 [2299331] J Mol Biol. 1981 Jan 5;145(1):215-50 [7265198] Science. 1991 Feb 22;251(4996):942-4 [2000495] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparative carcinogenicity of ethylene thiourea with or without perinatal exposure in rats and mice. AN - 72979879; 1597265 AB - Chronic toxicity and carcinogenicity studies of ethylene thiourea (ETU), 97% pure, were conducted in F344/N rats and B6C3F1 mice of each sex. The major objective of the study was to determine if incorporation of perinatal exposure, in addition to the conventional exposure of young adult animals for 2 years, enhances the sensitivity of the bioassay in identification of the carcinogenic potential of chemicals when compared to the conventional exposure of animals to a chemical for 2 years, usually beginning at the age of 6-8 weeks. The studies were designed to determine (1) the toxic and carcinogenic effects of dietary ETU in rats and mice receiving perinatal exposure up to 8 weeks of age followed by control diet for 2 years, (2) the effects of ETU in rats and mice receiving exposure for 2 years beginning at the age of 8 weeks, and (3) the effects of combined perinatal/adult exposure to ETU (perinatal exposure to 8 weeks of age followed by the adult exposure for 2 years). During the perinatal period, rats were exposed to dietary ETU concentrations ranging from 9 to 90 ppm and adult exposure concentrations ranged from 25 to 250 ppm. In the mice, the perinatal exposure concentrations of ETU in the diet ranged from 33 to 330 ppm, and in the adults the concentrations were 100 to 1000 ppm. A total of eight exposure groups (including controls) were used with 60 animals in each group. Ten animals from each group were killed at Month 9 of the study for interim evaluation. The thyroid gland in rats and mice and the liver in mice were identified as target organs of ETU toxicity at the 9-month interim evaluation. The perinatal only exposure to ETU was not carcinogenic in rats or mice, while adult or perinatal/adult combination exposures to ETU were carcinogenic both in rats and in mice. The thyroid gland was the major site of ETU carcinogenicity both in rats and in mice. The liver and pituitary glands were other major sites of ETU carcinogenicity in mice. The carcinogenic effects of ETU were generally similar by adult and perinatal/adult combination protocols except that the incidences of thyroid tumors were slightly higher in the rats receiving the perinatal/adult combination of ETU exposure in the diet. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Chhabra, R S AU - Eustis, S AU - Haseman, J K AU - Kurtz, P J AU - Carlton, B D AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 405 EP - 417 VL - 18 IS - 3 SN - 0272-0590, 0272-0590 KW - Carcinogens KW - 0 KW - Hormones KW - Thyroid Hormones KW - Ethylenethiourea KW - 24FOJ4N18S KW - Index Medicus KW - Thyroid Neoplasms -- chemically induced KW - Animals KW - Hormones -- blood KW - Mice KW - Neoplasms, Experimental -- pathology KW - Pregnancy KW - Rats KW - Rats, Inbred F344 KW - Body Weight -- drug effects KW - Mice, Inbred C57BL KW - Thyroid Neoplasms -- pathology KW - Diet KW - Thyroid Hormones -- blood KW - Species Specificity KW - Female KW - Organ Size -- drug effects KW - Prenatal Exposure Delayed Effects KW - Ethylenethiourea -- toxicity KW - Carcinogens -- administration & dosage KW - Carcinogens -- toxicity KW - Ethylenethiourea -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72979879?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=Comparative+carcinogenicity+of+ethylene+thiourea+with+or+without+perinatal+exposure+in+rats+and+mice.&rft.au=Chhabra%2C+R+S%3BEustis%2C+S%3BHaseman%2C+J+K%3BKurtz%2C+P+J%3BCarlton%2C+B+D&rft.aulast=Chhabra&rft.aufirst=R&rft.date=1992-04-01&rft.volume=18&rft.issue=3&rft.spage=405&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-07 N1 - Date created - 1992-07-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Applications of crude incidence curves. AN - 72978666; 1594819 AB - Crude incidence curves display the cumulative number of failures of interest as a function of time. With competing causes of failure, they are distinct from cause-specific incidence curves that treat secondary types of failures as censored observations. After briefly reviewing their definition and estimation, we present five applications of crude incidence curves to show their utility in a broad range of studies. In some of these applications it is helpful to model survival-time distributions with use of two different time metameters, for example, time from diagnosis and age of the patient. We describe how one can incorporate published vital statistics into the models when secondary types of failure correspond to common causes of death. JF - Statistics in medicine AU - Korn, E L AU - Dorey, F J AD - Biometric Research Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 813 EP - 829 VL - 11 IS - 6 SN - 0277-6715, 0277-6715 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Prosthesis Failure KW - Prostatectomy -- adverse effects KW - Humans KW - Male KW - Female KW - Radiotherapy -- adverse effects KW - Proportional Hazards Models KW - Hip Prosthesis -- adverse effects KW - Antineoplastic Agents -- adverse effects KW - Treatment Outcome KW - Incidence KW - Cause of Death KW - Survival Analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72978666?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Statistics+in+medicine&rft.atitle=Applications+of+crude+incidence+curves.&rft.au=Korn%2C+E+L%3BDorey%2C+F+J&rft.aulast=Korn&rft.aufirst=E&rft.date=1992-04-01&rft.volume=11&rft.issue=6&rft.spage=813&rft.isbn=&rft.btitle=&rft.title=Statistics+in+medicine&rft.issn=02776715&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-01 N1 - Date created - 1992-07-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Smoking and risk of leukemia. AN - 72974231; 1595675 AB - The relation between tobacco use and leukemia was evaluated in a population-based case-control study of 578 white men with leukemia and 820 controls conducted in Iowa and Minnesota during 1981-1984. Risks were significantly elevated for all leukemia (odds ratio (OR) = 1.4) and chronic lymphocytic leukemia (OR = 1.6) for both tobacco users and cigarette smokers. There were significantly elevated risks for cigarette smokers of longest duration for all leukemia (OR = 1.6), chronic myelogenous leukemia (OR = 3.3), and chronic lymphocytic leukemia (OR = 1.6). Thus, the findings of this study provide additional support for an association between smoking and the risk of several types of leukemia. JF - American journal of epidemiology AU - Brown, L M AU - Gibson, R AU - Blair, A AU - Burmeister, L F AU - Schuman, L M AU - Cantor, K P AU - Fraumeni, J F AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/04/01/ PY - 1992 DA - 1992 Apr 01 SP - 763 EP - 768 VL - 135 IS - 7 SN - 0002-9262, 0002-9262 KW - Index Medicus KW - Plants, Toxic KW - Odds Ratio KW - Risk Factors KW - Humans KW - Adult KW - Tobacco, Smokeless -- adverse effects KW - Case-Control Studies KW - Aged KW - Middle Aged KW - Male KW - Leukemia -- epidemiology KW - Smoking -- adverse effects KW - Leukemia -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72974231?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+epidemiology&rft.atitle=Smoking+and+risk+of+leukemia.&rft.au=Brown%2C+L+M%3BGibson%2C+R%3BBlair%2C+A%3BBurmeister%2C+L+F%3BSchuman%2C+L+M%3BCantor%2C+K+P%3BFraumeni%2C+J+F&rft.aulast=Brown&rft.aufirst=L&rft.date=1992-04-01&rft.volume=135&rft.issue=7&rft.spage=763&rft.isbn=&rft.btitle=&rft.title=American+journal+of+epidemiology&rft.issn=00029262&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-30 N1 - Date created - 1992-06-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pneumocystis carinii pneumonia (PCP) and your child: a parent information booklet. AN - 72970935; 1594471 AB - A parent education booklet describing Pneumocystis carinii pneumonia (PCP) was prepared by the Pediatric Branch of the National Cancer Institute. In addition to information about prophylaxis and treatment of PCP, the booklet discusses overall care of children infected with human immunodeficiency virus. JF - Oncology nursing forum AU - Wiener, L AU - Leyden, C G AU - Pizzo, P A AU - Ognibene, F P AU - Rosenthal, C AU - Schubert, W AD - Pediatric Branch, National Cancer Institute (NCI), National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 507 EP - 509 VL - 19 IS - 3 SN - 0190-535X, 0190-535X KW - Pentamidine KW - 673LC5J4LQ KW - Trimethoprim, Sulfamethoxazole Drug Combination KW - 8064-90-2 KW - Index Medicus KW - Nursing KW - AIDS/HIV KW - Humans KW - Trimethoprim, Sulfamethoxazole Drug Combination -- therapeutic use KW - Sputum -- parasitology KW - Pentamidine -- adverse effects KW - Child KW - Biopsy KW - Bronchoalveolar Lavage Fluid -- parasitology KW - Trimethoprim, Sulfamethoxazole Drug Combination -- adverse effects KW - Pentamidine -- therapeutic use KW - Parents -- education KW - Acquired Immunodeficiency Syndrome -- complications KW - Pneumonia, Pneumocystis -- drug therapy KW - Pneumonia, Pneumocystis -- diagnosis KW - Pneumonia, Pneumocystis -- complications KW - Pamphlets UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72970935?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncology+nursing+forum&rft.atitle=Pneumocystis+carinii+pneumonia+%28PCP%29+and+your+child%3A+a+parent+information+booklet.&rft.au=Wiener%2C+L%3BLeyden%2C+C+G%3BPizzo%2C+P+A%3BOgnibene%2C+F+P%3BRosenthal%2C+C%3BSchubert%2C+W&rft.aulast=Wiener&rft.aufirst=L&rft.date=1992-04-01&rft.volume=19&rft.issue=3&rft.spage=507&rft.isbn=&rft.btitle=&rft.title=Oncology+nursing+forum&rft.issn=0190535X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-01 N1 - Date created - 1992-07-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - CONF T1 - Criteria for judging the relative toxicity of chemicals from developmental toxicity data: a workshop summary. AN - 72970149; 1350114 AB - In summary, participants of this workshop confirmed that many criteria need to be considered when interpreting the results of developmental toxicity studies. All aspects of developmental toxicity are of interest, but their importance to the consideration varies along the continuum from hazard detection to risk estimation. As with many other manifestations of toxicity, potential developmental risk to humans is a function of exposure and developmental toxicity, the latter reflecting the inherent potential of a substance to cause an adverse effect under some defined condition. All of the criteria discussed in this workshop were considered to be of some importance in characterizing the developmental toxicity of a substance, their relative importance being a function of the question under consideration. Proper interpretation of developmental toxicity data, which must include prenatal as well as postnatal observations to be considered complete, should take into account the differential toxicity to the mother and the conceptus, the nature of the developmental toxicity observed, and the consistency of response between species. The proximity of human exposure levels to dose levels that are developmentally toxic in animals is a major determinant of the potential for hazard to humans. Mechanistic and pharmacokinetic knowledge can modulate interpretation of descriptive data and refine the prediction of human hazard. Recognizing that in vitro studies will never completely recapitulate the results of in vivo studies, the committee to update the "Smith list" will move forward taking the discussions of this workshop into account. JF - Teratology AU - Schwetz, B A Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 337 EP - 339 VL - 45 IS - 4 KW - Teratogens KW - 0 KW - Index Medicus KW - Animals KW - Toxicology -- standards KW - Humans KW - Reference Standards KW - Drug Evaluation, Preclinical KW - Teratogens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72970149?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=Teratology&rft.atitle=Criteria+for+judging+the+relative+toxicity+of+chemicals+from+developmental+toxicity+data%3A+a+workshop+summary.&rft.au=Schwetz%2C+B+A&rft.aulast=Schwetz&rft.aufirst=B&rft.date=1992-04-01&rft.volume=45&rft.issue=4&rft.spage=337&rft.isbn=&rft.btitle=&rft.title=Teratology&rft.issn=00403709&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-12 N1 - Date created - 1992-06-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Application of molecular encapsulation for toxicology studies: comparative toxicity of p-Chloro-alpha, alpha, alpha-trifluorotoluene in alpha-cyclodextrin vehicle versus corn oil vehicle in male and female Fischer 344 rats and B6C3F1 mice. AN - 72967993; 1375921 AB - The application of alpha-cyclodextrin (alpha-CD) as an alternative vehicle for water insoluble and volatile chemicals was investigated in toxicity studies of p-chloro-alpha, alpha, alpha-trifluorotoluene (CTFT). Groups of F344 rats and B6C3F1 mice of each sex were administered CTFT (97% pure) by gavage in either corn oil or alpha-CD aqueous formulations daily for 14 consecutive days. The dose levels used were 10 (mice only), 50, 400, and 1000 mg/kg for corn oil vehicle and 10, 50, and 400 mg/kg (maximum achievable dose at gavage volume of 5 ml/kg) for alpha-CD vehicle. With both vehicles CTFT and alpha 2u-globulin were found to accumulate in the male rat kidney after 14 days of exposure and a dose-related toxic nephropathy was observed at dose of 50 mg/kg or higher. The hepatocellular hypertrophy and cytoplasmic vacuolation of the adrenal cortex which appeared in dosed male and female rats were also found to be independent of vehicle. Clinical pathology findings suggested a mild anemia and cholestasis in rats. With both vehicles no tissue bioaccumulation of CTFT was found in male or female mice. Vehicle-independent hepatocellular hypertrophy and cholestasis were also observed in mice at doses of 400 and 1000 mg/kg. In conclusion, the alpha-CD vehicle does not affect the toxic responses of CTFT in both sexes of both species. The results of the studies suggest that alpha-CD may be an appropriate alternative vehicle for toxicity studies. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Yuan, J AU - Jameson, C W AU - Goehl, T J AU - Elwell, M R AU - Leininger, J R AU - Thompson, M B AU - Corniffe, G AU - Carlton, T AD - National Institutes of Health, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 460 EP - 470 VL - 18 IS - 3 SN - 0272-0590, 0272-0590 KW - Alpha-Globulins KW - 0 KW - Capsules KW - Cyclodextrins KW - Pharmaceutical Vehicles KW - Proteins KW - alpha 2u globulin KW - alpha-Cyclodextrins KW - Toluene KW - 3FPU23BG52 KW - 4-chloro-alpha,alpha,alpha-trifluorotoluene KW - 694YO34JHC KW - Corn Oil KW - 8001-30-7 KW - alpha-cyclodextrin KW - Z1LH97KTRM KW - Index Medicus KW - Alpha-Globulins -- biosynthesis KW - Animals KW - Liver -- pathology KW - Kidney -- metabolism KW - Kidney -- pathology KW - Humans KW - Infant, Newborn KW - Kidney -- drug effects KW - Liver -- metabolism KW - Mice KW - Proteins -- metabolism KW - Blood Cell Count KW - Rats KW - Mice, Inbred Strains KW - Rats, Inbred F344 KW - Liver -- drug effects KW - Body Weight -- drug effects KW - Alpha-Globulins -- immunology KW - Species Specificity KW - Male KW - Female KW - Organ Size -- drug effects KW - Toluene -- analogs & derivatives KW - Toluene -- administration & dosage KW - Toluene -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72967993?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=Application+of+molecular+encapsulation+for+toxicology+studies%3A+comparative+toxicity+of+p-Chloro-alpha%2C+alpha%2C+alpha-trifluorotoluene+in+alpha-cyclodextrin+vehicle+versus+corn+oil+vehicle+in+male+and+female+Fischer+344+rats+and+B6C3F1+mice.&rft.au=Yuan%2C+J%3BJameson%2C+C+W%3BGoehl%2C+T+J%3BElwell%2C+M+R%3BLeininger%2C+J+R%3BThompson%2C+M+B%3BCorniffe%2C+G%3BCarlton%2C+T&rft.aulast=Yuan&rft.aufirst=J&rft.date=1992-04-01&rft.volume=18&rft.issue=3&rft.spage=460&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-07 N1 - Date created - 1992-07-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Glutamatergic therapy of Huntington's chorea. AN - 72966479; 1350513 AB - Preclinical evidence suggests that hypofunction of the glutamatergic subthalamopallidal tract may contribute to the hyperkinesis in Huntington's chorea. The clinical effects of milacemide, a glycine prodrug, were studied in seven patients with Huntington's disease under double-blind, placebo-controlled conditions. Oral doses of 1,200 mg/day did not alter chorea or cognitive dysfunction. Specific modulatory effects of glycine on the NMDA subtype of glutamate receptors, rather than the AMPA receptors, which may predominate among target neurons of the subthalamus, may explain the therapeutic failure of milacemide. JF - Clinical neuropharmacology AU - Giuffra, M E AU - Mouradian, M M AU - Chase, T N AD - Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 148 EP - 151 VL - 15 IS - 2 SN - 0362-5664, 0362-5664 KW - Acetamides KW - 0 KW - Glutamates KW - Monoamine Oxidase Inhibitors KW - milacemide KW - 0HXT24RECU KW - Glutamic Acid KW - 3KX376GY7L KW - Index Medicus KW - Synaptic Transmission -- drug effects KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Female KW - Monoamine Oxidase Inhibitors -- adverse effects KW - Glutamates -- physiology KW - Huntington Disease -- drug therapy KW - Acetamides -- therapeutic use KW - Monoamine Oxidase Inhibitors -- therapeutic use KW - Acetamides -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72966479?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+neuropharmacology&rft.atitle=Glutamatergic+therapy+of+Huntington%27s+chorea.&rft.au=Giuffra%2C+M+E%3BMouradian%2C+M+M%3BChase%2C+T+N&rft.aulast=Giuffra&rft.aufirst=M&rft.date=1992-04-01&rft.volume=15&rft.issue=2&rft.spage=148&rft.isbn=&rft.btitle=&rft.title=Clinical+neuropharmacology&rft.issn=03625664&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-29 N1 - Date created - 1992-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DSM-III-R and the proposed DSM-IV alcohol use disorders, United States 1988: a nosological comparison. AN - 72959431; 1590542 AB - The purpose of the present study was to compare DSM-III-R and the proposed DSM-IV diagnostic criteria for alcohol abuse and dependence in a representative sample of the United States general population. Alcohol abuse and dependence diagnostic categories were contrasted in terms of prevalence and overlap. The prevalence of DSM-III-R diagnoses of alcohol abuse and dependence combined (8.63%) was greater than the corresponding DSM-IV diagnoses (6.00%). Disaggregation of abuse and dependence diagnoses showed that the major discrepancy between the classification systems resided between the abuse categories. Reasons for the discrepancies are discussed in terms of differences in the content of the DSM-III-R and DSM-IV abuse categories, in the relationship that each abuse category shares with its respective dependence category, and the impact of the DSM-III-R duration criterion. JF - Alcoholism, clinical and experimental research AU - Grant, B F AU - Harford, T C AU - Hasin, D S AU - Chou, P AU - Pickering, R AD - Division of Biometry and Epidemiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 215 EP - 221 VL - 16 IS - 2 SN - 0145-6008, 0145-6008 KW - Index Medicus KW - Alcohol Withdrawal Delirium -- classification KW - Humans KW - Alcohol Drinking -- adverse effects KW - Aged KW - Alcohol Withdrawal Delirium -- diagnosis KW - Alcohol Drinking -- epidemiology KW - Alcohol Withdrawal Delirium -- epidemiology KW - Cross-Sectional Studies KW - Adult KW - Alcohol Drinking -- psychology KW - Alcohol Withdrawal Delirium -- psychology KW - Incidence KW - Middle Aged KW - Adolescent KW - United States -- epidemiology KW - Male KW - Female KW - Alcoholism -- epidemiology KW - Alcoholism -- diagnosis KW - Alcoholism -- classification KW - Psychiatric Status Rating Scales -- statistics & numerical data KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72959431?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%2C+clinical+and+experimental+research&rft.atitle=DSM-III-R+and+the+proposed+DSM-IV+alcohol+use+disorders%2C+United+States+1988%3A+a+nosological+comparison.&rft.au=Grant%2C+B+F%3BHarford%2C+T+C%3BHasin%2C+D+S%3BChou%2C+P%3BPickering%2C+R&rft.aulast=Grant&rft.aufirst=B&rft.date=1992-04-01&rft.volume=16&rft.issue=2&rft.spage=215&rft.isbn=&rft.btitle=&rft.title=Alcoholism%2C+clinical+and+experimental+research&rft.issn=01456008&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-22 N1 - Date created - 1992-06-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Empirical subtypes of DSM-III-R alcohol dependence: United States, 1988. AN - 72958636; 1591982 AB - The purpose of the present study was to quantify the degree of heterogeneity of the DSM-III-R alcohol dependence category by comparing the number of potential subtypes of dependence to those empirically observed in a general population survey. Forty-one percent (n = 189) of the 466 potential subtypes of DSM-III-R alcohol dependence were observed, indicating that the category is indeed heterogeneous, but not as heterogeneous as theoretically predicted. Variations in the number, percent and configuration of empirical subtypes of dependence are discussed in terms of coincident morbidity, premature death from alcoholism or death from other competing causes, reporting biases and differences in drinking patterns. The predominance of the 'tolerance' 'withdrawal' and 'impaired control over drinking' criteria among the empirically observed subtypes of dependence are examined within the context of the physiological dependence subtype proposed for the DSM-IV category of alcohol dependence and difficulties encountered in operationalizing these diagnostic criteria. The relevance of study findings to the validation of diagnostic categories in psychiatry is also highlighted. JF - Drug and alcohol dependence AU - Grant, B F AU - Chou, S P AU - Pickering, R P AU - Hasin, D S AD - Division of Biometry and Epidemiology, National Institute on Alcohol, Abuse and Alcoholism, Rockville, MD 20852. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 75 EP - 84 VL - 30 IS - 1 SN - 0376-8716, 0376-8716 KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Substance Withdrawal Syndrome -- diagnosis KW - Humans KW - Substance Withdrawal Syndrome -- classification KW - Aged KW - Psychometrics KW - Drug Tolerance KW - Ethanol -- adverse effects KW - Adult KW - Alcohol Drinking -- psychology KW - Substance Withdrawal Syndrome -- psychology KW - Middle Aged KW - Adolescent KW - Female KW - Male KW - Alcoholism -- diagnosis KW - Alcoholism -- classification KW - Psychiatric Status Rating Scales -- statistics & numerical data KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72958636?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+and+alcohol+dependence&rft.atitle=Empirical+subtypes+of+DSM-III-R+alcohol+dependence%3A+United+States%2C+1988.&rft.au=Grant%2C+B+F%3BChou%2C+S+P%3BPickering%2C+R+P%3BHasin%2C+D+S&rft.aulast=Grant&rft.aufirst=B&rft.date=1992-04-01&rft.volume=30&rft.issue=1&rft.spage=75&rft.isbn=&rft.btitle=&rft.title=Drug+and+alcohol+dependence&rft.issn=03768716&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-01 N1 - Date created - 1992-07-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Supersensitivity to naloxone following acute morphine pretreatment in humans: behavioral, hormonal and physiological effects. AN - 72958601; 1591977 AB - The effects of naloxone (10 mg/70 kg) given 6 h following acute exposure to morphine (4, 8, 16 mg/70 kg) were assessed in 5 opiate-abusing volunteers who were not physically dependent upon entering the study. Naloxone increased cortisol plasma levels more following morphine than placebo pretreatment. Naloxone reversed the effects of morphine on pupil diameter and oral temperature and decreased skin temperature as a function of morphine pretreatment. Subjects' ability to detect the effects of naloxone, their scores on an opiate-withdrawal questionnaire, and their visual-analog ratings of 'bad effects', 'chills', 'confused' and 'restlessness' increased when naloxone followed pretreatment with 8 and 16 mg, but not 4 mg, of morphine. Performance on the Digit Symbol Substitution Test was not discernibly affected under any of the dose conditions. Overall, results from the present study provide further evidence in humans that the administration of naloxone shortly following acute morphine pretreatment increases naloxone sensitivity, produces signs and symptoms typical of opiate withdrawal and that these effects are dependent on the dose of morphine administered. JF - Drug and alcohol dependence AU - Higgins, S T AU - Preston, K L AU - Cone, E J AU - Henningfield, J E AU - Jaffe, J H AD - Addiction Research Center/National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 13 EP - 26 VL - 30 IS - 1 SN - 0376-8716, 0376-8716 KW - Naloxone KW - 36B82AMQ7N KW - Morphine KW - 76I7G6D29C KW - Prolactin KW - 9002-62-4 KW - Dextroamphetamine KW - TZ47U051FI KW - Hydrocortisone KW - WI4X0X7BPJ KW - Index Medicus KW - Double-Blind Method KW - Dose-Response Relationship, Drug KW - Humans KW - Injections, Intramuscular KW - Respiration -- drug effects KW - Opioid-Related Disorders -- rehabilitation KW - Dextroamphetamine -- pharmacology KW - Body Temperature Regulation -- drug effects KW - Heart Rate -- drug effects KW - Reflex, Pupillary -- drug effects KW - Adult KW - Blood Pressure -- drug effects KW - Male KW - Naloxone -- pharmacology KW - Prolactin -- blood KW - Morphine -- antagonists & inhibitors KW - Substance Withdrawal Syndrome -- etiology KW - Arousal -- drug effects KW - Naloxone -- toxicity KW - Neurologic Examination -- drug effects KW - Substance Withdrawal Syndrome -- blood KW - Hydrocortisone -- blood KW - Morphine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72958601?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+and+alcohol+dependence&rft.atitle=Supersensitivity+to+naloxone+following+acute+morphine+pretreatment+in+humans%3A+behavioral%2C+hormonal+and+physiological+effects.&rft.au=Higgins%2C+S+T%3BPreston%2C+K+L%3BCone%2C+E+J%3BHenningfield%2C+J+E%3BJaffe%2C+J+H&rft.aulast=Higgins&rft.aufirst=S&rft.date=1992-04-01&rft.volume=30&rft.issue=1&rft.spage=13&rft.isbn=&rft.btitle=&rft.title=Drug+and+alcohol+dependence&rft.issn=03768716&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-01 N1 - Date created - 1992-07-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alcohol use and dependence among employed men and women in the United States in 1988. AN - 72956657; 1590533 AB - This paper provides estimates of alcohol consumption and alcohol dependence among employed men and women in the United States. Data from the 1988 National Health Interview Survey indicate that the percentages of drinkers in white-collar occupations are higher than the percentages of drinkers in blue-collar occupations among both men and women; however, the men and women in blue-collar occupations who drink have a higher average daily consumption than drinkers in white-collar occupations. DSM-III-R criteria were used to classify respondents as alcohol-dependent. Consistent with an earlier survey of employed adults in Detroit, the prevalence of alcohol dependence is highest in certain blue-collar occupations (craftsmen, laborers, and service workers among men; machine operators, laborers, and service workers among women). Directions for further research on the occupational and drinking experiences of employed men and women are discussed. JF - Alcoholism, clinical and experimental research AU - Harford, T C AU - Parker, D A AU - Grant, B F AU - Dawson, D A AD - Division of Biometry and Epidemiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 146 EP - 148 VL - 16 IS - 2 SN - 0145-6008, 0145-6008 KW - Index Medicus KW - Cross-Sectional Studies KW - Humans KW - Incidence KW - Occupations -- statistics & numerical data KW - United States -- epidemiology KW - Male KW - Female KW - Alcoholism -- rehabilitation KW - Alcoholism -- epidemiology KW - Occupational Diseases -- rehabilitation KW - Occupational Diseases -- epidemiology KW - Alcohol Drinking -- prevention & control KW - Alcohol Drinking -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72956657?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%2C+clinical+and+experimental+research&rft.atitle=Alcohol+use+and+dependence+among+employed+men+and+women+in+the+United+States+in+1988.&rft.au=Harford%2C+T+C%3BParker%2C+D+A%3BGrant%2C+B+F%3BDawson%2C+D+A&rft.aulast=Harford&rft.aufirst=T&rft.date=1992-04-01&rft.volume=16&rft.issue=2&rft.spage=146&rft.isbn=&rft.btitle=&rft.title=Alcoholism%2C+clinical+and+experimental+research&rft.issn=01456008&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-22 N1 - Date created - 1992-06-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alterations in macrophage free radical and tumor necrosis factor production by a potassium channel activator. AN - 72950651; 1534387 AB - The potassium channel activator nicorandil, under evaluation for antianginal management, has been shown to decrease neutrophil respiratory burst. Since our laboratory has demonstrated that reactive oxygen species (ROS) increase tumor necrosis factor (TNF) production, we hypothesized that nicorandil might decrease TNF production from a lipopolysaccharide (LPS) challenge via reduction of respiratory burst. Macrophage viability and TNF production were determined after an 18-hr exposure to 5.0 micrograms/ml LPS and varying concentrations of nicorandil. Nicorandil was not toxic to macrophages below 12 mM (94 +/- 3% viability versus control) and decreased ROS and TNF production. Intracellular superoxide production decreased from 164 +/- 24 OD550 to 99 +/- 6 OD550 with 10 mM nicorandil and extracellular superoxide decreased from 3108 +/- 111 to 1760 +/- 210 nM. Hydrogen peroxide production was also decreased by 10 mM nicorandil. TNF production in response to 5 micrograms/ml LPS decreased from 6.8 +/- 0.6 to 2.7 +/- 0.4 ng/ml with 10 mM nicorandil. Northern and slot blot analyses demonstrate that nicorandil acts at a post-transcriptional site. These data imply that nicorandil decreases macrophage TNF production from an LPS challenge, possibly through a reduction in respiratory burst. Such compounds may prove useful in the treatment of conditions thought to be associated with free radical-lymphokine interactions such as ischemia-reperfusion injury, oxygen toxicity, adult respiratory distress syndrome, and septic shock. JF - The Journal of surgical research AU - Pogrebniak, H W AU - Matthews, W AU - Pass, H I AD - Thoracic Oncology Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 395 EP - 400 VL - 52 IS - 4 SN - 0022-4804, 0022-4804 KW - Free Radicals KW - 0 KW - Potassium Channels KW - Tumor Necrosis Factor-alpha KW - Niacinamide KW - 25X51I8RD4 KW - Nicorandil KW - 260456HAM0 KW - Oxygen KW - S88TT14065 KW - Index Medicus KW - Animals KW - Transcription, Genetic KW - Cell Survival KW - Niacinamide -- pharmacology KW - Oxygen -- metabolism KW - Niacinamide -- analogs & derivatives KW - Macrophages -- physiology KW - Tumor Necrosis Factor-alpha -- biosynthesis KW - Potassium Channels -- physiology KW - Potassium Channels -- drug effects KW - Tumor Necrosis Factor-alpha -- genetics KW - Macrophages -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72950651?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+surgical+research&rft.atitle=Alterations+in+macrophage+free+radical+and+tumor+necrosis+factor+production+by+a+potassium+channel+activator.&rft.au=Pogrebniak%2C+H+W%3BMatthews%2C+W%3BPass%2C+H+I&rft.aulast=Pogrebniak&rft.aufirst=H&rft.date=1992-04-01&rft.volume=52&rft.issue=4&rft.spage=395&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+surgical+research&rft.issn=00224804&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-30 N1 - Date created - 1992-06-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The epidemiology of multiple myeloma. AN - 72941609; 1582971 AB - Multiple myeloma is a relatively rare cancer that primarily affects older individuals. In the United States, the highest rates of myeloma are found in black individuals and these rates continue to outpace the rate of myeloma in white individuals. The causes of myeloma are largely unknown. The strongest potential risk factors include radiation and agricultural exposures. JF - Hematology/oncology clinics of North America AU - Riedel, D A AU - Pottern, L M AD - Environmental Epidemiology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 225 EP - 247 VL - 6 IS - 2 SN - 0889-8588, 0889-8588 KW - Index Medicus KW - Occupational Exposure KW - Survival Rate KW - Humans KW - Environmental Exposure KW - United States -- epidemiology KW - Radiation Injuries KW - Multiple Myeloma -- chemically induced KW - Multiple Myeloma -- etiology KW - Multiple Myeloma -- genetics KW - Multiple Myeloma -- epidemiology KW - Multiple Myeloma -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72941609?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hematology%2Foncology+clinics+of+North+America&rft.atitle=The+epidemiology+of+multiple+myeloma.&rft.au=Riedel%2C+D+A%3BPottern%2C+L+M&rft.aulast=Riedel&rft.aufirst=D&rft.date=1992-04-01&rft.volume=6&rft.issue=2&rft.spage=225&rft.isbn=&rft.btitle=&rft.title=Hematology%2Foncology+clinics+of+North+America&rft.issn=08898588&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-16 N1 - Date created - 1992-06-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Biologic correlates of suicidal risk and aggressive behavioral traits. AN - 72927742; 1374432 JF - Journal of clinical psychopharmacology AU - Linnoila, M AU - Virkkunen, M AD - Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 19S EP - 20S VL - 12 IS - 2 Suppl SN - 0271-0749, 0271-0749 KW - Serotonin KW - 333DO1RDJY KW - Hydroxyindoleacetic Acid KW - 54-16-0 KW - Index Medicus KW - Humans KW - Hydroxyindoleacetic Acid -- cerebrospinal fluid KW - Alcoholism -- physiopathology KW - Violence KW - Alcoholism -- psychology KW - Brain -- physiopathology KW - Impulsive Behavior -- physiopathology KW - Serotonin -- physiology KW - Depressive Disorder -- psychology KW - Aggression -- psychology KW - Impulsive Behavior -- psychology KW - Depressive Disorder -- physiopathology KW - Suicide -- psychology KW - Aggression -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72927742?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+psychopharmacology&rft.atitle=Biologic+correlates+of+suicidal+risk+and+aggressive+behavioral+traits.&rft.au=Linnoila%2C+M%3BVirkkunen%2C+M&rft.aulast=Linnoila&rft.aufirst=M&rft.date=1992-04-01&rft.volume=12&rft.issue=2+Suppl&rft.spage=19S&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+psychopharmacology&rft.issn=02710749&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-09 N1 - Date created - 1992-06-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Peroxidase-mediated glutathione conjugation of benzo[a]pyrene-7,8-dihydrodiol is enhanced by benzo[a]pyrene phenols in vitro. AN - 72925614; 1576701 AB - We reported previously that glutathione (GSH) is oxidized by peroxidases to a thiyl radical that can react with a number of chemicals, including the penultimate carcinogenic metabolite benzo[a]pyrene-7,8-dihydrodiol (7,8-B[a]PD), to give GSH conjugates. Here, we report that phenolic metabolites of benzo[a]pyrene (B[a]P) enhance the peroxidase-mediated formation of glutathione conjugates of 7,8-B[a]PD. The GSH conjugation of 7,8-B[a]PD in a horseradish peroxidase/peroxide system was increased over control values as follows: 9-OH-B[a]P by 4-fold, 7-OH-B[a]P by 3-fold, 1-OH-B[a]P by 2-fold. In contrast 3-OH-B[a]P was ineffective. A phenolic derivative of another polycyclic aromatic hydrocarbon (PAH), benz[a]anthracene, also enhanced GSH conjugation of 7,8-B[a]PD. The enhancement was dependent upon the presence of the phenol, horseradish peroxidase and peroxide. The phenolic compounds, including 3-OH-B[a]P, were also efficient reducing cofactors for the peroxidase. With the exception of 3-OH-B[a]P, the phenolic metabolites of PAH enhanced peroxidase-mediated formation of thiyl radical as detected by electron spin resonance spectrometry. Since both phenols and dihydrodiols are metabolites of B[a]P catalyzed by the cytochromes P450 system, enhancement of peroxidase-dependent 7,8-B[a]PD-GSH conjugation by phenols suggests a possible interaction between peroxidases and cytochromes P450 systems. This interaction may contribute to the detoxication of the penultimate carcinogenic PAH-dihydrodiols and other chemicals. JF - Carcinogenesis AU - Foureman, G L AU - Knecht, K T AU - Eling, T E AD - Laboratory of Molecular Biophysics, National Institute of Environmental, Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 515 EP - 518 VL - 13 IS - 4 SN - 0143-3334, 0143-3334 KW - Dihydroxydihydrobenzopyrenes KW - 0 KW - Free Radicals KW - Phenols KW - benzo(a)pyrene 7,8-dihydrodiol KW - 13345-25-0 KW - Benzo(a)pyrene KW - 3417WMA06D KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Peroxidases KW - EC 1.11.1.- KW - Glutathione KW - GAN16C9B8O KW - Index Medicus KW - Cytochrome P-450 Enzyme System -- pharmacology KW - Peroxidases -- pharmacology KW - Phenols -- pharmacology KW - Glutathione -- metabolism KW - Dihydroxydihydrobenzopyrenes -- metabolism KW - Benzo(a)pyrene -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72925614?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Peroxidase-mediated+glutathione+conjugation+of+benzo%5Ba%5Dpyrene-7%2C8-dihydrodiol+is+enhanced+by+benzo%5Ba%5Dpyrene+phenols+in+vitro.&rft.au=Foureman%2C+G+L%3BKnecht%2C+K+T%3BEling%2C+T+E&rft.aulast=Foureman&rft.aufirst=G&rft.date=1992-04-01&rft.volume=13&rft.issue=4&rft.spage=515&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-05 N1 - Date created - 1992-06-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Engineered disulfide bond greatly increases specific activity of recombinant murine interferon-beta. AN - 72922649; 1578187 AB - Unlike other species of interferon-beta (IFN-beta) mouse (Mu) IFN-beta has no naturally occurring intramolecular disulfide bond. When expressed in Escherichia coli, MuIFN-beta appears to exhibit instability and low activity. To increase its activity, we engineered a pair of cysteines into recombinant MuIFN-beta to test whether this change would improve its antiviral activity. In the absence of detailed structural data, the optimal placement of cysteines was determined by sequence comparison with other species of IFN-beta. While MuIFN-beta has only a single cysteine (at position 17), other species of IFN-beta have three cysteines, at positions 17, 31, and 141 (numbering based on consensus sequence), a disulfide bond being formed between the latter two residues. Thus, we introduced cysteines into MuIFN-beta at positions 29 and 136, which correspond to positions 31 and 141 of the consensus sequence. When the variant form of MuIFN-beta was expressed in bacteria and purified, we found that the additional cysteines greatly increased the antiviral activity. Further improvement was obtained by replacement of the Cys-17 with a serine. In this manner a specific activity approximately 15-fold that of the wild-type recombinant molecule was achieved. JF - Journal of interferon research AU - Day, C AU - Schwartz, B AU - Li, B L AU - Pestka, S AD - National Institutes of Health, Institute of Allergies & Infectious Diseases, Rockville, MD 20852. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 139 EP - 143 VL - 12 IS - 2 SN - 0197-8357, 0197-8357 KW - Disulfides KW - 0 KW - Recombinant Proteins KW - Interferon-beta KW - 77238-31-4 KW - Index Medicus KW - L Cells (Cell Line) KW - Animals KW - Escherichia coli -- metabolism KW - Base Sequence KW - Viral Plaque Assay KW - Protein Engineering KW - Mutagenesis, Site-Directed -- genetics KW - Molecular Sequence Data KW - Mice KW - Disulfides -- chemistry KW - Recombinant Proteins -- pharmacology KW - Interferon-beta -- pharmacology KW - Interferon-beta -- chemistry KW - Recombinant Proteins -- chemistry KW - Recombinant Proteins -- genetics KW - Interferon-beta -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72922649?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+interferon+research&rft.atitle=Engineered+disulfide+bond+greatly+increases+specific+activity+of+recombinant+murine+interferon-beta.&rft.au=Day%2C+C%3BSchwartz%2C+B%3BLi%2C+B+L%3BPestka%2C+S&rft.aulast=Day&rft.aufirst=C&rft.date=1992-04-01&rft.volume=12&rft.issue=2&rft.spage=139&rft.isbn=&rft.btitle=&rft.title=Journal+of+interferon+research&rft.issn=01978357&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-10 N1 - Date created - 1992-06-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vitro mutagenesis and the search for structure-function relationships among G protein-coupled receptors. AN - 72896455; 1314560 JF - The Biochemical journal AU - Savarese, T M AU - Fraser, C M AD - Section on Molecular Neurobiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852. Y1 - 1992/04/01/ PY - 1992 DA - 1992 Apr 01 SP - 1 EP - 19 VL - 283 ( Pt 1) SN - 0264-6021, 0264-6021 KW - Receptors, Neurotransmitter KW - 0 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Index Medicus KW - Sequence Homology, Nucleic Acid KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Structure-Activity Relationship KW - Receptors, Neurotransmitter -- physiology KW - Receptors, Neurotransmitter -- genetics KW - GTP-Binding Proteins -- physiology KW - Mutagenesis -- genetics KW - GTP-Binding Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72896455?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Biochemical+journal&rft.atitle=In+vitro+mutagenesis+and+the+search+for+structure-function+relationships+among+G+protein-coupled+receptors.&rft.au=Savarese%2C+T+M%3BFraser%2C+C+M&rft.aulast=Savarese&rft.aufirst=T&rft.date=1992-04-01&rft.volume=283+%28+Pt+1%29&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=The+Biochemical+journal&rft.issn=02646021&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-19 N1 - Date created - 1992-05-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1988 Jul 25;263(21):10267-71 [2899076] Science. 1986 Apr 11;232(4747):193-202 [2937147] Nature. 1985 Sep 12-18;317(6033):124-9 [2993919] Proc Natl Acad Sci U S A. 1986 Mar;83(5):1174-8 [3006038] Proc Natl Acad Sci U S A. 1986 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1989 Apr;12(4):148-51 [2470172] J Biol Chem. 1989 Oct 5;264(28):16786-92 [2476447] Biochem Biophys Res Commun. 1989 Dec 15;165(2):695-702 [2480781] Proc Natl Acad Sci U S A. 1989 Dec;86(24):9762-6 [2532362] J Biol Chem. 1989 May 5;264(13):7564-9 [2540197] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Serum-, TPA-, and Ras-induced expression from Ap-1/Ets-driven promoters requires Raf-1 kinase. AN - 72879598; 1313769 AB - Raf-1 serine-threonine protein kinase has the hallmarks of a critical switch that connects growth factor receptor activation at the cell membrane with transcriptional events in the nucleus. We show by use of Raf-1 dominant-negative mutants that Raf-1 is required for serum-, TPA-, and Ras-induced expression from the oncogene-responsive element in the polyomavirus enhancer. The minimal region of Raf-1 that displays this dominant-negative phenotype (Raf-C4) contains a cysteine finger motif. Raf-C4 appears to function by titrating out a Raf-1-activating factor that is induced by Ras following serum or TPA treatment of NIH-3T3 cells. In addition, we show that Raf-1 and Ras cooperate in trans-activation through the oncogene-responsive element and that the cysteine-rich region is necessary for this effect. JF - Genes & development AU - Bruder, J T AU - Heidecker, G AU - Rapp, U R AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 545 EP - 556 VL - 6 IS - 4 SN - 0890-9369, 0890-9369 KW - Proto-Oncogene Proteins KW - 0 KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Proto-Oncogene Proteins c-raf KW - EC 2.7.11.1 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Animals KW - 3T3 Cells KW - Base Sequence KW - Sequence Homology, Nucleic Acid KW - Enhancer Elements, Genetic KW - Polyomavirus -- genetics KW - Molecular Sequence Data KW - Mice KW - Genes, Viral KW - Amino Acid Sequence KW - Mutation KW - Transcriptional Activation KW - Genes, ras KW - Promoter Regions, Genetic KW - Proto-Oncogene Proteins -- metabolism KW - Gene Expression KW - Tetradecanoylphorbol Acetate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72879598?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genes+%26+development&rft.atitle=Serum-%2C+TPA-%2C+and+Ras-induced+expression+from+Ap-1%2FEts-driven+promoters+requires+Raf-1+kinase.&rft.au=Bruder%2C+J+T%3BHeidecker%2C+G%3BRapp%2C+U+R&rft.aulast=Bruder&rft.aufirst=J&rft.date=1992-04-01&rft.volume=6&rft.issue=4&rft.spage=545&rft.isbn=&rft.btitle=&rft.title=Genes+%26+development&rft.issn=08909369&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-12 N1 - Date created - 1992-05-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alteration of a protease-sensitive region of Pseudomonas exotoxin prolongs its survival in the circulation of mice. AN - 72874916; 1557414 AB - Pseudomonas exotoxin A (PE) is a single-chain 66-kDa polypeptide that kills eukaryotic cells by ADP-ribosylation of translational elongation factor 2. PE is composed of three major structural domains whose functions are binding of cells (I), translocation (II), and ADP-ribosylation (III). Here we describe a protease cleavage target that is located near arginine-490 on the surface of domain III. We made several different types of mutations near arginine-490. Deletion of arginine-490 or replacement of arginine-490 and -492 with serine and lysine or with two lysines resulted in protease-resistant molecules that were fully cytotoxic and had normal ADP-ribosylation activity. However, the half-life in mouse blood of the PE delta 490 mutant was 24 min whereas that of PE was 13 min. Furthermore, two PE mutants that were protease-hypersensitive, PEGlu246,247,249 and PEGlu57,246,247,249 (in which glutamate residues replace basic residues at the indicated positions), had very short half-lives. These data indicate that protease sensitivity is an important determinant in the half-life of PE in the circulation and suggest that the half-life of other proteins may be prolonged by removal of protease sites. Deletion of arginine-492 or the replacement of amino acids 486-491 with three glycines markedly diminished ADP-ribosylation activity and cytotoxicity, indicating that this region of domain III is also important for catalytic activity. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Brinkmann, U AU - Pai, L H AU - FitzGerald, D J AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/04/01/ PY - 1992 DA - 1992 Apr 01 SP - 3065 EP - 3069 VL - 89 IS - 7 SN - 0027-8424, 0027-8424 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - Bacterial Toxins -- pharmacokinetics KW - Molecular Sequence Data KW - Bacterial Toxins -- chemistry KW - Mice KW - Bacterial Toxins -- toxicity KW - Amino Acid Sequence KW - Pseudomonas aeruginosa KW - Structure-Activity Relationship KW - Protein Conformation KW - Exotoxins -- toxicity KW - Exotoxins -- chemistry KW - Exotoxins -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72874916?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Alteration+of+a+protease-sensitive+region+of+Pseudomonas+exotoxin+prolongs+its+survival+in+the+circulation+of+mice.&rft.au=Brinkmann%2C+U%3BPai%2C+L+H%3BFitzGerald%2C+D+J%3BPastan%2C+I&rft.aulast=Brinkmann&rft.aufirst=U&rft.date=1992-04-01&rft.volume=89&rft.issue=7&rft.spage=3065&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-06 N1 - Date created - 1992-05-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1986 Mar;83(5):1320-4 [3006045] J Biol Chem. 1988 Sep 15;263(26):13203-7 [2901411] J Cell Biochem. 1986;32(3):169-78 [3097031] J Mol Biol. 1986 May 5;189(1):113-30 [3537305] Nature. 1970 Aug 15;227(5259):680-5 [5432063] Proc Natl Acad Sci U S A. 1984 May;81(9):2645-9 [6201861] Biochem J. 1984 Feb 15;218(1):119-24 [6231920] Cell. 1987 Jan 16;48(1):129-36 [3098436] Proc Natl Acad Sci U S A. 1987 Jul;84(13):4538-42 [3299371] Cell. 1986 Dec 5;47(5):641-8 [3536124] Proc Natl Acad Sci U S A. 1975 Jun;72(6):2284-8 [166383] Science. 1991 Nov 22;254(5035):1173-7 [1683495] Cell. 1991 Mar 8;64(5):1017-23 [1900455] J Biol Chem. 1990 May 25;265(15):8636-41 [2111323] J Biol Chem. 1990 Sep 25;265(27):16306-10 [2118903] J Biol Chem. 1990 Nov 25;265(33):20678-85 [2122978] J Biol Chem. 1989 Sep 25;264(27):15953-9 [2506173] Biochim Biophys Acta. 1989 Aug 15;1012(3):231-6 [2547438] J Natl Cancer Inst. 1989 Oct 4;81(19):1455-63 [2550658] J Bacteriol. 1987 Nov;169(11):4967-71 [2889718] FEBS Lett. 1987 Mar 23;213(2):254-60 [3030813] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutant p53 can induce tumorigenic conversion of human bronchial epithelial cells and reduce their responsiveness to a negative growth factor, transforming growth factor beta 1. AN - 72874631; 1557382 AB - Loss of normal functions and gain of oncogenic functions when the p53 tumor suppressor gene is mutated are considered critical events in the development of the majority of human cancers. Human bronchial epithelial cells (BEAS-2B) provide an in vitro model system to study growth, differentiation, and neoplastic transformation of progenitor cells of lung carcinoma. When wild-type (WT) or mutant (MT; codon 143Val-Ala) human p53 cDNA was transfected into nontumorigenic BEAS-2B cells, we observed that (i) transfected WT p53 suppresses and MT p53 enhances the colony-forming efficiency of these cells, (ii) MT p53 increases resistance to transforming growth factor beta 1, and (iii) clones of MT p53 transfected BEAS-2B cells are tumorigenic when inoculated into athymic nude mice. These results are consistent with the hypothesis that certain mutations in p53 may function in multistage lung carcinogenesis by reducing the responsiveness of bronchial epithelial cells to negative growth factors. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Gerwin, B I AU - Spillare, E AU - Forrester, K AU - Lehman, T A AU - Kispert, J AU - Welsh, J A AU - Pfeifer, A M AU - Lechner, J F AU - Baker, S J AU - Vogelstein, B AD - Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/04/01/ PY - 1992 DA - 1992 Apr 01 SP - 2759 EP - 2763 VL - 89 IS - 7 SN - 0027-8424, 0027-8424 KW - Transforming Growth Factor beta KW - 0 KW - Tumor Suppressor Protein p53 KW - Index Medicus KW - Neoplasm Transplantation KW - Animals KW - Tumor Cells, Cultured KW - Genes, p53 KW - Transfection KW - Humans KW - In Vitro Techniques KW - Cell Division -- drug effects KW - Mice, Nude KW - Mice KW - Transforming Growth Factor beta -- pharmacology KW - Carcinoma, Bronchogenic -- pathology KW - Tumor Suppressor Protein p53 -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72874631?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Mutant+p53+can+induce+tumorigenic+conversion+of+human+bronchial+epithelial+cells+and+reduce+their+responsiveness+to+a+negative+growth+factor%2C+transforming+growth+factor+beta+1.&rft.au=Gerwin%2C+B+I%3BSpillare%2C+E%3BForrester%2C+K%3BLehman%2C+T+A%3BKispert%2C+J%3BWelsh%2C+J+A%3BPfeifer%2C+A+M%3BLechner%2C+J+F%3BBaker%2C+S+J%3BVogelstein%2C+B&rft.aulast=Gerwin&rft.aufirst=B&rft.date=1992-04-01&rft.volume=89&rft.issue=7&rft.spage=2759&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-06 N1 - Date created - 1992-05-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell. 1989 Jun 30;57(7):1083-93 [2525423] Cell Growth Differ. 1990 Dec;1(12):571-80 [2288874] Oncogene. 1987 May;1(2):201-11 [2830579] Proc Natl Acad Sci U S A. 1988 Jul;85(14):5146-50 [2839831] Proc Natl Acad Sci U S A. 1986 Apr;83(8):2438-42 [2871553] Oncogene. 1988 Nov;3(5):501-7 [2978867] J Biol Chem. 1986 Apr 15;261(11):5003-9 [3007486] J Virol. 1988 Oct;62(10):3903-6 [3047431] Cell. 1990 Oct 19;63(2):245-7 [2208284] Am J Pathol. 1990 Oct;137(4):833-43 [2221015] Oncogene. 1990 Dec;5(12):1829-32 [2284102] Cancer Res. 1988 Mar 15;48(6):1596-602 [2449957] Cancer Res. 1988 Apr 1;48(7):1904-9 [2450641] J Virol. 1989 Apr;63(4):1792-9 [2522559] Environ Health Perspect. 1989 Mar;80:209-20 [2538323] Cell. 1989 May 5;57(3):379-92 [2541911] J Natl Cancer Inst. 1989 May 10;81(10):745-57 [2654404] Mol Cell Biol. 1988 Feb;8(2):531-9 [2832726] Differentiation. 1988 Jun;38(1):60-6 [2846394] Mol Cell Biol. 1988 Sep;8(9):3740-7 [2851728] Adv Cancer Res. 1988;51:107-45 [2906217] Oncogene. 1988 Nov;3(5):595-603 [2978869] Nucleic Acids Res. 1985 Mar 11;13(5):1431-42 [2987824] Mol Cell Biol. 1987 May;7(5):2031-4 [3037341] Mol Cell Biol. 1987 Aug;7(8):2863-9 [3313006] Nature. 1979 Mar 15;278(5701):261-3 [218111] Cancer Res. 1991 Oct 1;51(19):5232-7 [1717142] Oncogene. 1991 Jan;6(1):131-6 [1846954] Nature. 1991 Jul 25;352(6333):345-7 [1852210] Science. 1991 Jul 5;253(5015):49-53 [1905840] Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3412-5 [2014262] Cell. 1979 May;17(1):43-52 [222475] Cell. 1991 Jun 14;65(6):1083-91 [1646078] Mol Cell Endocrinol. 1991 Apr;76(1-3):13-21 [1820969] Proc Natl Acad Sci U S A. 1991 May 15;88(10):4128-32 [1851994] Cancer Res. 1991 Aug 1;51(15):4090-6 [1855224] Oncogene. 1991 Aug;6(8):1471-6 [1886718] J Cell Physiol. 1991 Sep;148(3):391-5 [1918170] Cell. 1991 May 31;65(5):765-74 [2040013] Nature. 1991 Jun 6;351(6326):453-6 [2046748] Genes Dev. 1990 Jan;4(1):1-8 [2137806] Proc Natl Acad Sci U S A. 1990 Aug;87(16):6166-70 [2143581] Science. 1990 Aug 24;249(4971):912-5 [2144057] Science. 1990 Aug 31;249(4972):1046-9 [2144363] Oncogene. 1990 Jul;5(7):973-80 [2165234] Crit Rev Oncol Hematol. 1990;10(2):181-209 [2193649] Mol Cell Biol. 1988 Aug;8(8):3088-93 [2463471] Science. 1991 Jun 21;252(5013):1708-11 [2047879] Cell. 1990 Jun 1;61(5):777-85 [2140528] Cell. 1990 Aug 24;62(4):671-80 [2143698] Science. 1990 Aug 31;249(4972):1049-51 [2144364] Proc Natl Acad Sci U S A. 1990 May;87(10):3758-62 [2187192] Science. 1990 Oct 5;250(4977):113-6 [2218501] Mol Cell Biol. 1990 Nov;10(11):5772-81 [2233717] J Virol. 1989 Feb;63(2):739-46 [2642977] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Halothane hepatitis 28 years after primary exposure. AN - 72873238; 1554130 JF - Anesthesia and analgesia AU - Martin, J L AU - Dubbink, D A AU - Plevak, D J AU - Peronne, A AU - Taswell, H F AU - Hay, E J AU - Pumford, N R AU - Pohl, L R AD - Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 605 EP - 608 VL - 74 IS - 4 SN - 0003-2999, 0003-2999 KW - Halothane KW - UQT9G45D1P KW - Abridged Index Medicus KW - Index Medicus KW - Drug Hypersensitivity -- immunology KW - Drug Hypersensitivity -- etiology KW - Humans KW - Middle Aged KW - Time Factors KW - Male KW - Chemical and Drug Induced Liver Injury -- etiology KW - Halothane -- adverse effects KW - Chemical and Drug Induced Liver Injury -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72873238?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Anesthesia+and+analgesia&rft.atitle=Halothane+hepatitis+28+years+after+primary+exposure.&rft.au=Martin%2C+J+L%3BDubbink%2C+D+A%3BPlevak%2C+D+J%3BPeronne%2C+A%3BTaswell%2C+H+F%3BHay%2C+E+J%3BPumford%2C+N+R%3BPohl%2C+L+R&rft.aulast=Martin&rft.aufirst=J&rft.date=1992-04-01&rft.volume=74&rft.issue=4&rft.spage=605&rft.isbn=&rft.btitle=&rft.title=Anesthesia+and+analgesia&rft.issn=00032999&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-24 N1 - Date created - 1992-04-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Independent domain folding of Pseudomonas exotoxin and single-chain immunotoxins: influence of interdomain connections. AN - 72873069; 1557415 AB - We have studied the refolding of completely unfolded and reduced Pseudomonas exotoxin (PE) and of recombinant single-chain immunotoxins made with monoclonal antibody B3 that are composed of a heavy-chain variable region connected by a flexible linker to the corresponding light-chain variable region (Fv), which is in turn fused to a truncated form of PE. We have found by direct activity assays that different functional domains of these multifunctional proteins fold independently with different kinetics. The ADP-ribosylation domain of PE and of the recombinant immunotoxin fold rapidly, whereas the assembly of the binding and/or translocation domains is regained more slowly. The complete refolding of native PE occurs more rapidly than the refolding of the recombinant immunotoxins. To determine the influence of the connector region between the B3(Fv) moiety and the toxin on the folding process of the recombinant immunotoxin B3(Fv)-PE38KDEL, we have made two different mutations in the peptide that connects the single-chain Fv domain to domain II of PE. These molecules show different folding kinetics, differences in their propensity to aggregate, and different yields of correctly folded molecules. A mutation that decreases aggregation increases the rate of formation and the yield of active immunotoxin molecules. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Brinkmann, U AU - Buchner, J AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/04/01/ PY - 1992 DA - 1992 Apr 01 SP - 3075 EP - 3079 VL - 89 IS - 7 SN - 0027-8424, 0027-8424 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Immunotoxins KW - Macromolecular Substances KW - Oligodeoxyribonucleotides KW - Recombinant Fusion Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - Poly(ADP-ribose) Polymerases KW - EC 2.4.2.30 KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Poly(ADP-ribose) Polymerases -- chemistry KW - Protein Denaturation KW - Amino Acid Sequence KW - Poly(ADP-ribose) Polymerases -- metabolism KW - Protein Binding KW - Recombinant Fusion Proteins -- chemistry KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Oligodeoxyribonucleotides -- chemistry KW - Molecular Sequence Data KW - Bacterial Toxins -- chemistry KW - Pseudomonas aeruginosa KW - Immunotoxins -- chemistry KW - Exotoxins -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72873069?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Independent+domain+folding+of+Pseudomonas+exotoxin+and+single-chain+immunotoxins%3A+influence+of+interdomain+connections.&rft.au=Brinkmann%2C+U%3BBuchner%2C+J%3BPastan%2C+I&rft.aulast=Brinkmann&rft.aufirst=U&rft.date=1992-04-01&rft.volume=89&rft.issue=7&rft.spage=3075&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-06 N1 - Date created - 1992-05-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1989 Sep 25;264(27):15953-9 [2506173] J Biol Chem. 1989 Aug 25;264(24):14256-61 [2503515] J Biol Chem. 1988 Sep 15;263(26):13203-7 [2901411] Proc Natl Acad Sci U S A. 1984 May;81(9):2645-9 [6201861] Biochemistry. 1981 Mar 3;20(5):1396-401 [7225337] Infect Immun. 1977 Jun;16(3):832-41 [19354] Science. 1991 Jul 5;253(5015):54-8 [1648264] J Biol Chem. 1991 Sep 15;266(26):17376-81 [1910044] Biochemistry. 1991 Mar 19;30(11):2790-7 [2007117] Proc Natl Acad Sci U S A. 1990 Jan;87(1):308-12 [2104981] J Biol Chem. 1990 Nov 25;265(33):20678-85 [2122978] Nature. 1989 Jun 1;339(6223):394-7 [2498664] J Biol Chem. 1989 Sep 15;264(26):15157-60 [2504717] J Bacteriol. 1987 Nov;169(11):4967-71 [2889718] Proc Natl Acad Sci U S A. 1986 Mar;83(5):1320-4 [3006045] Prog Biophys Mol Biol. 1987;49(2-3):117-237 [3327098] Biochemistry. 1987 May 19;26(10):2785-90 [3606993] Adv Biophys. 1984;18:91-113 [6242326] Cell. 1987 Jan 16;48(1):129-36 [3098436] J Biol Chem. 1988 Jul 5;263(19):9470-5 [3132465] J Mol Biol. 1986 May 5;189(1):113-30 [3537305] Proc Natl Acad Sci U S A. 1975 Jun;72(6):2284-8 [166383] Curr Opin Biotechnol. 1991 Aug;2(4):532-8 [1367672] Biotechnology (N Y). 1991 Feb;9(2):157-62 [1369317] Cancer Res. 1991 Jul 15;51(14):3781-7 [1648444] Proc Natl Acad Sci U S A. 1991 Oct 1;88(19):8616-20 [1924323] Biochemistry. 1991 Oct 22;30(42):10117-25 [1931943] Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3358-62 [2014255] Proc Natl Acad Sci U S A. 1990 Feb;87(3):1066-70 [2105495] J Biol Chem. 1990 Sep 25;265(27):16306-10 [2118903] Science. 1988 Jan 29;239(4839):487-91 [2448875] Proc Natl Acad Sci U S A. 1989 Nov;86(21):8545-9 [2510169] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Biochemical modulation of fluorouracil with leucovorin and interferon: preclinical and clinical investigations. AN - 72871939; 1557656 AB - Leucovorin and interferon are capable of modulating the cytotoxicity of fluorouracil (5-FU). Preclinical studies demonstrate that d,l-leucovorin is rapidly metabolized in human breast and colon cells into the various one-carbon substituted folate pools and to the polyglutamated state. While increases in intracellular folate pools are proportional to the exposure concentration of leucovorin, relatively large increases in leucovorin concentrations (50- to 100-fold) are required to produce small intracellular changes (twofold). Polyglutamation is favored by prolonged exposures to leucovorin. Polyglutamate forms have a prolonged intracellular retention and a higher affinity for the target enzyme, thymidylate synthase. Ratios of up to 20:1 inactive to active leucovorin stereo-isomers had essentially no effect on the intracellular metabolism of the active isomer. Interferon gamma interacts with 5-FU in H630 colon cancer cells at the level of thymidylate synthase and enhances cytotoxicity of 5-FU by eliminating the 5-FU-induced acute overexpression of the target enzyme. No alterations in the intracellular metabolism or nucleic acid incorporation of 5-FU could be demonstrated with the addition of interferon gamma. A clinical trial combining interferon-alfa-2a (IFN-alpha-2a) (subcutaneous days 1 to 7) with 5-FU and leucovorin (given IV days 2 to 6) demonstrated that these agents could be combined with acceptable toxicity. While the addition of interferon did not allow dose escalation of 5-FU, it resulted in a significant increase in drug exposure (1.5-fold) compared with matched cycles of 5-FU plus leucovorin without interferon. The overall response rate in this pilot study of 13 untreated patients with gastrointestinal adenocarcinoma was 46%, including two complete responses. There were no responses in eight patients who had previously failed therapy with 5-FU. JF - Seminars in oncology AU - Grem, J L AU - Chu, E AU - Boarman, D AU - Balis, F M AU - Murphy, R F AU - McAtee, N AU - Allegra, C J AD - Medicine Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 36 EP - 44 VL - 19 IS - 2 Suppl 3 SN - 0093-7754, 0093-7754 KW - Interferon-alpha KW - 0 KW - Recombinant Proteins KW - Tetrahydrofolates KW - 5,10-methylenetetrahydrofolic acid KW - 0SXY5ET48B KW - interferon alfa-2a KW - 47RRR83SK7 KW - Interferon-gamma KW - 82115-62-6 KW - Leucovorin KW - Q573I9DVLP KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - Drug Interactions KW - Drug Administration Schedule KW - Pancreatic Neoplasms -- therapy KW - Pancreatic Neoplasms -- metabolism KW - Tumor Cells, Cultured KW - Neoplasms, Unknown Primary -- therapy KW - Humans KW - Neoplasms, Unknown Primary -- metabolism KW - Interferon-alpha -- pharmacology KW - Stomach Neoplasms -- metabolism KW - Interferon-alpha -- administration & dosage KW - Tetrahydrofolates -- metabolism KW - Colorectal Neoplasms -- metabolism KW - Leucovorin -- administration & dosage KW - Interferon-gamma -- pharmacology KW - Leucovorin -- metabolism KW - Fluorouracil -- administration & dosage KW - Fluorouracil -- adverse effects KW - Colonic Neoplasms -- therapy KW - Colorectal Neoplasms -- therapy KW - Stomach Neoplasms -- therapy KW - Leucovorin -- pharmacology KW - Colonic Neoplasms -- metabolism KW - Fluorouracil -- metabolism KW - Fluorouracil -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72871939?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+oncology&rft.atitle=Biochemical+modulation+of+fluorouracil+with+leucovorin+and+interferon%3A+preclinical+and+clinical+investigations.&rft.au=Grem%2C+J+L%3BChu%2C+E%3BBoarman%2C+D%3BBalis%2C+F+M%3BMurphy%2C+R+F%3BMcAtee%2C+N%3BAllegra%2C+C+J&rft.aulast=Grem&rft.aufirst=J&rft.date=1992-04-01&rft.volume=19&rft.issue=2+Suppl+3&rft.spage=36&rft.isbn=&rft.btitle=&rft.title=Seminars+in+oncology&rft.issn=00937754&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-01 N1 - Date created - 1992-05-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retinoic acid mimics transforming growth factor beta in the regulation of human immunodeficiency virus expression in monocytic cells. AN - 72871249; 1372988 AB - Retinoic acid (RA) exerts potent suppressive and upregulatory effects on human immunodeficiency virus (HIV) expression in mononuclear phagocytes, strikingly similar to the effects of the cytokine transforming growth factor beta (TGF-beta). RA significantly inhibited phorbol ester-mediated, but not tumor necrosis factor alpha-mediated, induction of HIV transcription in the chronically infected promonocytic U1 cell line. RA and TGF-beta also completely suppressed the induction of virus production in U1 cells by interleukin 6 alone or in combination with glucocorticoids, which predominantly upregulate virus expression at the posttranscriptional level. Despite the close parallel to TGF-beta-induced effects, no evidence was obtained that RA mediated its effect by inducing secretion of active TGF-beta 1, -beta 2, or -beta 3. As with chronically infected U1 cells, similar inhibitory effects were also observed in primary monocyte-derived macrophages previously infected with HIV and then exposed to either RA or TGF-beta. In contrast, stimulation of monocyte-derived macrophages or U937 cells (the parental cell line of U1) with either RA or TGF-beta prior to in vitro infection resulted in the enhancement of virus production. Given the already successful use of retinoids in the treatment of several malignancies and the present demonstration of their capability of blocking the induction of HIV expression in infected mononuclear phagocytes, it would be of interest to pursue the potential role of this class of compounds in the development of strategies aimed at the pharmacologic regulation of HIV expression. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Poli, G AU - Kinter, A L AU - Justement, J S AU - Bressler, P AU - Kehrl, J H AU - Fauci, A S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/04/01/ PY - 1992 DA - 1992 Apr 01 SP - 2689 EP - 2693 VL - 89 IS - 7 SN - 0027-8424, 0027-8424 KW - Transforming Growth Factor beta KW - 0 KW - Tretinoin KW - 5688UTC01R KW - RNA-Directed DNA Polymerase KW - EC 2.7.7.49 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - AIDS/HIV KW - Tumor Cells, Cultured KW - Virus Replication -- drug effects KW - Humans KW - In Vitro Techniques KW - Tetradecanoylphorbol Acetate -- pharmacology KW - RNA-Directed DNA Polymerase -- metabolism KW - Time Factors KW - Transforming Growth Factor beta -- administration & dosage KW - HIV -- growth & development KW - Tretinoin -- pharmacology KW - Transforming Growth Factor beta -- pharmacology KW - Tretinoin -- administration & dosage KW - Monocytes -- microbiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72871249?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Retinoic+acid+mimics+transforming+growth+factor+beta+in+the+regulation+of+human+immunodeficiency+virus+expression+in+monocytic+cells.&rft.au=Poli%2C+G%3BKinter%2C+A+L%3BJustement%2C+J+S%3BBressler%2C+P%3BKehrl%2C+J+H%3BFauci%2C+A+S&rft.aulast=Poli&rft.aufirst=G&rft.date=1992-04-01&rft.volume=89&rft.issue=7&rft.spage=2689&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-06 N1 - Date created - 1992-05-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1985 Dec 6;230(4730):1126-32 [2999973] J Exp Med. 1991 Apr 1;173(4):981-91 [2007861] J Exp Med. 1987 Aug 1;166(2):571-6 [3110354] N Engl J Med. 1988 Jun 23;318(25):1633-7 [3287161] Blood. 1983 Dec;62(6):1211-7 [6580050] Cell Regul. 1989 Nov;1(1):87-97 [2519621] J Immunol. 1989 Jun 15;142(12):4295-300 [2542408] J Cell Biochem. 1989 Feb;39(2):175-84 [2654150] J Exp Med. 1986 May 1;163(5):1037-50 [2871125] J Immunol. 1986 Dec 15;137(12):3855-60 [2878044] J Virol. 1986 Aug;59(2):284-91 [3016298] Science. 1988 Sep 23;241(4873):1673-5 [3047875] J Exp Med. 1988 Apr 1;167(4):1428-41 [3258626] J Exp Med. 1988 Aug 1;168(2):737-50 [3261777] Cancer Res. 1983 Jul;43(7):3034-40 [6189589] Proc Natl Acad Sci U S A. 1981 Sep;78(9):5339-43 [6975480] Virology. 1990 Dec;179(2):749-58 [1700541] Cell Regul. 1990 Oct;1(11):791-809 [1708287] J Virol. 1991 Jul;65(7):3968-71 [1710293] Blood. 1991 Mar 15;77(6):1248-55 [1848114] N Engl J Med. 1991 May 16;324(20):1385-93 [1850498] J Immunol. 1991 Jan 1;146(1):377-83 [1984449] J Immunol. 1991 Jan 1;146(1):81-4 [1984454] J Clin Invest. 1991 Mar;87(3):1010-6 [1999481] Nature. 1990 May 17;345(6272):224-9 [2159111] J Exp Med. 1990 Jul 1;172(1):151-8 [2193094] J Clin Invest. 1990 Dec;86(6):1976-84 [2254455] Med Microbiol Immunol. 1987;176(4):189-98 [2441239] Immunol Today. 1989 Aug;10(8):258-61 [2478145] Adv Immunol. 1989;47:377-431 [2573256] Nature. 1987 Dec 3-9;330(6147):444-50 [2825025] Mol Endocrinol. 1991 Jan;5(1):3-7 [2017191] Ann Oncol. 1991 Mar;2(3):234-5 [2043496] Blood. 1990 Nov 15;76(10):1980-8 [2173633] Blood. 1990 Oct 1;76(7):1315-22 [2207308] Growth Factors. 1990;2(4):283-7 [2337474] Cell. 1990 Jun 29;61(7):1271-6 [2364429] J Immunol. 1988 Feb 15;140(4):1117-22 [2449497] Proc Natl Acad Sci U S A. 1990 Nov;87(21):8321-5 [1700428] J Exp Med. 1991 Mar 1;173(3):589-97 [1705278] Cancer Res. 1991 Feb 15;51(4):1158-64 [1847657] Blood. 1991 Apr 15;77(8):1657-9 [1849758] J Immunol. 1991 Aug 15;147(4):1201-7 [1869819] J Virol. 1991 Mar;65(3):1291-303 [1995944] Nature. 1988 Jul 21;334(6179):260-2 [3041283] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Disruption of either the E1 or the E2 regulatory gene of human papillomavirus type 16 increases viral immortalization capacity. AN - 72870802; 1313584 AB - The "high-risk" human papillomavirus types 16 (HPV-16) and 18 (HPV-18) have been etiologically implicated in the majority of human cervical carcinomas. In these cancers, the viral DNAs are often integrated into the host genome so that expression of the E1 and the E2 genes is lost, suggesting that disruption of these regulatory genes plays an important role in carcinogenic progression. Previous studies defining the viral genes affecting HPV-16 transformation functions have used the "prototype" viral genome, which was cloned from a human cervical carcinoma and later discovered to harbor a mutation in the E1 gene. In this study, we have corrected this mutation and have evaluated the effect of mutations of either the E1 or the E2 gene on the efficiency of HPV-16 immortalization of human keratinocytes. Mutation of either the E1 gene or the E2 gene in the background of a "wild-type" HPV-16 genome markedly increased immortalization capacity. Mutations were also generated in the E2-binding sites located upstream of the P97 promoter, which directs synthesis of the viral E6 and E7 transforming genes. E2 negatively regulates the P97 promoter through binding at adjacent sites. Surprisingly, the mutation of these sites only partially relieved the negative effect of E2 on viral immortalization, implicating additional mechanisms in the E2 repression of viral immortalization functions. Our results provide genetic evidence that the E1 and E2 gene products each can repress HPV-16 immortalization and support the hypothesis that a selective growth advantage is provided by integration of the viral genome in a manner that causes the loss of expression of either E1 or E2. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Romanczuk, H AU - Howley, P M AD - Laboratory of Tumor Virus Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/04/01/ PY - 1992 DA - 1992 Apr 01 SP - 3159 EP - 3163 VL - 89 IS - 7 SN - 0027-8424, 0027-8424 KW - DNA, Viral KW - 0 KW - DNA-Binding Proteins KW - E2 protein, Human papillomavirus type 16 KW - Oncogene Proteins, Viral KW - Repressor Proteins KW - Viral Structural Proteins KW - Index Medicus KW - Promoter Regions, Genetic KW - Base Sequence KW - Humans KW - In Vitro Techniques KW - Molecular Sequence Data KW - Repressor Proteins -- genetics KW - Mutation KW - Keratinocytes -- microbiology KW - DNA, Viral -- genetics KW - Papillomaviridae -- pathogenicity KW - Papillomaviridae -- genetics KW - Oncogene Proteins, Viral -- physiology KW - Genes, Viral KW - Viral Structural Proteins -- genetics KW - Cell Transformation, Viral KW - Genes, Regulator UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72870802?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Disruption+of+either+the+E1+or+the+E2+regulatory+gene+of+human+papillomavirus+type+16+increases+viral+immortalization+capacity.&rft.au=Romanczuk%2C+H%3BHowley%2C+P+M&rft.aulast=Romanczuk&rft.aufirst=H&rft.date=1992-04-01&rft.volume=89&rft.issue=7&rft.spage=3159&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-06 N1 - Date created - 1992-05-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Virol. 1987 May;61(5):1630-8 [3033289] J Virol. 1987 Apr;61(4):962-71 [3029430] J Virol. 1987 Oct;61(10):3295-8 [3041049] Proc Natl Acad Sci U S A. 1983 Jun;80(12):3812-5 [6304740] EMBO J. 1984 May;3(5):1151-7 [6329740] EMBO J. 1987 Dec 1;6(12):3745-53 [2448139] New Biol. 1991 Jan;3(1):90-100 [1645591] J Biol Chem. 1991 Oct 5;266(28):18411-4 [1655748] Nature. 1991 Aug 29;352(6338):824-7 [1715519] J Virol. 1991 Feb;65(2):606-12 [1846186] J Virol. 1991 Feb;65(2):649-56 [1846189] EMBO J. 1991 Feb;10(2):449-57 [1846806] Cell. 1991 May 3;65(3):493-505 [1850324] New Biol. 1990 May;2(5):450-63 [1963084] J Virol. 1990 Feb;64(2):519-26 [2153221] Virology. 1990 Feb;174(2):557-75 [2154890] J Virol. 1990 Jun;64(6):2849-59 [2159546] Virology. 1990 Sep;178(1):254-62 [2167553] J Virol. 1990 Nov;64(11):5577-84 [2170687] Science. 1990 Dec 21;250(4988):1694-9 [2176744] J Virol. 1987 Apr;61(4):1061-6 [2434663] J Virol. 1988 Jun;62(6):1917-24 [2452896] Proc Natl Acad Sci U S A. 1988 Oct;85(19):7169-73 [2459699] EMBO J. 1988 Oct;7(10):3181-7 [2460337] J Virol. 1989 Oct;63(10):4317-24 [2476572] J Virol. 1989 Oct;63(10):4417-21 [2476573] J Virol. 1989 Mar;63(3):1247-55 [2536832] J Virol. 1989 Apr;63(4):1775-82 [2538656] EMBO J. 1989 Dec 1;8(12):3905-10 [2555178] EMBO J. 1987 Nov;6(11):3391-7 [2828029] EMBO J. 1987 Dec 1;6(12):3735-43 [2828035] J Virol. 1988 Mar;62(3):1022-7 [2828651] Oncogene. 1987;1(3):251-6 [2838778] J Virol. 1988 Nov;62(11):4009-15 [2845119] Nature. 1985 Mar 7-13;314(6006):111-4 [2983228] Virology. 1985 Aug;145(1):181-5 [2990099] J Gen Virol. 1985 Jul;66 ( Pt 7):1515-22 [2991428] Proc Natl Acad Sci U S A. 1986 Jul;83(13):4680-4 [3014503] EMBO J. 1986 Sep;5(9):2285-92 [3023067] Nature. 1987 Jan 1-7;325(6099):70-3 [3025749] EMBO J. 1987 Apr;6(4):989-92 [3036495] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Zinc, a neurotoxin to cultured neurons, contaminates cycad flour prepared by traditional guamanian methods. AN - 72870331; 1556606 AB - We have used cultured ventral mesencephalic and cerebellar granule cells to test the toxicity of extracts of cycad seeds (genus Cycas) and cycad-derived flours traditionally prepared in Guam. There was no significant difference in the toxicity of extracts prepared from the female gametophyte tissue of C. circinalis, C. revoluta, and C. media, common wheat flour, and 13 of 17 cycad flour samples. However, extracts prepared from 4 of 17 Guamanian flour samples exhibited marked dose-dependent neurotoxicity to mesencephalic and granule cell cultures. There was no correlation between toxicity and 2-amino-3-(methylamino)-propanoic acid (BMAA) content, and the concentration of BMAA in the medium arising from these extracts was far below that required to be neurotoxic. Toxicity of extracts was not blocked by the NMDA receptor antagonist MK-801 or the non-NMDA receptor antagonist 6-cyano-7-dinitroquinoxaline-2,3-dione, indicating that toxicity was not mediated by excitatory amino acid receptors. Analysis of the four toxic processed flour samples indicated high zinc content. Zinc produced a concentration-dependent neurotoxic response in mesencephalic and granule cell cultures that paralleled the calculated concentrations of zinc in the cultures derived from the four toxic flour samples. When sliced C. circinalis gametophyte tissue was "processed" in our laboratory by soaking in a galvanized container, there was a time-dependent increase in zinc content. JF - The Journal of neuroscience : the official journal of the Society for Neuroscience AU - Duncan, M W AU - Marini, A M AU - Watters, R AU - Kopin, I J AU - Markey, S P AD - Intramural Research Program, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 1523 EP - 1537 VL - 12 IS - 4 SN - 0270-6474, 0270-6474 KW - Neurotoxins KW - 0 KW - Plant Extracts KW - Zinc KW - J41CSQ7QDS KW - Index Medicus KW - Mesencephalon -- drug effects KW - Animals KW - Cerebellum -- cytology KW - Plants -- metabolism KW - Neurons -- drug effects KW - Guam KW - Cerebellum -- drug effects KW - Granulocytes -- drug effects KW - Plant Extracts -- poisoning KW - Plant Extracts -- chemistry KW - Mesencephalon -- cytology KW - Zinc -- pharmacology KW - Zinc -- analysis KW - Zinc -- pharmacokinetics KW - Cooking KW - Food Contamination KW - Neurotoxins -- pharmacology KW - Flour UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72870331?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+neuroscience+%3A+the+official+journal+of+the+Society+for+Neuroscience&rft.atitle=Zinc%2C+a+neurotoxin+to+cultured+neurons%2C+contaminates+cycad+flour+prepared+by+traditional+guamanian+methods.&rft.au=Duncan%2C+M+W%3BMarini%2C+A+M%3BWatters%2C+R%3BKopin%2C+I+J%3BMarkey%2C+S+P&rft.aulast=Duncan&rft.aufirst=M&rft.date=1992-04-01&rft.volume=12&rft.issue=4&rft.spage=1523&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+neuroscience+%3A+the+official+journal+of+the+Society+for+Neuroscience&rft.issn=02706474&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-06 N1 - Date created - 1992-05-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vivo T-cell ablation by a holo-immunotoxin directed at human CD3. AN - 72867593; 1372981 AB - We have evaluated the in vivo efficacy of anti-CD3-CRM9, a holo-immunotoxin constructed with a diphtheria toxin binding-site mutant. Eighty percent of established human T-cell subcutaneous tumors in nude mice completely regressed following intraperitoneal injection of immunotoxin at a dose set at half the minimum lethal dose assayed in toxin-sensitive animals. Similar regressions produced by a 137Cs source required a dose in excess of 500 cGy. The high degree of in vivo T-cell ablation produced by this immunotoxin is apparently due to maintenance of the toxin translocation function provided by CRM9 and a necessary intracellular routing function supplied by CD3. This immunotoxin may be useful in treating conditions caused by pathologic oligoclonal T-cell expansion such as graft-versus-host disease, autoimmune diseases, and possibly AIDS. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Neville, D M AU - Scharff, J AU - Srinivasachar, K AD - Section on Biophysical Chemistry, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1992/04/01/ PY - 1992 DA - 1992 Apr 01 SP - 2585 EP - 2589 VL - 89 IS - 7 SN - 0027-8424, 0027-8424 KW - Antigens, CD KW - 0 KW - Antigens, CD3 KW - Antigens, CD5 KW - Antigens, Differentiation, T-Lymphocyte KW - Diphtheria Toxin KW - Immunotoxins KW - Receptors, Antigen, T-Cell KW - Index Medicus KW - Neoplasm Transplantation KW - Animals KW - Leukemia, T-Cell -- therapy KW - Diphtheria Toxin -- administration & dosage KW - Tumor Cells, Cultured KW - Immunotherapy KW - Mice, Nude KW - Mice KW - Antigens, CD -- immunology KW - Immunotoxins -- toxicity KW - Lymphocyte Depletion KW - Receptors, Antigen, T-Cell -- immunology KW - Antigens, Differentiation, T-Lymphocyte -- immunology KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72867593?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=In+vivo+T-cell+ablation+by+a+holo-immunotoxin+directed+at+human+CD3.&rft.au=Neville%2C+D+M%3BScharff%2C+J%3BSrinivasachar%2C+K&rft.aulast=Neville&rft.aufirst=D&rft.date=1992-04-01&rft.volume=89&rft.issue=7&rft.spage=2585&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-06 N1 - Date created - 1992-05-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 1990 Jan 1;50(1):84-8 [2152774] Nature. 1990 Jun 14;345(6276):636-40 [1971917] Rheumatol Int. 1990;10(1):21-9 [2353150] J Biol Chem. 1989 Sep 5;264(25):14653-61 [2475487] Ann Intern Med. 1989 Dec 15;111(12):973-81 [2512828] J Neurosurg. 1989 Feb;70(2):240-8 [2783608] Cancer Treat Res. 1988;37:39-73 [2908634] J Biol Chem. 1988 Nov 15;263(32):17122-7 [3182838] J Biol Chem. 1988 Jan 25;263(3):1295-300 [3257214] Cancer Res. 1988 Sep 1;48(17):4862-7 [3261627] Ann N Y Acad Sci. 1987;507:165-71 [3327410] J Biol Chem. 1986 Mar 5;261(7):3030-5 [3485093] Annu Rev Biochem. 1986;55:195-224 [3527042] J Biol Chem. 1971 Mar 10;246(5):1504-10 [5545093] Eur J Immunol. 1981 Apr;11(4):329-34 [6788570] J Immunol. 1980 Aug;125(2):725-31 [6993560] Science. 1991 Oct 18;254(5030):423-7 [1925601] Science. 1991 Jan 18;251(4991):305-8 [1987646] Cell. 1990 Apr 20;61(2):213-22 [2331748] Eur J Immunol. 1986 Aug;16(8):975-9 [2427342] Methods Enzymol. 1989;178:404-22 [2513466] Science. 1988 Dec 23;242(4886):1706-9 [2904703] Bone Marrow Transplant. 1988 May;3(3):185-92 [3048485] Scand J Immunol. 1988 May;27(5):533-40 [3259720] Adv Immunol. 1976;24:215-335 [14486] Bioconjug Chem. 1991 Jul-Aug;2(4):207-10 [1685330] Transplantation. 1987 Jul;44(1):62-9 [3299923] Science. 1987 Oct 23;238(4826):536-9 [3498987] Biochim Biophys Acta. 1987 Aug 7;902(1):24-30 [3607056] J Virol. 1981 Mar;37(3):936-45 [6785449] Bacteriol Rev. 1975 Mar;39(1):54-85 [164179] J Biol Chem. 1977 Feb 25;252(4):1505-14 [190236] Cancer Res. 1990 May 15;50(10):2929-35 [1692251] Blood. 1990 Apr 1;75(7):1426-32 [2180494] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dopamine stimulates [3H]phorbol 12,13-dibutyrate binding in cultured striatal cells. AN - 72859371; 1312574 AB - The effect of dopamine (DA) on the binding of [3H]phorbol 12,13-dibutyrate ([3H]PdBu) in cultured rat striatal cells was examined. DA maximally increased specific [3H]PdBu binding by 70 +/- 10%, an increase comparable to that observed with norepinephrine (NE). This finding suggests that DA activates protein kinase C in cultured striatal cells, because increases in [3H]PdBu binding reflect translocation of protein kinase C. Half-maximal stimulation was observed with 10(-6) M DA. The peak response was observed at 2-3 min after addition of 10(-4) M DA, but [3H]PdBu binding was still increased above basal at 30 min. DA was not acting via an adrenergic receptor. Prazosin (10(-6) M) blocked the response to NE, suggesting mediation by an alpha 1-adrenergic receptor, but had little effect on the response to DA. Conversely, the D1 receptor antagonist SCH-23390 (10(-6) M) blocked the response to DA, but only partially inhibited the response to NE. Morphine (10(-6) M) inhibited the response to DA by 46 +/- 14%, but did not affect significantly the response to NE. The DA effect on [3H]PdBu binding is apparently independent of the increase in cyclic AMP seen on D1 receptor activation. Forskolin, apomorphine, and the D1 agonist SKF-38393 all increased cyclic AMP in striatal cells, but were less effective than DA in stimulating [3H]PdBu binding. The D2 agonist quinpirole was ineffective in stimulating either cyclic AMP or [3H]PdBu binding. JF - Journal of neurochemistry AU - McMillian, M K AU - He, X P AU - Hong, J S AU - Pennypacker, K R AD - Neuropharmacology Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 1308 EP - 1312 VL - 58 IS - 4 SN - 0022-3042, 0022-3042 KW - Receptors, Dopamine KW - 0 KW - Receptors, Dopamine D1 KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Morphine KW - 76I7G6D29C KW - Cyclic AMP KW - E0399OZS9N KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Animals KW - Receptors, Dopamine -- physiology KW - Norepinephrine -- pharmacology KW - Cells, Cultured KW - Cyclic AMP -- antagonists & inhibitors KW - Cyclic AMP -- metabolism KW - Cyclic AMP -- physiology KW - Morphine -- pharmacology KW - Corpus Striatum -- cytology KW - Dopamine -- pharmacology KW - Phorbol 12,13-Dibutyrate -- metabolism KW - Corpus Striatum -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72859371?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=Dopamine+stimulates+%5B3H%5Dphorbol+12%2C13-dibutyrate+binding+in+cultured+striatal+cells.&rft.au=McMillian%2C+M+K%3BHe%2C+X+P%3BHong%2C+J+S%3BPennypacker%2C+K+R&rft.aulast=McMillian&rft.aufirst=M&rft.date=1992-04-01&rft.volume=58&rft.issue=4&rft.spage=1308&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-17 N1 - Date created - 1992-04-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mouse mammary tumor gene int-3: a member of the notch gene family transforms mammary epithelial cells. AN - 72859326; 1312643 AB - Expression of a 2.3-kb RNA species is induced in mammary tumors as a consequence of insertional mutagenesis at the int-3 locus by the mouse mammary tumor virus. The nucleotide sequence and biological activity of this mammary tumor-specific int-3 RNA species were determined. It contains an open reading frame which encodes a 57-kDa protein. The translated protein possesses six nearly contiguous 32-amino-acid repeats which are related to a similar motif in the Saccharomyces cerevisiae cdc-10-encoded cell cycle protein. In addition, the int-3 cdc-10 repeats are bounded by the PEST amino acid sequence motif which is commonly found in proteins having a rapid turnover and may represent sites for phosphorylation. The int-3 cdc-10 repeat sequences are 50% identical to a portion of the intracellular domain of the neurogenic Drosophila notch gene product. Activation of expression of a recombinant int-3 genomic DNA fragment encoding the 2.3-kb RNA species in HC11 mouse mammary epithelial cells in vitro induces anchorage-independent growth in soft agar. JF - Journal of virology AU - Robbins, J AU - Blondel, B J AU - Gallahan, D AU - Callahan, R AD - Laboratory of Tumor Immunology and Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 2594 EP - 2599 VL - 66 IS - 4 SN - 0022-538X, 0022-538X KW - DNA, Viral KW - 0 KW - Insect Hormones KW - Membrane Proteins KW - Proto-Oncogene Proteins KW - Receptors, Cell Surface KW - Receptors, Notch KW - Notch4 protein, mouse KW - 146991-60-8 KW - Index Medicus KW - Animals KW - Transcription, Genetic KW - Amino Acid Sequence KW - Mice KW - Base Sequence KW - Sequence Alignment KW - Epithelial Cells KW - Mammary Glands, Animal -- cytology KW - Restriction Mapping KW - Molecular Sequence Data KW - Repetitive Sequences, Nucleic Acid KW - Cell Line KW - Multigene Family KW - Cell Transformation, Viral -- genetics KW - Receptors, Cell Surface -- genetics KW - Membrane Proteins -- genetics KW - Proto-Oncogene Proteins -- genetics KW - Insect Hormones -- genetics KW - Mammary Tumor Virus, Mouse -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72859326?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Mouse+mammary+tumor+gene+int-3%3A+a+member+of+the+notch+gene+family+transforms+mammary+epithelial+cells.&rft.au=Robbins%2C+J%3BBlondel%2C+B+J%3BGallahan%2C+D%3BCallahan%2C+R&rft.aulast=Robbins&rft.aufirst=J&rft.date=1992-04-01&rft.volume=66&rft.issue=4&rft.spage=2594&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-17 N1 - Date created - 1992-04-17 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M80456; GENBANK N1 - SuppNotes - Cited By: Cell. 1987 Aug 28;50(5):729-37 [2957062] Nature. 1987 Oct 15-21;329(6140):651-4 [2821408] J Virol. 1987 Jan;61(1):66-74 [3023708] EMBO J. 1988 Jul;7(7):2089-95 [3416834] Nature. 1987 Apr 30-May 6;326(6116):833 [3574458] Cell. 1985 Dec;43(3 Pt 2):567-81 [3935325] J Mol Appl Genet. 1982;1(4):327-41 [6286831] Nature. 1984 Feb 9-15;307(5951):521-7 [6320011] Cell. 1984 Jun;37(2):529-36 [6327073] Proc Natl Acad Sci U S A. 1984 Jun;81(12):3756-60 [6587390] Development. 1991 Sep;113(1):199-205 [1764995] Science. 1991 Aug 16;253(5021):789-92 [1876836] Nature. 1990 Mar 1;344(6261):36-42 [2137557] Cell. 1990 May 4;61(3):523-34 [2185893] Nature. 1990 Nov 1;348(6296):76-80 [2234062] Science. 1990 Sep 21;249(4975):1438-41 [2402639] Anal Biochem. 1987 Apr;162(1):156-9 [2440339] J Cell Biol. 1989 Feb;108(2):229-41 [2645293] Cell. 1989 Aug 11;58(3):553-63 [2758466] Science. 1986 Oct 17;234(4774):364-8 [2876518] Nucleic Acids Res. 1985 Mar 11;13(5):1431-42 [2987824] Cell. 1987 Aug 14;50(4):649-57 [3111720] Cell. 1987 Feb 13;48(3):389-97 [3542227] EMBO J. 1985 Feb;4(2):457-63 [4018034] Cell. 1982 Nov;31(1):99-109 [6297757] Nucleic Acids Res. 1984 Jan 11;12(1 Pt 1):387-95 [6546423] Cell. 1991 Jun 28;65(7):1281-9 [1829648] Cell. 1991 Aug 23;66(4):649-61 [1831692] Science. 1991 Aug 16;253(5021):762-8 [1876833] New Biol. 1990 Jul;2(7):595-600 [2083251] Proc Natl Acad Sci U S A. 1990 Jun;87(12):4519-23 [2162045] Cell. 1990 Mar 23;60(6):991-7 [2180580] Cell. 1990 Sep 7;62(5):1007-18 [2203531] Cell Growth Differ. 1990 Oct;1(10):463-72 [2278877] Cell. 1990 Mar 23;60(6):981-90 [2317869] Proc Natl Acad Sci U S A. 1986 Oct;83(20):7806-10 [2429320] Proc Natl Acad Sci U S A. 1989 Aug;86(15):5678-82 [2548184] Cell. 1989 Apr 7;57(1):21-9 [2649246] Nature. 1989 Dec 14;342(6251):830-3 [2689885] Proc Natl Acad Sci U S A. 1987 Oct;84(20):7305-9 [2959959] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Overexpression of the p185erB-2 tyrosine kinase growth factor receptor: control or chaos. AN - 72856689; 1347998 JF - American journal of respiratory cell and molecular biology AU - Gerwin, B I AD - Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 357 EP - 358 VL - 6 IS - 4 SN - 1044-1549, 1044-1549 KW - Proto-Oncogene Proteins KW - 0 KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Receptor, ErbB-2 KW - Index Medicus KW - Breast Neoplasms -- genetics KW - Lung Neoplasms -- enzymology KW - Humans KW - Gene Expression KW - Lung Neoplasms -- genetics KW - Breast Neoplasms -- enzymology KW - Female KW - Protein-Tyrosine Kinases -- genetics KW - Proto-Oncogenes KW - Proto-Oncogene Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72856689?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+respiratory+cell+and+molecular+biology&rft.atitle=Overexpression+of+the+p185erB-2+tyrosine+kinase+growth+factor+receptor%3A+control+or+chaos.&rft.au=Gerwin%2C+B+I&rft.aulast=Gerwin&rft.aufirst=B&rft.date=1992-04-01&rft.volume=6&rft.issue=4&rft.spage=357&rft.isbn=&rft.btitle=&rft.title=American+journal+of+respiratory+cell+and+molecular+biology&rft.issn=10441549&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-24 N1 - Date created - 1992-04-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phenylacetate: a novel nontoxic inducer of tumor cell differentiation. AN - 72854551; 1372534 AB - Sodium phenylacetate was found to affect the growth and differentiation of tumor cells in vitro at concentrations that have been achieved in humans with no significant adverse effects. Treatment of promyelocytic leukemia HL-60 cells resulted in the rapid decline of myc oncogene expression followed by growth arrest and granulocyte differentiation. Phenylacetate also induced highly efficient adipocyte conversion in immortalized mesenchymal C3H 10T1/2 cultures; yet, unlike the differentiating chemotherapeutic drug 5-aza-2'-deoxycytidine, phenylacetate did not cause neoplastic transformation in these susceptible cells. The results indicate that phenylacetate is both effective in inducing tumor cell maturation and free of cytotoxic and carcinogenic effects, a combination that warrants attention to its potential use in cancer intervention. JF - Cancer research AU - Samid, D AU - Shack, S AU - Sherman, L T AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/04/01/ PY - 1992 DA - 1992 Apr 01 SP - 1988 EP - 1992 VL - 52 IS - 7 SN - 0008-5472, 0008-5472 KW - myc KW - Antineoplastic Agents KW - 0 KW - Phenylacetates KW - RNA, Ribosomal KW - decitabine KW - 776B62CQ27 KW - phenylacetic acid KW - ER5I1W795A KW - Azacitidine KW - M801H13NRU KW - Index Medicus KW - Gene Expression -- drug effects KW - Animals KW - Azacitidine -- pharmacology KW - Azacitidine -- analogs & derivatives KW - Humans KW - Mice KW - Mice, Nude KW - RNA, Ribosomal -- drug effects KW - RNA, Ribosomal -- genetics KW - Leukemia, Promyelocytic, Acute KW - Genes, myc -- drug effects KW - Antineoplastic Agents -- pharmacology KW - Cell Line KW - Phenylacetates -- pharmacology KW - Adipose Tissue -- cytology KW - Cell Division -- drug effects KW - Adipose Tissue -- drug effects KW - Cell Differentiation -- drug effects KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72854551?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Phenylacetate%3A+a+novel+nontoxic+inducer+of+tumor+cell+differentiation.&rft.au=Samid%2C+D%3BShack%2C+S%3BSherman%2C+L+T&rft.aulast=Samid&rft.aufirst=D&rft.date=1992-04-01&rft.volume=52&rft.issue=7&rft.spage=1988&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-28 N1 - Date created - 1992-04-28 N1 - Date revised - 2017-01-13 N1 - Gene symbol - myc N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Stable expression of human cytochrome P450IIE1 in mammalian cells: metabolic activation of nitrosodimethylamine and formation of adducts with cellular DNA. AN - 72853543; 1551111 AB - To introduce cytochrome P450IIE1 DNA stably into the chromosomal DNA of mammalian cells, we constructed recombinant retroviruses containing the full-length complementary DNA for human cytochrome P450IIE1 and a selectable neo gene. Rat and mouse cells were infected with these viruses, and clones expressing the neo marker gene product were selected in G418-containing medium. Analysis of the DNA of the clones by Southern blotting showed that the viral DNA was integrated into the cellular DNA. Enzymatic analysis of the clones showed that the transduced DNA directed the expression of enzymatically active cytochrome P450IIE1. Treatment of the cells with the carcinogen [14C]-nitrosodimethylamine and analysis of the cellular DNA by CsCl equilibrium density gradients showed incorporation of the label into DNA, indicating the formation of covalent adducts with the cell DNA. Construction of recombinant cell lines constitutively expressing cytochrome P450IIE1 provides a permanent source for this enzyme and can aid in the analysis of its catalytic properties, such as the metabolic activation of chemical mutagens/carcinogens, and the consequent cytotoxic and genotoxic effects of these compounds. JF - Cancer research AU - Nouso, K AU - Thorgeirsson, S S AU - Battula, N AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/04/01/ PY - 1992 DA - 1992 Apr 01 SP - 1796 EP - 1800 VL - 52 IS - 7 SN - 0008-5472, 0008-5472 KW - Recombinant Proteins KW - 0 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Cytochrome P-450 CYP2E1 KW - EC 1.14.13.- KW - Oxidoreductases, N-Demethylating KW - EC 1.5.- KW - Dimethylnitrosamine KW - M43H21IO8R KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Humans KW - Mice KW - Rats KW - Rats, Inbred F344 KW - Transfection KW - Biotransformation KW - Cells, Cultured KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Epithelium -- metabolism KW - Oxidoreductases, N-Demethylating -- genetics KW - DNA -- isolation & purification KW - Cytochrome P-450 Enzyme System -- genetics KW - DNA -- metabolism KW - Liver -- metabolism KW - Cytochrome P-450 Enzyme System -- metabolism KW - Dimethylnitrosamine -- metabolism KW - Oxidoreductases, N-Demethylating -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72853543?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Stable+expression+of+human+cytochrome+P450IIE1+in+mammalian+cells%3A+metabolic+activation+of+nitrosodimethylamine+and+formation+of+adducts+with+cellular+DNA.&rft.au=Nouso%2C+K%3BThorgeirsson%2C+S+S%3BBattula%2C+N&rft.aulast=Nouso&rft.aufirst=K&rft.date=1992-04-01&rft.volume=52&rft.issue=7&rft.spage=1796&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-28 N1 - Date created - 1992-04-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Delayed reactions to contrast media after interleukin-2 immunotherapy. AN - 72853420; 1549655 AB - A prospective study was conducted by means of a questionnaire to determine the prevalence of delayed reactions to contrast media administered intravenously (iopamidol) and orally (diatrizoate sodium) in 170 patients who had received interleukin-2 (IL-2) and in 631 patients who did not. Another control group of 100 non-IL-2 patients received only oral contrast medium. Delayed reactions (eg, fever rash, flulike symptoms, joint pain, flushing, pruritus, and dizziness) were reported in 3.9% (25 of 631) of non-IL-2 patients and in 11.8% (20 of 170) of IL-2 patients. Reactions were mild in the non-IL-2 patients but were more severe in the IL-2 patients. Two IL-2 patients required hospitalization. Only rash, flulike symptoms, and pruritus were statistically more common in IL-2 patients than in non-IL-2 patients. The prevalence of delayed reactions to nonionic contrast medium is higher in patients who have received IL-2 than in the general population. Most delayed reactions do not require therapy, but, when necessary, therapy is usually limited to relief of symptoms. JF - Radiology AU - Choyke, P L AU - Miller, D L AU - Lotze, M T AU - Whiteis, J M AU - Ebbitt, B AU - Rosenberg, S A AD - Diagnostic Radiology Department, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 111 EP - 114 VL - 183 IS - 1 SN - 0033-8419, 0033-8419 KW - Interleukin-2 KW - 0 KW - Diatrizoate KW - 117-96-4 KW - Iopamidol KW - JR13W81H44 KW - Abridged Index Medicus KW - Index Medicus KW - Administration, Oral KW - Prospective Studies KW - Injections, Intravenous KW - Immunotherapy KW - Humans KW - Time Factors KW - Diatrizoate -- adverse effects KW - Interleukin-2 -- therapeutic use KW - Iopamidol -- adverse effects KW - Diatrizoate -- administration & dosage KW - Iopamidol -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72853420?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Radiology&rft.atitle=Delayed+reactions+to+contrast+media+after+interleukin-2+immunotherapy.&rft.au=Choyke%2C+P+L%3BMiller%2C+D+L%3BLotze%2C+M+T%3BWhiteis%2C+J+M%3BEbbitt%2C+B%3BRosenberg%2C+S+A&rft.aulast=Choyke&rft.aufirst=P&rft.date=1992-04-01&rft.volume=183&rft.issue=1&rft.spage=111&rft.isbn=&rft.btitle=&rft.title=Radiology&rft.issn=00338419&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-17 N1 - Date created - 1992-04-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tempol, a stable free radical, is a novel murine radiation protector. AN - 72853225; 1551104 AB - Nitroxide compounds are stable free radicals which were previously investigated as hypoxic cell radiosensitizers. The stable nitroxide 4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl (Tempol) has recently been shown to protect aerated cells in culture against superoxide generated from hypoxanthine/xanthine oxidase, hydrogen peroxide, and radiation-induced cytotoxicity and to modestly sensitive hypoxic cultured cells. To extend these observations from the cellular level to the whole animal, the toxicity, pharmacology, and in vivo radioprotective effects of Tempol were studied in C3H mice. The maximum tolerated dose of Tempol administered i.p. was found to be 275 mg/kg, which resulted in maximal Tempol levels in whole blood 5-10 min after injection. Mice were exposed to whole-body radiation in the absence or presence of injected Tempol (275 mg/kg) 5-10 min after administration. Tempol treatment provided significant radioprotection (P less than 0.0001); the dose of radiation at which 50% of Tempol-treated mice die at 30 days was 9.97 Gy, versus 7.84 Gy for control mice. Tempol represents a new class of in vivo, non-sulfur-containing radiation protectors. Given the potential for hypoxic radiosensitization and aerobic cell radioprotection, Temporal or other analogues may have potential therapeutic application. JF - Cancer research AU - Hahn, S M AU - Tochner, Z AU - Krishna, C M AU - Glass, J AU - Wilson, L AU - Samuni, A AU - Sprague, M AU - Venzon, D AU - Glatstein, E AU - Mitchell, J B AD - Radiation Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/04/01/ PY - 1992 DA - 1992 Apr 01 SP - 1750 EP - 1753 VL - 52 IS - 7 SN - 0008-5472, 0008-5472 KW - Cyclic N-Oxides KW - 0 KW - Free Radicals KW - Radiation-Protective Agents KW - Spin Labels KW - tempol KW - U78ZX2F65X KW - Index Medicus KW - Animals KW - Whole-Body Irradiation KW - Mice, Inbred C3H KW - Metabolic Clearance Rate KW - Mice KW - Dose-Response Relationship, Radiation KW - Time Factors KW - Female KW - Cyclic N-Oxides -- toxicity KW - Cyclic N-Oxides -- pharmacology KW - Radiation-Protective Agents -- pharmacology KW - Cyclic N-Oxides -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72853225?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Tempol%2C+a+stable+free+radical%2C+is+a+novel+murine+radiation+protector.&rft.au=Hahn%2C+S+M%3BTochner%2C+Z%3BKrishna%2C+C+M%3BGlass%2C+J%3BWilson%2C+L%3BSamuni%2C+A%3BSprague%2C+M%3BVenzon%2C+D%3BGlatstein%2C+E%3BMitchell%2C+J+B&rft.aulast=Hahn&rft.aufirst=S&rft.date=1992-04-01&rft.volume=52&rft.issue=7&rft.spage=1750&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-28 N1 - Date created - 1992-04-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Acquisition of a growth-inhibitory response to phorbol ester involves DNA damage. AN - 72852429; 1372531 AB - TPA (12-O-tetradecanoylphorbol-13-acetate), a potent tumor promoter, has been shown to stimulate or inhibit cell growth depending on the cell type investigated. We recently found that RT101 cells, a transformed mouse JB6 epidermal cell line, acquired a greater growth inhibition response to TPA during conventional subcultivation. The growth of low-passage RT101 cells was slightly inhibited by TPA in monolayer culture but stimulated in soft agar. In contrast, the growth of high-passage cells was greatly inhibited by TPA in both monolayer culture and in soft agar. Inhibition was dose dependent, directly correlated with protein kinase C-activating activities of tumor promoters, and was found to be reversible. TPA-treated high-passage cells were greatly reduced in volume, showed extensive abnormal mitoses, and were more susceptible to detachment. High-passage cells were also found to be less tumorigenic as indicated by in vivo tumorigenicity assay in nude mice. TPA treatment rendered cells still less tumorigenic in the case of both cell lines. The mechanism for acquisition of increased sensitivity to TPA of RT101 cells during subculture was investigated; it involved nonrandom DNA damage and detachment of nonviable cells. The results suggest the possibility that early-passage RT101 cells contained two subpopulations, one TPA-sensitive and one TPA-resistant population. Conventional subcultivation may have selected for the former subpopulation. The sensitive subpopulation may have been irreversibly inhibited as a result of TPA-induced cell killing, possibly apoptosis. JF - Cancer research AU - Sun, Y AU - Pommier, Y AU - Colburn, N H AD - Biological Carcinogenesis and Development Program, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1992/04/01/ PY - 1992 DA - 1992 Apr 01 SP - 1907 EP - 1915 VL - 52 IS - 7 SN - 0008-5472, 0008-5472 KW - fos KW - jun KW - Lyngbya Toxins KW - 0 KW - Tumor Necrosis Factor-alpha KW - teleocidins KW - 27974YJ83L KW - Epidermal Growth Factor KW - 62229-50-9 KW - RNA KW - 63231-63-0 KW - DNA KW - 9007-49-2 KW - Catalase KW - EC 1.11.1.6 KW - Glutathione Peroxidase KW - EC 1.11.1.9 KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Benzoyl Peroxide KW - W9WZN9A0GM KW - Index Medicus KW - Animals KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Superoxide Dismutase -- metabolism KW - Mice, Nude KW - Mice KW - Epidermal Growth Factor -- pharmacology KW - Genes, fos -- drug effects KW - Lyngbya Toxins -- pharmacology KW - Neoplasm Transplantation KW - Catalase -- metabolism KW - DNA -- isolation & purification KW - Glutathione Peroxidase -- metabolism KW - Benzoyl Peroxide -- pharmacology KW - DNA -- genetics KW - RNA -- isolation & purification KW - Genes, jun -- drug effects KW - Cell Line, Transformed KW - RNA -- genetics KW - DNA Damage KW - Cell Division -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72852429?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Acquisition+of+a+growth-inhibitory+response+to+phorbol+ester+involves+DNA+damage.&rft.au=Sun%2C+Y%3BPommier%2C+Y%3BColburn%2C+N+H&rft.aulast=Sun&rft.aufirst=Y&rft.date=1992-04-01&rft.volume=52&rft.issue=7&rft.spage=1907&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-28 N1 - Date created - 1992-04-28 N1 - Date revised - 2017-01-13 N1 - Gene symbol - fos; jun N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of human immunodeficiency virus type 1 Tat activity by coexpression of heterologous trans activators. AN - 72852092; 1312617 AB - We examined the mechanism of Tat-mediated trans activation through competition experiments employing Tat proteins of human immunodeficiency virus type 1 (HIV-1) and equine infectious anemia virus (EIAV). EIAV Tat, as well as chimeric EIAV/HIV-1 Tat proteins, inhibited HIV-1 Tat-mediated trans activation in a cell-type-dependent fashion. Furthermore, these proteins inhibited trans activation by Tat-bacteriophage R17 coat protein chimeras. Inhibition resulted from competition between activation domains of effectors and competitors for a limiting cellular cofactor. The context in which competitor activation domains were expressed contributed to the extent of inhibition. In transfected cells, EIAV Tat and all chimeric competitors were located primarily in the cytoplasm, whereas HIV-1 Tat was primarily located in the nucleus. These data are consistent with a model for trans activation in which the activation domain of Tat associates with and conveys a cellular factor to the transcription complex via the trans-acting-responsive element (TAR). JF - Journal of virology AU - Carroll, R AU - Peterlin, B M AU - Derse, D AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 2000 EP - 2007 VL - 66 IS - 4 SN - 0022-538X, 0022-538X KW - tat KW - Gene Products, tat KW - 0 KW - Trans-Activators KW - tat Gene Products, Human Immunodeficiency Virus KW - Index Medicus KW - AIDS/HIV KW - Bacteriophages -- metabolism KW - HeLa Cells KW - Humans KW - Binding, Competitive KW - Bacteriophages -- genetics KW - Molecular Sequence Data KW - Infectious Anemia Virus, Equine -- genetics KW - Amino Acid Sequence KW - Plasmids KW - Transcriptional Activation KW - Cloning, Molecular KW - Trans-Activators -- metabolism KW - HIV-1 -- metabolism KW - HIV-1 -- genetics KW - Gene Products, tat -- antagonists & inhibitors KW - Trans-Activators -- genetics KW - HIV Long Terminal Repeat -- genetics KW - Gene Products, tat -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72852092?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Inhibition+of+human+immunodeficiency+virus+type+1+Tat+activity+by+coexpression+of+heterologous+trans+activators.&rft.au=Carroll%2C+R%3BPeterlin%2C+B+M%3BDerse%2C+D&rft.aulast=Carroll&rft.aufirst=R&rft.date=1992-04-01&rft.volume=66&rft.issue=4&rft.spage=2000&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-17 N1 - Date created - 1992-04-17 N1 - Date revised - 2017-01-13 N1 - Gene symbol - tat N1 - SuppNotes - Cited By: Science. 1990 Sep 14;249(4974):1281-5 [2205002] Science. 1990 Jun 29;248(4963):1650-3 [2194290] Proc Natl Acad Sci U S A. 1990 Nov;87(22):8985-9 [2247474] Genes Dev. 1989 Apr;3(4):547-58 [2470647] J Virol. 1989 Jan;63(1):1-8 [2535718] Genes Dev. 1989 Mar;3(3):265-82 [2542124] Cell. 1989 Oct 20;59(2):283-92 [2553266] Cell. 1989 Jul 14;58(1):215-23 [2752420] J Virol. 1988 Mar;62(3):673-9 [2828663] Science. 1985 Jul 5;229(4708):69-73 [2990040] Science. 1985 Jul 5;229(4708):74-7 [2990041] Nature. 1988 Oct 20;335(6192):683-9 [3050531] J Virol. 1991 Jul;65(7):3460-7 [1645777] New Biol. 1991 Aug;3(8):759-68 [1931822] New Biol. 1991 Jan;3(1):82-9 [2039768] J Virol. 1990 Apr;64(4):1616-24 [2157047] Virology. 1990 May;176(1):178-83 [2184574] Proc Natl Acad Sci U S A. 1990 Jul;87(13):5079-83 [2195547] Cell. 1990 Nov 16;63(4):655-7 [2225069] J Virol. 1990 Dec;64(12):6018-26 [2243385] Proc Natl Acad Sci U S A. 1989 Sep;86(18):6925-9 [2476805] J Virol. 1989 Mar;63(3):1181-7 [2536828] Cell. 1989 Oct 20;59(2):229-30 [2680105] Nature. 1987 Dec 3-9;330(6147):489-93 [2825027] Cell. 1985 Jul;41(3):813-23 [2988790] J Virol. 1986 Nov;60(2):385-93 [3021973] Biochemistry. 1987 Mar 24;26(6):1563-8 [3297131] Cell. 1987 Feb 27;48(4):691-701 [3643816] Nature. 1970 Aug 15;227(5259):680-5 [5432063] Methods Enzymol. 1987;154:367-82 [3323813] Virology. 1973 Apr;52(2):456-67 [4705382] Science. 1984 Dec 7;226(4679):1165-71 [6095449] J Virol. 1991 Jul;65(7):3468-74 [1645778] J Virol. 1991 Dec;65(12):7012-5 [1658392] Proc Natl Acad Sci U S A. 1990 Aug;87(15):5817-21 [1696012] J Virol. 1991 Mar;65(3):1392-9 [1995949] Cell. 1990 Aug 24;62(4):769-76 [2117500] Nucleic Acids Res. 1990 Dec 11;18(23):6903-7 [2124673] Virology. 1990 May;176(1):280-8 [2158694] Nature. 1990 Jun 14;345(6276):640-2 [2190099] Genes Dev. 1990 Aug;4(8):1365-73 [2227414] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Natural history of intraepithelial neoplasia in humans with implications for cancer chemoprevention strategy. AN - 72851756; 1551096 AB - Intraepithelial neoplasia is of critical importance to the cancer chemoprevention field because it is a target condition for which drugs must be sought that will prevent its development or stop its progression. The term "dysplasia" refers to the morphological alterations that characterize intraepithelial neoplasia and according to many authors consists of seven basic morphological changes that occur in the majority of human epithelia, as well as in the epithelium of mouse skin papillomas induced by 7,12-dimethylbenz(a)anthracene and 12-O-tetradecanoylphorbol-13-acetate: increased nuclear size; altered nuclear shape; increased nuclear stain uptake; nuclear pleomorphism (increased variation in nuclear size, shape, and stain uptake); increased mitoses; abnormal mitoses; and disordered or absent maturation. Clonal evolution appears to begin early in the neoplastic process during intraepithelial neoplasia. Aneuploidy has been found during intraepithelial neoplasia in many human epithelia, and, in association with other forms of genetic instability, may provide the increase in genetically variant cells required for clonal evolution to occur. It is postulated that two major factors affecting the rate of progression of intraepithelial neoplasia are the cellular mutation rate, which is enhanced by environmental carcinogens, and the cellular proliferation rate, which is enhanced by agents that include sex hormones, inducers of chronic inflammation, and irritant chemicals which stimulate reactive hyperproliferation. A preferred chemoprevention strategy should consist of the development of drugs and drug combinations which will block mutagenic carcinogens or prevent epithelial hyperproliferation or its causes. Two examples of the induction of regression of intraepithelial neoplasia by chemopreventive drugs are the regression of oral leukoplakia produced by beta-carotene and the regression of colorectal polyps in patients with familial polyposis produced by sulindac. It is evident that there is a strong need for more research on the induction of regression of intraepithelial neoplasia with chemopreventive agents. There is also a critical need to identify and develop biomarkers that correlate with the appearance and regression of intraepithelial neoplasia. JF - Cancer research AU - Boone, C W AU - Kelloff, G J AU - Steele, V E AD - Chemoprevention Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/04/01/ PY - 1992 DA - 1992 Apr 01 SP - 1651 EP - 1659 VL - 52 IS - 7 SN - 0008-5472, 0008-5472 KW - Antineoplastic Agents KW - 0 KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Humans KW - Epithelium -- pathology KW - Skin Neoplasms -- physiopathology KW - Precancerous Conditions -- physiopathology KW - Papilloma -- prevention & control KW - Papilloma -- pathology KW - Carcinoma -- pathology KW - Skin Neoplasms -- chemically induced KW - Precancerous Conditions -- prevention & control KW - Carcinoma -- prevention & control KW - Carcinoma -- physiopathology KW - Skin Neoplasms -- pathology KW - Papilloma -- physiopathology KW - Antineoplastic Agents -- therapeutic use KW - Skin Neoplasms -- prevention & control KW - Precancerous Conditions -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72851756?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Natural+history+of+intraepithelial+neoplasia+in+humans+with+implications+for+cancer+chemoprevention+strategy.&rft.au=Boone%2C+C+W%3BKelloff%2C+G+J%3BSteele%2C+V+E&rft.aulast=Boone&rft.aufirst=C&rft.date=1992-04-01&rft.volume=52&rft.issue=7&rft.spage=1651&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-28 N1 - Date created - 1992-04-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Angiotensin II receptors are coupled to omega-conotoxin-sensitive calcium influx in bovine adrenal medullary chromaffin cells. AN - 72851420; 1548465 AB - The contribution of an omega-conotoxin GVIA (omega Cgtx)-sensitive Ca2+ influx pathway to the effects of angiotensin II (AII) receptor activation was examined in bovine adrenal medullary (BAM) cells. Pretreatment of BAM cells with 10(-6) M omega Cgtx blocked stimulation of exocytosis by the degradation-resistant analogue, sarcosine1-angiotensin II (S1-AII). In contrast, omega Cgtx had no effect on basal secretion, nor did it inhibit [3H]norepinephrine and [32P]ATP release in response to bradykinin, another phospholipase C-linked receptor agonist. Similarly, omega Cgtx pretreatment inhibited the stimulation of 45Ca2+ uptake by S1-AII, but did not affect the response to bradykinin. This selective inhibition did not appear to be due to blockade of AII receptors by omega Cgtx, as the accumulation of 3H-labeled inositol phosphates in response to S1-AII was not inhibited. The peak S1-AII-stimulated increase in the intracellular free Ca2+ concentration (Cai) in fura 2-loaded BAM cells also was not significantly reduced by omega Cgtx (or by stimulating in nominally Ca(2+)-free buffer), indicating that this response is dependent on intracellular Ca2+ pools. However, a small omega Cgtx-sensitive Cai response was detected after depletion of intracellular Ca2+ pools with ionomycin. This study shows that AII receptors, but not bradykinin receptors, are linked to an omega Cgtx-sensitive Ca2+ influx pathway in BAM cells. JF - Journal of neurochemistry AU - McMillian, M K AU - Tuominen, R K AU - Hudson, P M AU - Suh, H H AU - Hong, J S AD - Neuropharmacology Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 1285 EP - 1291 VL - 58 IS - 4 SN - 0022-3042, 0022-3042 KW - Calcium Channel Blockers KW - 0 KW - Peptides, Cyclic KW - Receptors, Angiotensin KW - Angiotensin II KW - 11128-99-7 KW - angiotensin II, Sar(1)-Ile(5)- KW - 51833-69-3 KW - Ionomycin KW - 56092-81-0 KW - omega-Conotoxin GVIA KW - 92078-76-7 KW - Bradykinin KW - S8TIM42R2W KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Exocytosis -- drug effects KW - Animals KW - Angiotensin II -- analogs & derivatives KW - Cattle KW - Angiotensin II -- metabolism KW - Calcium Channel Blockers -- pharmacology KW - Cells, Cultured KW - Ionomycin -- pharmacology KW - Bradykinin -- pharmacology KW - Angiotensin II -- pharmacology KW - Calcium -- metabolism KW - Receptors, Angiotensin -- metabolism KW - Adrenal Medulla -- cytology KW - Adrenal Medulla -- metabolism KW - Chromaffin System -- metabolism KW - Peptides, Cyclic -- pharmacology KW - Chromaffin System -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72851420?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=Angiotensin+II+receptors+are+coupled+to+omega-conotoxin-sensitive+calcium+influx+in+bovine+adrenal+medullary+chromaffin+cells.&rft.au=McMillian%2C+M+K%3BTuominen%2C+R+K%3BHudson%2C+P+M%3BSuh%2C+H+H%3BHong%2C+J+S&rft.aulast=McMillian&rft.aufirst=M&rft.date=1992-04-01&rft.volume=58&rft.issue=4&rft.spage=1285&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-17 N1 - Date created - 1992-04-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Topoisomerase I alteration in a camptothecin-resistant cell line derived from Chinese hamster DC3F cells in culture. AN - 72849918; 1312902 AB - Camptothecin-resistant DC3F Chinese hamster lung fibroblast cell lines were obtained after mutagenic treatment with ethylmethanesulfonate and subsequent exposure to 1 microM camptothecin (CPT). The most resistant cell line, which was obtained after exposure to CPT for 10 days, was designated DC3F/C-10. Comparison of 50% inhibitory concentration values after 8-h CPT treatments showed that DC3F/C-10 cells were 134-fold resistant to CPT. Resistance was associated with marked reduction of CPT-induced DNA single-strand breaks and DNA-protein cross-links. This reduction was not due to reduced amounts of immunoreactive DNA topoisomerase I protein, although nuclear extracts from DC3F/C-10 cells had less enzyme catalytic activity than those from DC3F cells. Also, fast protein liquid chromatography-purified DNA topoisomerase I from DC3F/C-10 had lower specific catalytic activity than that from DC3F cells. DNA topoisomerase I from DC3F/C-10 was resistant to inhibition of catalytic activity and induction of DNA cleavage by CPT. These results suggest that CPT resistance in DC3F/C-10 cells is due to qualitative alteration of DNA topoisomerase I. JF - Cancer research AU - Tanizawa, A AU - Pommier, Y AD - Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/04/01/ PY - 1992 DA - 1992 Apr 01 SP - 1848 EP - 1854 VL - 52 IS - 7 SN - 0008-5472, 0008-5472 KW - Antineoplastic Agents KW - 0 KW - DNA Topoisomerases, Type I KW - EC 5.99.1.2 KW - Camptothecin KW - XT3Z54Z28A KW - Index Medicus KW - Immunoblotting KW - Animals KW - Cell Nucleus -- enzymology KW - Cricetulus KW - Cell Survival -- drug effects KW - Lung KW - Electrophoresis, Polyacrylamide Gel KW - Kinetics KW - Drug Resistance KW - Molecular Weight KW - Cell Line KW - Cricetinae KW - DNA Topoisomerases, Type I -- isolation & purification KW - Camptothecin -- pharmacology KW - Antineoplastic Agents -- pharmacology KW - DNA Topoisomerases, Type I -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72849918?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Topoisomerase+I+alteration+in+a+camptothecin-resistant+cell+line+derived+from+Chinese+hamster+DC3F+cells+in+culture.&rft.au=Tanizawa%2C+A%3BPommier%2C+Y&rft.aulast=Tanizawa&rft.aufirst=A&rft.date=1992-04-01&rft.volume=52&rft.issue=7&rft.spage=1848&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-28 N1 - Date created - 1992-04-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Benzoquinonoid ansamycins possess selective tumoricidal activity unrelated to src kinase inhibition. AN - 72849711; 1551101 AB - The benzoquinonoid ansamycin antibiotics herbimycin A and geldanamycin have been shown to reverse the oncogenic phenotype of pp60v-src transformed cells as well as induce differentiation in a number of in vitro model systems, reportedly due to their inhibition of src family protein tyrosine kinases. We now report that these agents are potent cytotoxins in vitro against a panel of highly malignant human tumor cell lines possessing primitive neural features. Proliferation and/or survival of fibroblasts, primary neuronal cultures, and several leukemia cell lines are unaffected at concentrations resulting in greater than 99% cell loss in sensitive lines. The tumorigenicity in nude mice of sensitive cell lines can also be markedly reduced by either systemic or topical administration of these agents without apparent toxicity to the whole animal. The cytocidal action of these ansamycins is initiated very rapidly, is irreversible, and is clearly distinct from the delayed inhibition of src family kinases that has been reported previously. Due to their potency, relative selectivity, and novel mechanism(s) of action, these drugs could prove clinically useful in the therapy of a number of human cancers of neural derivation. JF - Cancer research AU - Whitesell, L AU - Shifrin, S D AU - Schwab, G AU - Neckers, L M AD - Tumor Cell Biology Section, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/04/01/ PY - 1992 DA - 1992 Apr 01 SP - 1721 EP - 1728 VL - 52 IS - 7 SN - 0008-5472, 0008-5472 KW - v-src KW - Antibiotics, Antineoplastic KW - 0 KW - Benzoquinones KW - Lactams, Macrocyclic KW - Quinones KW - Rifabutin KW - 1W306TDA6S KW - herbimycin KW - 70563-58-5 KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Oncogene Protein pp60(v-src) KW - EC 2.7.10.2 KW - geldanamycin KW - Z3K3VJ16KU KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Drug Screening Assays, Antitumor KW - Rifabutin -- analogs & derivatives KW - Dose-Response Relationship, Drug KW - Humans KW - Mice KW - Transfection KW - Kinetics KW - Cell Line, Transformed KW - Cell Line KW - Protein-Tyrosine Kinases -- antagonists & inhibitors KW - Cell Survival -- drug effects KW - Antibiotics, Antineoplastic -- pharmacology KW - Cell Division -- drug effects KW - Quinones -- pharmacology KW - Oncogene Protein pp60(v-src) -- antagonists & inhibitors KW - Oncogene Protein pp60(v-src) -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72849711?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Benzoquinonoid+ansamycins+possess+selective+tumoricidal+activity+unrelated+to+src+kinase+inhibition.&rft.au=Whitesell%2C+L%3BShifrin%2C+S+D%3BSchwab%2C+G%3BNeckers%2C+L+M&rft.aulast=Whitesell&rft.aufirst=L&rft.date=1992-04-01&rft.volume=52&rft.issue=7&rft.spage=1721&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-28 N1 - Date created - 1992-04-28 N1 - Date revised - 2017-01-13 N1 - Gene symbol - v-src N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Facilitated transport of the neurotoxin, beta-N-methylamino-L-alanine, across the blood-brain barrier. AN - 72849573; 1548467 AB - beta-N-Methylamino-L-alanine (BMAA) is a neurotoxic plant amino acid that has been implicated in the pathogenesis of the high incidence amyotrophic lateral sclerosis and related parkinsonism dementia of the western Pacific. Previous studies have demonstrated that BMAA is taken up into brain following intravenous or oral administration. To examine the kinetics and mechanism of brain transfer, BMAA influx across the blood-brain barrier was measured in rats using an in situ brain perfusion technique. BMAA influx was found to be saturable with a maximal transfer rate (Vmax) of 1.6 +/- 0.3 x 10(-3) mumol/s/g and a half-saturation constant (Km) of 2.9 +/- 0.7 mM based on total perfusate BMAA concentration. Uptake was sodium independent and inhibitable by excess L-leucine, but not by L-lysine, L-glutamate, or methylaminoisobutyric acid, indicative of transfer by the cerebrovascular large neutral amino acid carrier. L-BMAA competitively reduced brain influx of L-[14C]leucine, as expected for cross-inhibition. The results demonstrate that BMAA is taken up into brain by the large neutral amino acid carrier of the blood-brain barrier and suggest that uptake may be sensitive to the same factors that affect neutral amino acid transport, such as diet, metabolism, disease, and age. JF - Journal of neurochemistry AU - Smith, Q R AU - Nagura, H AU - Takada, Y AU - Duncan, M W AD - Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 1330 EP - 1337 VL - 58 IS - 4 SN - 0022-3042, 0022-3042 KW - Amino Acid Transport Systems KW - 0 KW - Amino Acids KW - Amino Acids, Diamino KW - Carrier Proteins KW - Neurotoxins KW - beta-N-methylamino-L-alanine KW - 108SA6URTV KW - Sodium Chloride KW - 451W47IQ8X KW - Sodium KW - 9NEZ333N27 KW - Leucine KW - GMW67QNF9C KW - Lysine KW - K3Z4F929H6 KW - Index Medicus KW - Animals KW - Carrier Proteins -- metabolism KW - Leucine -- pharmacokinetics KW - Amino Acids -- pharmacokinetics KW - Biological Transport KW - Lysine -- pharmacokinetics KW - Sodium -- pharmacology KW - Rats KW - Rats, Inbred Strains KW - Kinetics KW - Gas Chromatography-Mass Spectrometry KW - Male KW - Sodium Chloride -- pharmacology KW - Neurotoxins -- pharmacokinetics KW - Amino Acids, Diamino -- pharmacology KW - Amino Acids, Diamino -- pharmacokinetics KW - Brain -- metabolism KW - Blood-Brain Barrier UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72849573?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=Facilitated+transport+of+the+neurotoxin%2C+beta-N-methylamino-L-alanine%2C+across+the+blood-brain+barrier.&rft.au=Smith%2C+Q+R%3BNagura%2C+H%3BTakada%2C+Y%3BDuncan%2C+M+W&rft.aulast=Smith&rft.aufirst=Q&rft.date=1992-04-01&rft.volume=58&rft.issue=4&rft.spage=1330&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-17 N1 - Date created - 1992-04-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interleukin-1 alpha and tumor necrosis factor-alpha differentially regulate enkephalin, vasoactive intestinal polypeptide, neurotensin, and substance P biosynthesis in chromaffin cells. AN - 72845360; 1372239 AB - The pattern of expression of at least four neuropeptides contained in adrenomedullary chromaffin cells is altered by exposure to the cytokines interleukin-1 alpha (IL-1 alpha) and tumor necrosis factor-alpha (TNF alpha), alone or in combination with stimulation of other second messenger pathways. Vasoactive intestinal polypeptide (VIP) was elevated 2- to 3-fold by 1 nM IL-1 alpha within 48 h of exposure, while neurotensin and substance P synthesis were unaffected, and met-enkephalin levels were decreased 25-35%. Stimulation of VIP and substance P biosynthesis by forskolin was markedly enhanced by IL-1 alpha, while forskolin stimulation of enkephalin and neurotensin biosynthesis was unaffected. IL-1 alpha amplified the effect of phorbol myristate acetate to increase the VIP content of chromaffin cells, but antagonized phorbol ester-induced elevation of neurotensin levels. TNF alpha also demonstrated a neuropeptide-specific pattern of modulation of second-messenger effects on chromaffin cell neuropeptide levels similar to those seen with IL-1 alpha. The neuroendocrine actions of IL-1 alpha described above, unlike IL-1 action in the immune system, do not appear to be mediated through IL-2 as this cytokine did not affect VIP or enkephalin expression in the presence or absence of protein kinase stimulation. Neither IL-1 alpha nor TNF alpha affected the calcium-coupled stimulation of neuropeptide secretion and biosynthesis that occurs in response to cell depolarization in these and other neuroendocrine cells in vitro and in vivo. These data provide a functional demonstration of IL-1 and TNF receptors in chromaffin cell cultures and suggest a physiological role for cytokine production in the adrenal medulla. Since both the magnitude and direction of neuropeptide synthesis modulation by IL-1 alpha and TNF alpha are highly peptide-specific, it appears that these cytokines do not merely augment second messenger pathways that affect neuropeptide synthesis, but potentially regulate the activity of factors controlling the pattern of neuropeptide gene expression in chromaffin cells. JF - Endocrinology AU - Eskay, R L AU - Eiden, L E AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 2252 EP - 2258 VL - 130 IS - 4 SN - 0013-7227, 0013-7227 KW - Interleukin-1 KW - 0 KW - Interleukin-2 KW - Tumor Necrosis Factor-alpha KW - Colforsin KW - 1F7A44V6OU KW - Substance P KW - 33507-63-0 KW - Vasoactive Intestinal Peptide KW - 37221-79-7 KW - Neurotensin KW - 39379-15-2 KW - Enkephalin, Methionine KW - 58569-55-4 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Colforsin -- pharmacology KW - Cattle KW - Cells, Cultured KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Interleukin-2 -- biosynthesis KW - Vasoactive Intestinal Peptide -- biosynthesis KW - Interleukin-1 -- pharmacology KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Neurotensin -- biosynthesis KW - Chromaffin Granules -- metabolism KW - Substance P -- biosynthesis KW - Enkephalin, Methionine -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72845360?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrinology&rft.atitle=Interleukin-1+alpha+and+tumor+necrosis+factor-alpha+differentially+regulate+enkephalin%2C+vasoactive+intestinal+polypeptide%2C+neurotensin%2C+and+substance+P+biosynthesis+in+chromaffin+cells.&rft.au=Eskay%2C+R+L%3BEiden%2C+L+E&rft.aulast=Eskay&rft.aufirst=R&rft.date=1992-04-01&rft.volume=130&rft.issue=4&rft.spage=2252&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-22 N1 - Date created - 1992-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Accumulation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in cultured cerebellar astrocytes. AN - 72842962; 1548462 AB - Cultured cerebellar astrocytes rapidly accumulate 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) from the incubation medium, reaching a plateau within 10 min, whereas within that time negligible amounts of 1-methyl-4-phenylpyridinium (MPP+) have entered the astrocytes. MPTP accumulation is essentially independent of temperature and is proportional to extracellular concentration at steady state: The steady-state concentration achieved within these cells is about 50-fold higher at relatively low extracellular concentrations. MPTP appears to accumulate intracellularly within lysosomes, because lysosomotropic agents such as ammonium chloride and chloroquine markedly diminish the accumulation. Moreover, a proton gradient is required, because MPTP accumulation is abolished by the hydrogen ion antiporter monensin. Over an interval of several days, MPTP is converted to MPP+ intracellularly, with a concomitant decrease in medium MPTP and increase in medium MPP+. A constant, small but significant amount of MPP+ is retained intracellularly over a 72-h interval. Increasing the medium MPTP concentrations results in increased conversion of MPTP and enhanced intracellular retention of MPTP and MPP+. Neither MPTP nor MPP+ is neurotoxic to cultured cerebellar astrocytes as determined by cell counts and rate of conversion of MPTP to MPP+. JF - Journal of neurochemistry AU - Marini, A M AU - Lipsky, R H AU - Schwartz, J P AU - Kopin, I J AD - Clinical Neuroscience Branch, NINDS, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 1250 EP - 1258 VL - 58 IS - 4 SN - 0022-3042, 0022-3042 KW - Ammonium Chloride KW - 01Q9PC255D KW - Chloroquine KW - 886U3H6UFF KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Index Medicus KW - Animals KW - Cerebellum -- cytology KW - Chloroquine -- pharmacology KW - Cells, Cultured KW - 1-Methyl-4-phenylpyridinium -- metabolism KW - Lysosomes -- drug effects KW - Ammonium Chloride -- pharmacology KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- metabolism KW - Astrocytes -- drug effects KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- pharmacology KW - Astrocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72842962?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=Accumulation+of+1-methyl-4-phenyl-1%2C2%2C3%2C6-tetrahydropyridine+in+cultured+cerebellar+astrocytes.&rft.au=Marini%2C+A+M%3BLipsky%2C+R+H%3BSchwartz%2C+J+P%3BKopin%2C+I+J&rft.aulast=Marini&rft.aufirst=A&rft.date=1992-04-01&rft.volume=58&rft.issue=4&rft.spage=1250&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-17 N1 - Date created - 1992-04-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cholecystokinin-octapeptide stimulates hypothalamic-pituitary-adrenal function in rats: role of corticotropin-releasing hormone. AN - 72842241; 1312423 AB - Peripherally-administered cholecystokinin (CCK) is a profound suppressor of food intake, can promote anxiety, and causes the acute release of ACTH into plasma. Centrally administered corticotropin-releasing hormone (CRH), on the other hand, not only represents the principal stimulus to the pituitary corticotroph cell, but also has been shown to suppress appetite and to be profoundly anxiogenic. Because of the overlap in the effects of peripherally administered CCK and of centrally administered CRH, we report here a study to determine whether sulphated CCK octapeptide (CCK-8) could induce the release of CRH within the central nervous system. To accomplish this task, we first assessed the dose-related effects of CCK-8 on ACTH release. Graded doses of CCK-8 (0.1-10 micrograms/kg BW) given in an i.v. bolus to freely moving male rats, resulted in a dose-dependent increase of plasma immunoreactive (IR)-ACTH (ED50: 1-10 micrograms/kg BW). The lowest maximal stimulatory dose of CCK-8 (5 micrograms/kg BW) was used in all subsequent experiments. To evaluate whether CCK-induced ACTH secretion was mediated by a peripheral CCK receptor, an i.v. bolus injection of vehicle or L-364,718 (1 mg/kg BW), a specific, highly potent peripheral CCK receptor antagonist, was given before the i.v. administration of CCK-8 or vehicle. Plasma IR-ACTH response to CCK-8 was significantly attenuated by L-364,718. A role for the vagal afferents that contain CCK receptors in peripherally administered CCK-mediated hypothalamic-pituitary-adrenal (HPA) axis activation was examined in animals that had been pretreated with capsaicin, a potent neurotoxin that destroys vagal afferents. Plasma IR-ACTH and IR-corticosterone responses in capsaicin-treated animals were significantly lower than those in vehicle treated rats. In subsequent in vivo experiments, pituitary stalk-transected and sham-operated animals were used to evaluate whether CCK-8 stimulates the HPA axis via a centrally mediated mechanism. IR-ACTH and IR-corticosterone responses to i.v. CCK-8 were significantly reduced in the pituitary stalk-transected compared to sham-operated animals. In further effort to determine whether the central nervous system was involved in the plasma IR-ACTH response to the peripheral administration of i.v. CCK-8, we compared the effects of the i.v. administration of CRH antisera vs. normal rabbit serum on this parameter. IR-ACTH and IR-corticosterone responses to i.v. CCK-8 were significantly reduced in the context of pretreatment with CRH antisera compared to the administration of normal rabbit serum.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Endocrinology AU - Kamilaris, T C AU - Johnson, E O AU - Calogero, A E AU - Kalogeras, K T AU - Bernardini, R AU - Chrousos, G P AU - Gold, P W AD - Clinical Neuroendocrinology Branch, National Institute of Mental Health, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 1764 EP - 1774 VL - 130 IS - 4 SN - 0013-7227, 0013-7227 KW - Receptors, Cholecystokinin KW - 0 KW - Adrenocorticotropic Hormone KW - 9002-60-2 KW - Corticotropin-Releasing Hormone KW - 9015-71-8 KW - Sincalide KW - M03GIQ7Z6P KW - Abridged Index Medicus KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Adrenocorticotropic Hormone -- secretion KW - Dose-Response Relationship, Drug KW - Receptors, Cholecystokinin -- physiology KW - Male KW - Hypothalamo-Hypophyseal System -- drug effects KW - Corticotropin-Releasing Hormone -- physiology KW - Pituitary-Adrenal System -- drug effects KW - Sincalide -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72842241?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrinology&rft.atitle=Cholecystokinin-octapeptide+stimulates+hypothalamic-pituitary-adrenal+function+in+rats%3A+role+of+corticotropin-releasing+hormone.&rft.au=Kamilaris%2C+T+C%3BJohnson%2C+E+O%3BCalogero%2C+A+E%3BKalogeras%2C+K+T%3BBernardini%2C+R%3BChrousos%2C+G+P%3BGold%2C+P+W&rft.aulast=Kamilaris&rft.aufirst=T&rft.date=1992-04-01&rft.volume=130&rft.issue=4&rft.spage=1764&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-22 N1 - Date created - 1992-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Metabolic activation and genotoxicity of heterocyclic arylamines. AN - 72834069; 1544147 AB - Because of the potential for human exposure to mutagenic and carcinogenic heterocyclic arylamines in the diet, the carcinogenicity of three HAAs, 2-amino-3-methylimidazo[4,5-f]quinoline, 2-amino-3,8-dimethyl-imidazo[4,5-f]quinoxaline, and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, is being evaluated in nonhuman primates, especially cynomolgus monkeys. Concomitant with the carcinogenicity studies, the metabolic processing, disposition, and DNA-adduct formation of these compounds are being examined in these monkeys. This report highlights the results from studies in monkeys and from in vitro models examining metabolic activation and genotoxicity of HAAs. The extent of in vivo activation of HAAs in monkeys was assessed by measuring DNA adducts in various tissues. Both 2-amino-3-methylimidazo[4,5-f]quinoline and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine form high levels of DNA adducts in a number of organs, particularly the liver, kidney, and heart. The implications of metabolic activation and DNA-adduct formation to the carcinogenicity of HAAs are discussed. JF - Cancer research AU - Snyderwine, E G AU - Schut, H A AU - Adamson, R H AU - Thorgeirsson, U P AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/04/01/ PY - 1992 DA - 1992 Apr 01 SP - 2099s EP - 2102s VL - 52 IS - 7 Suppl SN - 0008-5472, 0008-5472 KW - Heterocyclic Compounds KW - 0 KW - Imidazoles KW - Polychlorinated Dibenzodioxins KW - Quinolines KW - Quinoxalines KW - 2-amino-3-methylimidazo(4,5-f)quinoline KW - 30GL3D3T0G KW - 2-amino-3,8-dimethylimidazo(4,5-f)quinoxaline KW - 77500-04-0 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine KW - 909C6UN66T KW - Index Medicus KW - Salmonella -- drug effects KW - Animals KW - Mutagenicity Tests KW - Biotransformation KW - Mice, Inbred C57BL KW - Cytochrome P-450 Enzyme System -- metabolism KW - Mice KW - Quinolines -- toxicity KW - Imidazoles -- pharmacokinetics KW - Imidazoles -- toxicity KW - Heterocyclic Compounds -- pharmacokinetics KW - DNA -- metabolism KW - Quinoxalines -- toxicity KW - Quinoxalines -- pharmacokinetics KW - Heterocyclic Compounds -- toxicity KW - Quinolines -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72834069?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Metabolic+activation+and+genotoxicity+of+heterocyclic+arylamines.&rft.au=Snyderwine%2C+E+G%3BSchut%2C+H+A%3BAdamson%2C+R+H%3BThorgeirsson%2C+U+P%3BThorgeirsson%2C+S+S&rft.aulast=Snyderwine&rft.aufirst=E&rft.date=1992-04-01&rft.volume=52&rft.issue=7+Suppl&rft.spage=2099s&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-15 N1 - Date created - 1992-04-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Adaptive chaos and AIDS. AN - 72741844; 15335977 JF - Current biology : CB AU - O'Brien, S J AU - Mann, D L AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, National Institutes of Health, Frederick, Maryland 21762, USA. Y1 - 1992/04// PY - 1992 DA - April 1992 SP - 203 EP - 205 VL - 2 IS - 4 SN - 0960-9822, 0960-9822 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72741844?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+biology+%3A+CB&rft.atitle=Adaptive+chaos+and+AIDS.&rft.au=O%27Brien%2C+S+J%3BMann%2C+D+L&rft.aulast=O%27Brien&rft.aufirst=S&rft.date=1992-04-01&rft.volume=2&rft.issue=4&rft.spage=203&rft.isbn=&rft.btitle=&rft.title=Current+biology+%3A+CB&rft.issn=09609822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2005-03-01 N1 - Date created - 2004-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Structural and functional analysis of human germ cell alkaline phosphatase by site-specific mutagenesis. AN - 72862765; 1554693 AB - Human germ cell alkaline phosphatase (GCAP), which shares 98% amino acid sequence identity with the placental AP (PLAP), is expressed by malignant trophoblasts. Protein sequence analysis suggests that the Ser residue at position 92 is the putative active site of GCAP which contains two recognition sequences (Asn122-Thr-Thr124 and Asn249-Arg-Thr251) for asparagine-linked glycosylation. To examine the roles of the Ser residue and glycan moieties on GCAP activity and processing, we altered the GCAP cDNA by site-directed mutagenesis and expressed the GCAP mutants in COS-1 cells. Substitution of Ser-92 with either a Thr (S92T) or an Ala (S92A) residue yielded a GCAP devoid of catalytic activity, suggesting that the Ser codon 92 is the active site of GCAP. Six GCAP mutants that lack one or both glycosylation sites were constructed by substituting either Asn-122 or Asn-249 with an Asp residue or either Thr-124 or Thr-251 with an Ala residue. The mature GCAP migrated as a 65-kDa product, but GCAP mutants lacking one or both glycosylation sites migrated as 62- or 58-kDa polypeptides, respectively, indicating that both sites were glycosylated. All six glycosylated mutants were active enzymatically and, in addition, were equally sensitive to heat, L-leucine, and EDTA inhibition as the parental enzyme. GCAP as well as its two active-site and six glycosylation mutants could be released from the plasma membrane of transfected COS-1 cells by the proteinase bromelain.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Biochemistry AU - Watanabe, T AU - Wada, N AU - Chou, J Y AD - Human Genetics Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1992/03/31/ PY - 1992 DA - 1992 Mar 31 SP - 3051 EP - 3058 VL - 31 IS - 12 SN - 0006-2960, 0006-2960 KW - Isoenzymes KW - 0 KW - Membrane Proteins KW - germ-cell AP isoenzyme KW - Serine KW - 452VLY9402 KW - Alkaline Phosphatase KW - EC 3.1.3.1 KW - Index Medicus KW - Animals KW - Membrane Proteins -- chemistry KW - Humans KW - Membrane Proteins -- genetics KW - Glycosylation KW - Serine -- chemistry KW - Germ Cells -- chemistry KW - Structure-Activity Relationship KW - Binding Sites KW - Base Sequence KW - Kinetics KW - Cercopithecus aethiops KW - Molecular Sequence Data KW - Kidney KW - Cell Line KW - Germ Cells -- enzymology KW - Mutagenesis, Site-Directed KW - Isoenzymes -- chemistry KW - Alkaline Phosphatase -- chemistry KW - Isoenzymes -- biosynthesis KW - Alkaline Phosphatase -- biosynthesis KW - Alkaline Phosphatase -- genetics KW - Isoenzymes -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72862765?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=Structural+and+functional+analysis+of+human+germ+cell+alkaline+phosphatase+by+site-specific+mutagenesis.&rft.au=Watanabe%2C+T%3BWada%2C+N%3BChou%2C+J+Y&rft.aulast=Watanabe&rft.aufirst=T&rft.date=1992-03-31&rft.volume=31&rft.issue=12&rft.spage=3051&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-01 N1 - Date created - 1992-05-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Recovery in hemiparkinsonian rats following intrastriatal implantation of activated leukocytes. AN - 73167500; 1515912 AB - Behavioral improvement has been seen in hemiparkinsonian animals after surgical lesions of the denervated caudate nucleus. This study was designed to investigate the role of inflammatory cells in injury-induced recovery. A hemiparkinsonian syndrome was induced in rats by unilateral injections of 6-hydroxydopamine into the pars compacta of the substantia nigra. Phytohemagglutinin-stimulated rat peritoneal cells, predominantly T cells and macrophages, were stereotactically implanted in the lesioned caudate-putamen, and amphetamine-induced turning was used to assess recovery. Animals receiving implants of activated peritoneal cells showed a 47% decrease in amphetamine-induced turning 8 weeks after implantation, which was not seen in control or sham-operated animals. Immunocytochemistry revealed increased tyrosine hydroxylase reactive fibers in the leukocyte-implanted striatum. We conclude that implantation of activated leukocytes promotes functional recovery in hemiparkinsonian rats. JF - Brain research AU - Ewing, S E AU - Weber, R J AU - Zauner, A AU - Plunkett, R J AD - Surgical Neurology Branch, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/03/27/ PY - 1992 DA - 1992 Mar 27 SP - 42 EP - 48 VL - 576 IS - 1 SN - 0006-8993, 0006-8993 KW - Lectins KW - 0 KW - Oxidopamine KW - 8HW4YBZ748 KW - Dextroamphetamine KW - TZ47U051FI KW - Index Medicus KW - Animals KW - Ganglia, Spinal -- physiology KW - T-Lymphocytes -- transplantation KW - Macrophage Activation KW - Denervation KW - Dextroamphetamine -- pharmacology KW - Lymphocyte Activation KW - Rats KW - Rats, Inbred Strains KW - Macrophages -- transplantation KW - Oxidopamine -- toxicity KW - Male KW - Leukocyte Transfusion KW - Substantia Nigra -- physiopathology KW - Corpus Striatum -- physiopathology KW - Substantia Nigra -- pathology KW - Caudate Nucleus -- physiopathology KW - Corpus Striatum -- drug effects KW - Caudate Nucleus -- drug effects KW - Stereotyped Behavior -- drug effects KW - Parkinson Disease -- physiopathology KW - Parkinson Disease -- surgery UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73167500?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Recovery+in+hemiparkinsonian+rats+following+intrastriatal+implantation+of+activated+leukocytes.&rft.au=Ewing%2C+S+E%3BWeber%2C+R+J%3BZauner%2C+A%3BPlunkett%2C+R+J&rft.aulast=Ewing&rft.aufirst=S&rft.date=1992-03-27&rft.volume=576&rft.issue=1&rft.spage=42&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-06 N1 - Date created - 1992-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A pregnancy-specific mammary nuclear factor involved in the repression of the mouse beta-casein gene transcription by progesterone. AN - 72872171; 1556095 AB - The sequence-specific binding pattern of mammary nuclear proteins to the 545-base pair (bp) 5'-flanking region of the mouse beta-casein gene was compared between pregnant and lactating mice by a gel mobility shift assay. By using appropriate probes, two complexes were detected only during pregnancy, whereas an additional four complexes were detected during both pregnancy and lactation. The two pregnancy-specific complexes showed identical electrophoretic mobility and were cross-competed with two unlabeled DNA fragments used to generate the probes. Methylation interference experiments indicated that the two binding regions involved guanosine residues at nucleotides -350 and -8, and the sequences around each guanosine residue have a common palindromic sequence, 5'-TGAT/ATCA-3'. This binding factor is termed pregnancy-specific mammary nuclear factor. In gene transfection experiments, expression of the chimeric beta-casein-CAT gene linked to the 545 bp of mouse beta-casein gene promoter region was maximally induced when transfected mammary epithelial cells were cultured with the lactogenic hormones prolactin, hydrocortisone, and insulin, whereas it was very low when insulin alone was added. The addition of progesterone together with the lactogenic hormones inhibited the hormonal induction of the chimeric gene, whereas co-transfection with an oligonucleotide containing the pregnancy-specific mammary nuclear factor binding site substantially overcome the progesterone-mediated repression of transcription. Furthermore, mutation of the pregnancy-specific mammary nuclear factor binding sites of the chimeric beta-casein-CAT gene resulted in attenuation of the inhibitory effect of progesterone without blocking the stimulatory effect of the lactogenic hormones. These results indicate the presence of a pregnancy-specific mammary nuclear factor(s) that bind to two separate sites of the beta-casein gene promoter and suggest that it may serve as a repressor that mediates the inhibitory action of progesterone on beta-casein gene transcription. JF - The Journal of biological chemistry AU - Lee, C S AU - Oka, T AD - Laboratory of Molecular and Cellular Biology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/03/25/ PY - 1992 DA - 1992 Mar 25 SP - 5797 EP - 5801 VL - 267 IS - 9 SN - 0021-9258, 0021-9258 KW - Caseins KW - 0 KW - Insulin KW - Nuclear Proteins KW - Oligodeoxyribonucleotides KW - Progesterone KW - 4G7DS2Q64Y KW - Prolactin KW - 9002-62-4 KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Hydrocortisone KW - WI4X0X7BPJ KW - Index Medicus KW - Animals KW - Insulin -- pharmacology KW - Mice KW - Plasmids KW - Chloramphenicol O-Acetyltransferase -- metabolism KW - Pregnancy KW - Mutagenesis, Site-Directed KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Hydrocortisone -- pharmacology KW - Promoter Regions, Genetic KW - Base Sequence KW - Transfection KW - Cells, Cultured KW - Restriction Mapping KW - Mice, Inbred C3H KW - Molecular Sequence Data KW - Prolactin -- pharmacology KW - Methylation KW - Female KW - Lactation -- physiology KW - Transcription, Genetic -- drug effects KW - Caseins -- genetics KW - Mammary Glands, Animal -- physiology KW - Progesterone -- pharmacology KW - Gene Expression Regulation -- drug effects KW - Nuclear Proteins -- metabolism KW - Pregnancy, Animal -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72872171?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=A+pregnancy-specific+mammary+nuclear+factor+involved+in+the+repression+of+the+mouse+beta-casein+gene+transcription+by+progesterone.&rft.au=Lee%2C+C+S%3BOka%2C+T&rft.aulast=Lee&rft.aufirst=C&rft.date=1992-03-25&rft.volume=267&rft.issue=9&rft.spage=5797&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-04 N1 - Date created - 1992-05-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Structure and function of the 5'-flanking sequence of the human cytosolic selenium-dependent glutathione peroxidase gene (hgpx1). AN - 72871440; 1556108 AB - Human selenium-dependent glutathione peroxidase (hGPx1) (EC 1.11.1.9) is thought to be involved in many critical cellular functions as a result of its role in glutathione-mediated reduction of toxic peroxides, and it is implicated as a mechanism of resistance against oxygen free radicals. Previous studies have demonstrated that the gene encoding hGPx1 (hgpx1) is more highly expressed in multidrug-resistant AdrR MCF-7 human breast cancer cells than in the parental WT MCF-7 cell line. In order to further study the transcriptional regulation of hgpx1, we have cloned the genomic hgpx1 gene and determined its nucleotide sequence. The 2550-base pair (bp) 5'-flanking sequence of hgpx1 contained the terminal 511 bp of the 3' end of a previously reported rhoH12 cDNA (Yeramian, P., Chardin, P., Madaule, P., and Tavitian, A. (1987) Nucleic Acids Res. 15, 1989), a ras-related oncogene. Further downstream from rhoH12, but before the start of transcription of hgpx1, RNase protection analysis revealed a transcribed sequence of at least 270 bp which we have called mid. RNA transcripts homologous to both rhoH12 (1.8 and 1.5 kilobase pairs (kb)) and mid (1.8 kb) are also more highly expressed in AdrR MCF-7 cells than in WT MCF-7 cells. We screened an AdrR MCF-7 cDNA library with the mid sequence and isolated a partial cDNA clone which contains both mid and rhoH12 sequences and is colinear with the genomic sequence which extends from 10 bp 3' to the rhoH12 stop codon to 810 bp 5' to the start of transcription of hgpx1. The start of transcription of hgpx1 in AdrR MCF-7 cells was determined by primer extension analysis. The promoter and 2 kb of the 5'-flanking sequence of hgpx1 was fused to the bacterial chloramphenicol acetyltransferase gene (hGPx1-CAT1). Analysis of deletion constructs of hGPx1-CAT1 revealed three possible cis-acting regulatory regions. The transcriptional regulation of hgpx1 was examined using the hGPx1-CAT hybrid genes and nuclear run-on studies. We found no evidence that increased mRNA transcript formation could account for different levels of hgpx1 RNA either in different breast cancer cell lines or in response to selenium. JF - The Journal of biological chemistry AU - Moscow, J A AU - Morrow, C S AU - He, R AU - Mullenbach, G T AU - Cowan, K H AD - Medicine Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/03/25/ PY - 1992 DA - 1992 Mar 25 SP - 5949 EP - 5958 VL - 267 IS - 9 SN - 0021-9258, 0021-9258 KW - hgpx1 KW - mid KW - rhoH12 KW - DNA Probes KW - 0 KW - DNA, Neoplasm KW - Oligodeoxyribonucleotides KW - Glutathione Peroxidase KW - EC 1.11.1.9 KW - Selenium KW - H6241UJ22B KW - Index Medicus KW - Blotting, Northern KW - Cytosol -- enzymology KW - Humans KW - Amino Acid Sequence KW - DNA, Neoplasm -- isolation & purification KW - Genomic Library KW - Cloning, Molecular KW - Leukocytes -- enzymology KW - Selenium -- metabolism KW - Base Sequence KW - Blotting, Southern KW - Restriction Mapping KW - Molecular Sequence Data KW - DNA, Neoplasm -- genetics KW - Male KW - Cell Line KW - Genes KW - Glutathione Peroxidase -- genetics KW - Genes, Regulator UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72871440?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Structure+and+function+of+the+5%27-flanking+sequence+of+the+human+cytosolic+selenium-dependent+glutathione+peroxidase+gene+%28hgpx1%29.&rft.au=Moscow%2C+J+A%3BMorrow%2C+C+S%3BHe%2C+R%3BMullenbach%2C+G+T%3BCowan%2C+K+H&rft.aulast=Moscow&rft.aufirst=J&rft.date=1992-03-25&rft.volume=267&rft.issue=9&rft.spage=5949&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-04 N1 - Date created - 1992-05-04 N1 - Date revised - 2017-01-13 N1 - Gene symbol - hgpx1; mid; rhoH12 N1 - Genetic sequence - L01675; GENBANK; M83677; M83678; M83676; M83094; M83679; L01676; L01677; M83680; M83681 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retroviral vectors containing putative internal ribosome entry sites: development of a polycistronic gene transfer system and applications to human gene therapy. AN - 19628646; 8743660 AB - Recombinant retroviral vectors producing multicistronic mRNAs were constructed. Picornavirus putative internal ribosome entry sites (IRES) were used to confer cap-independent translation of an internal cistron. Internal cistrons were engineered by ligation of various lengths of the IRES of encephalomyocarditis (EMC) virus or polio virus to the E. coli chloramphenicol acetyltransferase (CAT) gene. The IRES/CAT fusions were introduced into retroviral vectors 3' to the translation stop codon of the neomycin phosphotransferase (NEO) gene, and the molecular constructs transfected into retroviral vector packaging lines. Retroviral vector producer cells efficiently express the internal CAT gene product only when the full length IRES is used. Both the EMC/CAT and polio/CAT retroviral vectors produced high titer vector supernatant capable of productive transduction of target cells. To test the generality of this gene transfer system, a retroviral vector containing an IRES fusion to the human adenosine deaminase (ADA) gene was constructed. Producer cell supernatant was used to transduce NIH/3T3 cells, and transduced cells were shown to express NEO, and ADA. Novel three-gene-containing retroviral vectors were constructed by introducing the EMC/ADA fusion into either an existing internal-promoter-containing vector, or a polio/CAT bicistronic vector. Producer cell clones of the three-gene vectors synthesize all three gene products, were of high titer, and could productively transduce NIH/3T3 cells. By utilizing cap-independent translation units, IRES vectors can produce polycistronic mRNAs which enhance the ability of retroviral-mediated gene transfer to engineer cells to produce multiple foreign proteins. Images JF - Nucleic Acids Research AU - Morgan, R A AU - Couture, L AU - Elroy-Stein, O AU - Ragheb, J AU - Moss, B AU - Anderson, W F AD - Molecular Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/03/25/ PY - 1992 DA - 1992 Mar 25 SP - 1293 EP - 1299 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 20 IS - 6 SN - 0305-1048, 0305-1048 KW - Genetics Abstracts; Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - Translation KW - Poliovirus KW - Picornavirus KW - Gene therapy KW - Producer cells KW - ADA gene KW - Expression vectors KW - Cistrons KW - Stop codon KW - Chloramphenicol O-acetyltransferase KW - NEO gene KW - CAT gene KW - Escherichia coli KW - Internal ribosome entry site KW - Adenosine deaminase KW - Packaging KW - neomycin phosphotransferase KW - W 30905:Medical Applications KW - G 07880:Human Genetics KW - V 22320:Replication KW - N 14810:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19628646?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+Acids+Research&rft.atitle=Retroviral+vectors+containing+putative+internal+ribosome+entry+sites%3A+development+of+a+polycistronic+gene+transfer+system+and+applications+to+human+gene+therapy.&rft.au=Morgan%2C+R+A%3BCouture%2C+L%3BElroy-Stein%2C+O%3BRagheb%2C+J%3BMoss%2C+B%3BAnderson%2C+W+F&rft.aulast=Morgan&rft.aufirst=R&rft.date=1992-03-25&rft.volume=20&rft.issue=6&rft.spage=1293&rft.isbn=&rft.btitle=&rft.title=Nucleic+Acids+Research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2008-12-01 N1 - Last updated - 2015-03-27 N1 - SubjectsTermNotLitGenreText - Translation; Gene therapy; Producer cells; ADA gene; Expression vectors; Cistrons; Chloramphenicol O-acetyltransferase; Stop codon; NEO gene; CAT gene; Internal ribosome entry site; neomycin phosphotransferase; Packaging; Adenosine deaminase; Poliovirus; Picornavirus; Escherichia coli ER - TY - JOUR T1 - Search for neurotoxins structurally related to 1-methyl-4-phenylpyridine (MPP+) in the pathogenesis of Parkinson's disease. AN - 72908908; 1571786 AB - Immunoassays sensitive to a broad range of compounds structurally related to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP) and 1-methyl-4-phenylpyridine (MPP+) have been developed and used to test for the presence of possible chemically related neurotoxins in the brains of Parkinson's disease patients. The sensitivity and chemical reactivity of the polyclonal antibodies used in these assays have been characterized with a range of endogenous and chemically related materials. Two methods were developed and tested for extraction followed by chromatographic separation which would be applicable to stored or accumulated substances. The immunoassays were tested and applied to the assay of tissue extracts from MPTP or MPTP-analogue exposed animals, and indicated detectability of MPP(+)-immunoreactivity greater than 8 weeks after exposure to MPTP in monkey brain. No difference in immunoactivity was measured in extracts from human brains of Parkinson's disease patients or controls, and particularly low levels of immunoreactivity were found in the striatum relative to the levels measured in several cortical regions. From these studies, there is no evidence for the role of an environmental neurotoxin chemically related to MPTP in the pathogenesis of Parkinson's disease. JF - Brain research AU - Ikeda, H AU - Markey, C J AU - Markey, S P AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1992/03/20/ PY - 1992 DA - 1992 Mar 20 SP - 285 EP - 298 VL - 575 IS - 2 SN - 0006-8993, 0006-8993 KW - Neurotoxins KW - 0 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Index Medicus KW - Animals KW - 1-Methyl-4-phenylpyridinium -- analysis KW - Humans KW - Dogs KW - Neurotoxins -- analysis KW - Enzyme-Linked Immunosorbent Assay KW - Adrenal Glands -- chemistry KW - 1-Methyl-4-phenylpyridinium -- chemistry KW - Haplorhini KW - Chromatography, High Pressure Liquid KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- analysis KW - Brain Chemistry KW - Parkinson Disease -- metabolism KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72908908?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Search+for+neurotoxins+structurally+related+to+1-methyl-4-phenylpyridine+%28MPP%2B%29+in+the+pathogenesis+of+Parkinson%27s+disease.&rft.au=Ikeda%2C+H%3BMarkey%2C+C+J%3BMarkey%2C+S+P&rft.aulast=Ikeda&rft.aufirst=H&rft.date=1992-03-20&rft.volume=575&rft.issue=2&rft.spage=285&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-29 N1 - Date created - 1992-05-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cancer in the contralateral breast after radiotherapy for breast cancer. AN - 72827653; 1538720 AB - Patients with breast cancer have a threefold increase in the risk that a second breast cancer will develop. Radiation treatment for the initial cancer can result in moderately high doses to the contralateral breast, possibly contributing to this heightened risk. We conducted a case-control study in a cohort of 41,109 women diagnosed with breast cancer between 1935 and 1982 in Connecticut. We reviewed the medical records of 655 women in whom a second breast cancer developed five or more years after the initial tumor and compared their radiation exposure with that of 1189 matched controls from the cohort who did not have a second cancer. The dose of radiation to the contralateral breast was estimated from the original radiotherapy records. Among the exposed women, the average radiation dose to the contralateral breast was 2.82 Gy (maximum, 7.10). Overall, 23 percent of the women who had a second breast cancer and 20 percent of the controls had received radiotherapy (relative risk of a second breast cancer associated with radiotherapy, 1.19). Among women who survived for at least 10 years, radiation treatment was associated with a small but marginally significant elevation in the risk of a second breast cancer (relative risk, 1.33); the risk increased significantly with the dose of radiation. An increase in risk in association with radiotherapy was evident only among women who were under 45 years of age when they were treated (relative risk, 1.59) and not among older women (relative risk, 1.01). Radiotherapy for breast cancer contributes little to the already high risk of a second cancer in the opposite breast. Fewer than 3 percent of all second breast cancers in this study could be attributed to previous radiation treatment; the risk, however, was significantly increased among women who underwent irradiation at a relatively young age (less than 45 years). Radiation exposure after the age of 45 entails little, if any, risk of radiation-induced breast cancer. JF - The New England journal of medicine AU - Boice, J D AU - Harvey, E B AU - Blettner, M AU - Stovall, M AU - Flannery, J T AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, Md. Y1 - 1992/03/19/ PY - 1992 DA - 1992 Mar 19 SP - 781 EP - 785 VL - 326 IS - 12 SN - 0028-4793, 0028-4793 KW - Abridged Index Medicus KW - Index Medicus KW - Risk KW - Age Factors KW - Radiotherapy Dosage KW - Humans KW - Adult KW - Case-Control Studies KW - Middle Aged KW - Time Factors KW - Recurrence KW - Female KW - Radiotherapy -- adverse effects KW - Neoplasms, Radiation-Induced -- etiology KW - Breast Neoplasms -- etiology KW - Breast Neoplasms -- radiotherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72827653?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+New+England+journal+of+medicine&rft.atitle=Cancer+in+the+contralateral+breast+after+radiotherapy+for+breast+cancer.&rft.au=Boice%2C+J+D%3BHarvey%2C+E+B%3BBlettner%2C+M%3BStovall%2C+M%3BFlannery%2C+J+T&rft.aulast=Boice&rft.aufirst=J&rft.date=1992-03-19&rft.volume=326&rft.issue=12&rft.spage=781&rft.isbn=&rft.btitle=&rft.title=The+New+England+journal+of+medicine&rft.issn=00284793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-27 N1 - Date created - 1992-03-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: N Engl J Med. 1992 Aug 6;327(6):430; author reply 431-2 [1625721] N Engl J Med. 1992 Aug 6;327(6):431; author reply 431-2 [1625724] N Engl J Med. 1992 Aug 6;327(6):431; author reply 431-2 [1625723] N Engl J Med. 1992 Aug 6;327(6):430; author reply 431-2 [1625722] Int J Radiat Oncol Biol Phys. 2003 Jul 15;56(4):920-1 [12829125] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phosphatase activity against neurofilament proteins from bovine spinal cord: effect of aluminium and neuropsychoactive drugs. AN - 73056085; 1320755 AB - Protein phosphatase activity associated with neurofilament (NF) rich (Triton X-100 insoluble) fraction was extracted and partially characterised by using known inhibitors of protein phosphatases such as vanadate and fluoride. Protein phosphatase activity was demonstrated with reference to the dephosphorylation of endogenous substrate, NF protein and exogenous protein substrates, casein and phosvitin. Phosphoamino acids and beta-glycerophosphate were found to be poor substrates. Further, new observations have been made regarding the in vitro inhibitory effect of aluminium and the differential effects of some of the neuropsychoactive drugs. The findings could possibly lead to studies explaining the biochemical basis of aluminium induced neurotoxicity as well as the side effects associated with the long term medication of neuropsychoactive drugs. JF - Neuroscience letters AU - Shetty, K T AU - Veeranna AU - Guru, S C AD - Department of Neurochemistry, National Institute of Mental Health and Neuro Science, Bangalore, India. Y1 - 1992/03/16/ PY - 1992 DA - 1992 Mar 16 SP - 83 EP - 86 VL - 137 IS - 1 SN - 0304-3940, 0304-3940 KW - Aldehydes KW - 0 KW - Aluminum Compounds KW - Cations KW - Chlorides KW - Nerve Tissue Proteins KW - Neurofilament Proteins KW - Phosphoproteins KW - Psychotropic Drugs KW - aluminum chloride KW - 3CYT62D3GA KW - Vanadates KW - 3WHH0066W5 KW - Ditiocarb KW - 99Z2744345 KW - propionaldehyde KW - AMJ2B4M67V KW - Aluminum KW - CPD4NFA903 KW - Phosphoprotein Phosphatases KW - EC 3.1.3.16 KW - Glutathione KW - GAN16C9B8O KW - Acetaldehyde KW - GO1N1ZPR3B KW - Ascorbic Acid KW - PQ6CK8PD0R KW - Fluorides KW - Q80VPU408O KW - Index Medicus KW - Ditiocarb -- pharmacology KW - Animals KW - Cattle KW - Phosphorylation KW - Acetaldehyde -- pharmacology KW - Vanadates -- pharmacology KW - Fluorides -- pharmacology KW - Substrate Specificity KW - Ascorbic Acid -- pharmacology KW - Glutathione -- pharmacology KW - Aldehydes -- pharmacology KW - Phosphoprotein Phosphatases -- antagonists & inhibitors KW - Phosphoprotein Phosphatases -- isolation & purification KW - Aluminum -- pharmacology KW - Nerve Tissue Proteins -- isolation & purification KW - Neurofilament Proteins -- metabolism KW - Psychotropic Drugs -- pharmacology KW - Phosphoprotein Phosphatases -- metabolism KW - Spinal Cord -- chemistry KW - Nerve Tissue Proteins -- metabolism KW - Neurofilament Proteins -- isolation & purification KW - Phosphoproteins -- isolation & purification KW - Cations -- pharmacology KW - Phosphoproteins -- metabolism KW - Chlorides -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73056085?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+letters&rft.atitle=Phosphatase+activity+against+neurofilament+proteins+from+bovine+spinal+cord%3A+effect+of+aluminium+and+neuropsychoactive+drugs.&rft.au=Shetty%2C+K+T%3BVeeranna%3BGuru%2C+S+C&rft.aulast=Shetty&rft.aufirst=K&rft.date=1992-03-16&rft.volume=137&rft.issue=1&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=Neuroscience+letters&rft.issn=03043940&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-07 N1 - Date created - 1992-08-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - RNA-dependent RNA polymerase consensus sequence of the L-A double-stranded RNA virus: definition of essential domains. AN - 72852789; 1549580 AB - The L-A double-stranded RNA virus of Saccharomyces cerevisiae makes a gag-pol fusion protein by a -1 ribosomal frameshift. The pol amino acid sequence includes consensus patterns typical of the RNA-dependent RNA polymerases (EC 2.7.7.48) of (+) strand and double-stranded RNA viruses of animals and plants. We have carried out "alanine-scanning mutagenesis" of the region of L-A including the two most conserved polymerase motifs, SG...T...NT..N (. = any amino acid) and GDD. By constructing and analyzing 46 different mutations in and around the RNA polymerase consensus regions, we have precisely defined the extent of domains and specific residues essential for viral replication. Assuming that this highly conserved region has a common secondary structure among different viruses, we predict a largely beta-sheet structure. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Ribas, J C AU - Wickner, R B AD - Section on the Genetics of Simple Eukaryotes, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/03/15/ PY - 1992 DA - 1992 Mar 15 SP - 2185 EP - 2189 VL - 89 IS - 6 SN - 0027-8424, 0027-8424 KW - RNA, Double-Stranded KW - 0 KW - RNA, Viral KW - RNA Replicase KW - EC 2.7.7.48 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Polymerase Chain Reaction KW - RNA, Double-Stranded -- genetics KW - Sindbis Virus -- genetics KW - Sequence Homology, Nucleic Acid KW - Sindbis Virus -- enzymology KW - Genetic Vectors KW - Molecular Sequence Data KW - Amino Acid Sequence KW - RNA, Viral -- genetics KW - Protein Conformation KW - Saccharomyces cerevisiae -- genetics KW - RNA Viruses -- enzymology KW - Saccharomyces cerevisiae -- enzymology KW - RNA Viruses -- genetics KW - RNA Replicase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72852789?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=RNA-dependent+RNA+polymerase+consensus+sequence+of+the+L-A+double-stranded+RNA+virus%3A+definition+of+essential+domains.&rft.au=Ribas%2C+J+C%3BWickner%2C+R+B&rft.aulast=Ribas&rft.aufirst=J&rft.date=1992-03-15&rft.volume=89&rft.issue=6&rft.spage=2185&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-17 N1 - Date created - 1992-04-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1977 Dec 25;252(24):9010-7 [336627] Genetics. 1976 Mar 25;82(3):429-42 [773743] J Virol. 1991 Jan;65(1):155-61 [1985195] Proc Natl Acad Sci U S A. 1991 Jan 1;88(1):174-8 [1986362] Protein Eng. 1990 May;3(6):461-7 [2196557] Cell. 1988 Nov 18;55(4):663-71 [2460245] J Virol. 1991 Sep;65(9):4565-72 [1651402] Cell. 1990 Aug 24;62(4):819-28 [2117501] Science. 1988 Jan 29;239(4839):487-91 [2448875] Nucleic Acids Res. 1988 Nov 11;16(21):9909-16 [2461550] J Mol Biol. 1989 Feb 20;205(4):751-64 [2538637] EMBO J. 1989 Dec 1;8(12):3867-74 [2555175] EMBO J. 1989 Mar;8(3):947-54 [2656262] Virology. 1988 Mar;163(1):240-2 [2831661] Virology. 1989 Mar;169(1):194-203 [2922925] J Virol. 1987 Dec;61(12):3946-9 [3316709] Proc Natl Acad Sci U S A. 1987 Jul;84(14):4767-71 [3474623] Science. 1983 Feb 11;219(4585):620-5 [6186023] J Bacteriol. 1983 Jan;153(1):163-8 [6336730] J Bacteriol. 1980 Jul;143(1):463-70 [6995444] J Biol Chem. 1988 Jan 5;263(1):454-60 [3275647] J Virol. 1988 Apr;62(4):1180-5 [3346944] J Virol. 1987 Dec;61(12):3809-19 [3479621] Proc Natl Acad Sci U S A. 1985 Jan;82(2):488-92 [3881765] Nucleic Acids Res. 1984 Sep 25;12(18):7269-82 [6207485] Cell. 1982 Dec;31(2 Pt 1):429-41 [6819084] Science. 1989 Jun 2;244(4908):1081-5 [2471267] Proc Natl Acad Sci U S A. 1989 Jul;86(13):4803-7 [2472634] Virology. 1989 Jul;171(1):131-40 [2545026] J Virol. 1989 Dec;63(12):5302-9 [2585606] J Biol Chem. 1989 Apr 25;264(12):6716-23 [2651431] J Biol Chem. 1989 Jun 25;264(18):10872-7 [2659596] Nucleic Acids Res. 1988 Dec 23;16(24):11759-67 [2850542] Yeast. 1988 Mar;4(1):17-26 [3059710] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Proc Natl Acad Sci U S A. 1976 Oct;73(10):3651-5 [790391] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The interleukin 2 receptor (IL-2R): the IL-2R alpha subunit alters the function of the IL-2R beta subunit to enhance IL-2 binding and signaling by mechanisms that do not require binding of IL-2 to IL-2R alpha subunit. AN - 72852742; 1549576 AB - Interleukin 2 (IL-2)-mediated signaling through its high-affinity receptor involves a complex interrelationship between IL-2 and two IL-2-binding chains, IL-2R alpha and beta chains. Previously with the reagents available it was difficult to define functional interactions between these two IL-2R subunits involved in IL-2 binding and signal transduction. To extend our understanding of the interplay between the two binding subunits we have done studies with the monoclonal antibody HIEI, which interferes with interaction of IL-2R alpha and beta chains (IL-2R alpha and IL-2R beta, respectively). Furthermore, we used two forms of IL-2, recombinant native IL-2 and F42A, an IL-2 analog (Phe-42----Ala substitution) that binds only to IL-2R beta. Analog F42A manifested 75-100% of the bioactivity of wild-type IL-2. This observation is inconsistent with the strict hierarchical IL-2-binding affinity conversion model previously proposed by Saito and coworkers [Saito Y., Sabe, H., Suzuki, N., Kondo, S., Ogura, T., Shimizu, A. & Honjo, T. (1988) J. Exp. Med. 168, 1563-1572] that predicted an ordered sequence of events in which IL-2 must first bind to IL-2R alpha before its interaction with IL-2R beta. Previous investigations using IL-2 variants were interpreted to show that IL-2R alpha merely acts to concentrate IL-2 to the cell surface and that no other meaningful interaction occurred between IL-2R alpha and IL-2R beta. However, our data are inconsistent with this view. We draw this conclusion on the basis of our observation that antibody HIEI, which reacts with an epitope of IL-2R alpha and interferes with interaction of this chain and IL-2R beta, inhibits the IL-2-dependent proliferative effects mediated by analog F42A. Furthermore, by blocking interaction of IL-2R alpha and IL-2R beta with the antibody HIEI, a decrease in the affinity of radiolabeled analog F42A for IL-2R beta was seen. In our proposed model IL-2R alpha contributes several functions to IL-2-mediated signaling through the high-affinity IL-2R. These functions include concentration of IL-2 within the two-dimensional surface of the plasma membrane as well as alteration of the functional capacity of IL-2R beta, an effect that does not require prior binding of IL-2R to IL-2R alpha. The IL-2R alpha-mediated augmentation of IL-2R beta functions involves affinity conversion of IL-2R beta, increasing its affinity for IL-2, and may involve facilitation of Il-2-mediated signaling after binding of IL-2 to this IL-2R beta. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Grant, A J AU - Roessler, E AU - Ju, G AU - Tsudo, M AU - Sugamura, K AU - Waldmann, T A AD - Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/03/15/ PY - 1992 DA - 1992 Mar 15 SP - 2165 EP - 2169 VL - 89 IS - 6 SN - 0027-8424, 0027-8424 KW - Antibodies, Monoclonal KW - 0 KW - Interleukin-2 KW - Macromolecular Substances KW - Receptors, Interleukin-2 KW - Recombinant Proteins KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Lymphocyte Activation -- drug effects KW - Animals KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Humans KW - Mice KW - Amino Acid Sequence KW - Cytotoxicity, Immunologic -- drug effects KW - Cell Line KW - Interleukin-2 -- pharmacology KW - Receptors, Interleukin-2 -- metabolism KW - Interleukin-2 -- metabolism KW - Receptors, Interleukin-2 -- physiology KW - Receptors, Interleukin-2 -- genetics KW - Signal Transduction UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72852742?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=The+interleukin+2+receptor+%28IL-2R%29%3A+the+IL-2R+alpha+subunit+alters+the+function+of+the+IL-2R+beta+subunit+to+enhance+IL-2+binding+and+signaling+by+mechanisms+that+do+not+require+binding+of+IL-2+to+IL-2R+alpha+subunit.&rft.au=Grant%2C+A+J%3BRoessler%2C+E%3BJu%2C+G%3BTsudo%2C+M%3BSugamura%2C+K%3BWaldmann%2C+T+A&rft.aulast=Grant&rft.aufirst=A&rft.date=1992-03-15&rft.volume=89&rft.issue=6&rft.spage=2165&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-17 N1 - Date created - 1992-04-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Immunol. 1991 Nov 15;147(10):3396-401 [1940342] J Exp Med. 1987 Oct 1;166(4):1055-69 [3116143] Proc Natl Acad Sci U S A. 1991 Jun 1;88(11):4636-40 [2052547] J Clin Immunol. 1990 Nov;10(6 Suppl):19S-28S; discussion 28S-29S [2081786] Trends Biochem Sci. 1990 Jul;15(7):265-70 [2166365] Proc Natl Acad Sci U S A. 1990 Sep;87(18):6934-8 [2169613] Microbiol Immunol. 1985;29(10):959-72 [2417094] EMBO J. 1989 Sep;8(9):2583-90 [2583124] Cell. 1989 Dec 1;59(5):837-45 [2590941] J Exp Med. 1989 Apr 1;169(4):1323-32 [2784485] J Exp Med. 1989 Jul 1;170(1):291-6 [2787381] Science. 1986 Nov 14;234(4778):859-63 [3095922] Proc Natl Acad Sci U S A. 1986 Dec;83(24):9694-8 [3099289] Proc Natl Acad Sci U S A. 1987 Aug;84(15):5394-8 [3110786] J Exp Med. 1987 Oct 1;166(4):1156-61 [3116145] Proc Natl Acad Sci U S A. 1988 Aug;85(15):5654-8 [3135551] J Exp Med. 1986 Sep 1;164(3):814-25 [3489062] J Immunol. 1981 Apr;126(4):1393-7 [6970774] Immunology. 1989 Jan;66(1):117-24 [15493273] Hybridoma. 1985 Summer;4(2):91-102 [2408992] Proc Natl Acad Sci U S A. 1989 Mar;86(6):1982-6 [2467293] Eur J Biochem. 1989 Mar 15;180(2):295-300 [2647490] Science. 1989 May 5;244(4904):551-6 [2785715] Proc Natl Acad Sci U S A. 1986 Dec;83(23):9026-9 [3097640] J Biol Chem. 1987 Apr 25;262(12):5723-31 [3106342] J Exp Med. 1988 Nov 1;168(5):1563-72 [3263463] Proc Natl Acad Sci U S A. 1983 Nov;80(22):6957-61 [6417659] J Biol Chem. 1991 Feb 15;266(5):2681-4 [1993646] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - IL-10 inhibits parasite killing and nitrogen oxide production by IFN-gamma-activated macrophages. AN - 72827744; 1541819 AB - IL-10, a cytokine produced by CD4+ T lymphocytes belonging to the Th-2 subset, has previously been shown to inhibit the synthesis of IFN-gamma by both T cells and NK cells. We now demonstrate that IL-10 can also down-regulate IFN-gamma-dependent immunity by blocking the ability of that lymphokine to activate macrophages. Thus, IL-10, in a dose-dependent manner, inhibits the microbicidal activity of IFN-gamma-treated inflammatory macrophages against intracellular Toxoplasma gondii as well as the extracellular killing of schistosomula of Schistosoma mansoni. This suppression correlates with the inhibition by IL-10 of IFN-gamma-induced production of toxic nitrogen oxide metabolites, an effector mechanism previously implicated in the killing by macrophages of both parasite targets. IL-10 inhibition of nitric oxide production was shown to occur when the cytokine is given before or together with the IFN-gamma-activating stimulus, but not after its removal from the cultures and to require 12 h of contact for maximal suppressive effect on macrophage function. These results, taken together with previous findings on the down-regulation of Th1 lymphokine production by IL-10, indicate that the induction of IL-10 may be an important strategy by which parasites evade IFN-gamma-dependent, cell-mediated immune destruction. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Gazzinelli, R T AU - Oswald, I P AU - James, S L AU - Sher, A AD - Immunology and Cell Biology Section, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/03/15/ PY - 1992 DA - 1992 Mar 15 SP - 1792 EP - 1796 VL - 148 IS - 6 SN - 0022-1767, 0022-1767 KW - Nitrogen Oxides KW - 0 KW - Interleukin-10 KW - 130068-27-8 KW - Interferon-gamma KW - 82115-62-6 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Toxoplasma -- immunology KW - Schistosoma mansoni -- immunology KW - In Vitro Techniques KW - Mice, Inbred C57BL KW - Immunity, Cellular -- drug effects KW - Interferon-gamma -- pharmacology KW - Mice KW - Cytotoxicity, Immunologic -- drug effects KW - Macrophages -- immunology KW - Nitrogen Oxides -- metabolism KW - Toxoplasmosis, Animal -- immunology KW - Interleukin-10 -- pharmacology KW - Macrophages -- drug effects KW - Schistosomiasis mansoni -- immunology KW - Macrophage Activation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72827744?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=IL-10+inhibits+parasite+killing+and+nitrogen+oxide+production+by+IFN-gamma-activated+macrophages.&rft.au=Gazzinelli%2C+R+T%3BOswald%2C+I+P%3BJames%2C+S+L%3BSher%2C+A&rft.aulast=Gazzinelli&rft.aufirst=R&rft.date=1992-03-15&rft.volume=148&rft.issue=6&rft.spage=1792&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-09 N1 - Date created - 1992-04-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reduced blood clearance and increased urinary excretion of N-nitrosodimethylamine in patas monkeys exposed to ethanol or isopropyl alcohol. AN - 72827385; 1540953 AB - Low concentrations of N-nitrosodimethylamine are metabolized in rodent and human liver by cytochrome P450IIE1, an activity competitively inhibitable by ethanol. In rodents coadministration of ethanol with N-nitrosodimethylamine results in increased tumorigenicity in extrahepatic organs, probably as a result of reduced hepatic clearance. To test this concept in a primate, the effects of ethanol cotreatment on the pharmacokinetics of N-nitrosodimethylamine were measured in male patas monkeys. Ethanol, 1.2 g/kg given p.o. before i.v. N-nitrosodimethylamine (1 mg/kg) or concurrently with an intragastric dose resulted in a 10-50-fold increase in the area under the blood concentration versus time curves and a 4-13-fold increase in mean residence times for N-nitrosodimethylamine. Isopropyl alcohol, 3.2 g/kg 24 h before N-nitrosodimethylamine, also increased these parameters 7-10-fold; this effect was associated with persistence of isopropyl alcohol and its metabolic product acetone, both IIE1 inhibitors, in the blood. While no N-nitrosodimethylamine was detected in expired air, trace amounts were found in urine. Ethanol and isopropyl alcohol pretreatment increased the maximum urinary N-nitrosodimethylamine concentration 15-50-fold and the percentage of the dose excreted in the urine by 100-800-fold. Thus ethanol and isopropyl alcohol greatly increase systemic exposure of extrahepatic organs to N-nitrosodimethylamine in a primate. JF - Cancer research AU - Anderson, L M AU - Koseniauskas, R AU - Burak, E S AU - Moskal, T J AU - Gombar, C T AU - Phillips, J M AU - Sansone, E B AU - Keimig, S AU - Magee, P N AU - Rice, J M AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, Maryland. Y1 - 1992/03/15/ PY - 1992 DA - 1992 Mar 15 SP - 1463 EP - 1468 VL - 52 IS - 6 SN - 0008-5472, 0008-5472 KW - Acetone KW - 1364PS73AF KW - Ethanol KW - 3K9958V90M KW - 1-Propanol KW - 96F264O9SV KW - Dimethylnitrosamine KW - M43H21IO8R KW - Index Medicus KW - Animals KW - Premedication KW - Erythrocebus patas KW - Acetone -- blood KW - Male KW - Ethanol -- blood KW - Dimethylnitrosamine -- blood KW - Dimethylnitrosamine -- pharmacokinetics KW - 1-Propanol -- pharmacology KW - Ethanol -- pharmacology KW - 1-Propanol -- blood KW - Dimethylnitrosamine -- urine UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72827385?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Reduced+blood+clearance+and+increased+urinary+excretion+of+N-nitrosodimethylamine+in+patas+monkeys+exposed+to+ethanol+or+isopropyl+alcohol.&rft.au=Anderson%2C+L+M%3BKoseniauskas%2C+R%3BBurak%2C+E+S%3BMoskal%2C+T+J%3BGombar%2C+C+T%3BPhillips%2C+J+M%3BSansone%2C+E+B%3BKeimig%2C+S%3BMagee%2C+P+N%3BRice%2C+J+M&rft.aulast=Anderson&rft.aufirst=L&rft.date=1992-03-15&rft.volume=52&rft.issue=6&rft.spage=1463&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-09 N1 - Date created - 1992-04-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A model for initiated mouse skin: suppression of papilloma but not carcinoma formation by normal epidermal cells in grafts on athymic nude mice. AN - 72826258; 1540951 AB - The availability of a skin grafting system on nude mouse hosts and of epidermal cell lines which form papillomas when grafted has made possible the creation of a model for initiated skin in vivo from cultured cells. When grafted with 6-8 x 10(6) primary dermal fibroblasts, 10 x 10(6) primary epidermal cells form an apparently normal skin, and cell line SP-1 (0.5 x 10(6) cells) forms papillomas. Cell line SP-1 was derived from papillomas produced on SENCAR mice by initiation with 7,12-dimethylbenzaadaa]anthracene and promotion with 12-O-tetradecanoylphorbol-13-acetate. Grafting of 0.5 x 10(6) SP-1 cells along with 10 x 10(6) SENCAR newborn primary epidermal cells resulted in a 90% reduction in the average papilloma volume per mouse compared to controls without primary epidermal cells. Suppression occurred specifically with epidermal cells, either cultured or freshly prepared, and was not seen when an equivalent number of SENCAR primary dermal fibroblasts was grafted in place of epidermal cells. Nor did suppression occur when primary epidermal cells were replaced with a carcinogen-altered cell line, SCR722. SCR722 cells have a normal-skin phenotype when grafted. Furthermore, suppression of tumor formation did not occur when a malignant variant of SP-1 cells replaced benign SP-1 cells in grafts. Repeated treatment of suppressed grafts with 12-O-tetradecanoylphorbol-13-acetate resulted in an increased number of mice with papillomas and a larger mean papilloma volume per mouse compared to controls treated with solvent alone, whereas treatment of nonsuppressed grafts of papilloma cells with promoter produced no change in tumor size. These results support the concepts that normal epidermal cells suppress the growth of initiated cells and that repeated treatment with phorbol ester tumor promoters overcomes the suppression, leading to benign tumor formation. JF - Cancer research AU - Strickland, J E AU - Ueda, M AU - Hennings, H AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/03/15/ PY - 1992 DA - 1992 Mar 15 SP - 1439 EP - 1444 VL - 52 IS - 6 SN - 0008-5472, 0008-5472 KW - fos KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Fibroblasts -- transplantation KW - Cocarcinogenesis KW - Mice, Nude KW - Mice KW - Genes, fos KW - Mice, Inbred BALB C KW - Male KW - Papilloma -- prevention & control KW - Skin Neoplasms -- chemically induced KW - Carcinoma -- prevention & control KW - Skin Transplantation KW - Skin Neoplasms -- prevention & control KW - Papilloma -- chemically induced KW - Carcinoma -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72826258?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=A+model+for+initiated+mouse+skin%3A+suppression+of+papilloma+but+not+carcinoma+formation+by+normal+epidermal+cells+in+grafts+on+athymic+nude+mice.&rft.au=Strickland%2C+J+E%3BUeda%2C+M%3BHennings%2C+H%3BYuspa%2C+S+H&rft.aulast=Strickland&rft.aufirst=J&rft.date=1992-03-15&rft.volume=52&rft.issue=6&rft.spage=1439&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-09 N1 - Date created - 1992-04-09 N1 - Date revised - 2017-01-13 N1 - Gene symbol - fos N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Wegener granulomatosis: an analysis of 158 patients. AN - 72804000; 1739240 AB - To prospectively study the clinical features, pathophysiology, treatment and prognosis of Wegener granulomatosis. Of the 180 patients with Wegener granulomatosis referred to the National Institute of Allergy and Infectious Diseases during the past 24 years, 158 have been followed for 6 months to 24 years (a total of 1229 patient-years). Characteristics of clinical presentation, surgical pathology, course of illness, laboratory and radiographic findings, and the results of medical and surgical treatment have been recorded in a computer-based information retrieval system. The Warren Magnuson Clinical Center of the National Institutes of Health. Men and women were equally represented; 97% of patients were white, and 85% were more than 19 years of age. The mean period of follow-up was 8 years. One hundred and thirty-three patients (84%) received "standard" therapy with daily low-dose cyclophosphamide and glucocorticoids. Eight (5.0%) received only low-dose cyclophosphamide. Six (4.0%) never received cyclophosphamide and were treated with other cytotoxic agents and glucocorticoids. Ten patients (6.0%) were treated with only glucocorticoids. Ninety-one percent of patients experienced marked improvement, and 75% achieved complete remission. Fifty percent of remissions were associated with one or more relapses. Of 99 patients followed for greater than 5 years, 44% had remissions of greater than 5 years duration. Thirteen percent of patients died of Wegener granulomatosis, treatment-related causes, or both. Almost all patients had serious morbidity from irreversible features of their disease (86%) or side effects of treatment (42%). The course of Wegener granulomatosis has been dramatically improved by daily treatment with cyclophosphamide and glucocorticoids. Nonetheless, disease- and treatment-related morbidity is often profound. Alternative forms of therapy have not yet achieved the high rates of remission induction and successful maintenance that have been reported with daily cyclophosphamide treatment. Despite continued therapeutic success with cyclophosphamide, our long-term follow-up of patients with Wegener granulomatosis has led to increasing concerns about toxicity resulting from prolonged cyclophosphamide therapy and has encouraged investigation of other therapeutic regimens. JF - Annals of internal medicine AU - Hoffman, G S AU - Kerr, G S AU - Leavitt, R Y AU - Hallahan, C W AU - Lebovics, R S AU - Travis, W D AU - Rottem, M AU - Fauci, A S AD - National Institutes of Health, Bethesda, Maryland. Y1 - 1992/03/15/ PY - 1992 DA - 1992 Mar 15 SP - 488 EP - 498 VL - 116 IS - 6 SN - 0003-4819, 0003-4819 KW - Cyclophosphamide KW - 8N3DW7272P KW - Prednisone KW - VB0R961HZT KW - Abridged Index Medicus KW - Index Medicus KW - Opportunistic Infections -- epidemiology KW - Humans KW - Aged KW - Biopsy KW - Child KW - Recurrence KW - Morbidity KW - Drug Therapy, Combination KW - Adult KW - Treatment Outcome KW - Follow-Up Studies KW - Middle Aged KW - Adolescent KW - Female KW - Male KW - Remission Induction KW - Prednisone -- adverse effects KW - Cyclophosphamide -- therapeutic use KW - Prednisone -- therapeutic use KW - Granulomatosis with Polyangiitis -- complications KW - Granulomatosis with Polyangiitis -- mortality KW - Granulomatosis with Polyangiitis -- diagnosis KW - Granulomatosis with Polyangiitis -- drug therapy KW - Cyclophosphamide -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72804000?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+internal+medicine&rft.atitle=Wegener+granulomatosis%3A+an+analysis+of+158+patients.&rft.au=Hoffman%2C+G+S%3BKerr%2C+G+S%3BLeavitt%2C+R+Y%3BHallahan%2C+C+W%3BLebovics%2C+R+S%3BTravis%2C+W+D%3BRottem%2C+M%3BFauci%2C+A+S&rft.aulast=Hoffman&rft.aufirst=G&rft.date=1992-03-15&rft.volume=116&rft.issue=6&rft.spage=488&rft.isbn=&rft.btitle=&rft.title=Annals+of+internal+medicine&rft.issn=00034819&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-16 N1 - Date created - 1992-03-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Ann Intern Med. 1992 Oct 1;117(7):619-20; author reply 620-1 [1524345] Ann Intern Med. 1992 Oct 1;117(7):619; author reply 620-1 [1524344] Ann Intern Med. 1992 Oct 1;117(7):620; author reply 620-1 [1524346] Ann Intern Med. 1992 Oct 1;117(7):620; author reply 620-1 [1482486] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Protection against dendrotoxin-induced clonic seizures in mice by anticonvulsant drugs. AN - 73133136; 1504773 AB - Various anticonvulsant drugs were evaluated for their ability to protect against clonic seizures induced in mice by intraventricular injection of the K+ channel blocking peptide dendrotoxin (DTX). Phenytoin, the phenytoin-like anticonvulsant carbamazepine and the broad spectrum drug valproate were effective in this model, whereas the GABA-enhancers diazepam and tiagabine, the NMDA antagonists (+/-)-CPP and (+)-MK-801, the AMPA antagonist NBQX, the antiabsence drug ethosuximide and the Ca2+ channel antagonist nimodipine were inactive. In contrast to the lack of activity of other NMDA antagonists, phencyclidine and ADCI [(+/-)-aminocarbonyl-10,11-dihydro-5H-dibenzo [a,d]cyclohepten-5,10-imine] were potent antagonists of DTX-induced seizures. JF - Brain research AU - Coleman, M H AU - Yamaguchi, S AU - Rogawski, M A AD - Neuronal Excitability Section, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892. Y1 - 1992/03/13/ PY - 1992 DA - 1992 Mar 13 SP - 138 EP - 142 VL - 575 IS - 1 SN - 0006-8993, 0006-8993 KW - Anticonvulsants KW - 0 KW - Elapid Venoms KW - Neurotoxins KW - dendrotoxin KW - 74811-93-1 KW - Index Medicus KW - Animals KW - Mice KW - Male KW - Injections, Intraventricular KW - Elapid Venoms -- antagonists & inhibitors KW - Anticonvulsants -- therapeutic use KW - Neurotoxins -- antagonists & inhibitors KW - Epilepsy, Tonic-Clonic -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73133136?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Protection+against+dendrotoxin-induced+clonic+seizures+in+mice+by+anticonvulsant+drugs.&rft.au=Coleman%2C+M+H%3BYamaguchi%2C+S%3BRogawski%2C+M+A&rft.aulast=Coleman&rft.aufirst=M&rft.date=1992-03-13&rft.volume=575&rft.issue=1&rft.spage=138&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-24 N1 - Date created - 1992-09-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mapping rat brain structures activated during ethanol withdrawal: role of glutamate and NMDA receptors. AN - 73159366; 1355445 AB - Brain structures activated during ethanol withdrawal have been mapped by visualizing c-fos mRNA expression. The regional distribution of c-fos mRNA in brain during ethanol withdrawal can be mimicked by acute injection of N-methyl-D-aspartic acid (NMDA) and is stereospecifically blocked by the NMDA receptor antagonist, MK-801. The findings reveal that the dentate gyrus and piriform cortex are selectively activated during ethanol withdrawal and suggest that this may be mediated by glutamate activation of NMDA receptors. JF - European journal of pharmacology AU - Morgan, P F AU - Nadi, N S AU - Karanian, J AU - Linnoila, M AD - Laboratory of Clinical Studies, National Institute of Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/03/12/ PY - 1992 DA - 1992 Mar 12 SP - 217 EP - 223 VL - 225 IS - 3 SN - 0014-2999, 0014-2999 KW - Glutamates KW - 0 KW - Proto-Oncogene Proteins c-fos KW - RNA, Messenger KW - Receptors, N-Methyl-D-Aspartate KW - Ethanol KW - 3K9958V90M KW - Glutamic Acid KW - 3KX376GY7L KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Stereoisomerism KW - Second Messenger Systems -- physiology KW - Second Messenger Systems -- drug effects KW - RNA, Messenger -- analysis KW - Brain -- physiology KW - Male KW - Proto-Oncogene Proteins c-fos -- biosynthesis KW - Dizocilpine Maleate -- pharmacology KW - Brain Chemistry -- physiology KW - Ethanol -- blood KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Brain Mapping KW - Substance Withdrawal Syndrome -- physiopathology KW - Glutamates -- physiology KW - Ethanol -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73159366?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+pharmacology&rft.atitle=Mapping+rat+brain+structures+activated+during+ethanol+withdrawal%3A+role+of+glutamate+and+NMDA+receptors.&rft.au=Morgan%2C+P+F%3BNadi%2C+N+S%3BKaranian%2C+J%3BLinnoila%2C+M&rft.aulast=Morgan&rft.aufirst=P&rft.date=1992-03-12&rft.volume=225&rft.issue=3&rft.spage=217&rft.isbn=&rft.btitle=&rft.title=European+journal+of+pharmacology&rft.issn=00142999&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-06 N1 - Date created - 1992-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutations of p53 and ras genes in radon-associated lung cancer from uranium miners. AN - 72816817; 1347094 AB - Radon increases the risk of lung cancer in smoking and non-smoking underground miners. To investigate the mutational spectrum associated with exposure to high levels of radon, we sequenced exons 5-9 of the p53 tumour suppressor gene and codons 12-13 of the Ki-ras protooncogene in 19 lung cancers from uranium miners exposed to radon and tobacco smoke. Mutations were not found in Ki-ras, but 9 p53 mutations, including 2 deletions, were found in 7 patients by direct DNA sequencing after polymerase chain reaction amplification of DNA from formalin-fixed, paraffin-embedded tissue. In tumours from 5 patients, the mutation produced an aminoacid change and an increased nuclear content of p53 protein. The tumours with either a stop codon or frame-shift deletion in the p53 gene were negative by immunohistochemistry. None of the mutations were G:C to T:A transversions in the coding strand of the p53 gene, which are the most frequent base substitutions associated with tobacco smoking, and none were found at the hotspot codons described in lung cancer. The observed differences from the usual lung cancer mutational spectrum may reflect the genotoxic effects of radon. JF - Lancet (London, England) AU - Vähäkangas, K H AU - Samet, J M AU - Metcalf, R A AU - Welsh, J A AU - Bennett, W P AU - Lane, D P AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/03/07/ PY - 1992 DA - 1992 Mar 07 SP - 576 EP - 580 VL - 339 IS - 8793 SN - 0140-6736, 0140-6736 KW - p53 KW - ras KW - Codon KW - 0 KW - DNA, Neoplasm KW - Uranium KW - 4OC371KSTK KW - Radon KW - Q74S4N8N1G KW - Abridged Index Medicus KW - Index Medicus KW - Polymerase Chain Reaction KW - Chromosome Deletion KW - Base Sequence KW - Codon -- genetics KW - Humans KW - Molecular Sequence Data KW - Smoking -- adverse effects KW - Aged KW - Middle Aged KW - DNA, Neoplasm -- analysis KW - Occupational Diseases -- genetics KW - Genes, ras -- genetics KW - Carcinoma -- pathology KW - Genes, p53 -- genetics KW - Mutation -- genetics KW - Lung Neoplasms -- genetics KW - Neoplasms, Radiation-Induced -- genetics KW - Mining KW - Radon -- adverse effects KW - Lung Neoplasms -- pathology KW - Carcinoma -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72816817?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lancet+%28London%2C+England%29&rft.atitle=Mutations+of+p53+and+ras+genes+in+radon-associated+lung+cancer+from+uranium+miners.&rft.au=V%C3%A4h%C3%A4kangas%2C+K+H%3BSamet%2C+J+M%3BMetcalf%2C+R+A%3BWelsh%2C+J+A%3BBennett%2C+W+P%3BLane%2C+D+P%3BHarris%2C+C+C&rft.aulast=V%C3%A4h%C3%A4kangas&rft.aufirst=K&rft.date=1992-03-07&rft.volume=339&rft.issue=8793&rft.spage=576&rft.isbn=&rft.btitle=&rft.title=Lancet+%28London%2C+England%29&rft.issn=01406736&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-31 N1 - Date created - 1992-03-31 N1 - Date revised - 2017-01-13 N1 - Gene symbol - p53; ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nitric oxide does not mediate the neurotrophic effects of excitatory amino acids in cultured cerebellar granule neurons. AN - 72991102; 1318207 AB - Excitatory amino acids, such as N-methyl-D-aspartate (NMDA) and kainate, promote neuritogenesis and viability in primary cultures of cerebellar granule cells. In view of the recent demonstration that excitatory amino acids activate the synthesis of nitric oxide, the present study examined a potential role of nitric oxide in mediating the neurotrophic effects of excitatory amino acids. NMDA enhanced the viability of 8-day-old cerebellar granule cell cultures in a concentration-dependent fashion, whereas kainate showed a concentration-dependent biphasic effect. A specific inhibitor of nitric oxide synthase, NG-nitroarginine (0.5 mM), did not antagonize the neurotrophic effects of NMDA (0.5 mM) or kainate (0.05 mM). The concentration of NG-nitroarginine was sufficient to inhibit NMDA or kainate stimulated nitric oxide synthesis and was stable in the culture media throughout the 8-day culture period. Using a specific chemiluminescence detection method, endogenous nitric oxide was directly measured in the headspace gas phase of homogenized cultured cerebellar granule cells, and was not detected when homogenates were incubated with NG-nitroarginine (0.5 mM). Furthermore, addition of a nitric oxide precursor, S-nitroso-N-acetylpenicillamine (1-200 microM), was not neurotrophic, but rather, was neurotoxic in granule cells. These findings indicate that nitric oxide is not a neurotrophic factor in primary cultures of cerebellar granule cells. JF - European journal of pharmacology AU - Boje, K M AU - Skolnick, P AD - Laboratory of Neuroscience, National Institute of Diabetes, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/03/03/ PY - 1992 DA - 1992 Mar 03 SP - 151 EP - 158 VL - 212 IS - 2-3 SN - 0014-2999, 0014-2999 KW - Nitroarginine KW - 2149-70-4 KW - Nitric Oxide KW - 31C4KY9ESH KW - N-Methylaspartate KW - 6384-92-5 KW - S-Nitroso-N-Acetylpenicillamine KW - 79032-48-7 KW - Arginine KW - 94ZLA3W45F KW - Penicillamine KW - GNN1DV99GX KW - Cyclic GMP KW - H2D2X058MU KW - Kainic Acid KW - SIV03811UC KW - Index Medicus KW - Animals KW - Arginine -- analysis KW - Drug Stability KW - Penicillamine -- analogs & derivatives KW - Penicillamine -- pharmacology KW - Rats KW - Rats, Inbred Strains KW - Cyclic GMP -- metabolism KW - Cells, Cultured KW - Arginine -- analogs & derivatives KW - Cell Survival -- physiology KW - Kainic Acid -- pharmacology KW - Cerebellum -- cytology KW - N-Methylaspartate -- pharmacology KW - Cerebellum -- drug effects KW - Nitric Oxide -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72991102?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+pharmacology&rft.atitle=Nitric+oxide+does+not+mediate+the+neurotrophic+effects+of+excitatory+amino+acids+in+cultured+cerebellar+granule+neurons.&rft.au=Boje%2C+K+M%3BSkolnick%2C+P&rft.aulast=Boje&rft.aufirst=K&rft.date=1992-03-03&rft.volume=212&rft.issue=2-3&rft.spage=151&rft.isbn=&rft.btitle=&rft.title=European+journal+of+pharmacology&rft.issn=00142999&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-13 N1 - Date created - 1992-07-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lipreading in patients with schizophrenia. AN - 85263462; pmid-1588334 AB - This study was designed to explore whether schizophrenic patients who are able to maintain their gaze with adequate persistence could competently lip-read. Four lipreading tests, designed to assess recognition of syllables, words, and overlearned sentences, were administered to 15 schizophrenic and 15 normal subjects matched for age, sex, and educational level. The patients proved to be competent lip-readers susceptible to the blend illusion and were inferior only in lipreading of overlearned sentences. The latter difficulty may tentatively be attributed to the inadequacy of the patient's premorbid social network for establishing contextual cues that aid in the recognition of overlearned sentences. JF - The Journal of Nervous and Mental DIsease AU - Myslobodsky, M S AU - Goldberg, T AU - Johnson, F AU - Hicks, L AU - Weinberger, D R AD - Clinical Brain Disorder Branch, NIMH Neuroscience Center, St. Elizabeth's Hospital. PY - 1992 SP - 168 EP - 171 VL - 180 IS - 3 SN - 0022-3018, 0022-3018 KW - Videotape Recording KW - Age Factors KW - Educational Status KW - Sex Factors KW - Human KW - Brain KW - Overlearning KW - Schizophrenia KW - Adult KW - Schizophrenic Psychology KW - Laterality KW - Male KW - Female KW - Lipreading UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85263462?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+Nervous+and+Mental+DIsease&rft.atitle=Lipreading+in+patients+with+schizophrenia.&rft.au=Myslobodsky%2C+M+S%3BGoldberg%2C+T%3BJohnson%2C+F%3BHicks%2C+L%3BWeinberger%2C+D+R&rft.aulast=Myslobodsky&rft.aufirst=M&rft.date=1992-03-01&rft.volume=180&rft.issue=3&rft.spage=168&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Nervous+and+Mental+DIsease&rft.issn=00223018&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - From the National Institute on Deafness and Other Communication Disorders. AN - 85214307; pmid-1589225 JF - Otolaryngology--Head and Neck Surgery AU - Snow, J B AD - National Institute on Deafness and other Communication Disorders, Bethesda, Maryland 20892, USA. PY - 1992 SP - 311 EP - 314 VL - 106 IS - 3 SN - 0194-5998, 0194-5998 KW - United States KW - Human KW - Neurobiology KW - Research KW - Hearing KW - Deafness KW - National Institutes of Health (U.S.) KW - Communication Disorders UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85214307?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Otolaryngology--Head+and+Neck+Surgery&rft.atitle=From+the+National+Institute+on+Deafness+and+Other+Communication+Disorders.&rft.au=Snow%2C+J+B&rft.aulast=Snow&rft.aufirst=J&rft.date=1992-03-01&rft.volume=106&rft.issue=3&rft.spage=311&rft.isbn=&rft.btitle=&rft.title=Otolaryngology--Head+and+Neck+Surgery&rft.issn=01945998&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - No evidence of hearing loss in humans due to transcranial magnetic stimulation. AN - 85161000; pmid-1549231 AB - Prompted by the description of hearing loss in rabbits exposed to the acoustic artifact of magnetic stimulation, we compared the results of audiologic studies before and after exposure to transcranial magnetic stimulation in humans. We found no evidence of temporary or permanent threshold shifts in any of the subjects, even in those exposed to transcranial magnetic stimulation repeatedly for several years. Risk of hearing loss from the acoustic artifact of magnetic stimulation, as evaluated by audiograms, tympanograms, acoustic reflexes, and auditory evoked potentials, seems to be small in humans. JF - Neurology AU - Pascual-Leone, A AU - Cohen, L G AU - Shotland, L I AU - Dang, N AU - Pikus, A AU - Wassermann, E M AU - Brasil-Neto, J P AU - Valls-Solé J AU - Hallett, M AD - Human Cortical Physiology Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. PY - 1992 SP - 647 EP - 651 VL - 42 IS - 3 Pt 1 SN - 0028-3878, 0028-3878 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85161000?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurology&rft.atitle=No+evidence+of+hearing+loss+in+humans+due+to+transcranial+magnetic+stimulation.&rft.au=Pascual-Leone%2C+A%3BCohen%2C+L+G%3BShotland%2C+L+I%3BDang%2C+N%3BPikus%2C+A%3BWassermann%2C+E+M%3BBrasil-Neto%2C+J+P%3BValls-Sol%C3%A9+J%3BHallett%2C+M&rft.aulast=Pascual-Leone&rft.aufirst=A&rft.date=1992-03-01&rft.volume=42&rft.issue=3+Pt+1&rft.spage=647&rft.isbn=&rft.btitle=&rft.title=Neurology&rft.issn=00283878&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - The polymerase chain reaction. History, methods, and applications. AN - 75537175; 1342955 AB - The polymerase chain reaction (PCR) uses in vitro enzymatic synthesis to amplify specific DNA sequences. PCR amplification can produce approximately 100 billion copies of one molecule of DNA in a few hours. PCR has revolutionized research in the biological sciences and medicine, and has influenced criminology and law. Several major scientific discoveries, including purification of DNA polymerase and elucidation of the mechanism of DNA replication, were essential for development of the present PCR technology. An overview of these discoveries and early work on in vitro DNA synthesis are presented. Basic PCR methodology, instrumentation, advanced PCR techniques, and applications are also discussed in this review. Several new amplification systems are mentioned. PCR is an extremely important and simple technology for research and diagnostic analyses of DNA and RNA. PCR technology and other amplification procedures will continue to produce novel applications in basic research and clinical medicine. JF - Diagnostic molecular pathology : the American journal of surgical pathology, part B AU - Templeton, N S AD - Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 58 EP - 72 VL - 1 IS - 1 SN - 1052-9551, 1052-9551 KW - DNA Primers KW - 0 KW - DNA KW - 9007-49-2 KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - Index Medicus KW - History of medicine KW - Base Sequence KW - History, 20th Century KW - DNA Primers -- genetics KW - Humans KW - DNA -- genetics KW - Molecular Sequence Data KW - DNA -- biosynthesis KW - DNA Replication KW - Mutagenesis KW - Gene Amplification KW - Polymerase Chain Reaction -- methods KW - Polymerase Chain Reaction -- history UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75537175?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Diagnostic+molecular+pathology+%3A+the+American+journal+of+surgical+pathology%2C+part+B&rft.atitle=The+polymerase+chain+reaction.+History%2C+methods%2C+and+applications.&rft.au=Templeton%2C+N+S&rft.aulast=Templeton&rft.aufirst=N&rft.date=1992-03-01&rft.volume=1&rft.issue=1&rft.spage=58&rft.isbn=&rft.btitle=&rft.title=Diagnostic+molecular+pathology+%3A+the+American+journal+of+surgical+pathology%2C+part+B&rft.issn=10529551&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-02-22 N1 - Date created - 1994-02-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - MPTP-induced "parkinsonism" in the goldfish. AN - 75524246; 1365442 JF - Neurochemistry international AU - Youdim, M B AU - Dhariwal, K AU - Levine, M AU - Markey, C J AU - Markey, S AU - Caohuy, H AU - Adeyemo, O M AU - Pollard, H B AD - Laboratory of Cell Biology and Genetics, NIDDK, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 275S EP - 278S VL - 20 Suppl SN - 0197-0186, 0197-0186 KW - Biogenic Monoamines KW - 0 KW - Catecholamines KW - Tranylcypromine KW - 3E3V44J4Z9 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Monoamine Oxidase KW - EC 1.4.3.4 KW - Index Medicus KW - Brain -- enzymology KW - Behavior, Animal -- drug effects KW - Animals KW - Tranylcypromine -- pharmacology KW - Eye -- metabolism KW - Catecholamines -- metabolism KW - Goldfish KW - Brain -- metabolism KW - Monoamine Oxidase -- metabolism KW - Biogenic Monoamines -- metabolism KW - Parkinson Disease, Secondary -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75524246?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurochemistry+international&rft.atitle=MPTP-induced+%22parkinsonism%22+in+the+goldfish.&rft.au=Youdim%2C+M+B%3BDhariwal%2C+K%3BLevine%2C+M%3BMarkey%2C+C+J%3BMarkey%2C+S%3BCaohuy%2C+H%3BAdeyemo%2C+O+M%3BPollard%2C+H+B&rft.aulast=Youdim&rft.aufirst=M&rft.date=1992-03-01&rft.volume=20+Suppl&rft.issue=&rft.spage=275S&rft.isbn=&rft.btitle=&rft.title=Neurochemistry+international&rft.issn=01970186&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1995-01-30 N1 - Date created - 1995-01-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A report on the National Commission on Cytotoxic Exposure. AN - 73065109; 10118896 JF - The Journal of pharmacy technology : jPT : official publication of the Association of Pharmacy Technicians AU - Gallelli, J F AD - Warren G. Magnuson Clinical Center, National Institutes of Health, Bethesda, MD 20892. PY - 1992 SP - 55 EP - 64 VL - 8 IS - 2 SN - 8755-1225, 8755-1225 KW - Antineoplastic Agents KW - 0 KW - Hazardous Substances KW - Health administration KW - United States KW - Mutagenicity Tests KW - Humans KW - National Institutes of Health (U.S.) KW - Protective Devices -- standards KW - Protective Devices -- utilization KW - Personnel, Hospital -- standards KW - Occupational Exposure -- prevention & control KW - Antineoplastic Agents -- standards KW - Antineoplastic Agents -- poisoning KW - Pharmacy Service, Hospital -- standards KW - Drug Compounding -- standards KW - Hazardous Substances -- standards KW - Antineoplastic Agents -- urine UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73065109?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacy+technology+%3A+jPT+%3A+official+publication+of+the+Association+of+Pharmacy+Technicians&rft.atitle=A+report+on+the+National+Commission+on+Cytotoxic+Exposure.&rft.au=Gallelli%2C+J+F&rft.aulast=Gallelli&rft.aufirst=J&rft.date=1992-03-01&rft.volume=8&rft.issue=2&rft.spage=55&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacy+technology+%3A+jPT+%3A+official+publication+of+the+Association+of+Pharmacy+Technicians&rft.issn=87551225&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-14 N1 - Date created - 1992-08-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Brown-Séquard syndrome due to Semple antirabies vaccine: case report. AN - 73055998; 1630845 JF - Paraplegia AU - Swamy, H S AU - Vasanth, A AU - Sasikumar AD - Department of Neurology, National Institute of Mental Health and Neuro Sciences, Bangalore, India. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 181 EP - 183 VL - 30 IS - 3 SN - 0031-1758, 0031-1758 KW - Rabies Vaccines KW - 0 KW - Dexamethasone KW - 7S5I7G3JQL KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - Drug Therapy, Combination KW - Nervous System Diseases -- drug therapy KW - Dexamethasone -- therapeutic use KW - Cyclophosphamide -- therapeutic use KW - Nervous System Diseases -- etiology KW - Evoked Potentials KW - Syndrome KW - Humans KW - Adult KW - Neural Conduction KW - Nervous System Diseases -- physiopathology KW - Male KW - Rabies Vaccines -- adverse effects KW - Paralysis -- drug therapy KW - Paralysis -- etiology KW - Sensation KW - Paralysis -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73055998?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Paraplegia&rft.atitle=Brown-S%C3%A9quard+syndrome+due+to+Semple+antirabies+vaccine%3A+case+report.&rft.au=Swamy%2C+H+S%3BVasanth%2C+A%3BSasikumar&rft.aulast=Swamy&rft.aufirst=H&rft.date=1992-03-01&rft.volume=30&rft.issue=3&rft.spage=181&rft.isbn=&rft.btitle=&rft.title=Paraplegia&rft.issn=00311758&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-18 N1 - Date created - 1992-08-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Typing of HLA-DQA1 and DQB1 using DNA single-strand conformation polymorphism. AN - 73052318; 1618658 AB - The technique of single-strand conformation polymorphism (SSCP), which is capable of distinguishing DNA sequence variability, was adapted to the identification of the HLA-DQA1 and DQB1 alleles. Eight DQA1 alleles and 12 DQB1 alleles were distinguished by amplifying the second exon of the genes in the presence of radioactive deoxynucleotide, denaturing the products with heat, and separating the single strands by electrophoresis in nondenaturing gels. For DQA1, it was possible to distinguish the eight alleles with standard bis-acrylamide or with a Hydrolink gel matrix. Twelve DQB1 alleles were identified by a protocol employing a combination of oligohybridization and SSCP using products amplified by specific DQB1 primers. JF - Human immunology AU - Carrington, M AU - Miller, T AU - White, M AU - Gerrard, B AU - Stewart, C AU - Dean, M AU - Mann, D AD - Biological Carcinogenesis and Development Program, Program Resources, Inc./DynCorp, NCI-Frederick Cancer Research, MD 21702. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 208 EP - 212 VL - 33 IS - 3 SN - 0198-8859, 0198-8859 KW - DNA, Single-Stranded KW - 0 KW - HLA-DQ Antigens KW - HLA-DQ alpha-Chains KW - HLA-DQ beta-Chains KW - HLA-DQA1 antigen KW - HLA-DQB1 antigen KW - Index Medicus KW - Base Sequence KW - Alleles KW - Humans KW - Molecular Sequence Data KW - HLA-DQ Antigens -- genetics KW - DNA, Single-Stranded -- chemistry KW - Nucleic Acid Conformation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73052318?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+immunology&rft.atitle=Typing+of+HLA-DQA1+and+DQB1+using+DNA+single-strand+conformation+polymorphism.&rft.au=Carrington%2C+M%3BMiller%2C+T%3BWhite%2C+M%3BGerrard%2C+B%3BStewart%2C+C%3BDean%2C+M%3BMann%2C+D&rft.aulast=Carrington&rft.aufirst=M&rft.date=1992-03-01&rft.volume=33&rft.issue=3&rft.spage=208&rft.isbn=&rft.btitle=&rft.title=Human+immunology&rft.issn=01988859&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-04 N1 - Date created - 1992-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - MPTP lesions of the nigrostriatal dopaminergic projection decrease [3H]1-[1-(2-thienyl)cyclohexyl]piperidine binding to PCP site 2: further evidence that PCP site 2 is associated with the biogenic amine reuptake complex. AN - 73048829; 1320214 AB - Our previous studies have demonstrated that, using membranes of guinea pig brain, [3H]1-[1-(2-thienyl)cyclohexyl]piperidine ([3H]TCP) labels not only the phencyclidine binding site associated with the NMDA receptor (PCP site 1), but also a second high affinity binding site which is associated with the biogenic amine reuptake carrier (termed PCP site 2). To test this hypothesis, the binding of [3H]GBR12935 to the dopamine transporter, and [3H]TCP binding to PCP sites 1 and 2 were measured in caudates harvested from control, MPTP-treated and reserpine-treated dogs. MPTP treatment decreased dopamine levels by over 99%, decreased [3H]GBR12935 binding by over 90%, decreased [3H]TCP binding to PCP site 2 by about 50%, and had no significant effect on [3H]TCP binding to PCP site 1. These data are consistent with the hypothesis that a portion of PCP site 2 is associated with dopaminergic nerve terminals in dog caudate. JF - Neurochemical research AU - Akunne, H C AU - Johannessen, J N AU - de Costa, B R AU - Rice, K C AU - Rothman, R B AD - Laboratory of Medicinal Chemistry, NIDDK, Bethesda, MD 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 261 EP - 264 VL - 17 IS - 3 SN - 0364-3190, 0364-3190 KW - Biogenic Amines KW - 0 KW - Receptors, Neurotransmitter KW - Receptors, Phencyclidine KW - Reserpine KW - 8B1QWR724A KW - tenocyclidine KW - 8BQ45Q6VCL KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Phencyclidine KW - J1DOI7UV76 KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Reserpine -- pharmacology KW - Animals KW - Dopamine -- physiology KW - Dogs KW - Neural Pathways -- drug effects KW - Female KW - Biogenic Amines -- metabolism KW - Phencyclidine -- metabolism KW - Substantia Nigra -- drug effects KW - Receptors, Neurotransmitter -- drug effects KW - Corpus Striatum -- drug effects KW - Phencyclidine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73048829?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurochemical+research&rft.atitle=MPTP+lesions+of+the+nigrostriatal+dopaminergic+projection+decrease+%5B3H%5D1-%5B1-%282-thienyl%29cyclohexyl%5Dpiperidine+binding+to+PCP+site+2%3A+further+evidence+that+PCP+site+2+is+associated+with+the+biogenic+amine+reuptake+complex.&rft.au=Akunne%2C+H+C%3BJohannessen%2C+J+N%3Bde+Costa%2C+B+R%3BRice%2C+K+C%3BRothman%2C+R+B&rft.aulast=Akunne&rft.aufirst=H&rft.date=1992-03-01&rft.volume=17&rft.issue=3&rft.spage=261&rft.isbn=&rft.btitle=&rft.title=Neurochemical+research&rft.issn=03643190&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-05 N1 - Date created - 1992-08-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Diclofenac does not modify morphine bioavailability in cancer patients. AN - 72969254; 1594262 AB - We determined morphine plasma concentrations in 6 cancer patients before and with administration of diclofenac for 5 days. The non-steroidal anti-inflammatory drug does not modify morphine bioavailability. This observation suggests that diclofenac can be used in association with morphine during cancer pain treatment, without increasing the risk of overdosage or side effects of the opiate. JF - Pain AU - De Conno, F AU - Ripamonti, C AU - Bianchi, M AU - Ventafridda, V AU - Panerai, A E AD - Pain Therapy and Palliative Care Division, National Cancer Institute, Milan, Italy. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 401 EP - 402 VL - 48 IS - 3 SN - 0304-3959, 0304-3959 KW - Diclofenac KW - 144O8QL0L1 KW - Morphine KW - 76I7G6D29C KW - Index Medicus KW - Drug Interactions KW - Half-Life KW - Humans KW - Aged KW - Middle Aged KW - Chromatography, High Pressure Liquid KW - Biological Availability KW - Pain -- etiology KW - Pain -- drug therapy KW - Morphine -- therapeutic use KW - Morphine -- pharmacokinetics KW - Diclofenac -- adverse effects KW - Neoplasms -- physiopathology KW - Pain -- metabolism KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72969254?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pain&rft.atitle=Diclofenac+does+not+modify+morphine+bioavailability+in+cancer+patients.&rft.au=De+Conno%2C+F%3BRipamonti%2C+C%3BBianchi%2C+M%3BVentafridda%2C+V%3BPanerai%2C+A+E&rft.aulast=De+Conno&rft.aufirst=F&rft.date=1992-03-01&rft.volume=48&rft.issue=3&rft.spage=401&rft.isbn=&rft.btitle=&rft.title=Pain&rft.issn=03043959&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-26 N1 - Date created - 1992-06-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ibotenic acid lesions of medial prefrontal cortex augment swim-stress-induced locomotion. AN - 72956896; 1584841 AB - Locomotor activity of rats with sham or ibotenic acid lesions of the medial prefrontal cortex (MPFC) was assessed after animals were exposed to a 15-min swim or control stress. Swim-stress-induced locomotor activity was augmented in the MPFC-lesioned rats. These and other data suggest that lesions of the MPFC are followed by an exaggeration of the normal behavioral response to stress. Dysregulation of dopamine transmission in the basal ganglia may be involved. JF - Pharmacology, biochemistry, and behavior AU - Jaskiw, G E AU - Weinberger, D R AD - Clinical Brain Disorders Branch, National Institutes of Mental Health Intramural Research Program, NIMH Research Center, Washington, DC 20032. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 607 EP - 609 VL - 41 IS - 3 SN - 0091-3057, 0091-3057 KW - Ibotenic Acid KW - 2552-55-8 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Swimming KW - Motor Activity -- physiology KW - Male KW - Frontal Lobe -- physiopathology KW - Frontal Lobe -- drug effects KW - Locomotion -- physiology KW - Ibotenic Acid -- toxicity KW - Stress, Physiological -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72956896?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology%2C+biochemistry%2C+and+behavior&rft.atitle=Ibotenic+acid+lesions+of+medial+prefrontal+cortex+augment+swim-stress-induced+locomotion.&rft.au=Jaskiw%2C+G+E%3BWeinberger%2C+D+R&rft.aulast=Jaskiw&rft.aufirst=G&rft.date=1992-03-01&rft.volume=41&rft.issue=3&rft.spage=607&rft.isbn=&rft.btitle=&rft.title=Pharmacology%2C+biochemistry%2C+and+behavior&rft.issn=00913057&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-18 N1 - Date created - 1992-06-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Liver carcinogenesis by methyl carbamate in F344 rats and not in B6C3F1 mice. AN - 72947489; 1582888 AB - Short-term and long-term carcinogenicity of methyl carbamate (MCB) was evaluated in F344 rats and B6C3F1 mice. In experiments lasting 6, 12, and 18 months, MCB was given in water by gavage to groups of 10 male and 10 female rats at 0 or 400 mg/kg body weight, 5 days per week, and to similar groups of mice at 0 or 1,000 mg/kg. At 6 months, MCB induced atypical mitoses, cytologic alterations, cytomegaly, pigmentation, necrosis, and neoplastic nodules of the liver in rats. At 12 and 18 months, carcinomas of the liver were induced by MCB in 80-90% of male rats and in 60-80% of female rats. None was observed in control rats or in mice. In the 2-year studies, MCB was given to groups of 50 male and 50 female rats at 0, 100, or 200 mg/kg and to similar groups of mice at 0, 500, or 1,000 mg/kg, 5 days/week. Chronic focal inflammation, cytologic alteration, hyperplasia, and neoplastic nodules and carcinomas (200 mg/kg groups only) of the liver were induced by MCB in rats. Liver tumor incidence data for combined experiments in rats were: males--5% in controls, 0% in 100 mg/kg group, 14% in 200 mg/kg group, and 77% in 400 mg/kg group; females--5% in controls, 0% in controls, 0% in 100 mg/kg group, 12% in 200 mg/kg group, and 63% in 400 mg/kg group. MCB was not shown to be carcinogenic in mice. JF - Japanese journal of cancer research : Gann AU - Chan, P C AU - Huff, J AU - Haseman, J K AU - Quest, J A AU - Hall, W AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 258 EP - 263 VL - 83 IS - 3 SN - 0910-5050, 0910-5050 KW - Carbamates KW - 0 KW - methyl carbamate KW - 9WFX634X2T KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Liver -- drug effects KW - Body Weight -- drug effects KW - Carcinogenicity Tests KW - Mice KW - Time Factors KW - Species Specificity KW - Male KW - Female KW - Liver Neoplasms, Experimental -- mortality KW - Liver Neoplasms, Experimental -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72947489?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Japanese+journal+of+cancer+research+%3A+Gann&rft.atitle=Liver+carcinogenesis+by+methyl+carbamate+in+F344+rats+and+not+in+B6C3F1+mice.&rft.au=Chan%2C+P+C%3BHuff%2C+J%3BHaseman%2C+J+K%3BQuest%2C+J+A%3BHall%2C+W&rft.aulast=Chan&rft.aufirst=P&rft.date=1992-03-01&rft.volume=83&rft.issue=3&rft.spage=258&rft.isbn=&rft.btitle=&rft.title=Japanese+journal+of+cancer+research+%3A+Gann&rft.issn=09105050&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-18 N1 - Date created - 1992-06-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Heterogeneous calcium currents and transmitter release in cultured mouse spinal cord and dorsal root ganglion neurons. AN - 72928963; 1374458 AB - 1. Calcium currents and transmitter release were studied in cocultures of fetal mouse neurons from the ventral half of the spinal cord (VH neurons) and from dorsal root ganglion (DRG neurons). The effects of BayK 8644 and omega-conotoxin on calcium currents and transmitter release were compared. 2. The presence of low voltage-activated (LVA) calcium current in both VH and DRG neurons is variable. Some cells exhibit only high voltage-activated (HVA) currents, whereas others show both HVA and LVA currents. 3. BayK 8644 did not affect LVA currents but strongly augmented both steady and transient components of the HVA calcium conductance. 4. omega-Conotoxin GVIA reduces both transient and steady components of the HVA but does not abolish either component even after 3 h of application. 5. Calcium currents that were resistant to omega-contoxin were augmented by BayK 8644. 6. Synaptic transmission between pairs of spinal cord neurons from the ventral half of the spinal cord (VH-VH connections) or between dorsal root ganglion neurons and VH neurons (DRG-VH connections) were studied with two-cell recording and stimulation techniques. 7. In approximately 70% of VH-VH connections and 50% of DRG-VH connections, BayK 8644 or its active optical isomer failed to affect transmitter output. Substantial augmentation of the remainder of the connections could be reliably produced by the dihydropyridines. Raised calcium in the extracellular medium produced augmentation of synaptic connections in all cases. BayK 8644 produced substantial, consistent augmentation of voltage-sensitive calcium channels in both VH and DRG neurons. 8. The toxin, omega-conotoxin, produced no consistent effect on excitatory or inhibitory postsynaptic potentials (EPSPs or IPSPs) elicited in VH neurons by stimulation of nearby VH neurons. VH EPSPs elicited by stimulation of nearby DRG neurons were reduced to approximately 50% of control values after 10 min of omega-conotoxin perfusion. Spontaneous and evoked synaptic activity could be recorded in VH neurons as long as 2 h after cultures were incubated in 0.5 microM omega-conotoxin. omega-Conotoxin produced a modest reduction in HVA currents in both VH and DRG neurons. 9. BayK 8644 did not produce consistent augmentation of transmission at the frog neuromuscular junction. omega-Conotoxin produced total blockade of transmission in this preparation. 10. We conclude that neither sustained nor inactivating high-threshold voltage-sensitive (HVA) calcium channels sensitive to BayK 8644 or omega-conotoxin such as those measured in the neuronal cell bodies are responsible for action-potential-evoked transmitter release from the majority of VH neurons.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Journal of neurophysiology AU - Yu, C AU - Lin, P X AU - Fitzgerald, S AU - Nelson, P AD - Laboratory of Developmental Neurobiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 561 EP - 575 VL - 67 IS - 3 SN - 0022-3077, 0022-3077 KW - Calcium Channel Blockers KW - 0 KW - Calcium Channels KW - Culture Media KW - Neurotransmitter Agents KW - Peptides, Cyclic KW - 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester KW - 71145-03-4 KW - omega-Conotoxin GVIA KW - 92078-76-7 KW - Index Medicus KW - Animals KW - Synapses -- drug effects KW - Calcium Channel Blockers -- pharmacology KW - Cells, Cultured KW - Synaptic Transmission -- drug effects KW - Anura KW - 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester -- pharmacology KW - Mice KW - Action Potentials -- drug effects KW - Peptides, Cyclic -- pharmacology KW - Ganglia, Spinal -- cytology KW - Calcium Channels -- physiology KW - Neurotransmitter Agents -- physiology KW - Ganglia, Spinal -- physiology KW - Calcium Channels -- drug effects KW - Neurons -- physiology KW - Spinal Cord -- physiology KW - Spinal Cord -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72928963?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurophysiology&rft.atitle=Heterogeneous+calcium+currents+and+transmitter+release+in+cultured+mouse+spinal+cord+and+dorsal+root+ganglion+neurons.&rft.au=Yu%2C+C%3BLin%2C+P+X%3BFitzgerald%2C+S%3BNelson%2C+P&rft.aulast=Yu&rft.aufirst=C&rft.date=1992-03-01&rft.volume=67&rft.issue=3&rft.spage=561&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurophysiology&rft.issn=00223077&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-10 N1 - Date created - 1992-06-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Detection of multiple tumor suppressor genes for Syrian hamster fibrosarcomas by somatic cell hybridization. AN - 72918045; 1574739 AB - Identification of tumor suppressor gene loci in rodent cell culture systems has relied upon the use of somatic cell hybridization studies. Although normal rodent fibroblasts are capable of suppressing the tumorigenicity of a variety of tumor cells, the lack of complementation in tumor cell x tumor cell hybrids has left the possibility that a single tumor suppressor gene may be responsible for tumor suppression in a particular rodent cell culture system. Using this same approach, we found no evidence for complementation resulting in suppression of the transformed phenotype when three viral oncogene-transformed Syrian hamster embryo (SHE) cell lines and one spontaneously transformed baby hamster kidney (BHK) cell line were fused to benzo[a]pyrene-transformed SHE cells (BP6T-M3). However, v-src oncogene-transformed cell line (srcT) x BP6T-M3 hybrids did demonstrate limited suppression of the transformed phenotype, suggesting at least two complementing tumor suppressor genes in this system. We were able to confirm and extend this finding using another experimental approach with preneoplastic hamster cell lines that are immortal in culture but nontumorigenic in nude mice. We propose that fusion of these preneoplastic cells to various tumor cells may reveal tumor suppressor genes not evident in the tumor cell x tumor cell complementation studies. Subclones of two nontumorigenic, immortal hamster cell lines, 10W and DES4, displayed differing abilities to suppress BP6T-M3 cells in somatic cell hybrids, as quantitated by the ability of the hybrid cells to form colonies in soft agar. With a panel of preneoplastic hamster cell x BP6T-M3 hybrids, a distinct pattern of suppression or expression of the transformed phenotype was observed. Marked differences in this pattern were seen when the same 10W and DES4 subclones were fused to other hamster fibrosarcoma cell lines, indicating different tumor suppressing activities of multiple tumor suppressor genes. Analysis of this data suggests that as few as three or as many as six different tumor suppressor genes may be active in the Syrian hamster embryo cell culture system. Thus, this system may provide a useful model for identifying and studying the effects and regulation of a number of different tumor suppressor genes for fibrosarcomas. JF - Somatic cell and molecular genetics AU - Whitehead, R E AU - Sugawara, O AU - Maronpot, R R AU - Gladen, B C AU - Barrett, J C AD - National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 131 EP - 142 VL - 18 IS - 2 SN - 0740-7750, 0740-7750 KW - Benzo(a)pyrene KW - 3417WMA06D KW - Index Medicus KW - Animals KW - Mice KW - Mice, Nude KW - Neoplasm Transplantation KW - Genes, src -- genetics KW - Genes, ras -- genetics KW - Benzo(a)pyrene -- toxicity KW - Genes, p53 -- genetics KW - Genetic Complementation Test KW - Hybrid Cells KW - Mutation -- genetics KW - Mesocricetus KW - Tumor Stem Cell Assay KW - Embryo, Mammalian KW - Cricetinae KW - Genes, Tumor Suppressor -- genetics KW - Fibrosarcoma -- genetics KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72918045?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Somatic+cell+and+molecular+genetics&rft.atitle=Detection+of+multiple+tumor+suppressor+genes+for+Syrian+hamster+fibrosarcomas+by+somatic+cell+hybridization.&rft.au=Whitehead%2C+R+E%3BSugawara%2C+O%3BMaronpot%2C+R+R%3BGladen%2C+B+C%3BBarrett%2C+J+C&rft.aulast=Whitehead&rft.aufirst=R&rft.date=1992-03-01&rft.volume=18&rft.issue=2&rft.spage=131&rft.isbn=&rft.btitle=&rft.title=Somatic+cell+and+molecular+genetics&rft.issn=07407750&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-02 N1 - Date created - 1992-06-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Concordance of carcinogenic response between rodent species: potency dependence and potential underestimation. AN - 72916078; 1574611 AB - The use of average qualitative concordance between two bioassay endpoints is considered, with emphasis directed at agreement between rats and mice from results of long-term carcinogenicity studies. It is noted that concordance varies as a function of the underlying potency or toxicity of the chemicals over which the averaging is performed. Thus, the averaging process dilutes large observed concordances from potent chemicals, and possibly inflates lower observed concordances from weakly active chemicals. Stratification over some measure of potency is suggested as a method for taking these effects into account. Statistical simulations of concordance analyses limited to low-potency ranges are employed to examine the concordance measure in greater detail. It is seen that at low potencies, observed concordance is consistently underestimated, reaching maximum levels of only about 80%. JF - Risk analysis : an official publication of the Society for Risk Analysis AU - Piegorsch, W W AU - Carr, G J AU - Portier, C J AU - Hoel, D G AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 115 EP - 121 VL - 12 IS - 1 SN - 0272-4332, 0272-4332 KW - Carcinogens KW - 0 KW - Index Medicus KW - Rats KW - Risk KW - Animals KW - Computer Simulation KW - Databases, Factual KW - Carcinogens -- toxicity KW - Mice KW - Biological Assay -- statistics & numerical data KW - Species Specificity KW - Carcinogenicity Tests -- statistics & numerical data UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72916078?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Risk+analysis+%3A+an+official+publication+of+the+Society+for+Risk+Analysis&rft.atitle=Concordance+of+carcinogenic+response+between+rodent+species%3A+potency+dependence+and+potential+underestimation.&rft.au=Piegorsch%2C+W+W%3BCarr%2C+G+J%3BPortier%2C+C+J%3BHoel%2C+D+G&rft.aulast=Piegorsch&rft.aufirst=W&rft.date=1992-03-01&rft.volume=12&rft.issue=1&rft.spage=115&rft.isbn=&rft.btitle=&rft.title=Risk+analysis+%3A+an+official+publication+of+the+Society+for+Risk+Analysis&rft.issn=02724332&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-29 N1 - Date created - 1992-05-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alterations in hematopoietic responses in B6C3F1 mice caused by drinking a mixture of 25 groundwater contaminants. AN - 72909973; 1573557 AB - Myelotoxicity parameters were monitored in female B6C3F1 mice exposed to 0, 1, 5, and 10% of a chemical mixture stock in drinking water for 2.5 to 31.5 weeks. The mixture consisted of 25 groundwater contaminants frequently found near toxic waste dumps, as determined by U.S. Environmental Protection Agency (EPA) surveys. Water consumption, body and organ weights, and hematological and histopathological examinations were conducted. No animals developed overt signs of toxicity after 2.5 weeks of treatment. No significant effect on bone marrow cellularity was observed after 2.5, 15.5, or 31.5 weeks of exposure; however, mice exposed to 5% or higher concentrations of the chemical mixture stock solution for 15.5 weeks showed significant suppression of granulocyte-macrophage progenitor cells (CFU-GM) and erythroid precursors (CFU-E) with no changes in body weight, histopathological or hematological parameters. Decreases occurred in erythrocyte mean corpuscular volume of mice exposed to a 10% solution for 15.5 weeks and to 5 and 10% solutions following 31.5 weeks of treatment. In addition, dose-related decreases were found in body, liver, and thymus weights in the 5 and 10% solutions exposure groups after 31.5 weeks. These results suggest that bone marrow may be a sensitive indicator for long-term, low-level exposure of multiple chemicals in mice. Furthermore, long-term exposure to highly contaminated groundwater may present a subtle risk to the hematopoietic system. JF - Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer AU - Hong, H L AU - Yang, R S AU - Boorman, G A AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1992 SP - 1 EP - 10 VL - 11 IS - 2 SN - 0731-8898, 0731-8898 KW - Water Pollutants, Chemical KW - 0 KW - Index Medicus KW - Drinking KW - Animals KW - Liver -- pathology KW - Kidney -- pathology KW - Kidney -- drug effects KW - Thymus Gland -- pathology KW - Spleen -- pathology KW - Mice KW - Thymus Gland -- drug effects KW - Liver -- drug effects KW - Body Weight -- drug effects KW - Spleen -- drug effects KW - Female KW - Organ Size -- drug effects KW - Water Pollutants, Chemical -- toxicity KW - Hematopoietic Stem Cells -- cytology KW - Hematopoietic Stem Cells -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72909973?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+environmental+pathology%2C+toxicology+and+oncology+%3A+official+organ+of+the+International+Society+for+Environmental+Toxicology+and+Cancer&rft.atitle=Alterations+in+hematopoietic+responses+in+B6C3F1+mice+caused+by+drinking+a+mixture+of+25+groundwater+contaminants.&rft.au=Hong%2C+H+L%3BYang%2C+R+S%3BBoorman%2C+G+A&rft.aulast=Hong&rft.aufirst=H&rft.date=1992-03-01&rft.volume=11&rft.issue=2&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Journal+of+environmental+pathology%2C+toxicology+and+oncology+%3A+official+organ+of+the+International+Society+for+Environmental+Toxicology+and+Cancer&rft.issn=07318898&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-04 N1 - Date created - 1992-06-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of anticonvulsant drugs on 4-aminopyridine-induced seizures in mice. AN - 72898281; 1563341 AB - The K+ channel blocker 4-aminopyridine (4-AP) causes epileptiform activity in in vitro preparations and is a potent convulsant in animals and man. In mice, 4-AP produces behavioral activation, clonic limb movements and wild running, followed by tonic hindlimb extension and death (ED97, 13.3 mg/kg, s.c.). We evaluated the ability of a series of anticonvulsant drugs to protect against 4-AP-induced seizures using lethality as the endpoint. Drugs with a phenytoin-like profile of activity were protective with ED50 values (all in mg/kg, i.p.) of 34.4 for phenytoin, 18.6 for carbamazepine, 26.9 for felbamate, and 41.5 for zonisamide. Phenobarbital and valproate also protected against 4-AP-induced seizures and lethality (ED50s, 30.6 and 301, respectively). In contrast the NMDA antagonists (+/-)-CPP and (+)-MK-801 were inactive as were the GABA enhancers diazepam, vigabatrin and tiagabine; the antiabsence drug ethosuximide; and the L-type Ca2+ channel blocker nimodipine. We conclude that drugs like phenytoin which block seizure spread are effective antagonists of seizures induced by K+ channel blockade. Drugs with specific actions on other cellular targets may be weak or inactive, presumably because they are unable to attenuate the spread of intense (non-NMDA receptor mediated) excitation evoked by 4-AP. JF - Epilepsy research AU - Yamaguchi, S AU - Rogawski, M A AD - Neuronal Excitability Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 9 EP - 16 VL - 11 IS - 1 SN - 0920-1211, 0920-1211 KW - Anticonvulsants KW - 0 KW - 4-Aminopyridine KW - BH3B64OKL9 KW - Index Medicus KW - Behavior, Animal -- drug effects KW - Animals KW - Dose-Response Relationship, Drug KW - Mice KW - Male KW - Reaction Time KW - Seizures -- chemically induced KW - Anticonvulsants -- pharmacology KW - 4-Aminopyridine -- pharmacology KW - 4-Aminopyridine -- antagonists & inhibitors KW - Seizures -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72898281?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epilepsy+research&rft.atitle=Effects+of+anticonvulsant+drugs+on+4-aminopyridine-induced+seizures+in+mice.&rft.au=Yamaguchi%2C+S%3BRogawski%2C+M+A&rft.aulast=Yamaguchi&rft.aufirst=S&rft.date=1992-03-01&rft.volume=11&rft.issue=1&rft.spage=9&rft.isbn=&rft.btitle=&rft.title=Epilepsy+research&rft.issn=09201211&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-15 N1 - Date created - 1992-05-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selecting dose-intense drug combinations: metastatic breast cancer. AN - 72895974; 1349245 AB - A mathematical model previously described is applied to the problem of selecting drug combinations for metastatic breast cancer. The model accounts for the differing single-agent activities of the drugs as well as their differing profiles of toxicity. With no bone marrow protection, combinations with cisplatin offer a small improvement in total equivalent dose over therapy with the more active single-agents. Restricting consideration to the four most commonly used agents, single-agent doxorubicin has the greatest equivalent dose. With protection for leukopenia or willingness to accept a higher incidence of severe leukopenia, a combination with large doses of cyclophosphamide, doxorubicin, and fluorouracil, and a small dose of cisplatin has greatest equivalent dose. The doublets cyclophosphamide/fluorouracil or fluorouracil/cisplatin at higher doses are almost as good. With protection for leukopenia and thrombocytopenia, a cyclophosphamide/thiotepa combination at very high doses maximizes total equivalent dose. This approach can be used to identify regimens worthy of prospective evaluation. JF - Breast cancer research and treatment AU - Korn, E L AU - Simon, R AD - Biometric Research Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 155 EP - 166 VL - 20 IS - 3 SN - 0167-6806, 0167-6806 KW - Alkaloids KW - 0 KW - Antineoplastic Agents, Phytogenic KW - Paclitaxel KW - P88XT4IS4D KW - Index Medicus KW - Drug Screening Assays, Antitumor KW - Dose-Response Relationship, Drug KW - Humans KW - Blood Platelets -- drug effects KW - Neoplasm Metastasis KW - Organ Specificity KW - Antineoplastic Agents, Phytogenic -- administration & dosage KW - Female KW - Leukocytes -- drug effects KW - Alkaloids -- administration & dosage KW - Breast Neoplasms -- drug therapy KW - Breast Neoplasms -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Models, Biological UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72895974?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Breast+cancer+research+and+treatment&rft.atitle=Selecting+dose-intense+drug+combinations%3A+metastatic+breast+cancer.&rft.au=Korn%2C+E+L%3BSimon%2C+R&rft.aulast=Korn&rft.aufirst=E&rft.date=1992-03-01&rft.volume=20&rft.issue=3&rft.spage=155&rft.isbn=&rft.btitle=&rft.title=Breast+cancer+research+and+treatment&rft.issn=01676806&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-02 N1 - Date created - 1992-06-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Experimental antifungal chemotherapy in granulocytopenic animal models of disseminated candidiasis: approaches to understanding investigational antifungal compounds for patients with neoplastic diseases. AN - 72894001; 1562687 AB - Disseminated candidiasis is the most common life-threatening invasive fungal infection in granulocytopenic patients. A review of recent approaches to pre-clinical laboratory investigation of promising antifungal compounds, which may have potential utility in granulocytopenic patients is presented. A particularly useful strategy is the study of persistently granulocytopenic rabbit models of acute, subacute, and chronic forms of disseminated candidiasis. When the antifungal triazoles (fluconazole, itraconazole, and SCH 39304 [SCH 42427]) were each evaluated for use as preventive, early treatment, or delayed treatment in the different models, the triazoles were consistently more active when used for preventive and early treatment than for delayed treatment. These triazoles were as active as amphotericin B plus flucytosine (AB + FC) when used for early treatment but were less active than AB + FC when used for delayed treatment. Several lipid formulations of amphotericin B demonstrate reduced nephrotoxicity at higher safely achievable dosages in comparison to those of deoxycholate amphotericin B in several models of disseminated candidiasis. When administered to follow non-linear saturable Michaelis-Menten-type plasma pharmacokinetics, the antifungal activity of the echinocandin compound cilofungin was significantly augmented. Thoughtfully designed and carefully conducted laboratory investigations in appropriate animal models of disseminated candidiasis can provide a scientific foundation and guide for development of clinical protocols investigating new approaches to prevention and treatment of invasive candidiasis in granulocytopenic patients. JF - Clinical infectious diseases : an official publication of the Infectious Diseases Society of America AU - Walsh, T J AU - Lee, J W AU - Roilides, E AU - Francis, P AU - Bacher, J AU - Lyman, C A AU - Pizzo, P A AD - Infectious Diseases Section, Pediatric Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - S139 EP - S147 VL - 14 Suppl 1 SN - 1058-4838, 1058-4838 KW - Antifungal Agents KW - 0 KW - Drugs, Investigational KW - Index Medicus KW - Animals KW - Humans KW - Rabbits KW - Immunosuppression KW - Drugs, Investigational -- therapeutic use KW - Candidiasis -- drug therapy KW - Agranulocytosis -- complications KW - Neoplasms -- complications KW - Disease Models, Animal KW - Drugs, Investigational -- administration & dosage KW - Antifungal Agents -- administration & dosage KW - Candidiasis -- etiology KW - Antifungal Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72894001?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+infectious+diseases+%3A+an+official+publication+of+the+Infectious+Diseases+Society+of+America&rft.atitle=Experimental+antifungal+chemotherapy+in+granulocytopenic+animal+models+of+disseminated+candidiasis%3A+approaches+to+understanding+investigational+antifungal+compounds+for+patients+with+neoplastic+diseases.&rft.au=Walsh%2C+T+J%3BLee%2C+J+W%3BRoilides%2C+E%3BFrancis%2C+P%3BBacher%2C+J%3BLyman%2C+C+A%3BPizzo%2C+P+A&rft.aulast=Walsh&rft.aufirst=T&rft.date=1992-03-01&rft.volume=14+Suppl+1&rft.issue=&rft.spage=S139&rft.isbn=&rft.btitle=&rft.title=Clinical+infectious+diseases+%3A+an+official+publication+of+the+Infectious+Diseases+Society+of+America&rft.issn=10584838&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-19 N1 - Date created - 1992-05-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Calcium signaling and secretory responses in agonist-stimulated pituitary gonadotrophs. AN - 72886953; 1373299 AB - In cultured pituitary gonadotrophs, gonadotropin-releasing hormone (GnRH) caused dose-dependent and biphasic increases in cytoplasmic calcium concentration ([Ca2+]i) and LH release. Both extra- and intracellular calcium pools participate in GnRH-induced elevation of [Ca2+]i and LH secretion. The spike phase of the [Ca2+]i response represents the primary signal derived predominantly from the rapid mobilization of intracellular Ca2+. In contrast, the prolonged phase of the Ca2+ signal depends exclusively on Ca2+ entry from the extracellular pool. The influx of Ca2+ occurs partially through dihydropyridine-sensitive calcium channels. Both [Ca2+]i and LH responses to increasing concentrations of GnRH occur over very similar time scales, suggesting that increasing degrees of receptor occupancy are transduced into amplitude-modulated Ca2+ responses, which in turn activate exocytosis in a linear manner. However, several lines of evidence indicated the complexity over the relationship between Ca2+ signaling and LH exocytosis. In contrast to [Ca2+]i measurements in cell suspension, single cell Ca2+ measurements revealed the existence of a more complicated pattern of Ca2+ response to GnRH, with a biphasic response to high agonist doses and prominent oscillatory responses to lower GnRH concentrations, with a log-linear correlation between GnRH dose and the frequency of Ca2+ spiking. In addition, analysis of the magnitudes of the [Ca2+]i and LH responses of gonadotrophs to a wide range of GnRH concentrations in the presence and absence of extracellular Ca2+, and to K+ and phorbol ester stimulation, showed non-linearity between these parameters with amplification of [Ca2+]i-mediated exocytosis. Studies on cell depleted of protein kinase C under conditions that did not change the LH pool suggested the participation of protein kinase C in this amplification, especially during the plateau phase of the secretory response to GnRH. JF - The Journal of steroid biochemistry and molecular biology AU - Stojilković, S S AU - Torsello, A AU - Iida, T AU - Rojas, E AU - Catt, K J AD - Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 453 EP - 467 VL - 41 IS - 3-8 SN - 0960-0760, 0960-0760 KW - Calcium Channel Blockers KW - 0 KW - Calcium Channels KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 KW - Cobalt KW - 3G0H8C9362 KW - 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester KW - 71145-03-4 KW - Luteinizing Hormone KW - 9002-67-9 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Potassium KW - RWP5GA015D KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Reference Values KW - Calcium Channels -- metabolism KW - Perfusion KW - 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester -- pharmacology KW - Cobalt -- pharmacology KW - Rats, Inbred Strains KW - Rats KW - Protein Kinase C -- metabolism KW - Calcium Channel Blockers -- pharmacology KW - Cells, Cultured KW - Kinetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Membrane Potentials KW - Potassium -- pharmacology KW - Ovariectomy KW - Female KW - Luteinizing Hormone -- secretion KW - Calcium -- metabolism KW - Pituitary Gland, Anterior -- drug effects KW - Pituitary Gland, Anterior -- metabolism KW - Signal Transduction -- drug effects KW - Pituitary Gland, Anterior -- physiology KW - Calcium -- pharmacology KW - Gonadotropin-Releasing Hormone -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72886953?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+steroid+biochemistry+and+molecular+biology&rft.atitle=Calcium+signaling+and+secretory+responses+in+agonist-stimulated+pituitary+gonadotrophs.&rft.au=Stojilkovi%C4%87%2C+S+S%3BTorsello%2C+A%3BIida%2C+T%3BRojas%2C+E%3BCatt%2C+K+J&rft.aulast=Stojilkovi%C4%87&rft.aufirst=S&rft.date=1992-03-01&rft.volume=41&rft.issue=3-8&rft.spage=453&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+steroid+biochemistry+and+molecular+biology&rft.issn=09600760&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-18 N1 - Date created - 1992-05-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A prospective examination of octreotide-induced gall-bladder changes in acromegaly. AN - 72885541; 1563079 AB - We wished to determine the effects of octreotide acetate, a somatostatin analogue, on gall-bladder function during treatment of acromegaly. We used a prospective, open label trial of somatostatin analogue. Seventeen patients with acromegaly took part. Ultrasonographic evaluation of gall-bladder contents were performed pretreatment, after 1 month, and subsequently at intervals of 3-6 months. Non-shadowing floating echogenic particles were observed in the gall-bladder in 12 of 17 patients after (mean +/- SEM) 2.5 +/- 0.6 months of treatment. During long-term treatment (mean 20.8 +/- 4.3, median 13, range 1-59 months), ultrasound evidence for cholelithiasis was observed in four patients after 20 +/- 4 months (range 4.2-43) months of octreotide therapy. No symptoms of biliary tract disease have been observed. Duration of acromegaly, average GH, average IGF-I, gender, age at entry, dose of analogue, and concurrent use of non-steroidal anti-inflammatory drugs did not affect the occurrence of sludge or gallstones. Formation of non-shadowing, floating echogenic particles occurs commonly during the first 6 months of treatment with octreotide acetate. Cholelithiasis is a risk of long-term treatment. JF - Clinical endocrinology AU - Eastman, R C AU - Arakaki, R F AU - Shawker, T AU - Schock, R AU - Roach, P AU - Comi, R J AU - Gorden, P AD - Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 265 EP - 269 VL - 36 IS - 3 SN - 0300-0664, 0300-0664 KW - Octreotide KW - RWM8CCW8GP KW - Index Medicus KW - Prospective Studies KW - Humans KW - Adult KW - Middle Aged KW - Follow-Up Studies KW - Ultrasonography KW - Male KW - Female KW - Cholelithiasis -- diagnostic imaging KW - Gallbladder -- diagnostic imaging KW - Cholelithiasis -- chemically induced KW - Octreotide -- therapeutic use KW - Octreotide -- adverse effects KW - Acromegaly -- drug therapy KW - Gallbladder -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72885541?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+endocrinology&rft.atitle=A+prospective+examination+of+octreotide-induced+gall-bladder+changes+in+acromegaly.&rft.au=Eastman%2C+R+C%3BArakaki%2C+R+F%3BShawker%2C+T%3BSchock%2C+R%3BRoach%2C+P%3BComi%2C+R+J%3BGorden%2C+P&rft.aulast=Eastman&rft.aufirst=R&rft.date=1992-03-01&rft.volume=36&rft.issue=3&rft.spage=265&rft.isbn=&rft.btitle=&rft.title=Clinical+endocrinology&rft.issn=03000664&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-21 N1 - Date created - 1992-05-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Epidemiology of thrombocytopenia in HIV infection. AN - 72877056; 1348479 AB - Thrombocytopenia is a known complication of human immunodeficiency virus Type-1 (HIV-1) infection, and more data need to be collected on its frequency, severity, and clinical sequelae. We determined the frequency of thrombocytopenia and its relationship to other HIV infection characteristics from a review of records of 1004 HIV-infected patients attending two outpatient clinics in Washington, D.C. The self-reported sources of HIV-1 exposure were male homosexual activity (68%), bisexual activity (10%), heterosexual activity (6%), and intravenous drug use (15%). Fifty-nine percent of the individuals were white, 37% were black and 94% were male. Fifteen percent had AIDS. Thrombocytopenia occurred more frequently in subjects with AIDS (21.2%) than in HIV-infected individuals who did not fit clinical criteria for AIDS (9.2%) (p less than 0.001). Patients with few CD4-positive cells and an advanced stage of disease were more likely to have low platelet counts: 30% with an absolute CD4 cell count lower than 200/mm3 vs 8% with CD4 counts between 200 and 500 (p less than 0.00001), and 18.5% with Stage IV disease compared to 7.6% in Stage II (p less than 0.001) had platelet counts less than 150,000/mm3. Thrombocytopenia was more frequent in white males and older subjects. Although subjects infected by heterosexual exposure had a lower frequency of thrombocytopenia, intravenous drug users and homosexual men exhibited similar frequencies of thrombocytopenia. Of all subjects with platelet counts less than 50,000/mm3, 40% reported bleeding and 1 died of an intracranial hemorrhage. Thrombocytopenia occurs frequently in HIV-infected people, primarily in those with AIDS, low CD4 cell numbers, and advanced stages of diseases. JF - European journal of haematology AU - Sloand, E M AU - Klein, H G AU - Banks, S M AU - Vareldzis, B AU - Merritt, S AU - Pierce, P AD - National Heart, Lung, and Blood Institute, Bethesda, MD 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 168 EP - 172 VL - 48 IS - 3 SN - 0902-4441, 0902-4441 KW - Zidovudine KW - 4B9XT59T7S KW - Index Medicus KW - AIDS/HIV KW - Zidovudine -- therapeutic use KW - Bone Marrow -- pathology KW - Humans KW - Hemophilia A KW - CD4-Positive T-Lymphocytes -- pathology KW - Blood Transfusion KW - Homosexuality KW - Male KW - Leukocyte Count KW - Female KW - Substance Abuse, Intravenous KW - Acquired Immunodeficiency Syndrome -- complications KW - Thrombocytopenia -- pathology KW - Thrombocytopenia -- epidemiology KW - Thrombocytopenia -- complications KW - Acquired Immunodeficiency Syndrome -- transmission KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - HIV-1 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72877056?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+haematology&rft.atitle=Epidemiology+of+thrombocytopenia+in+HIV+infection.&rft.au=Sloand%2C+E+M%3BKlein%2C+H+G%3BBanks%2C+S+M%3BVareldzis%2C+B%3BMerritt%2C+S%3BPierce%2C+P&rft.aulast=Sloand&rft.aufirst=E&rft.date=1992-03-01&rft.volume=48&rft.issue=3&rft.spage=168&rft.isbn=&rft.btitle=&rft.title=European+journal+of+haematology&rft.issn=09024441&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-14 N1 - Date created - 1992-05-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Eur J Haematol. 1993 Apr;50(4):239-40 [8500608] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Drug abuse research and HIV/AIDS: a national perspective from the US. AN - 72876238; 1559034 AB - The National Institute on Drug Abuse (NIDA), the lead Federal agency charged with research on reducing the demand for illicit drugs in the US, has actively pursued the associated challenge of reducing drugs-related HIV transmission. Drug abuse-related spread of the virus occurs not only through sharing contaminated needles but also sexually to partners and perinatally from infected mothers to their offspring. Through a national research and demonstration program, NIDA supports primary AIDS risk reduction activities focused on identifying effective drug abuse prevention and treatment strategies. AIDS is increasingly a disease found in women, children, minorities, and people who live in rural areas. NIDA's efforts are clearly responsive to the changing nature of this epidemic. Among the many promising initiatives currently underway are a medications development program to find new pharmacotherapies for treating drug addiction; an array of National AIDS Outreach Demonstration Projects implementing alternative control strategies for drug abusers not attracted to or successful in drug abuse treatment; establishment of several treatment research units for designing and conducting studies on treatment effectiveness; and a variety of programs aimed at identifying and potentially reducing the risks of prenatal drug use to both mother and child. Effective dissemination of our findings is particularly critical to the overall impact of our research efforts. Collaborative activities teaming NIDA with a multitude of organizations also addressing AIDS related issues are designed to provide a synergistic impact on this complex and multifaceted public health crisis. JF - British journal of addiction AU - Schuster, C R AD - National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 355 EP - 361 VL - 87 IS - 3 SN - 0952-0481, 0952-0481 KW - Street Drugs KW - 0 KW - Index Medicus KW - AIDS/HIV KW - United States KW - HIV Seroprevalence -- trends KW - Risk Factors KW - Humans KW - National Institutes of Health (U.S.) KW - Research KW - Acquired Immunodeficiency Syndrome -- prevention & control KW - HIV Infections -- transmission KW - Substance Abuse, Intravenous -- rehabilitation KW - HIV Infections -- prevention & control KW - Acquired Immunodeficiency Syndrome -- transmission KW - Substance Abuse, Intravenous -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72876238?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+addiction&rft.atitle=Drug+abuse+research+and+HIV%2FAIDS%3A+a+national+perspective+from+the+US.&rft.au=Schuster%2C+C+R&rft.aulast=Schuster&rft.aufirst=C&rft.date=1992-03-01&rft.volume=87&rft.issue=3&rft.spage=355&rft.isbn=&rft.btitle=&rft.title=British+journal+of+addiction&rft.issn=09520481&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-14 N1 - Date created - 1992-05-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A nested case-control study of lung cancer among silica exposed workers in China. AN - 72868844; 1313281 AB - In an attempt to assess whether silica induces lung cancer, a nested case-control study of 316 male lung cancer cases and 1352 controls was carried out among pottery workers and tungsten, copper-iron, and tin miners from five provinces in south central China. Exposure to dust and silica for each study subject was evaluated quantitatively by cumulative exposure measures based on historical industrial hygiene records. Measurements on confounders such as inorganic arsenic, polycyclic aromatic hydrocarbons (PAHs), and radon were also collected from the worksites. Information on cigarette smoking was obtained by interviews of the subjects or their next of kin. A significant trend of increasing risk of lung cancer with exposure to silica was found for tin miners, but not for miners working in tungsten or copper-iron mines. Concomitant and highly correlated exposures to arsenic and PAHs among tin miners were also found. Risk of lung cancer among pottery workers was related to exposure to silica, although the dose-response gradient was not significant. Risks of lung cancer were significantly increased among silicotic subjects in iron-copper and tin mines, but not in pottery factories or tungsten mines. The results of this study provide only limited support for an aetiological association between silica and lung cancer. JF - British journal of industrial medicine AU - McLaughlin, J K AU - Chen, J Q AU - Dosemeci, M AU - Chen, R A AU - Rexing, S H AU - Wu, Z AU - Hearl, F J AU - McCawley, M A AU - Blot, W J AD - National Cancer Institute, Division of Cancer Etiology, Bethesda, Maryland 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 167 EP - 171 VL - 49 IS - 3 SN - 0007-1072, 0007-1072 KW - Polycyclic Compounds KW - 0 KW - Silicon Dioxide KW - 7631-86-9 KW - Arsenic KW - N712M78A8G KW - Radon KW - Q74S4N8N1G KW - Index Medicus KW - Arsenic -- adverse effects KW - Risk Factors KW - Humans KW - Case-Control Studies KW - Smoking -- adverse effects KW - Mining KW - Radon -- adverse effects KW - Polycyclic Compounds -- adverse effects KW - Male KW - China KW - Lung Neoplasms -- etiology KW - Lung Neoplasms -- epidemiology KW - Occupational Diseases -- etiology KW - Occupational Diseases -- epidemiology KW - Silicon Dioxide -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72868844?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+industrial+medicine&rft.atitle=A+nested+case-control+study+of+lung+cancer+among+silica+exposed+workers+in+China.&rft.au=McLaughlin%2C+J+K%3BChen%2C+J+Q%3BDosemeci%2C+M%3BChen%2C+R+A%3BRexing%2C+S+H%3BWu%2C+Z%3BHearl%2C+F+J%3BMcCawley%2C+M+A%3BBlot%2C+W+J&rft.aulast=McLaughlin&rft.aufirst=J&rft.date=1992-03-01&rft.volume=49&rft.issue=3&rft.spage=167&rft.isbn=&rft.btitle=&rft.title=British+journal+of+industrial+medicine&rft.issn=00071072&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-04 N1 - Date created - 1992-05-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Occup Med. 1981 Nov;23(11):779-84 [7320778] Comput Biomed Res. 1981 Apr;14(2):138-43 [7273715] S Afr Med J. 1969 Oct 25;43(43):1307-12 [4310754] Am J Epidemiol. 1987 Jan;125(1):35-43 [3024482] Am J Ind Med. 1986;10(1):57-62 [3017101] Regul Toxicol Pharmacol. 1990 Dec;12(3 Pt 1):224-37 [2077559] Br J Ind Med. 1990 Jan;47(1):4-9 [2155648] Int J Epidemiol. 1990 Mar;19(1):19-25 [2161807] Br J Ind Med. 1989 May;46(5):289-91 [2546576] Br J Ind Med. 1989 Dec;46(12):877-80 [2611162] Br J Ind Med. 1989 Dec;46(12):881-6 [2611163] N Engl J Med. 1963 Aug 8;269:284-9 [13998279] Am J Ind Med. 1985;7(4):285-94 [2986455] Int Arch Occup Environ Health. 1988;60(4):299-302 [2836314] Br J Ind Med. 1991 Jan;48(1):53-60 [1847069] Br J Ind Med. 1991 Feb;48(2):122-9 [1998606] Arch Environ Health. 1991 Mar-Apr;46(2):82-9 [2006898] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - An HLA-A2/beta 2-microglobulin/peptide complex assembled from subunits expressed separately in Escherichia coli. AN - 72867181; 1557046 AB - The human class I histocompatibility antigen HLA-A2 has been assembled from subunits expressed separately in E. coli. A peptide that is known to be recognized by human cytotoxic T lymphocytes (CTLs) in association with HLA-A2 is a necessary component of the reconstitution mixture. The N-terminal extracellular fragment of the HLA-A2 heavy chain is initially synthesised as an insoluble aggregate. The aggregate is solubilized in denaturant, mixed with the influenza nucleoprotein 85-94 decapeptide (NP peptide), and diluted into a solution containing human beta 2-microglobulin (beta 2 m) isolated from the E. coli periplasm. The HLA-A2 heavy chain becomes soluble in physiological solutions if both beta 2m and the NP peptide are present. The reconstituted HLA-A2 complex is recognised by a monoclonal antibody that is specific for the native HLA-A2/beta 2m heterodimer, and is also recognised by a monoclonal antibody that recognises beta 2m. When other peptides known from CTL studies to associate with HLA-A2 are used, a significantly lower yield of reconstituted complex is obtained. The isoelectric point of the reconstituted complex depends on which peptide is used, confirming that the peptide is a component of the reconstituted complex. JF - Molecular immunology AU - Parker, K C AU - Silver, M L AU - Wiley, D C AD - Biological Resources Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 371 EP - 378 VL - 29 IS - 3 SN - 0161-5890, 0161-5890 KW - HLA-A2 Antigen KW - 0 KW - Oligopeptides KW - Recombinant Proteins KW - Viral Proteins KW - beta 2-Microglobulin KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Transfection KW - Electrophoresis, Polyacrylamide Gel KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Plasmids KW - Cloning, Molecular KW - Escherichia coli -- genetics KW - HLA-A2 Antigen -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72867181?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+immunology&rft.atitle=An+HLA-A2%2Fbeta+2-microglobulin%2Fpeptide+complex+assembled+from+subunits+expressed+separately+in+Escherichia+coli.&rft.au=Parker%2C+K+C%3BSilver%2C+M+L%3BWiley%2C+D+C&rft.aulast=Parker&rft.aufirst=K&rft.date=1992-03-01&rft.volume=29&rft.issue=3&rft.spage=371&rft.isbn=&rft.btitle=&rft.title=Molecular+immunology&rft.issn=01615890&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-05 N1 - Date created - 1992-05-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Simulation modeling of carcinogenesis. AN - 72865152; 1553760 AB - A discrete-time simulation model of carcinogenesis is described mathematically using recursive relationships between time-varying model variables. The dynamics of cellular behavior is represented within a biological framework that encompasses two irreversible and heritable genetic changes. Empirical data and biological supposition dealing with both control and experimental animal groups are used together to establish values for model input variables. The estimation of these variables is integral to the simulation process as described in step-by-step detail. Hepatocarcinogenesis in male F344 rats provides the basis for seven modeling scenarios which illustrate the complexity of relationships among cell proliferation, genotoxicity, and tumor risk. JF - Toxicology and applied pharmacology AU - Ellwein, L B AU - Cohen, S M AD - National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 98 EP - 108 VL - 113 IS - 1 SN - 0041-008X, 0041-008X KW - Index Medicus KW - Rats KW - Liver Neoplasms, Experimental -- genetics KW - Animals KW - Rats, Inbred F344 KW - Age Factors KW - Liver Neoplasms, Experimental -- metabolism KW - Risk Factors KW - Mitosis KW - Cell Death KW - Male KW - Models, Biological KW - Neoplasms -- genetics KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72865152?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Simulation+modeling+of+carcinogenesis.&rft.au=Ellwein%2C+L+B%3BCohen%2C+S+M&rft.aulast=Ellwein&rft.aufirst=L&rft.date=1992-03-01&rft.volume=113&rft.issue=1&rft.spage=98&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=0041008X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-29 N1 - Date created - 1992-04-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Early menopause in long-term survivors of cancer during adolescence. AN - 72856363; 1550144 AB - We attempted to investigate the risk of early menopause after treatment for cancer during childhood or adolescence. We interviewed 1067 women in whom cancer was diagnosed before age 20, who were at least 5-year survivors, and who were still menstruating at age 21. Self-reported menopause status in survivors was compared with that in 1599 control women. Cancer survivors, with disease diagnosed between ages 13 and 19, had a risk of menopause four times greater than that of controls during the ages 21 to 25; the risk relative to controls declined thereafter. Significantly increased relative risks of menopause during the early 20s occurred after treatment with either radiotherapy alone (relative risk 3.7) or alkylating agents alone (relative risk 9.2). During ages 21 to 25 the risk of menopause increased 27-fold for women treated with both radiation below the diaphragm and alkylating agent chemotherapy. By age 31, 42% of these women had reached menopause compared with 5% for controls. Treatment for cancer during adolescence carries a substantial risk for early menopause among women still menstruating at age 21. Increasing use of radiation and chemotherapy, together with the continued trend toward delayed childbearing, suggests that these women should be made aware of their smaller window of fertility so that they can plan their families accordingly. JF - American journal of obstetrics and gynecology AU - Byrne, J AU - Fears, T R AU - Gail, M H AU - Pee, D AU - Connelly, R R AU - Austin, D F AU - Holmes, G F AU - Holmes, F F AU - Latourette, H B AU - Meigs, J W AD - Clinical Epidemiology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 788 EP - 793 VL - 166 IS - 3 SN - 0002-9378, 0002-9378 KW - Alkylating Agents KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Alkylating Agents -- therapeutic use KW - Risk Factors KW - Humans KW - Cohort Studies KW - Adult KW - Neoplasms, Radiation-Induced KW - Alkylating Agents -- adverse effects KW - Time Factors KW - Female KW - Survival Analysis KW - Hodgkin Disease -- etiology KW - Neoplasms -- mortality KW - Menopause, Premature KW - Neoplasms -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72856363?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+obstetrics+and+gynecology&rft.atitle=Early+menopause+in+long-term+survivors+of+cancer+during+adolescence.&rft.au=Byrne%2C+J%3BFears%2C+T+R%3BGail%2C+M+H%3BPee%2C+D%3BConnelly%2C+R+R%3BAustin%2C+D+F%3BHolmes%2C+G+F%3BHolmes%2C+F+F%3BLatourette%2C+H+B%3BMeigs%2C+J+W&rft.aulast=Byrne&rft.aufirst=J&rft.date=1992-03-01&rft.volume=166&rft.issue=3&rft.spage=788&rft.isbn=&rft.btitle=&rft.title=American+journal+of+obstetrics+and+gynecology&rft.issn=00029378&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-20 N1 - Date created - 1992-04-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - An Escherichia coli dnaE mutation with suppressor activity toward mutator mutD5. AN - 72850732; 1548237 AB - The Escherichia coli mutator mutD5 is a conditional mutator whose strength is moderate when the strain is growing in minimal medium but very strong when it is growing in rich medium. The primary defect of this strain resides in the dnaQ gene, which encodes the epsilon (exonucleolytic proofreading) subunit of the DNA polymerase III holoenzyme. In one of our mutD5 strains we discovered a mutation that suppressed the mutability of mutD5. Interestingly, the level of suppression was strong in minimal medium but weak in rich medium. The mutation was localized to the dnaE gene, which encodes the alpha (polymerase) subunit of the DNA polymerase III holoenzyme. This mutation, termed dnaE910, also conferred improved growth of the mutD5 strain and caused increased temperature sensitivity in both wild-type and dnaQ49 backgrounds. The reduction in mutator strength by dnaE910 was also observed when this allele was placed in a mutL, a mutT, or a dnaQ49 background. The results suggest that dnaE910 encodes an antimutator DNA polymerase whose effect might be mediated by improved insertion fidelity or by increased proofreading via its effect on the exonuclease activity. JF - Journal of bacteriology AU - Schaaper, R M AU - Cornacchio, R AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 1974 EP - 1982 VL - 174 IS - 6 SN - 0021-9193, 0021-9193 KW - dnaE KW - dnaQ KW - mutD5 KW - mutL KW - mutT KW - DNA Polymerase III KW - EC 2.7.7.- KW - Index Medicus KW - DNA Repair KW - Temperature KW - Mutation KW - Chromosome Mapping KW - DNA Replication KW - Genes, Bacterial KW - DNA Polymerase III -- genetics KW - Escherichia coli -- genetics KW - Genes, Suppressor KW - Mutagenesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72850732?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+bacteriology&rft.atitle=An+Escherichia+coli+dnaE+mutation+with+suppressor+activity+toward+mutator+mutD5.&rft.au=Schaaper%2C+R+M%3BCornacchio%2C+R&rft.aulast=Schaaper&rft.aufirst=R&rft.date=1992-03-01&rft.volume=174&rft.issue=6&rft.spage=1974&rft.isbn=&rft.btitle=&rft.title=Journal+of+bacteriology&rft.issn=00219193&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-23 N1 - Date created - 1992-04-23 N1 - Date revised - 2017-01-13 N1 - Gene symbol - dnaE; dnaQ; mutD5; mutL; mutT N1 - SuppNotes - Cited By: Mol Gen Genet. 1989 Oct;219(1-2):256-62 [2693944] Genetics. 1989 Feb;121(2):205-12 [2659431] Proc Natl Acad Sci U S A. 1987 Jul;84(13):4389-92 [3037519] Proc Natl Acad Sci U S A. 1988 Nov;85(21):8126-30 [3054881] Annu Rev Biochem. 1987;56:435-66 [3304141] Microbiol Rev. 1986 Jun;50(2):133-65 [3523187] Mol Gen Genet. 1986 Oct;205(1):9-13 [3540531] J Mol Biol. 1983 Apr 25;165(4):633-54 [6222197] J Bacteriol. 1982 Oct;152(1):351-6 [6288664] J Biol Chem. 1984 May 10;259(9):5567-73 [6325441] Proc Natl Acad Sci U S A. 1983 Apr;80(8):2189-92 [6340117] Proc Natl Acad Sci U S A. 1983 Dec;80(23):7085-9 [6359162] Proc Natl Acad Sci U S A. 1984 Dec;81(24):7747-51 [6393125] Mol Gen Genet. 1980;178(3):703-8 [6993863] Genetics. 1982 Jan;100(1):7-18 [7047297] Mol Gen Genet. 1978 Jul 25;163(3):277-83 [355854] Microbiol Rev. 1990 Jun;54(2):130-97 [2194094] EMBO J. 1989 Nov;8(11):3511-6 [2555167] J Bacteriol. 1989 Aug;171(8):4494-7 [2666405] Annu Rev Genet. 1986;20:523-38 [2949693] Annu Rev Biochem. 1988;57:519-50 [3052282] Biochemistry. 1988 Sep 6;27(18):6716-25 [3058205] Proc Natl Acad Sci U S A. 1987 Sep;84(17):6220-4 [3306672] J Bacteriol. 1974 Feb;117(2):477-87 [4590472] J Mol Biol. 1983 Jul 15;167(4):757-71 [6224021] J Bacteriol. 1983 Mar;153(3):1361-7 [6337996] Proc Natl Acad Sci U S A. 1983 Apr;80(8):2295-9 [6340119] J Biol Chem. 1984 Jun 25;259(12):7990-3 [6376496] Mutat Res. 1982 Mar;93(1):25-33 [7038468] J Biol Chem. 1956 Jan;218(1):97-106 [13278318] J Biol Chem. 1991 Mar 15;266(8):5055-61 [2002048] J Biol Chem. 1990 Jan 15;265(2):1171-8 [2153103] J Bacteriol. 1989 Oct;171(10):5572-80 [2551891] Proc Natl Acad Sci U S A. 1989 Jun;86(11):3949-52 [2657730] J Biol Chem. 1985 Oct 25;260(24):12987-92 [2997151] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Corticotropin-releasing hormone: potentiation of cocaine-kindled seizures and lethality. AN - 72847511; 1547754 AB - Carbamazepine (CBZ) blocks the development of local anesthetic seizures kindled by cocaine and lidocaine. Cocaine and lidocaine release corticotropin-releasing hormone (CRH) in hypothalamic cell cultures, and this effect is also blocked by CBZ. Because CRH administered intracerebroventricularly (i.c.v.) can produce seizures, its potential role in the development of cocaine seizures and in the anticonvulsant effects of CBZ was studied. CRH (at doses of 5, 10, and 100 micrograms) potentiated cocaine-kindled seizure development and lethality in a dose-related fashion. CRH also reversed the effects of CBZ on cocaine kindling and lethality, but only at the highest doses, which also affected cocaine kindling. Thus, a selective role for CRH in the anticonvulsant effects of CBZ was not demonstrated. The findings suggest a potentially important role for CRH in exacerbating cocaine-seizure evolution and its associated lethality and confirm the inhibition of cocaine kindling and lethality by CBZ. JF - Epilepsia AU - Weiss, S R AU - Nierenberg, J AU - Lewis, R AU - Post, R M AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, Maryland 20892. PY - 1992 SP - 248 EP - 254 VL - 33 IS - 2 SN - 0013-9580, 0013-9580 KW - Carbamazepine KW - 33CM23913M KW - Corticotropin-Releasing Hormone KW - 9015-71-8 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Animals KW - Dose-Response Relationship, Drug KW - Hypothalamus -- drug effects KW - Hypothalamus -- cytology KW - Injections, Intraventricular KW - Rats, Inbred Strains KW - Rats KW - Cells, Cultured KW - Hypothalamus -- metabolism KW - Carbamazepine -- pharmacology KW - Models, Neurological KW - Drug Antagonism KW - Drug Synergism KW - Male KW - Seizures -- chemically induced KW - Kindling, Neurologic -- drug effects KW - Seizures -- mortality KW - Seizures -- prevention & control KW - Corticotropin-Releasing Hormone -- administration & dosage KW - Cocaine -- pharmacology KW - Corticotropin-Releasing Hormone -- pharmacology KW - Corticotropin-Releasing Hormone -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72847511?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epilepsia&rft.atitle=Corticotropin-releasing+hormone%3A+potentiation+of+cocaine-kindled+seizures+and+lethality.&rft.au=Weiss%2C+S+R%3BNierenberg%2C+J%3BLewis%2C+R%3BPost%2C+R+M&rft.aulast=Weiss&rft.aufirst=S&rft.date=1992-03-01&rft.volume=33&rft.issue=2&rft.spage=248&rft.isbn=&rft.btitle=&rft.title=Epilepsia&rft.issn=00139580&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-20 N1 - Date created - 1992-04-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of an activated Notch-related int-3 transgene interferes with cell differentiation and induces neoplastic transformation in mammary and salivary glands. AN - 72847028; 1372276 AB - Expression of the int-3 locus is activated in mouse mammary tumors as a consequence of insertional mutagenesis by the mouse mammary tumor virus (MMTV). Integration of the MMTV provirus into the int-3 locus promotes the transcription and translation of flanking cellular int-3 sequences sharing significant homology with the intracellular domain of the neurogenic Notch gene of Drosophila, and with the yeast cell cycle regulatory genes cdc10 and SWI6. To determine the in vivo consequences of activated int-3 expression, transgenic mice were generated harboring a genomic tumor DNA fragment consisting of the MMTV LTR and the flanking cellular int-3 sequences. All six int-3 founder transgenic mice and the progeny of one established line exhibited similar dramatic phenotypic abnormalities in tissues in which the transgene was expressed. Focal and often multiple poorly differentiated mammary and salivary adenocarcinomas appeared in the majority of transgenic mice between 2 and 7 months of age. Significantly, mammary glands were arrested in development and were lactation deficient in all female int-3 mice. The salivary glands, glands of the nasal mucosa and maxillary sinus, the extraorbital lacrimal glands, and the Harderian glands of juvenile and adult transgenic mice all contained proliferating immature ductule cells and were incompletely differentiated. In addition, all male int-3 transgenic mice were sterile, apparently the result of severe hyperplasia of the epididymis. These findings demonstrate in vivo that expression of the activated Notch-related int-3 gene causes deregulation of normal developmental controls and hyperproliferation of glandular epithelia. JF - Genes & development AU - Jhappan, C AU - Gallahan, D AU - Stahle, C AU - Chu, E AU - Smith, G H AU - Merlino, G AU - Callahan, R AD - Division of Cancer Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 345 EP - 355 VL - 6 IS - 3 SN - 0890-9369, 0890-9369 KW - cdc10 KW - int-3 KW - sw16 KW - RNA KW - 63231-63-0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Hyperplasia -- genetics KW - DNA -- genetics KW - Mammary Neoplasms, Experimental -- genetics KW - Mice KW - Adenocarcinoma -- genetics KW - Salivary Gland Neoplasms -- genetics KW - Plasmids KW - Mice, Transgenic KW - Male KW - Female KW - RNA -- genetics KW - Mammary Glands, Animal -- pathology KW - Salivary Glands -- pathology KW - Gene Expression KW - Cell Differentiation -- genetics KW - Cell Transformation, Neoplastic -- genetics KW - Mammary Tumor Virus, Mouse -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72847028?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genes+%26+development&rft.atitle=Expression+of+an+activated+Notch-related+int-3+transgene+interferes+with+cell+differentiation+and+induces+neoplastic+transformation+in+mammary+and+salivary+glands.&rft.au=Jhappan%2C+C%3BGallahan%2C+D%3BStahle%2C+C%3BChu%2C+E%3BSmith%2C+G+H%3BMerlino%2C+G%3BCallahan%2C+R&rft.aulast=Jhappan&rft.aufirst=C&rft.date=1992-03-01&rft.volume=6&rft.issue=3&rft.spage=345&rft.isbn=&rft.btitle=&rft.title=Genes+%26+development&rft.issn=08909369&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-17 N1 - Date created - 1992-04-17 N1 - Date revised - 2017-01-13 N1 - Gene symbol - cdc10; int-3; sw16 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Maitotoxin effects are blocked by SK&F 96365, an inhibitor of receptor-mediated calcium entry. AN - 72840938; 1312215 AB - The dinoflagellate toxin maitotoxin (MTX) elicited a sustained increase of [Ca2+]i in C6 glioma cells. This response was inhibited by SK&F 96365, a blocker of receptor-mediated calcium entry. In C6 cells, endothelin-1 elicited a rapid but transient increase in [Ca2+]i, followed by a smaller sustained increase. SK&F 96365 inhibited the sustained increase in [Ca2+]i. In both C6 glioma cells and RIN insulinoma cells, MTX elicited a marked influx of 45Ca2+. SK&F 96365 inhibited MTX-induced 45Ca2+ influx by 95% at 30 microM. The L-type calcium channel blocker nifedipine, even at 10 microM, inhibited MTX-induced calcium uptake by only 20% in RIN cells and by only 10% in C6 cells. MTX elicited calcium-dependent phosphoinositide breakdown in both C6 and RIN cells. In both cell lines, the MTX-induced phosphoinositide breakdown was inhibited by 90% by SK&F 96365 at 30 microM. Endothelin-1 and carbamylcholine elicited phosphoinositide breakdown in C6 cells and RIN cells, respectively. The stimulations were unaffected by the presence of SK&F 96365 up to 100 microM. In RIN insulinoma cells, MTX elicited calcium-dependent release of insulin. SK&F 96365 at 30 microM inhibited MTX-induced insulin release by 75%, whereas nifedipine, even at 30 microM, inhibited release by only 10%. The blockade of MTX-induced responses by SK&F 96365 indicates that MTX increases intracellular calcium by interacting directly with a calcium-entry system that is similar, in its sensitivity to SK&F 96365, to the calcium-entry system activated by receptors that elicit phosphoinositide breakdown. Activation of phospholipase C and hormone release by MTX also are blocked by SK&F 96365 and, thus, may be secondary to the activation of such a calcium-entry system. JF - Molecular pharmacology AU - Soergel, D G AU - Yasumoto, T AU - Daly, J W AU - Gusovsky, F AD - Laboratory of Bioorganic Chemistry, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 487 EP - 493 VL - 41 IS - 3 SN - 0026-895X, 0026-895X KW - Calcium Channel Blockers KW - 0 KW - Endothelins KW - Imidazoles KW - Insulin KW - Marine Toxins KW - Oxocins KW - Phosphatidylinositols KW - Carbachol KW - 8Y164V895Y KW - maitotoxin KW - 9P59GES78D KW - 1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole KW - I61V87164A KW - Nifedipine KW - I9ZF7L6G2L KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Nifedipine -- pharmacology KW - Phosphatidylinositols -- metabolism KW - Endothelins -- pharmacology KW - Tumor Cells, Cultured KW - Insulin -- metabolism KW - Glioma -- metabolism KW - Radioimmunoassay KW - Carbachol -- pharmacology KW - Calcium -- metabolism KW - Imidazoles -- pharmacology KW - Calcium Channel Blockers -- pharmacology KW - Marine Toxins -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72840938?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=Maitotoxin+effects+are+blocked+by+SK%26amp%3BF+96365%2C+an+inhibitor+of+receptor-mediated+calcium+entry.&rft.au=Soergel%2C+D+G%3BYasumoto%2C+T%3BDaly%2C+J+W%3BGusovsky%2C+F&rft.aulast=Soergel&rft.aufirst=D&rft.date=1992-03-01&rft.volume=41&rft.issue=3&rft.spage=487&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=0026895X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-16 N1 - Date created - 1992-04-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Acute or chronic topical retinoic acid treatment of human skin in vivo alters the expression of epidermal transglutaminase, loricrin, involucrin, filaggrin, and keratins 6 and 13 but not keratins 1, 10, and 14. AN - 72839381; 1372028 AB - Histologic and immunocytochemical analyses were performed on cutaneous biopsies from 10 patients treated with retinoic acid under occlusion for 4 d compared to biopsies from 19 patients treated nightly for 16 weeks. Acute application of RA caused epidermal thickening (9 of 10 samples), stratum granulosum thickening (7 of 10), parakeratosis (4 of 10), a marked increase in the number of cell layers expressing epidermal transglutaminase (7 of 10), and focal expression of two non-epidermal keratins, K6 (8 of 10) and K13 (2 of 10), changes also observed with chronic treatment. Involucrin, filaggrin, and loricrin were also altered in samples from both acute and chronic treatment. An increased number of cell layers expressed both involucrin and filaggrin from both the acute (7 of 10) and chronic (14 of 19) treatment groups. In the acute group, loricrin expression was significantly reduced or absent in some regions of the epidermis (5 of 10), whereas most chronic samples showed an increased number of cell layers expressing loricrin (12 of 19). The pattern of expression of three major epidermal differentiation products, keratins K1, K10, and K14, was not significantly altered in any of the acute or chronic samples, although there was a slight reduction in the detection of K10 in two of the acute samples. Thus, acute topical RA treatment under occlusion caused substantial changes in the epidermis, and reproduced most, but not all of the effects of chronic treatment. JF - The Journal of investigative dermatology AU - Rosenthal, D S AU - Griffiths, C E AU - Yuspa, S H AU - Roop, D R AU - Voorhees, J J AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 343 EP - 350 VL - 98 IS - 3 SN - 0022-202X, 0022-202X KW - Intermediate Filament Proteins KW - 0 KW - Membrane Proteins KW - Protein Precursors KW - RNA, Messenger KW - filaggrin KW - loricrin KW - Tretinoin KW - 5688UTC01R KW - involucrin KW - 60108-77-2 KW - Keratins KW - 68238-35-7 KW - Transglutaminases KW - EC 2.3.2.13 KW - Index Medicus KW - Humans KW - RNA, Messenger -- analysis KW - Immunohistochemistry KW - Administration, Topical KW - Keratins -- genetics KW - Tretinoin -- pharmacology KW - Skin -- chemistry KW - Skin -- drug effects KW - Tretinoin -- administration & dosage KW - Transglutaminases -- analysis KW - Intermediate Filament Proteins -- analysis KW - Protein Precursors -- analysis KW - Membrane Proteins -- analysis KW - Keratins -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72839381?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+investigative+dermatology&rft.atitle=Acute+or+chronic+topical+retinoic+acid+treatment+of+human+skin+in+vivo+alters+the+expression+of+epidermal+transglutaminase%2C+loricrin%2C+involucrin%2C+filaggrin%2C+and+keratins+6+and+13+but+not+keratins+1%2C+10%2C+and+14.&rft.au=Rosenthal%2C+D+S%3BGriffiths%2C+C+E%3BYuspa%2C+S+H%3BRoop%2C+D+R%3BVoorhees%2C+J+J&rft.aulast=Rosenthal&rft.aufirst=D&rft.date=1992-03-01&rft.volume=98&rft.issue=3&rft.spage=343&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+investigative+dermatology&rft.issn=0022202X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-15 N1 - Date created - 1992-04-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: J Invest Dermatol 1992 Aug;99(2):145 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nonsedating antihistamines: pharmacology, clinical efficacy and adverse effects. AN - 72838052; 1347437 AB - Antihistamines are effective therapy for histamine-mediated conditions, including seasonal and perennial allergic rhinitis and chronic urticaria. Until recently, all antihistamines produced some degree of drowsiness, as well as anticholinergic side effects. Several nonsedating antihistamines have been developed. Two of these antihistamines--terfenadine and astemizole--are commercially available. The lack of central nervous system effects is attributed to the inability of these drugs to penetrate the blood-brain barrier. They also have no appreciable binding to cholinergic receptors. Clinical trials have demonstrated that the newer agents are as effective as classic antihistamines and that they have no greater incidence of central nervous system or anticholinergic side effects than placebo. JF - American family physician AU - Kaliner, M A AD - National Institute of Allergy and Infectious Diseases, Bethesda, Maryland. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 1337 EP - 1342 VL - 45 IS - 3 SN - 0002-838X, 0002-838X KW - Histamine H1 Antagonists KW - 0 KW - Cyproheptadine KW - 2YHB6175DO KW - Loratadine KW - 7AJO3BO7QN KW - Terfenadine KW - 7BA5G9Y06Q KW - Astemizole KW - 7HU6337315 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Astemizole -- therapeutic use KW - Astemizole -- pharmacology KW - Terfenadine -- adverse effects KW - Terfenadine -- pharmacology KW - Hypersensitivity, Immediate -- drug therapy KW - Astemizole -- adverse effects KW - Cyproheptadine -- pharmacology KW - Histamine H1 Antagonists -- adverse effects KW - Terfenadine -- therapeutic use KW - Cyproheptadine -- adverse effects KW - Cyproheptadine -- analogs & derivatives KW - Histamine H1 Antagonists -- pharmacology KW - Cyproheptadine -- therapeutic use KW - Histamine H1 Antagonists -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72838052?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+family+physician&rft.atitle=Nonsedating+antihistamines%3A+pharmacology%2C+clinical+efficacy+and+adverse+effects.&rft.au=Kaliner%2C+M+A&rft.aulast=Kaliner&rft.aufirst=M&rft.date=1992-03-01&rft.volume=45&rft.issue=3&rft.spage=1337&rft.isbn=&rft.btitle=&rft.title=American+family+physician&rft.issn=0002838X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-07 N1 - Date created - 1992-04-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Acute gastric mucosal injury associated with the systemic administration of interleukin-4. AN - 72834119; 1542854 AB - Seventy-three patients with advanced malignancy were treated with the recombinant lymphokine interleukin-4 either as the sole immunotherapeutic reagent or in combination with recombinant interleukin-2. Twelve of 84 courses of therapy were complicated by gastroduodenal erosion or ulceration. Three of these courses were associated with significant bleeding, which required multiple red blood cell transfusions and endoscopic therapy. No treatment-related deaths occurred. Eleven of 57 courses administered with concomitant indomethacin and 11 of 62 courses administered with ranitidine resulted in gastroduodenal mucosal injury. No acute change in gastric acid output occurred after one dose of interleukin-4 in patients prospectively evaluated with an indwelling nasogastric tube. An intravenous ranitidine infusion appropriately reduced acid output in these patients. In contrast, we have treated over 650 patients with interleukin-2 and indomethacin without interleukin-4, none of whom developed signs or symptoms of gastroduodenal ulceration. These observations suggest that systemically administered cytokines may exert an effect on the integrity of the gastroduodenal mucosa. JF - Surgery AU - Rubin, J T AU - Lotze, M T AD - Surgery Branch, National Cancer Institute, Bethesda, Md. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 274 EP - 280 VL - 111 IS - 3 SN - 0039-6060, 0039-6060 KW - Interleukin-2 KW - 0 KW - Interleukin-4 KW - 207137-56-2 KW - Abridged Index Medicus KW - Index Medicus KW - Drug Evaluation KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Female KW - Gastric Acid -- secretion KW - Interleukin-4 -- toxicity KW - Stomach Neoplasms -- secondary KW - Interleukin-2 -- therapeutic use KW - Stomach Neoplasms -- therapy KW - Gastric Mucosa -- drug effects KW - Interleukin-2 -- toxicity KW - Gastric Mucosa -- pathology KW - Interleukin-4 -- therapeutic use KW - Stomach Ulcer -- pathology KW - Stomach Ulcer -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72834119?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Surgery&rft.atitle=Acute+gastric+mucosal+injury+associated+with+the+systemic+administration+of+interleukin-4.&rft.au=Rubin%2C+J+T%3BLotze%2C+M+T&rft.aulast=Rubin&rft.aufirst=J&rft.date=1992-03-01&rft.volume=111&rft.issue=3&rft.spage=274&rft.isbn=&rft.btitle=&rft.title=Surgery&rft.issn=00396060&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-09 N1 - Date created - 1992-04-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Insulin-like growth factor I gene expression is induced in astrocytes during experimental demyelination. AN - 72832969; 1371885 AB - To investigate insulin-like growth factor I (IGF-I) and IGF-I receptor gene expression during experimental demyelination and myelin regeneration, young mice were fed cuprizone (( bis(cyclohexanone) oxaldihydrazone )). This copper-chelating agent produces demyelination in the corpus callosum and superior cerebellar peduncles, and when treatment is stopped, there is rapid remyelination. At intervals during cuprizone treatment and recovery, brain sections were hybridized with specific probes and immunostained with antibodies to determine the localization and relative amounts of IGF-I and IGF-I receptor mRNAs and peptides. In untreated littermates, IGF-I and IGF-I receptor mRNAs and peptides were not detected in white matter. In cuprizone-treated mice, high levels of both IGF-I mRNA and peptide were expressed by astrocytes in areas of myelin breakdown. Astrocyte IGF-I expression decreased rapidly during recovery and oligodendroglial expression of myelin-related genes increased. In severely demyelinated areas, immature oligodendroglia exhibited a transient increase in IGF-I receptor mRNA and peptide immunoreactivity during early recovery. This highly specific pattern of IGF-I induction in astrocytes during demyelination and the expression of the IGF-I receptor in regenerating oligodendrocytes during recovery suggest that IGF-I functions in the regulation of oligodendrocyte and myelin metabolism in vivo. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Komoly, S AU - Hudson, L D AU - Webster, H D AU - Bondy, C A AD - Laboratory of Experimental Neuropathology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/03/01/ PY - 1992 DA - 1992 Mar 01 SP - 1894 EP - 1898 VL - 89 IS - 5 SN - 0027-8424, 0027-8424 KW - Glial Fibrillary Acidic Protein KW - 0 KW - Myelin Basic Protein KW - Nerve Tissue Proteins KW - Proteolipids KW - RNA, Messenger KW - Receptors, Cell Surface KW - Receptors, Somatomedin KW - Cuprizone KW - 5N16U7E0AO KW - Insulin-Like Growth Factor I KW - 67763-96-6 KW - 2',3'-Cyclic-Nucleotide Phosphodiesterases KW - EC 3.1.4.- KW - Index Medicus KW - Animals KW - Cuprizone -- pharmacology KW - Gene Expression KW - Glial Fibrillary Acidic Protein -- metabolism KW - Mice KW - Proteolipids -- metabolism KW - Nucleic Acid Hybridization KW - RNA, Messenger -- genetics KW - Receptors, Cell Surface -- metabolism KW - 2',3'-Cyclic-Nucleotide Phosphodiesterases -- metabolism KW - Myelin Basic Protein -- metabolism KW - Nerve Tissue Proteins -- metabolism KW - Receptors, Cell Surface -- genetics KW - Immunoenzyme Techniques KW - Male KW - Insulin-Like Growth Factor I -- genetics KW - Demyelinating Diseases -- genetics KW - Astrocytes -- physiology KW - Demyelinating Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72832969?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Insulin-like+growth+factor+I+gene+expression+is+induced+in+astrocytes+during+experimental+demyelination.&rft.au=Komoly%2C+S%3BHudson%2C+L+D%3BWebster%2C+H+D%3BBondy%2C+C+A&rft.aulast=Komoly&rft.aufirst=S&rft.date=1992-03-01&rft.volume=89&rft.issue=5&rft.spage=1894&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-07 N1 - Date created - 1992-04-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell. 1985 Dec;43(3 Pt 2):721-7 [2416470] Nature. 1990 Sep 6;347(6288):103-4 [2395455] Cell. 1989 Oct 20;59(2):235-8 [2553265] Endocr Rev. 1989 Feb;10(1):68-91 [2666112] J Neurosci Res. 1988 Apr;19(4):483-90 [2838644] Annu Rev Physiol. 1985;47:425-42 [2986537] Endocrinology. 1988 Dec;123(6):2827-33 [3197646] Proc Natl Acad Sci U S A. 1988 Jan;85(1):265-9 [3422422] Proc Natl Acad Sci U S A. 1986 Feb;83(3):822-6 [3511475] J Neurol Sci. 1987 Apr;78(2):125-37 [3553434] Brain Res. 1986 Dec;387(3):231-41 [3828759] Acta Neuropathol. 1984;63(3):240-8 [6205535] Proc Natl Acad Sci U S A. 1978 May;75(5):2521-4 [353815] J Neurosci. 1991 Nov;11(11):3442-55 [1658250] J Neurosci Res. 1991 Jul;29(3):379-89 [1920534] J Cell Biol. 1990 Apr;110(4):1307-17 [2157718] Eur J Biochem. 1990 Jul 5;190(3):445-62 [2197088] Brain Res. 1985 Aug;353(2):257-64 [2412655] J Neurosci Res. 1988 Oct-Dec;21(2-4):210-9 [2464075] Science. 1989 Mar 17;243(4897):1450-5 [2648568] Proc Natl Acad Sci U S A. 1988 Jun;85(11):4066-70 [2897692] Brain Res. 1987 Mar 17;406(1-2):32-42 [3105814] J Neurosci Res. 1988 Oct-Dec;21(2-4):199-209 [3216421] J Neurosci. 1986 May;6(5):1211-9 [3519887] J Biol Chem. 1986 Nov 5;261(31):14539-44 [3771541] J Neurocytol. 1972 Dec;1(4):413-26 [8530973] Am J Pathol. 1979 Jun;95(3):683-96 [453329] Lab Invest. 1978 Dec;39(6):597-612 [739762] Brain Res Mol Brain Res. 1991 Apr;10(1):43-8 [1647481] J Neurosci Res. 1991 Feb;28(2):244-53 [1851850] Development. 1991 Jan;111(1):105-15 [2015788] J Neurosci Res. 1990 Nov;27(3):400-7 [2097382] Mol Endocrinol. 1990 Sep;4(9):1386-98 [2172801] J Neurol Sci. 1987 Jun;79(1-2):141-8 [2440995] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immunohistologic demonstration of myocardial proteins with applications. AN - 72829560; 1371901 AB - The authors used antibodies specific for creatine kinase MB isoenzyme (CK-MB) and myosin light chain-1 (MLC-1) for immunohistologic staining. At appropriate dilutions of antibody, frozen sections of human heart muscle were positive for both CK-MB and MLC-1, whereas sections of human skeletal muscle were negative for both proteins. Staining for both CK-MB and MLC-1 also was demonstrated in an immature teratoma. Furthermore, staining was localized to the rhabdomyosarcomatous elements within the teratoma; other components of the tumor did not stain for CK-MB or MLC-1. Biopsies of skeletal muscle revealed that regenerative, but not intact normal or degenerating, fibers also contained CK-MB and MLC-1. Immunohistologic stains for CK-MB and MLC-1 may be useful as tumor markers and as markers for regenerative muscle fibers. JF - American journal of clinical pathology AU - Emancipator, K AU - Urankar-Nagy, N AU - Leonard, K A AU - Bradford, G AU - Emancipator, S N AD - Clinical Pathology Department, Warren G. Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 376 EP - 380 VL - 97 IS - 3 SN - 0002-9173, 0002-9173 KW - Isoenzymes KW - 0 KW - Muscle Proteins KW - Neoplasm Proteins KW - Platelet-Derived Growth Factor KW - Creatine Kinase KW - EC 2.7.3.2 KW - Myosins KW - EC 3.6.4.1 KW - Abridged Index Medicus KW - Index Medicus KW - Space life sciences KW - Creatine Kinase -- analysis KW - Muscles -- chemistry KW - Rhabdomyosarcoma -- chemistry KW - Humans KW - Myosins -- analysis KW - Platelet-Derived Growth Factor -- analysis KW - Biopsy KW - Regeneration KW - Myosins -- chemistry KW - Muscles -- pathology KW - Teratoma -- chemistry KW - Neoplasm Proteins -- analysis KW - Staining and Labeling KW - Muscles -- physiology KW - Myocardium -- chemistry KW - Muscle Proteins -- analysis KW - Immunologic Techniques UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72829560?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+clinical+pathology&rft.atitle=Immunohistologic+demonstration+of+myocardial+proteins+with+applications.&rft.au=Emancipator%2C+K%3BUrankar-Nagy%2C+N%3BLeonard%2C+K+A%3BBradford%2C+G%3BEmancipator%2C+S+N&rft.aulast=Emancipator&rft.aufirst=K&rft.date=1992-03-01&rft.volume=97&rft.issue=3&rft.spage=376&rft.isbn=&rft.btitle=&rft.title=American+journal+of+clinical+pathology&rft.issn=00029173&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-08 N1 - Date created - 1992-04-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Construction of a umuDC operon substitution mutation in Escherichia coli. AN - 72827030; 1371846 AB - Using a specialized transducing lambda phage, the umuDC operon of Escherichia coli was deleted and replaced with the chloramphenicol acetyltransferase gene. The delta (umuDC)595::cat mutation was subsequently transferred by generalized P1 transduction into a variety of genetic backgrounds. It is concluded that the UmuDC proteins, which are normally required for inducible mutagenesis, are not essential for cell survival. JF - Mutation research AU - Woodgate, R AD - Section on Viruses and Cellular Biology, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 221 EP - 225 VL - 281 IS - 3 SN - 0027-5107, 0027-5107 KW - cat KW - umuDC KW - DNA, Bacterial KW - 0 KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - Genes, Bacterial KW - Blotting, Southern KW - Bacteriophage lambda -- genetics KW - Models, Genetic KW - DNA, Bacterial -- isolation & purification KW - DNA, Bacterial -- genetics KW - Transduction, Genetic KW - Restriction Mapping KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Chromosome Deletion KW - Operon KW - Escherichia coli -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72827030?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+research&rft.atitle=Construction+of+a+umuDC+operon+substitution+mutation+in+Escherichia+coli.&rft.au=Woodgate%2C+R&rft.aulast=Woodgate&rft.aufirst=R&rft.date=1992-03-01&rft.volume=281&rft.issue=3&rft.spage=221&rft.isbn=&rft.btitle=&rft.title=Mutation+research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-03 N1 - Date created - 1992-04-03 N1 - Date revised - 2017-01-13 N1 - Gene symbol - cat; umuDC N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Baculovirus-mediated expression and functional characterization of human NADPH-P450 oxidoreductase. AN - 72819876; 1536559 AB - Human NADPH-P450 oxidoreductase (OR) is an intrinsically membrane-bound flavoprotein that serves to transfer electrons from NADPH to cytochrome P450. OR is also involved in the metabolic activation of chemotherapeutic alkylating agents. The human OR cDNA was engineered into baculovirus and the recombinant virus was used to infect Spodoptera frugiperda (Sf9) cells. Approximately 3.3% of total protein of infected cells was human OR. The enzyme was purified by ion exchange and affinity chromatography to a specific activity of 20 units/mg protein. Baculovirus-expressed OR displayed an absolute spectrum typical of the protein purified from tissue sources. The purified enzyme was able to support P450 activity in a reconstituted lipid vesicle system where maximal P450 activity was achieved at an OR/P450 ratio of 2. When recombinant OR and P450 DNA-containing baculoviruses were used to coinfect Sf9 cells, the OR/P450 ratio needed to achieve half maximal P450 catalytic activity was less than 0.5. These studies demonstrate the utility of baculovirus to analyze the functional and structural relationship of OR and P450. JF - Archives of biochemistry and biophysics AU - Tamura, S AU - Korzekwa, K R AU - Kimura, S AU - Gelboin, H V AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 219 EP - 223 VL - 293 IS - 2 SN - 0003-9861, 0003-9861 KW - Recombinant Proteins KW - 0 KW - DNA KW - 9007-49-2 KW - NADPH-Ferrihemoprotein Reductase KW - EC 1.6.2.4 KW - Index Medicus KW - Animals KW - Recombinant Proteins -- biosynthesis KW - Electron Transport KW - Humans KW - Moths -- genetics KW - Recombinant Proteins -- genetics KW - DNA -- biosynthesis KW - Baculoviridae -- enzymology KW - NADPH-Ferrihemoprotein Reductase -- genetics KW - Baculoviridae -- genetics KW - NADPH-Ferrihemoprotein Reductase -- biosynthesis KW - Genetic Vectors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72819876?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+biochemistry+and+biophysics&rft.atitle=Baculovirus-mediated+expression+and+functional+characterization+of+human+NADPH-P450+oxidoreductase.&rft.au=Tamura%2C+S%3BKorzekwa%2C+K+R%3BKimura%2C+S%3BGelboin%2C+H+V%3BGonzalez%2C+F+J&rft.aulast=Tamura&rft.aufirst=S&rft.date=1992-03-01&rft.volume=293&rft.issue=2&rft.spage=219&rft.isbn=&rft.btitle=&rft.title=Archives+of+biochemistry+and+biophysics&rft.issn=00039861&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-24 N1 - Date created - 1992-03-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Iron chelation in myocardial preservation after ischemia-reperfusion injury: the importance of pretreatment and toxicity. AN - 72818995; 1540057 AB - Oxygen-derived free radicals have been implicated in myocardial ischemia-reperfusion injury. It has been proposed that deferoxamine, an iron chelator, improves myocardial preservation by reducing the iron-catalyzed production of the hydroxyl radical. The objectives of this study were to define the appropriate timing of iron chelation therapy and the dose-response properties of deferoxamine. Isolated working rat hearts were subjected to 25 minutes of normothermic global ischemia. Deferoxamine was given as pretreatment (n = 39; doses of 10 or 30 mg/kg), added to cardioplegic solution (n = 43; doses 0.46 to 1.90 mmol/L), or administered upon reperfusion (n = 52; doses 0.15 to 0.76 mmol/L) and compared with saline controls (n = 25). Deferoxamine pretreatment improved survival at each dose from a control value of 44% to 71% and 72% (p less than 0.05), respectively. A cardioplegia dose of 0.46 mmol/L improved survival from 48% to 75%. Higher doses reduced survival and implied a toxic effect. Reperfusion therapy did not alter survival. Regardless of time of administration, deferoxamine did not improve ventricular function or adenosine triphosphate levels. Deferoxamine given as pretreatment 1 hour before ischemia at doses of 30 mg/kg, and perhaps as low as 10 mg/kg, significantly improved survival. The addition of deferoxamine to cardioplegic solution was safe and may be protective at approximately 0.50 mmol/L; however, toxicity should be considered at concentrations greater than 0.76 mmol/L. These data support the postulate that iron catalysis is involved in the production of oxygen-derived free radicals during ischemia-reperfusion injury. We conclude that pretreatment before ischemia is an important component of iron chelation therapy in myocardial preservation. JF - The Annals of thoracic surgery AU - DeBoer, D A AU - Clark, R E AD - Surgery Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 412 EP - 418 VL - 53 IS - 3 SN - 0003-4975, 0003-4975 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Iron KW - E1UOL152H7 KW - Deferoxamine KW - J06Y7MXW4D KW - Abridged Index Medicus KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Dose-Response Relationship, Drug KW - Adenosine Triphosphate -- metabolism KW - Hemodynamics KW - Male KW - Deferoxamine -- toxicity KW - Chelation Therapy KW - Myocardial Reperfusion Injury -- therapy KW - Myocardial Reperfusion Injury -- metabolism KW - Deferoxamine -- administration & dosage KW - Heart -- physiopathology KW - Myocardial Reperfusion Injury -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72818995?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Annals+of+thoracic+surgery&rft.atitle=Iron+chelation+in+myocardial+preservation+after+ischemia-reperfusion+injury%3A+the+importance+of+pretreatment+and+toxicity.&rft.au=DeBoer%2C+D+A%3BClark%2C+R+E&rft.aulast=DeBoer&rft.aufirst=D&rft.date=1992-03-01&rft.volume=53&rft.issue=3&rft.spage=412&rft.isbn=&rft.btitle=&rft.title=The+Annals+of+thoracic+surgery&rft.issn=00034975&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-01 N1 - Date created - 1992-04-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - L-tryptophan-associated eosinophilic fasciitis prior to the 1989 eosinophilia-myalgia syndrome outbreak. AN - 72818685; 1536667 AB - To investigate the relationship between L-tryptophan (LT) ingestion and eosinophilic fasciitis (EF) occurring prior to the outbreak of eosinophilia-myalgia syndrome in 1989. Interviews and record reviews of 45 EF case-patients and 126 polymyositis patients (controls) diagnosed prior to 1988. Nine case-patients (20%) and no controls recalled taking LT before onset of the disease (odds ratio = infinity, 95% confidence interval = 8.3-infinity). Among EF case-patients, LT ingestion was associated with dyspnea. LT ingestion was associated with EF prior to the 1989 outbreak of eosinophilia-myalgia syndrome. Lung abnormalities may be a distinguishing feature of LT-mediated illness. JF - Arthritis and rheumatism AU - Hibbs, J R AU - Mittleman, B AU - Hill, P AU - Medsger, T A AD - NHLBI/CHB, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 299 EP - 303 VL - 35 IS - 3 SN - 0004-3591, 0004-3591 KW - Tryptophan KW - 8DUH1N11BX KW - Abridged Index Medicus KW - Index Medicus KW - Myositis -- diagnosis KW - Humans KW - Case-Control Studies KW - Middle Aged KW - Male KW - Female KW - Eosinophilia-Myalgia Syndrome -- epidemiology KW - Tryptophan -- adverse effects KW - Tryptophan -- administration & dosage KW - Eosinophilia -- chemically induced KW - Fasciitis -- chemically induced KW - Eosinophilia-Myalgia Syndrome -- etiology KW - Disease Outbreaks UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72818685?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Arthritis+and+rheumatism&rft.atitle=L-tryptophan-associated+eosinophilic+fasciitis+prior+to+the+1989+eosinophilia-myalgia+syndrome+outbreak.&rft.au=Hibbs%2C+J+R%3BMittleman%2C+B%3BHill%2C+P%3BMedsger%2C+T+A&rft.aulast=Hibbs&rft.aufirst=J&rft.date=1992-03-01&rft.volume=35&rft.issue=3&rft.spage=299&rft.isbn=&rft.btitle=&rft.title=Arthritis+and+rheumatism&rft.issn=00043591&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-26 N1 - Date created - 1992-03-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cholera toxin promotes the proliferation of anti-mu antibody-prestimulated human B cells. AN - 72817672; 1310902 AB - The predominant effect of cholera toxin (CT) on cell growth has been postulated to be inhibitory as a result of its induction of intracellular cAMP. We have recently reported that CT selectively enhances surface DR expression while it inhibits anti-mu antibody-induced B lymphocyte proliferation. In the present series of experiments we studied the effect of CT on in vitro preactivated highly purified (greater than 95% CD20+) human B cells. Cholera toxin enhanced thymidine incorporation of anti-mu antibody-preactivated but not of Staphylococcus aureus Cowan I or PMA + ionomycin-preactivated B cells. Concentrations of 100 pg/ml CT stimulated an enhancement of thymidine incorporation equivalent to that of optimal doses of BCGF. The growth factor-like effect of CT required the complete molecule, since binding of purified B subunit (B-CT) to GM1 ganglioside by itself did not reproduce the holotoxin effect. Moreover, B-CT pretreatment of anti-mu antibody-primed cells completely neutralized the holotoxin-enhancing effect. Both PGE2, a physiological agent that stimulates intracellular cAMP elevation, and the cAMP analogue, 8-bromo-cAMP, mimicked the growth-promoting effect of CT. However, the ED50 of CT required to augment proliferation in anti-mu antibody-preactivated human B cells was approximately 100 times less than the ED50 for cAMP formation. These results demonstrate a specific growth factor-like promoting effect of CT on sIg-preactivated highly purified human B cells that may be mediated at least in part through elevation in intracellular cAMP levels. Increased DR expression and stimulation of growth of sIg preactivated B cells may explain some of the adjuvant properties of CT following orally or parenterally administered antigens. JF - Cellular immunology AU - Anastassiou, E D AU - Yamada, H AU - Boumpas, D T AU - Tsokos, G C AU - Thyphronitis, G AU - Balow, J AU - Mond, J J AD - Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 237 EP - 247 VL - 140 IS - 1 SN - 0008-8749, 0008-8749 KW - Antibodies, Monoclonal KW - 0 KW - Interleukin-4 KW - 207137-56-2 KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Ionomycin KW - 56092-81-0 KW - Cholera Toxin KW - 9012-63-9 KW - Cyclic AMP KW - E0399OZS9N KW - Index Medicus KW - Dose-Response Relationship, Drug KW - Humans KW - Interleukin-4 -- pharmacology KW - Cells, Cultured -- immunology KW - Cell Division -- drug effects KW - Cyclic AMP -- analysis KW - Ionomycin -- pharmacology KW - Phorbol 12,13-Dibutyrate -- pharmacology KW - Antibodies, Monoclonal -- immunology KW - Lymphocyte Activation -- drug effects KW - B-Lymphocytes -- drug effects KW - Cholera Toxin -- pharmacology KW - B-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72817672?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cellular+immunology&rft.atitle=Cholera+toxin+promotes+the+proliferation+of+anti-mu+antibody-prestimulated+human+B+cells.&rft.au=Anastassiou%2C+E+D%3BYamada%2C+H%3BBoumpas%2C+D+T%3BTsokos%2C+G+C%3BThyphronitis%2C+G%3BBalow%2C+J%3BMond%2C+J+J&rft.aulast=Anastassiou&rft.aufirst=E&rft.date=1992-03-01&rft.volume=140&rft.issue=1&rft.spage=237&rft.isbn=&rft.btitle=&rft.title=Cellular+immunology&rft.issn=00088749&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-20 N1 - Date created - 1992-03-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - IL-4 regulation of a protein kinase C independent pathway for the generation of alpha CD3-induced activated killer cells. AN - 72817638; 1531452 AB - alpha CD3 induced the generation of activated killer cells from resting T cells. Pretreatment of the splenic responders with PMA, a phorbol ester, depleted protein kinase C and induced unresponsiveness to the generation of alpha CD3-induced activated killer (CD3-AK) cells. Addition of exogenous IL-4 (1 U/ml) restored the cytotoxic response, with the maximal effect achieved with 30 to 100 U/ml. The phenotypes of CD3-AK cells maintained in IL-2 or in IL-4, with or without PMA, were the same: Thy1+ and CD8+. These results were reproduced with purified T cells and purified CD8+ cells, indicating that both the effectors and precursors were CD8+ cells and IL-4 had a selective effect to upregulate the CD8+ cells. Similar results were obtained by using SSP (staurosporine), another PKC inhibitor. At 2 days prior to testing, switching the lymphokine added to 2-week PMA- and IL-2-maintained CD3-AK cells reversed their cytolytic activity: switching from IL-2 to IL-4 restored cytolytic activity, and switching from IL-4 to IL-2 reduced cytolytic activity. The cytolytic activity of these CD3-AK cells correlated with their ability to produce BLT-esterase. In the absence of PMA, CD3-AK cells cultured in either IL-2 or IL-4 were cytolytic and contained high levels of BLT-esterase. In contrast, in the presence of PMA, only the IL-4-maintained CD3-AK cells were cytolytic and produced significant amounts of BLT-esterase. The effect of IL-4 was abrogated by the alpha IL-4 antibody 11B11, which reduced the cytolytic activity of CD3-AK and the ability to produce BLT-esterase. The requirement of IL-2 was less stringent and its major role appeared to be maintaining the cell growth. These findings indicate that IL-4 may participate in the regulation of a PKC-independent pathway for the generation of CD3-AK cells by regulating the production of cytolytic granules. JF - Cellular immunology AU - Ting, C C AU - Hargrove, M E AD - Division of Cancer Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 130 EP - 144 VL - 140 IS - 1 SN - 0008-8749, 0008-8749 KW - Alkaloids KW - 0 KW - Antibodies KW - Antibodies, Monoclonal KW - Antigens, CD3 KW - Antigens, Differentiation, T-Lymphocyte KW - Interleukin-2 KW - Receptors, Antigen, T-Cell KW - Interleukin-4 KW - 207137-56-2 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Granzymes KW - EC 3.4.21.- KW - Serine Endopeptidases KW - Staurosporine KW - H88EPA0A3N KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Antibodies -- immunology KW - Interleukin-2 -- pharmacology KW - Spleen -- cytology KW - Killer Cells, Lymphokine-Activated -- immunology KW - Cell Division -- drug effects KW - Serine Endopeptidases -- analysis KW - Mice KW - Cells, Cultured -- drug effects KW - Protein Kinase C -- immunology KW - Antibodies, Monoclonal -- immunology KW - Lymphocyte Activation -- drug effects KW - Tumor Cells, Cultured -- immunology KW - Killer Cells, Lymphokine-Activated -- drug effects KW - Mice, Inbred C57BL KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Alkaloids -- pharmacology KW - Cytotoxicity, Immunologic -- drug effects KW - Female KW - Interleukin-4 -- pharmacology KW - T-Lymphocytes, Cytotoxic -- immunology KW - Receptors, Antigen, T-Cell -- immunology KW - Antigens, Differentiation, T-Lymphocyte -- immunology KW - T-Lymphocytes, Cytotoxic -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72817638?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cellular+immunology&rft.atitle=IL-4+regulation+of+a+protein+kinase+C+independent+pathway+for+the+generation+of+alpha+CD3-induced+activated+killer+cells.&rft.au=Ting%2C+C+C%3BHargrove%2C+M+E&rft.aulast=Ting&rft.aufirst=C&rft.date=1992-03-01&rft.volume=140&rft.issue=1&rft.spage=130&rft.isbn=&rft.btitle=&rft.title=Cellular+immunology&rft.issn=00088749&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-20 N1 - Date created - 1992-03-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Gene transfer demonstrates that the V gamma 1.1C gamma 4V delta 6C delta T cell receptor is essential for autoreactivity. AN - 72816602; 1371523 AB - Murine T cell lines and hybridomas derived from the epidermis that express the V gamma 1.1C gamma 4V delta 6C delta TCR and may, therefore, recognize an autoantigen, secrete cytokines spontaneously in culture. In addition, activation of these cells requires engagement of the vitronectin receptor (VNR) by extracellular matrix proteins. To further evaluate the role of the TCR, the VNR, and the putative autoantigen in the activation of this T cell subset, we cloned complete cDNA encoding the V gamma 1.1C gamma 4 and V delta 6C delta TCR and transfected the cDNA constructs into a TCR- murine hybridoma and into a TCR- variant of the human Jurkat line. The murine transfectant spontaneously produced IL-2 in culture and IL-2 production could be inhibited by anti-CD3, anticlonotypic mAb to the transfected TCR, and anti-VNR mAb, as well as by RGDS. These results demonstrate that transfection of the gamma delta TCR confers to recipient T cells the phenotype of constitutive activation, as well as dependence on engagement of the VNR as an accessory molecule. In contrast, the Jurkat gamma delta transfectant failed to produce cytokines spontaneously, although the transfected TCR was capable of signal transduction after stimulation by anti-TCR mAb. Surprisingly, neither the murine transfectant nor the human transfectant could be induced to respond to autoantigen bearing cells in coculture assays. One interpretation of these results is that coexpression on the surface of the same cell of the V gamma 1.1 V delta 6 TCR, the VNR, and a putative autoantigen are necessary for T cell activation in this system. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Kikuchi, G E AU - Roberts, K AU - Shevach, E M AU - Coligan, J E AD - Biological Resources Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/03/01/ PY - 1992 DA - 1992 Mar 01 SP - 1302 EP - 1307 VL - 148 IS - 5 SN - 0022-1767, 0022-1767 KW - Autoantigens KW - 0 KW - Interleukin-2 KW - Receptors, Antigen, T-Cell, gamma-delta KW - Receptors, Immunologic KW - Receptors, Vitronectin KW - Interleukin-4 KW - 207137-56-2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Base Sequence KW - Receptors, Immunologic -- physiology KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Interleukin-4 -- biosynthesis KW - Interleukin-2 -- biosynthesis KW - Mice KW - Autoantigens -- analysis KW - Lymphocyte Activation KW - Transfection KW - Receptors, Antigen, T-Cell, gamma-delta -- genetics KW - T-Lymphocytes -- immunology KW - Receptors, Antigen, T-Cell, gamma-delta -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72816602?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Gene+transfer+demonstrates+that+the+V+gamma+1.1C+gamma+4V+delta+6C+delta+T+cell+receptor+is+essential+for+autoreactivity.&rft.au=Kikuchi%2C+G+E%3BRoberts%2C+K%3BShevach%2C+E+M%3BColigan%2C+J+E&rft.aulast=Kikuchi&rft.aufirst=G&rft.date=1992-03-01&rft.volume=148&rft.issue=5&rft.spage=1302&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-30 N1 - Date created - 1992-03-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Developmental exposure to estrogens induces persistent changes in skeletal tissue. AN - 72815880; 1537323 AB - Short-term exposure to estrogens during development has been reported to cause irreversible changes including neoplasia in estrogen target tissues, i.e. reproductive tract and mammary gland. Moreover, it has been established that estrogens have a dramatic effect on bone turnover. The recent demonstration of a low level of estrogen receptor (ER) in bone cells strongly suggests that these estrogenic effects are direct. This report was designed to evaluate whether neonatal exposure to diethylstilbestrol (DES) induces irreversible changes in bone tissue as demonstrated in other specific target organs. We show that short-term exposure of newborn mice (day 1-5) to DES (2 micrograms/pup/day) induces permanent changes in skeletal tissue in adulthood; femurs of DES-treated animals were significantly shorter than age-matched control mice. Furthermore, a significant increment (1.5 fold) in the amount of bone in the femurs (representative of long bone) and vertebrae (representative of short bone) was observed in DES-exposed animals. These data provide further evidence that bone tissue is a specific estrogen target tissue. Finally, we postulate that physiological exposure to estrogens in childhood might be one of the key factors in determining the final peak bone density in adulthood. JF - Endocrinology AU - Migliaccio, S AU - Newbold, R R AU - Bullock, B C AU - McLachlan, J A AU - Korach, K S AD - Receptor Biology Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 1756 EP - 1758 VL - 130 IS - 3 SN - 0013-7227, 0013-7227 KW - Estrogens KW - 0 KW - Diethylstilbestrol KW - 731DCA35BT KW - Abridged Index Medicus KW - Index Medicus KW - Bone Density -- drug effects KW - Animals KW - Diethylstilbestrol -- pharmacology KW - Bone Density -- physiology KW - Mice KW - Animals, Newborn -- growth & development KW - Time Factors KW - Image Processing, Computer-Assisted KW - Female KW - Animals, Newborn -- physiology KW - Pregnancy KW - Estrogens -- pharmacology KW - Bone and Bones -- physiology KW - Bone and Bones -- drug effects KW - Bone Development -- physiology KW - Bone Development -- drug effects KW - Bone and Bones -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72815880?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrinology&rft.atitle=Developmental+exposure+to+estrogens+induces+persistent+changes+in+skeletal+tissue.&rft.au=Migliaccio%2C+S%3BNewbold%2C+R+R%3BBullock%2C+B+C%3BMcLachlan%2C+J+A%3BKorach%2C+K+S&rft.aulast=Migliaccio&rft.aufirst=S&rft.date=1992-03-01&rft.volume=130&rft.issue=3&rft.spage=1756&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-02 N1 - Date created - 1992-04-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of human T cell leukemia virus by the plant flavonoid baicalin (7-glucuronic acid, 5,6-dihydroxyflavone). AN - 72813435; 1371535 AB - The ability of baicalin (7-glucuronic acid, 5,6-dihydroxyflavone), a flavonoid compound purified from the Chinese medicinal herb, Scutellaria baicalensis georgi, to inhibit human T cell leukemia virus type I (HTLV-I) was examined. Baicalin produced concentration-dependent inhibition of HTLV-I replication in productively infected T and B cells. Moreover, baicalin treatment selectively reduced the detectable levels of HTLV-I p19 gag protein in infected cells by greater than 70% at concentrations that produced insignificant effects on total cellular protein and DNA synthesis with no loss in cell viability. Resistance to HTLV-I infection and virus-mediated transformation was noted in uninfected peripheral blood lymphocytes pretreated with baicalin before cocultivation with lethally irradiated chronically infected cells. Baicalin inhibited reverse transcriptase activity in HTLV-I-infected cells as well as the activity of purified reverse transcriptase from Moloney murine leukemia virus and Rous-associated virus type 2. These results suggest that baicalin may be a potential therapeutic agent against HTLV-I-associated T cell diseases. JF - The Journal of infectious diseases AU - Baylor, N W AU - Fu, T AU - Yan, Y D AU - Ruscetti, F W AD - Biological Carcinogenesis and Development Program, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 433 EP - 437 VL - 165 IS - 3 SN - 0022-1899, 0022-1899 KW - Anti-Infective Agents KW - 0 KW - Drugs, Chinese Herbal KW - Flavonoids KW - Gene Products, gag KW - HTLV-I Antigens KW - Retroviridae Proteins, Oncogenic KW - Reverse Transcriptase Inhibitors KW - gag Gene Products, Human Immunodeficiency Virus KW - p19 protein, Human T-lymphotropic virus 1 KW - baicalin KW - 347Q89U4M5 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Retroviridae Proteins, Oncogenic -- antagonists & inhibitors KW - Virus Replication -- drug effects KW - Cells, Cultured KW - Humans KW - Gene Expression Regulation, Viral -- drug effects KW - Gene Products, gag -- antagonists & inhibitors KW - Drugs, Chinese Herbal -- pharmacology KW - Cell Line KW - HTLV-I Antigens -- drug effects KW - Human T-lymphotropic virus 1 -- genetics KW - B-Lymphocytes -- microbiology KW - T-Lymphocytes -- microbiology KW - Human T-lymphotropic virus 1 -- drug effects KW - Anti-Infective Agents -- pharmacology KW - Flavonoids -- pharmacology KW - Human T-lymphotropic virus 1 -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72813435?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+infectious+diseases&rft.atitle=Inhibition+of+human+T+cell+leukemia+virus+by+the+plant+flavonoid+baicalin+%287-glucuronic+acid%2C+5%2C6-dihydroxyflavone%29.&rft.au=Baylor%2C+N+W%3BFu%2C+T%3BYan%2C+Y+D%3BRuscetti%2C+F+W&rft.aulast=Baylor&rft.aufirst=N&rft.date=1992-03-01&rft.volume=165&rft.issue=3&rft.spage=433&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=00221899&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-30 N1 - Date created - 1992-03-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Protein kinase C regulates endothelial cell tube formation on basement membrane matrix, Matrigel. AN - 72799505; 1370939 AB - Human umbilical vein endothelial cells differentiate within 12 h to form capillary-like networks of tube structures when the cells are plated on Matrigel, a mixture of basement membrane proteins. Nothing is known about the intracellular signaling events involved in this differentiation. As a first step to define the process, we investigated the possible role of protein kinase C activation by beta-phorbol 12-myristate 13-acetate (PMA) in regulating the formation of the tube structures. In this model, PMA increased tube formation several-fold in a dose-dependent manner with half-maximum stimulation of tube formation at approximately 5 nM PMA. In the absence of serum, essentially little or no tubes were formed on Matrigel unless PMA was added to the medium. Only active phorbol analogs increased tube formation, while the protein kinase C inhibitor, H-7, blocked tube formation. The protein kinase C activators and inhibitors were effective only when added at or just after plating of the cells and did not affect already formed tubes. This study suggests that protein kinase C is involved in the early events of in vitro endothelial cell tube formation on Matrigel. JF - Experimental cell research AU - Kinsella, J L AU - Grant, D S AU - Weeks, B S AU - Kleinman, H K AD - Laboratory of Cardiovascular Science, National Institute on Aging, Baltimore, Maryland 21224. Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 56 EP - 62 VL - 199 IS - 1 SN - 0014-4827, 0014-4827 KW - Drug Combinations KW - 0 KW - Isoquinolines KW - Laminin KW - Piperazines KW - Proteoglycans KW - matrigel KW - 119978-18-6 KW - 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine KW - 84477-87-2 KW - Collagen KW - 9007-34-5 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Isoquinolines -- pharmacology KW - Blood KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - Kinetics KW - Humans KW - Piperazines -- pharmacology KW - Cell Differentiation -- drug effects KW - Protein Kinase C -- metabolism KW - Protein Kinase C -- antagonists & inhibitors KW - Endothelium, Vascular -- cytology KW - Laminin -- physiology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Proteoglycans -- physiology KW - Neovascularization, Pathologic KW - Collagen -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72799505?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Experimental+cell+research&rft.atitle=Protein+kinase+C+regulates+endothelial+cell+tube+formation+on+basement+membrane+matrix%2C+Matrigel.&rft.au=Kinsella%2C+J+L%3BGrant%2C+D+S%3BWeeks%2C+B+S%3BKleinman%2C+H+K&rft.aulast=Kinsella&rft.aufirst=J&rft.date=1992-03-01&rft.volume=199&rft.issue=1&rft.spage=56&rft.isbn=&rft.btitle=&rft.title=Experimental+cell+research&rft.issn=00144827&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-10 N1 - Date created - 1992-03-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Thin section petrography and microcomputer-assisted image analysis AN - 50277630; 1994-015334 JF - Abstracts with Programs - Geological Society of America AU - Halsor, Sid P AU - Wolfe, Brian P AU - Rasband, Wayne S AU - Anonymous Y1 - 1992/03// PY - 1992 DA - March 1992 SP - 26 PB - Geological Society of America (GSA), Boulder, CO VL - 24 IS - 3 SN - 0016-7592, 0016-7592 KW - petrology KW - microscope methods KW - data processing KW - petrography KW - thin sections KW - image analysis KW - automated analysis KW - 05A:Igneous and metamorphic petrology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/50277630?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ageorefmodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Abstracts+with+Programs+-+Geological+Society+of+America&rft.atitle=Thin+section+petrography+and+microcomputer-assisted+image+analysis&rft.au=Halsor%2C+Sid+P%3BWolfe%2C+Brian+P%3BRasband%2C+Wayne+S%3BAnonymous&rft.aulast=Halsor&rft.aufirst=Sid&rft.date=1992-03-01&rft.volume=24&rft.issue=3&rft.spage=26&rft.isbn=&rft.btitle=&rft.title=Abstracts+with+Programs+-+Geological+Society+of+America&rft.issn=00167592&rft_id=info:doi/ LA - English DB - GeoRef N1 - Conference title - Geological Society of America, Northeastern Section, 27th annual meeting N1 - Copyright - GeoRef, Copyright 2012, American Geosciences Institute. N1 - Date revised - 1994-01-01 N1 - PubXState - CO N1 - Last updated - 2012-06-07 N1 - CODEN - GAAPBC N1 - SubjectsTermNotLitGenreText - automated analysis; data processing; image analysis; microscope methods; petrography; petrology; thin sections ER - TY - JOUR T1 - Heterogenous distribution of fluorescent phorbol ester signal in living sea urchin embryos. AN - 16422693; 2902279 AB - The major protein receptor for the active phorbol esters is the Ca super(2+)/phospholipid-dependent protein kinase (PKC). Limited studies in which fluorescent phorbol esters were employed have suggested that such probes may be useful for studying PKC function in living cells. The role of PKC in sea urchin egg activation has been well described. To gain further insight into PKC function during this process, we used established methods to examine the behavior of BODIPY phorbol-ester under different conditions in eggs from Lytichinus pictus . JF - Biological Bulletin, Marine Biological Laboratory, Woods Hole AU - Connor, J H AU - Olds, J L AU - Lester, D S AU - McPhie, D L AU - Senft, S L AU - Johnston, JA AU - Alkon, D L AD - NINDS/NIH, Bethesda, MD 20892, USA Y1 - 1992/03// PY - 1992 DA - Mar 1992 SP - 365 EP - 366 VL - 183 IS - 2 SN - 0006-3185, 0006-3185 KW - Lytechinus pictus KW - distribution KW - embryos KW - fluorescence KW - function KW - phorbol 12-myristate 13-acetate diesters KW - phorbol ester KW - protein kinase KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Oceanic Abstracts; ASFA 1: Biological Sciences & Living Resources KW - Marine KW - Q1 08246:Physiology, biochemistry, biophysics KW - O 1030:Invertebrates UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16422693?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=Biological+Bulletin%2C+Marine+Biological+Laboratory%2C+Woods+Hole&rft.atitle=Heterogenous+distribution+of+fluorescent+phorbol+ester+signal+in+living+sea+urchin+embryos.&rft.au=Connor%2C+J+H%3BOlds%2C+J+L%3BLester%2C+D+S%3BMcPhie%2C+D+L%3BSenft%2C+S+L%3BJohnston%2C+JA%3BAlkon%2C+D+L&rft.aulast=Connor&rft.aufirst=J&rft.date=1992-03-01&rft.volume=183&rft.issue=2&rft.spage=365&rft.isbn=&rft.btitle=&rft.title=Biological+Bulletin%2C+Marine+Biological+Laboratory%2C+Woods+Hole&rft.issn=00063185&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - embryos; fluorescence; distribution; Marine ER - TY - CONF T1 - CYP1A1 protein and mRNA in teleosts as an environmental bioindicator: Laboratory and environmental studies. AN - 16402108; 2882988 AB - Teleosts are exposed, in the environment, to a number of chemicals that are capable of inducing hepatic cytochrome P450 monooxygenase activity. This indication has been described as a most sensitive biological indicator of the presence of certain classes of chemicals in water. The concept of a bioindicator, as applied here, is derived from the idea that a toxic effect will be manifested at the subcellular level before effects will be apparent at higher levels of biological organization. Laboratory and environmental induction of hepatic cytochrome P450 CYP1A1 (P450IA1) was investigated using catalytic activity, immunodetection and nucleic acid hybridization. Rainbow trout and largemouth bass were exposed, under flow-through conditions, to beta -naphthoflavone ( beta -NF), a known CYP1A1 inducer, at concentrations ranging from 0 multiplied by 625 to 500 mu g beta -NF/liter for periods of 1 to 21 days. JF - Marine environmental research. London AU - Haasch, M L AU - Quardokus, E M AU - Sutherland, LA AU - Goodrich AU - Prince, R AU - Cooper, K R AU - Lech, J J Y1 - 1992/03// PY - 1992 DA - Mar 1992 SP - 139 EP - 145 VL - 34 IS - 1-2 KW - beta -naphthoflavone KW - cytochrome P450 KW - induction KW - RNA KW - bioindicators KW - Pollution Abstracts; Toxicology Abstracts KW - chemical pollution KW - toxicology KW - Pisces KW - environmental monitoring KW - proteins KW - X 24156:Environmental impact KW - P 6000:TOXICOLOGY AND HEALTH UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16402108?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Marine+environmental+research.+London&rft.atitle=CYP1A1+protein+and+mRNA+in+teleosts+as+an+environmental+bioindicator%3A+Laboratory+and+environmental+studies.&rft.au=Haasch%2C+M+L%3BQuardokus%2C+E+M%3BSutherland%2C+LA%3BGoodrich%3BPrince%2C+R%3BCooper%2C+K+R%3BLech%2C+J+J&rft.aulast=Haasch&rft.aufirst=M&rft.date=1992-03-01&rft.volume=34&rft.issue=1-2&rft.spage=139&rft.isbn=&rft.btitle=&rft.title=Marine+environmental+research.+London&rft.issn=01411136&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 ER - TY - JOUR T1 - Forensic Drug Testing For Opiates. IV. Analytical Sensitivity, Specificity, and Accuracy of Commercial Urine Opiate Immunoassays AN - 1093472298; 17185316 AB - Four commercial immunoassays, TDxA registered Opiates (TDx), Coat-A-CountA? Morphine in Urine (CAC), AbuscreenA? Radioimmunoassay for Morphine (ABUS) and EmitA? d.a.u.a,,? Opiate Assay (EMIT), were tested for sensitivity, specificity, and accuracy with urine specimens containing known amounts of opiates and opiate metabolites. The immunoassays were evaluated in a semiquantitative mode by comparison of morphine equivalents to GC/MS assay of free and total morphine and codeine or to target concentrations. In all cases, the apparent sensitivities of the assays were higher than those required for detection of morphine at cutoffs mandated by the Health and Human Services guidelines for testing of Federal workers. The apparent specificities of the immunoassays varied considerably. The CAC assay was found to be highly selective for free morphine, whereas TDx, ABUS, and EMIT demonstrated broad cross-reactivity with other opiates. Comparison of semiquantitative results from the immunoassays with GC/MS data indicated a high degree of accuracy for determination of morphine levels. Generally, the patterns of sensitivity and cross-reactivity were unique for each assay, indicating that a detailed knowledge of assay performance characteristics is necessary for accurate interpretation of forensic urine testing data. JF - Journal of Analytical Toxicology AU - Cone, Edward J AU - Dickerson, Sandra AU - Paul, Buddha D AU - Mitchell, John M AD - P.O. Box 5180, Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland 21224 Y1 - 1992/03// PY - 1992 DA - Mar 1992 SP - 72 EP - 78 PB - Preston Publications, Inc., 6600 W. Touhy Ave. Niles IL 60714 United States VL - 16 IS - 2 SN - 0146-4760, 0146-4760 KW - Toxicology Abstracts KW - Codeine KW - Cross-reactivity KW - Data processing KW - Drugs KW - Forensic science KW - Guanylate cyclase KW - Metabolites KW - Morphine KW - Opiates KW - Radioimmunoassay KW - Urine KW - Workers KW - X 24380:Social Poisons & Drug Abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1093472298?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Analytical+Toxicology&rft.atitle=Forensic+Drug+Testing+For+Opiates.+IV.+Analytical+Sensitivity%2C+Specificity%2C+and+Accuracy+of+Commercial+Urine+Opiate+Immunoassays&rft.au=Cone%2C+Edward+J%3BDickerson%2C+Sandra%3BPaul%2C+Buddha+D%3BMitchell%2C+John+M&rft.aulast=Cone&rft.aufirst=Edward&rft.date=1992-03-01&rft.volume=16&rft.issue=2&rft.spage=72&rft.isbn=&rft.btitle=&rft.title=Journal+of+Analytical+Toxicology&rft.issn=01464760&rft_id=info:doi/ L2 - http://www.ingentaconnect.com/content/oup/jat/1992/00000016/00000002/art00002 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2012-10-19 N1 - SubjectsTermNotLitGenreText - Workers; Guanylate cyclase; Morphine; Data processing; Cross-reactivity; Opiates; Urine; Forensic science; Metabolites; Drugs; Radioimmunoassay; Codeine ER - TY - JOUR T1 - The effects of dNTP pool imbalances on frameshift fidelity during DNA replication. AN - 72816342; 1371272 AB - The use of unequal concentrations of the four deoxynucleoside triphosphates (dNTPs) in DNA polymerization reactions alters base substitution error rates in a predictable way. Less is known about the effects of substrate imbalances on base addition and deletion error rates. Thus, we examined pool bias effects on frameshift fidelity during DNA synthesis catalyzed by replicative DNA polymerases. Imbalanced pools altered the frameshift fidelity of the human immunodeficiency virus type-1 reverse transcriptase. Both mutagenic and antimutagenic effects were observed for minus-one, plus-one, and minus-two nucleotide errors, in a highly sequence-specific manner. Most of this specificity can be rationalized by either of two models. One involves frameshifts initiated by pool bias-induced nucleotide misinsertion, and the other involves pool bias-initiated template-primer slippage. Several examples of complex mutations were also recovered more than once in small mutant collections. These contained closely spaced single-base substitution and minus-one base frameshift changes. The two changes occurred at a frequency much higher than predicted if they were generated independently. This suggests that when the polymerase makes one mistake, the probability that it will make a second mistake within the next few incorporations increases significantly. Perturbation of dNTP pools also affected the frameshift fidelity of the replicative yeast DNA polymerase alpha. In reactions containing a low concentration of one dNTP, the error rate increased for one-nucleotide deletions at homopolymeric template nucleotides complementary to the dNTP whose concentration was low. We extended this approach to determine the frameshift fidelity of simian virus 40 origin-dependent semiconservative replication of double-stranded DNA in extracts of human cells. In reactions performed with an equal concentration of all four dNTPs, replication was highly accurate for minus-one-nucleotide errors. However, when the concentration of one dNTP was decreased, the replication error rate increased at complementary, homopolymeric template positions. This response provides an approach for describing frameshift accuracy during replication of the leading and lagging strands. JF - The Journal of biological chemistry AU - Bebenek, K AU - Roberts, J D AU - Kunkel, T A AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/02/25/ PY - 1992 DA - 1992 Feb 25 SP - 3589 EP - 3596 VL - 267 IS - 6 SN - 0021-9258, 0021-9258 KW - Deoxyribonucleotides KW - 0 KW - DNA KW - 9007-49-2 KW - RNA-Directed DNA Polymerase KW - EC 2.7.7.49 KW - Index Medicus KW - AIDS/HIV KW - Base Sequence KW - HeLa Cells KW - Simian virus 40 -- genetics KW - Humans KW - Molecular Sequence Data KW - HIV-1 -- enzymology KW - RNA-Directed DNA Polymerase -- metabolism KW - Frameshift Mutation KW - Deoxyribonucleotides -- metabolism KW - DNA Replication UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72816342?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=The+effects+of+dNTP+pool+imbalances+on+frameshift+fidelity+during+DNA+replication.&rft.au=Bebenek%2C+K%3BRoberts%2C+J+D%3BKunkel%2C+T+A&rft.aulast=Bebenek&rft.aufirst=K&rft.date=1992-02-25&rft.volume=267&rft.issue=6&rft.spage=3589&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-24 N1 - Date created - 1992-03-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evidence that nucleosomes on the mouse mammary tumor virus promoter adopt specific translational positions. AN - 20742228; 8734159 AB - We have previously demonstrated that an array of six nucleosomes are phased on the mouse mammary tumor virus (MMTV) long terminal repeat (1,2). In this study, we devised a new assay to measure the translational positions of specific nucleosomes on the MMTV promoter. Nucleosome core particles were purified and shown to contain A and B nucleosomal DNA by Taq polymerase primer extension with nucleosome-specific primers. The 5' and 3' boundaries of A and B nucleosomes were measured by extending to the end of the core DNA with internal primers. This approach yielded results consistent with major translational positions of -23 to +123 and -221 to -75 for A and B nucleosomes, respectively. The micrococcal nuclease cleavage patterns of A and B nucleosome regions in isolated nuclei are conserved at base-pair resolution in multiple murine cell lines containing either stable MMTV-reporter chimeras or endogenous proviruses. As the refined nucleosome positions place important transcription factor binding sites at the 3' edge of the B nucleosome and in the nucleosome A/B linker, we propose that linker histone depletion and chromatin unfolding may be required to expose these cis-elements during steroid hormone-induced transcription initiation. Images JF - Nucleic Acids Research AU - Bresnick, E H AU - Rories, C AU - Hager, G L AD - Hormone Action & Oncogenesis Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/02/25/ PY - 1992 DA - 1992 Feb 25 SP - 865 EP - 870 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 20 IS - 4 SN - 0305-1048, 0305-1048 KW - Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - Translation KW - Histones KW - Chromatin KW - Long terminal repeat KW - Core particles KW - Nuclease KW - Steroid hormones KW - Transcription initiation KW - Chimeras KW - Promoters KW - Mouse mammary tumor virus KW - Nucleosomes KW - Transcription factors KW - Boundaries KW - DNA KW - Primers KW - Nuclei KW - Proviruses KW - J 02310:Genetics & Taxonomy KW - V 22300:Methods KW - N 14820:DNA Metabolism & Structure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/20742228?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+Acids+Research&rft.atitle=Evidence+that+nucleosomes+on+the+mouse+mammary+tumor+virus+promoter+adopt+specific+translational+positions.&rft.au=Bresnick%2C+E+H%3BRories%2C+C%3BHager%2C+G+L&rft.aulast=Bresnick&rft.aufirst=E&rft.date=1992-02-25&rft.volume=20&rft.issue=4&rft.spage=865&rft.isbn=&rft.btitle=&rft.title=Nucleic+Acids+Research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2008-12-01 N1 - Last updated - 2015-03-27 N1 - SubjectsTermNotLitGenreText - Translation; Histones; Chromatin; Long terminal repeat; Core particles; Nuclease; Steroid hormones; Transcription initiation; Promoters; Chimeras; Nucleosomes; Transcription factors; DNA; Boundaries; Primers; Nuclei; Proviruses; Mouse mammary tumor virus ER - TY - JOUR T1 - Low frequency of p53 gene mutation in tumors induced by aflatoxin B1 in nonhuman primates. AN - 72810915; 1310637 AB - Aflatoxin B1 has been suggested as a causative agent for a G to T mutation at codon 249 in the p53 gene in human hepatocellular carcinomas from southern Africa and Qidong in China. To test this hypothesis, nine tumors induced by aflatoxin B1 in nonhuman primates were analyzed for mutations in the p53 gene. These included four hepatocellular carcinomas, two cholangiocarcinomas, a spindle cell carcinoma of the bile duct, a hemangioendothelial sarcoma of the liver, and an osteogenic sarcoma of the tibia. None of the tumors showed changes at the third position of codon 249 by cleavage analysis of the HaeIII enzyme site at codon 249. A point mutation was identified in one hepatocellular carcinoma at the second position of codon 175 (G to T transversion) by sequencing analysis of the four conserved domains (II to V) in the p53 gene. These data suggest that mutations in the p53 gene are not necessary in aflatoxin B1 induced hepatocarcinogenesis in nonhuman primates. The occurrence of mutation in codon 249 of the p53 gene in selective samples of human hepatocellular cancers may indicate involvement of environmental carcinogens other than aflatoxin B1 or that hepatitis B virus-related hepatitis is a prerequisite for aflatoxin B1 induction of G to T transversion in codon 249. JF - Cancer research AU - Fujimoto, Y AU - Hampton, L L AU - Luo, L D AU - Wirth, P J AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/02/15/ PY - 1992 DA - 1992 Feb 15 SP - 1044 EP - 1046 VL - 52 IS - 4 SN - 0008-5472, 0008-5472 KW - p53 KW - DNA, Neoplasm KW - 0 KW - Oligodeoxyribonucleotides KW - Aflatoxin B1 KW - 9N2N2Y55MH KW - Index Medicus KW - Animals KW - Osteosarcoma -- chemically induced KW - Macaca fascicularis KW - Bile Duct Neoplasms -- chemically induced KW - Bone Neoplasms -- chemically induced KW - Exons KW - Liver Neoplasms -- chemically induced KW - Liver Neoplasms, Experimental -- chemically induced KW - DNA, Neoplasm -- isolation & purification KW - Hemangioendothelioma -- chemically induced KW - Polymerase Chain Reaction KW - Base Sequence KW - Adenoma, Bile Duct -- chemically induced KW - Molecular Sequence Data KW - Introns KW - DNA, Neoplasm -- genetics KW - Macaca mulatta KW - Carcinoma -- chemically induced KW - Genes, p53 -- drug effects KW - Neoplasms, Experimental -- genetics KW - Aflatoxin B1 -- toxicity KW - Mutagenesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72810915?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Low+frequency+of+p53+gene+mutation+in+tumors+induced+by+aflatoxin+B1+in+nonhuman+primates.&rft.au=Fujimoto%2C+Y%3BHampton%2C+L+L%3BLuo%2C+L+D%3BWirth%2C+P+J%3BThorgeirsson%2C+S+S&rft.aulast=Fujimoto&rft.aufirst=Y&rft.date=1992-02-15&rft.volume=52&rft.issue=4&rft.spage=1044&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-17 N1 - Date created - 1992-03-17 N1 - Date revised - 2017-01-13 N1 - Gene symbol - p53 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Diverse biologic properties imparted by the c-fgr proto-oncogene. AN - 72807973; 1737799 AB - The c-fgr proto-oncogene specifies a nonreceptor protein-tyrosine kinase, p55c-fgr, a member of the src family. In the present study, we have mutagenized c-fgr to mimic alterations found at the 3' end of the v-fgr oncogene and have investigated the biologic effects of normal and mutant p55c-fgr expression. Genes lacking 10 or 13 codons at the 3' end, as well as a gene encoding phenylalanine instead of tyrosine at codon 523, were potent oncogenes when transfected into NIH 3T3 cells. Specific enzymatic activities of the more highly transforming gene products were 3-4-fold greater than that of p55c-fgr. In vivo, the amount of tyrosine phosphorylation of cellular proteins was directly proportional to potency in focus-forming assays. These findings are the first to identify highly transforming mutations of the c-fgr proto-oncogene. The proto-oncogene was also active in transforming assays, demonstrably greater than that of a kinase-deficient mutant. Foci arising in c-fgr-transfected cultures expressed abundant enzyme that was normal by a number of criteria. In addition, growth rates for cells expressing p55c-fgr were restricted, as compared with cells expressing a kinase-deficient protein or cells transformed by proteins with high specific enzymatic activities. Thus, enzymatically active p55c-fgr can simultaneously activate transforming and growth inhibitory pathways. JF - The Journal of biological chemistry AU - Sartor, O AU - Moriuchi, R AU - Sameshima, J H AU - Severino, M AU - Gutkind, J S AU - Robbins, K C AD - Laboratory of Cellular Development and Oncology, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/02/15/ PY - 1992 DA - 1992 Feb 15 SP - 3460 EP - 3465 VL - 267 IS - 5 SN - 0021-9258, 0021-9258 KW - c-fgr KW - Oligodeoxyribonucleotides KW - 0 KW - Proto-Oncogene Proteins KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - proto-oncogene proteins c-fgr KW - EC 2.7.10.2 KW - src-Family Kinases KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Gene Expression KW - Mice KW - Plasmids KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Transfection KW - Kinetics KW - Molecular Sequence Data KW - Cell Transformation, Neoplastic KW - Cell Division KW - Proto-Oncogene Proteins -- biosynthesis KW - Protein-Tyrosine Kinases -- genetics KW - Proto-Oncogene Proteins -- isolation & purification KW - Proto-Oncogenes KW - Proto-Oncogene Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72807973?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Diverse+biologic+properties+imparted+by+the+c-fgr+proto-oncogene.&rft.au=Sartor%2C+O%3BMoriuchi%2C+R%3BSameshima%2C+J+H%3BSeverino%2C+M%3BGutkind%2C+J+S%3BRobbins%2C+K+C&rft.aulast=Sartor&rft.aufirst=O&rft.date=1992-02-15&rft.volume=267&rft.issue=5&rft.spage=3460&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-17 N1 - Date created - 1992-03-17 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-fgr N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Stem cell factor increases colony-forming unit-spleen number in vitro in synergy with interleukin-6, and in vivo in Sl/Sld mice as a single factor. AN - 72805201; 1371079 AB - Hematopoiesis is thought to be modulated by interactions of progenitor cells with hematopoietic growth factors. We have shown that colony-forming units-spleen (CFU-S) and repopulating stem cells require interleukin-3 (IL-3) to survive in vitro, and that CFU-S number and long-term repopulating ability can be increased by culture in the combination of IL-3 and IL-6. In this report, we describe the effects of stem cell factor (SCF) on CFU-S and repopulating stem cells. Injection of SCF into anemic Sl/Sld mice caused a twofold and 20-fold increase in CFU-S number in the bone marrow and spleen of treated animals, respectively. After 6 days in suspension culture, CFU-S number increased threefold in cultures supplemented with SCF and IL-6, or SCF, IL-3, and IL-6 relative to the number at day 0. The long-term repopulating ability of cells cultured in SCF, IL-3, and IL-6 was approximately sevenfold better than that of cells cultured in IL-3 or SCF. Similar experiments were performed on populations of bone marrow cells enriched for, or depleted of, CFU-S by elutriation and lineage subtraction. The combination of SCF and IL-6 increased CFU-S number approximately fourfold to eightfold in the CFU-S-enriched fraction, but had no effect on the CFU-S-depleted cells. These results show that SCF alone can increase CFU-S number in vivo, and in combination with other growth factors increases CFU-S numbers in vitro. JF - Blood AU - Bodine, D M AU - Orlic, D AU - Birkett, N C AU - Seidel, N E AU - Zsebo, K M AD - Clinical Hematology Branch NHLBI, Bethesda, MD 20892. Y1 - 1992/02/15/ PY - 1992 DA - 1992 Feb 15 SP - 913 EP - 919 VL - 79 IS - 4 SN - 0006-4971, 0006-4971 KW - Hematopoietic Cell Growth Factors KW - 0 KW - Interleukin-3 KW - Interleukin-6 KW - Recombinant Proteins KW - Stem Cell Factor KW - Abridged Index Medicus KW - Index Medicus KW - Bone Marrow Cells KW - Animals KW - Mice, Mutant Strains KW - Recombinant Proteins -- pharmacology KW - Cell Count KW - Cells, Cultured KW - Interleukin-3 -- pharmacology KW - Mice, Inbred C57BL KW - Mice KW - Drug Synergism KW - Colony-Forming Units Assay KW - Cell Division KW - Spleen -- cytology KW - Hematopoietic Stem Cells -- cytology KW - Interleukin-6 -- pharmacology KW - Hematopoietic Cell Growth Factors -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72805201?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Blood&rft.atitle=Stem+cell+factor+increases+colony-forming+unit-spleen+number+in+vitro+in+synergy+with+interleukin-6%2C+and+in+vivo+in+Sl%2FSld+mice+as+a+single+factor.&rft.au=Bodine%2C+D+M%3BOrlic%2C+D%3BBirkett%2C+N+C%3BSeidel%2C+N+E%3BZsebo%2C+K+M&rft.aulast=Bodine&rft.aufirst=D&rft.date=1992-02-15&rft.volume=79&rft.issue=4&rft.spage=913&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-16 N1 - Date created - 1992-03-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transplantation of bone marrow cells from transgenic mice expressing the human MDR1 gene results in long-term protection against the myelosuppressive effect of chemotherapy in mice. AN - 72801749; 1737094 AB - Many human cancers that are initially responsive to chemotherapy eventually fail to respond to treatment. For some drugs, dose escalation that may be required for a cure cannot be achieved because sensitive tissues such as bone marrow (BM) limit cytotoxic therapy. Approaches to prevent or circumvent BM toxicity are therefore a high priority of research on dose escalation protocols. In this study, we have transplanted BM cells from transgenic mice that constitutively express physiologic amounts of a functional human multidrug resistance (MDR1) cDNA to lethally irradiated C57BL/6 x SJL F1 mice (n = 36). From 6 weeks to 10 months after the transplant, all animals contained MDR1 DNA in spleen and BM specimens as indicated by Southern blot analysis, and expressed MDR1 messenger RNA in BM samples as detected by slot blot analysis. In addition, these animals were resistant to the myelosuppressive effect of doxorubicin, daunomycin, taxol, vinblastine, vincristine, etoposide, and actinomycin D, whereas control animals that were reconstituted with normal BM were drug sensitive. Finally, the chemoprotection afforded by the MDR1 gene could readily be reversed by adding chemosensitizers such as cyclosporin A and R-verapamil to chemotherapy. Hence, it appears that BM cells expressing the human MDR1 gene maintain this function after transplantation to host animals for a minimum of 10 months, and confer multidrug resistance to these BM recipients. This selective advantage conferred by expression of the MDR1 cDNA suggests a strategy for the use of MDR1 gene therapy in cancer chemotherapy and for the introduction of otherwise nonselectable genes into BM. JF - Blood AU - Mickisch, G H AU - Aksentijevich, I AU - Schoenlein, P V AU - Goldstein, L J AU - Galski, H AU - Stahle, C AU - Sachs, D H AU - Pastan, I AU - Gottesman, M M AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/02/15/ PY - 1992 DA - 1992 Feb 15 SP - 1087 EP - 1093 VL - 79 IS - 4 SN - 0006-4971, 0006-4971 KW - MDR1 KW - Antineoplastic Agents KW - 0 KW - RNA, Messenger KW - Cyclosporine KW - 83HN0GTJ6D KW - DNA KW - 9007-49-2 KW - Verapamil KW - CJ0O37KU29 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Spleen -- chemistry KW - Humans KW - DNA -- analysis KW - RNA, Messenger -- analysis KW - Mice KW - Verapamil -- pharmacology KW - Mice, Transgenic KW - Leukocyte Count KW - Blotting, Southern KW - Cyclosporine -- pharmacology KW - DNA -- genetics KW - Mice, Inbred C57BL KW - Time Factors KW - Drug Resistance -- genetics KW - Gene Expression KW - Bone Marrow -- chemistry KW - Bone Marrow -- drug effects KW - Antineoplastic Agents -- pharmacology KW - Bone Marrow Transplantation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72801749?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Blood&rft.atitle=Transplantation+of+bone+marrow+cells+from+transgenic+mice+expressing+the+human+MDR1+gene+results+in+long-term+protection+against+the+myelosuppressive+effect+of+chemotherapy+in+mice.&rft.au=Mickisch%2C+G+H%3BAksentijevich%2C+I%3BSchoenlein%2C+P+V%3BGoldstein%2C+L+J%3BGalski%2C+H%3BStahle%2C+C%3BSachs%2C+D+H%3BPastan%2C+I%3BGottesman%2C+M+M&rft.aulast=Mickisch&rft.aufirst=G&rft.date=1992-02-15&rft.volume=79&rft.issue=4&rft.spage=1087&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-16 N1 - Date created - 1992-03-16 N1 - Date revised - 2017-01-13 N1 - Gene symbol - MDR1 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - GTP but not GDP analogues promote association of ADP-ribosylation factors, 20-kDa protein activators of cholera toxin, with phospholipids and PC-12 cell membranes. AN - 72799606; 1737779 AB - ADP-ribosylation factors (ARFs) are a family of approximately 20-kDa guanine nucleotide-binding proteins initially identified by their ability to enhance cholera toxin ADP-ribosyltransferase activity in the presence of GTP. ARFs have been purified from both membrane and cytosolic fractions. ARF purified from bovine brain cytosol requires phospholipid plus detergent for high affinity guanine nucleotide binding and for optimal enhancement of cholera toxin ADP-ribosyltransferase activity. The phospholipid requirements, combined with a putative role for ARF in vesicular transport, suggested that the soluble protein might interact reversibly with membranes. A polyclonal antibody against purified bovine ARF (sARF II) was used to detect ARF by immunoblot in membrane and soluble fractions from rat pheochromocytoma (PC-12) cell homogenates. ARF was predominantly cytosolic but increased in membranes during incubation of homogenates with nonhydrolyzable GTP analogues guanosine 5'-O-(3-thiotriphosphate), guanylyl-(beta gamma-imido)-diphosphate, and guanylyl-(beta gamma-methylene)-diphosphate, and to a lesser extent, adenosine 5'-O-(3-thiotriphosphate). GTP, GDP, GMP, and ATP were inactive. Cytosolic ARF similarly associated with added phosphatidylserine, phosphatidylinositol, or cardiolipin in GTP gamma S-dependent fashion. ARF binding to phosphatidylserine was reversible and coincident with stimulation of cholera toxin-catalyzed ADP-ribosylation. These observations may reflect a mechanism by which ARF could cycle between soluble and membrane compartments in vivo. JF - The Journal of biological chemistry AU - Walker, M W AU - Bobak, D A AU - Tsai, S C AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/02/15/ PY - 1992 DA - 1992 Feb 15 SP - 3230 EP - 3235 VL - 267 IS - 5 SN - 0021-9258, 0021-9258 KW - Adenine Nucleotides KW - 0 KW - Carrier Proteins KW - Guanine Nucleotides KW - Membrane Lipids KW - Phospholipids KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Cholera Toxin KW - 9012-63-9 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - ADP-Ribosylation Factors KW - EC 3.6.5.2 KW - Index Medicus KW - Animals KW - Carrier Proteins -- metabolism KW - Electrophoresis, Polyacrylamide Gel KW - Adenosine Diphosphate Ribose -- metabolism KW - Protein Binding KW - Molecular Weight KW - PC12 Cells KW - Adenine Nucleotides -- pharmacology KW - GTP-Binding Proteins -- metabolism KW - GTP-Binding Proteins -- isolation & purification KW - Phospholipids -- metabolism KW - Membrane Lipids -- metabolism KW - Cholera Toxin -- pharmacology KW - Cell Membrane -- metabolism KW - Guanine Nucleotides -- pharmacology KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72799606?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=GTP+but+not+GDP+analogues+promote+association+of+ADP-ribosylation+factors%2C+20-kDa+protein+activators+of+cholera+toxin%2C+with+phospholipids+and+PC-12+cell+membranes.&rft.au=Walker%2C+M+W%3BBobak%2C+D+A%3BTsai%2C+S+C%3BMoss%2C+J%3BVaughan%2C+M&rft.aulast=Walker&rft.aufirst=M&rft.date=1992-02-15&rft.volume=267&rft.issue=5&rft.spage=3230&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-17 N1 - Date created - 1992-03-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A deletion in the extracellular domain of the alpha platelet-derived growth factor (PDGF) receptor differentially impairs PDGF-AA and PDGF-BB binding affinities. AN - 72795219; 1310677 AB - 32D cells transfected with the human alpha platelet-derived growth factor receptor (alpha PDGFR) bind PDGF-AA, -AB, and -BB isoforms with high affinity, and the binding of each can be efficiently competed by all three isoforms. In an effort to develop better understanding of spatial relationships of binding sites for PDGF-AA and -BB, we constructed an alpha PDGFR mutant which deleted amino acids 150-189 within its extracellular domain. This mutant showed a marked decrease in high affinity binding sites for PDGF-AA without comparable alteration in affinity for PDGF-BB. These findings imply that the high affinity binding sites for PDGF-AA and PDGF-BB in the alpha PDGFR extracellular domain are not structurally coincident. JF - The Journal of biological chemistry AU - Heidaran, M A AU - Yu, J C AU - Jensen, R A AU - Pierce, J H AU - Aaronson, S A AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/02/15/ PY - 1992 DA - 1992 Feb 15 SP - 2884 EP - 2887 VL - 267 IS - 5 SN - 0021-9258, 0021-9258 KW - Oligodeoxyribonucleotides KW - 0 KW - Platelet-Derived Growth Factor KW - Receptors, Cell Surface KW - Recombinant Proteins KW - Receptors, Platelet-Derived Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Humans KW - Amino Acid Sequence KW - Oligodeoxyribonucleotides -- chemical synthesis KW - DNA Replication -- drug effects KW - Binding Sites KW - Mutagenesis, Site-Directed KW - Polymerase Chain Reaction KW - Base Sequence KW - Transfection KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Molecular Sequence Data KW - Cell Line KW - Receptors, Cell Surface -- metabolism KW - Platelet-Derived Growth Factor -- metabolism KW - Chromosome Deletion KW - Platelet-Derived Growth Factor -- pharmacology KW - Receptors, Cell Surface -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72795219?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=A+deletion+in+the+extracellular+domain+of+the+alpha+platelet-derived+growth+factor+%28PDGF%29+receptor+differentially+impairs+PDGF-AA+and+PDGF-BB+binding+affinities.&rft.au=Heidaran%2C+M+A%3BYu%2C+J+C%3BJensen%2C+R+A%3BPierce%2C+J+H%3BAaronson%2C+S+A&rft.aulast=Heidaran&rft.aufirst=M&rft.date=1992-02-15&rft.volume=267&rft.issue=5&rft.spage=2884&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-17 N1 - Date created - 1992-03-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Requirement for GLY-60 of Escherichia coli adenylyl cyclase for ATP binding and catalytic activity. AN - 72824422; 1540166 AB - The region of Escherichia coli adenylyl cyclase spanned by glycine-55 to threonine-65 was tested for its importance for enzyme activity. Site-directed mutagenesis was used to replace glycine-55 and glycine-60 as well as lysine-59, leucine-63 and threonine-65 with other amino acids. While substitution of glycine-55 with aspartic acid produced no significant change in kinetic parameters, the change of glycine-60 to aspartic acid or asparagine eliminated binding to 8-azido-ATP and decreased the Vmax (two orders of magnitude) and Km (factor of four-five). Smaller effects on kinetic parameters were observed with substitutions of lysine-59, leucine-63 or threonine-65. JF - Biochemical and biophysical research communications AU - Amin, N AU - Peterkofsky, A AD - Laboratory of Biochemical Genetics, National Heart, Lung and Blood Institute, Bethesda, MD 20892. Y1 - 1992/02/14/ PY - 1992 DA - 1992 Feb 14 SP - 1218 EP - 1225 VL - 182 IS - 3 SN - 0006-291X, 0006-291X KW - Azides KW - 0 KW - Oligodeoxyribonucleotides KW - Recombinant Proteins KW - 8-azidoadenosine 5'-triphosphate KW - 53696-59-6 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Glycine KW - TE7660XO1C KW - Index Medicus KW - Recombinant Proteins -- isolation & purification KW - Azides -- metabolism KW - Base Sequence KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Restriction Mapping KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Plasmids KW - Binding Sites KW - Mutagenesis, Site-Directed KW - Adenosine Triphosphate -- analogs & derivatives KW - Adenosine Triphosphate -- metabolism KW - Adenylyl Cyclases -- metabolism KW - Escherichia coli -- genetics KW - Adenylyl Cyclases -- isolation & purification KW - Adenylyl Cyclases -- genetics KW - Escherichia coli -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72824422?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+biophysical+research+communications&rft.atitle=Requirement+for+GLY-60+of+Escherichia+coli+adenylyl+cyclase+for+ATP+binding+and+catalytic+activity.&rft.au=Amin%2C+N%3BPeterkofsky%2C+A&rft.aulast=Amin&rft.aufirst=N&rft.date=1992-02-14&rft.volume=182&rft.issue=3&rft.spage=1218&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+biophysical+research+communications&rft.issn=0006291X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-27 N1 - Date created - 1992-03-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ethanol inhibition of N-methyl-D-aspartate-activated ion current in rat hippocampal neurons is not competitive with glycine. AN - 73011310; 1377089 AB - The interaction of ethanol with glycine at the N-methyl-D-aspartate (NMDA)-activated ion channel was investigated in voltage-clamped rat cultured hippocampal neurons. As shown previously, glycine increased, and ethanol inhibited, the NMDA-activated current in these cells. Concentration-response data for glycine (0.1-100 microM) indicate that the inhibition of NMDA-activated current by ethanol does not involve a competitive interaction with glycine. Thus, ethanol appears to inhibit NMDA-activated current at a locus different from the glycine modulatory site. JF - Brain research AU - Peoples, R W AU - Weight, F F AD - Section of Electrophysiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852. Y1 - 1992/02/07/ PY - 1992 DA - 1992 Feb 07 SP - 342 EP - 344 VL - 571 IS - 2 SN - 0006-8993, 0006-8993 KW - Ion Channels KW - 0 KW - Ethanol KW - 3K9958V90M KW - N-Methylaspartate KW - 6384-92-5 KW - Glycine KW - TE7660XO1C KW - Index Medicus KW - Rats KW - Fetus KW - Animals KW - Drug Interactions KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - Kinetics KW - Hippocampus -- physiology KW - N-Methylaspartate -- pharmacology KW - Glycine -- pharmacology KW - Ethanol -- pharmacology KW - Neurons -- drug effects KW - Ion Channels -- drug effects KW - Neurons -- physiology KW - N-Methylaspartate -- antagonists & inhibitors KW - Ion Channels -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73011310?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Ethanol+inhibition+of+N-methyl-D-aspartate-activated+ion+current+in+rat+hippocampal+neurons+is+not+competitive+with+glycine.&rft.au=Peoples%2C+R+W%3BWeight%2C+F+F&rft.aulast=Peoples&rft.aufirst=R&rft.date=1992-02-07&rft.volume=571&rft.issue=2&rft.spage=342&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-24 N1 - Date created - 1992-07-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of growth by transforming growth factor-beta following fusion of two nonresponsive human carcinoma cell lines. Implication of the type II receptor in growth inhibitory responses. AN - 72786796; 1370826 AB - Loss of growth regulation by transforming growth factor-beta (TGF-beta) may be an important step in carcinogenesis. We have used a cell fusion system to show that inhibition of growth by TGF-beta can be restored to carcinoma cell lines that are unresponsive to the inhibitory effects of TGF-beta. In a previous study, the EJ bladder carcinoma line was fused to the SW480 colon adenocarcinoma line and found to produce nontumorigenic hybrid cells along with one hybrid cell clone of low tumorigenicity. Here we show that the capacity of the nontumorigenic hybrid cells to respond to either TGF-beta 1 or TGF-beta 2 has been restored, while the parental or tumorigenic hybrid cells show little or no inhibition of growth following TGF-beta treatment. Cross-linking analyses with labeled TGF-beta 1 demonstrated much higher levels of the type II (85 kDa) receptor in the hybrid cells compared with the parental tumor lines. Both the parental and tumorigenic hybrid cell lines were capable of responding to TGF-beta as evidenced by increased levels of mRNA for fibronectin, type IV collagenase, and plasminogen activator inhibitor after treatment with TGF-beta 1. These results suggest that the type II receptor is necessary for mediating the effects of TGF-beta on inhibition of growth but not on gene activation of the hybrid cells. JF - The Journal of biological chemistry AU - Geiser, A G AU - Burmester, J K AU - Webbink, R AU - Roberts, A B AU - Sporn, M B AD - Laboratory of Chemoprevention, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/02/05/ PY - 1992 DA - 1992 Feb 05 SP - 2588 EP - 2593 VL - 267 IS - 4 SN - 0021-9258, 0021-9258 KW - Receptors, Cell Surface KW - 0 KW - Receptors, Transforming Growth Factor beta KW - Transforming Growth Factor beta KW - RNA KW - 63231-63-0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Blotting, Northern KW - Tumor Cells, Cultured KW - Humans KW - Electrophoresis, Agar Gel KW - Nucleic Acid Hybridization KW - DNA -- biosynthesis KW - Transforming Growth Factor beta -- physiology KW - Cell Division -- physiology KW - Transforming Growth Factor beta -- metabolism KW - Receptors, Cell Surface -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72786796?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Inhibition+of+growth+by+transforming+growth+factor-beta+following+fusion+of+two+nonresponsive+human+carcinoma+cell+lines.+Implication+of+the+type+II+receptor+in+growth+inhibitory+responses.&rft.au=Geiser%2C+A+G%3BBurmester%2C+J+K%3BWebbink%2C+R%3BRoberts%2C+A+B%3BSporn%2C+M+B&rft.aulast=Geiser&rft.aufirst=A&rft.date=1992-02-05&rft.volume=267&rft.issue=4&rft.spage=2588&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-03 N1 - Date created - 1992-03-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Labelling and recording from dissociated target-specific rat superior cervical ganglion neurons. AN - 73050403; 1378213 AB - A population of neurons was retrogradely labelled in the superior cervical ganglia (SCG) of the adult rat following the injection of the fluorescent dye Fast blue into the submandibular salivary glands (SMG). The neurons retained the fluorescent label following dissociation and culture. Electrical and chemosensitive properties of the labelled neurons were studied with the whole-cell patch-clamp technique. JF - Neuroscience letters AU - Luebke, J I AU - Weight, F F AU - Aguayo, L G AD - Section of Electrophysiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852. Y1 - 1992/02/03/ PY - 1992 DA - 1992 Feb 03 SP - 210 EP - 214 VL - 135 IS - 2 SN - 0304-3940, 0304-3940 KW - Amidines KW - 0 KW - Ion Channels KW - diamidino compound 253-50 KW - Tetrodotoxin KW - 4368-28-9 KW - Acetylcholine KW - N9YNS0M02X KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Submandibular Gland -- anatomy & histology KW - Ion Channels -- drug effects KW - Submandibular Gland -- innervation KW - Acetylcholine -- pharmacology KW - Electrophysiology KW - Tetrodotoxin -- pharmacology KW - Ganglia, Sympathetic -- cytology KW - Neurons -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73050403?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+letters&rft.atitle=Labelling+and+recording+from+dissociated+target-specific+rat+superior+cervical+ganglion+neurons.&rft.au=Luebke%2C+J+I%3BWeight%2C+F+F%3BAguayo%2C+L+G&rft.aulast=Luebke&rft.aufirst=J&rft.date=1992-02-03&rft.volume=135&rft.issue=2&rft.spage=210&rft.isbn=&rft.btitle=&rft.title=Neuroscience+letters&rft.issn=03043940&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-07 N1 - Date created - 1992-08-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Housing, Gentrification and Urban Regeneration Policies AN - 918041046; 13500504 AB - The paper examines the role of housing in recent urban regeneration policies and the question of whether this involves a process of gentrification. Using examples from Tyneside, it notes the emphasis on riverside and city centre locations away from established residential areas, and on high-cost housing for sale. It is suggested, though, that this is not gentrification in the most direct sense, in that it does not displace or reduce housing opportunities for low-income residents. Evaluation must take account of non-housing issues, such as the employment effects and the political and ideological implications of these housing policies. JF - Urban Studies AU - Cameron, Stuart AD - Department of Town and Country Planning, University of Newcastle upon Tyne, Newcastle upon Tyne NEI 7RU, UK Y1 - 1992/02// PY - 1992 DA - Feb 1992 SP - 3 EP - 14 PB - Sage Publications, Inc., 2455 Teller Road Thousand Oaks CA 91320 USA VL - 29 IS - 1 SN - 0042-0980, 0042-0980 KW - Environment Abstracts KW - employment KW - Housing KW - Politics KW - Socioeconomics KW - urban renewal KW - Residential areas KW - housing policy KW - Urban areas KW - ENA 09:Land Use & Planning UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/918041046?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvabstractsmodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Urban+Studies&rft.atitle=Housing%2C+Gentrification+and+Urban+Regeneration+Policies&rft.au=Cameron%2C+Stuart&rft.aulast=Cameron&rft.aufirst=Stuart&rft.date=1992-02-01&rft.volume=29&rft.issue=1&rft.spage=3&rft.isbn=&rft.btitle=&rft.title=Urban+Studies&rft.issn=00420980&rft_id=info:doi/10.1080%2F00420989220080011 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-01-01 N1 - Last updated - 2012-03-29 N1 - SubjectsTermNotLitGenreText - urban renewal; employment; Housing; Politics; Residential areas; housing policy; Socioeconomics; Urban areas DO - http://dx.doi.org/10.1080/00420989220080011 ER - TY - JOUR T1 - Simple reaction time to focal transcranial magnetic stimulation. Comparison with reaction time to acoustic, visual and somatosensory stimuli. AN - 85230550; pmid-1559148 AB - We studied the effect of different go-signals on the reaction time in nine normal human subjects trained to respond by rapidly flexing one arm. Reaction times to auditory stimuli were shorter than those to visual or somatosensory stimuli, and were inversely correlated with the stimulus intensity. The reaction time was longest to a transcranial (magnetic or electric) stimulus delivered over the contralateral motor cortex that was sufficiently strong to induce a motor evoked potential in the responding biceps. Conversely, reaction time was shortest to either subthreshold transcranial stimulation over the same scalp position or to transcranial stimulation over the ipsilateral motor cortex regardless of intensity. Suprathreshold transcranial stimulation to the motor cortex seems to transiently inhibit the neurons responsible for initiation of motor programs involving muscles in which motor evoked potentials have been induced, thereby prolonging the reaction time. On the other hand, a subthreshold stimulus either disinhibits or directly activates such neurons leading to a shorter reaction time. Transcallosal connections between the motor cortices may account for the short reaction time to ipsilateral transcranial stimulation. JF - Brain AU - Pascual-Leone, A AU - Brasil-Neto, J P AU - Valls-Solé J AU - Cohen, L G AU - Hallett, M AD - Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 109 EP - 122 VL - 115 Pt 1 SN - 0006-8950, 0006-8950 KW - Somatosensory Cortex KW - Human KW - Electric Stimulation KW - Evoked Potentials, Somatosensory KW - Auditory Perception KW - Motor Cortex KW - Evoked Potentials, Visual KW - Adult KW - Motor Activity KW - Evoked Potentials, Auditory KW - Support, Non-U.S. Gov't KW - Acoustic Stimulation KW - Male KW - Female KW - Visual Perception KW - Reaction Time KW - Magnetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85230550?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain&rft.atitle=Simple+reaction+time+to+focal+transcranial+magnetic+stimulation.+Comparison+with+reaction+time+to+acoustic%2C+visual+and+somatosensory+stimuli.&rft.au=Pascual-Leone%2C+A%3BBrasil-Neto%2C+J+P%3BValls-Sol%C3%A9+J%3BCohen%2C+L+G%3BHallett%2C+M&rft.aulast=Pascual-Leone&rft.aufirst=A&rft.date=1992-02-01&rft.volume=115+Pt+1&rft.issue=&rft.spage=109&rft.isbn=&rft.btitle=&rft.title=Brain&rft.issn=00068950&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Characteristics of late responses to superior laryngeal nerve stimulation in humans. AN - 85176756; pmid-1739256 AB - To characterize human thyroarytenoid and cricothyroid muscle responses to stimulation of the internal (sensory) and external (motor) branches of the superior laryngeal nerve (SLN), three awake subjects were studied at rest and during muscle activation with stimulation at different current levels. When only the external branch was stimulated, direct cricothyroid muscle responses were obtained without responses in either thyroarytenoid muscle. When only the internal branch was stimulated, no cricothyroid responses were obtained, but two late thyroarytenoid responses occurred (R1 and R2). The R1 response was usually ipsilateral and had a mean onset latency of 18 milliseconds, while the R2 response was bilateral and occurred between 66 and 70 milliseconds. Both responses tended to decrease in latency and increase in amplitude with increased stimulation level. The similarity of R1 to the adductor response and R2 to other late responses is discussed. JF - The Annals of Otology, Rhinology, and Laryngology AU - Ludlow, Christy L AU - Van Pelt F AU - Koda, J AD - Laryngeal and Speech Section, National Institute of Neurological Disorders and Stroke PY - 1992 SP - 127 EP - 134 VL - 101 IS - 2 Pt 1 SN - 0003-4894, 0003-4894 KW - Laryngeal Nerves KW - Reference Values KW - Laryngeal Muscles KW - Humans KW - Electrodes KW - Electromyography KW - Middle Aged KW - Adolescent KW - Electric Stimulation KW - Time Factors KW - Male KW - Reaction Time UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85176756?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Annals+of+Otology%2C+Rhinology%2C+and+Laryngology&rft.atitle=Characteristics+of+late+responses+to+superior+laryngeal+nerve+stimulation+in+humans.&rft.au=Ludlow%2C+Christy+L%3BVan+Pelt+F%3BKoda%2C+J&rft.aulast=Ludlow&rft.aufirst=Christy&rft.date=1992-02-01&rft.volume=101&rft.issue=2+Pt+1&rft.spage=127&rft.isbn=&rft.btitle=&rft.title=The+Annals+of+Otology%2C+Rhinology%2C+and+Laryngology&rft.issn=00034894&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Tumour necrosis factor mediates the survival benefit of interleukin 2 in a murine pulmonary metastases model. AN - 75529240; 1341229 AB - Antibody to tumour necrosis factor (TNF Ab) markedly decreases the toxicity of systemic interleukin-2 (IL-2) in mice but does not completely abrogate the anti-tumour response in terms of number of pulmonary metastases. Experiments were performed with a murine model of pulmonary metastases treated with high-dose IL-2 and concomitant TNF Ab or control antibody (CON Ab) to determine the effects of TNF Ab on survival. Mice were given either equal doses of IL-2 and TNF Ab or CON Ab or equitoxic doses of IL-2. In four consecutive experiments mice given TNF Ab tolerated 5 to 6 additional IL-2 doses (a 40-60% increase in total doses) in the equitoxic IL-2 dose group compared to the maximally tolerated dose with CON Ab. In all four experiments TNF Ab-treated mice had decreased survival compared to the CON Ab group given equal doses of IL-2 and in two of four experiments this difference was statistically significant (P2 < 0.01). Mice given 40-60% additional doses of IL-2 with TNF Ab had no improvement in survival compared with equitoxic doses of IL-2 with CON Ab in three of four experiments (P2 = 0.32, P2 = 0.67, P2 = 0.69). The TNF Ab preparation had no direct inhibition of IL-2 activity in an in vitro IL-2 proliferation bioassay. TNF Ab consistently blocks IL-2 toxicity and it also abrogates IL-2 therapeutic efficacy such that survival parallels treatment toxicity in this experimental model. JF - Surgical oncology AU - Fraker, D L AU - Thom, A K AU - Doherty, G M AU - Langstein, H N AU - Buresh, C M AU - Norton, J A AD - Surgical Metabolism Section, Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 1 EP - 9 VL - 1 IS - 1 SN - 0960-7404, 0960-7404 KW - Antibodies KW - 0 KW - Interleukin-2 KW - Recombinant Proteins KW - Tumor Necrosis Factor-alpha KW - Index Medicus KW - Recombinant Proteins -- toxicity KW - Neoplasm Transplantation KW - Drug Screening Assays, Antitumor KW - Animals KW - Drug Interactions KW - Dose-Response Relationship, Drug KW - Mice, Inbred C57BL KW - Mice KW - Recombinant Proteins -- therapeutic use KW - Female KW - Antibodies -- therapeutic use KW - Lung Neoplasms -- secondary KW - Interleukin-2 -- therapeutic use KW - Tumor Necrosis Factor-alpha -- immunology KW - Lung Neoplasms -- therapy KW - Disease Models, Animal KW - Lung Neoplasms -- mortality KW - Antibodies -- isolation & purification KW - Interleukin-2 -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75529240?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Surgical+oncology&rft.atitle=Tumour+necrosis+factor+mediates+the+survival+benefit+of+interleukin+2+in+a+murine+pulmonary+metastases+model.&rft.au=Fraker%2C+D+L%3BThom%2C+A+K%3BDoherty%2C+G+M%3BLangstein%2C+H+N%3BBuresh%2C+C+M%3BNorton%2C+J+A&rft.aulast=Fraker&rft.aufirst=D&rft.date=1992-02-01&rft.volume=1&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Surgical+oncology&rft.issn=09607404&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-01-13 N1 - Date created - 1994-01-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Monitoring tricyclic antidepressant therapy. AN - 75527727; 10147108 JF - PharmacoEconomics AU - Rudorfer, M V AD - National Institute of Mental Health, Rockville, Maryland. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 148 EP - 150 VL - 1 IS - 2 SN - 1170-7690, 1170-7690 KW - Antidepressive Agents, Tricyclic KW - 0 KW - Health technology assessment KW - Humans KW - Cost-Benefit Analysis KW - Antidepressive Agents, Tricyclic -- blood KW - Depression -- drug therapy KW - Antidepressive Agents, Tricyclic -- adverse effects KW - Drug Monitoring -- economics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75527727?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PharmacoEconomics&rft.atitle=Monitoring+tricyclic+antidepressant+therapy.&rft.au=Rudorfer%2C+M+V&rft.aulast=Rudorfer&rft.aufirst=M&rft.date=1992-02-01&rft.volume=1&rft.issue=2&rft.spage=148&rft.isbn=&rft.btitle=&rft.title=PharmacoEconomics&rft.issn=11707690&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-07-28 N1 - Date created - 1994-07-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Nonresponsiveness of the rat liver to alkylating carcinogens given by gavage. AN - 75526542; 1344210 AB - Carcinogenic alkylating agents administered orally are metabolized in the liver and alkylate DNA in liver cells of rats and hamsters. They frequently, but not always, induce liver tumors, in addition to tumors of other organs. Directly acting alkylating agents, such as alkylnitrosoureas and alkylnitrosocarbamates, rarely induce liver tumors, although they alkylate DNA in liver cells. The methylating agents nitrosodimethylamine and azoxymethane induce high incidences of liver tumors in rats when given in drinking water, but few or no liver tumors when given by gavage, although the total dose and the weekly dose were the same in either regimen. In contrast, methylnitrosoethylamine and nitrosodiethylamine give rise to liver tumors in rats in high incidences whether given by gavage or in drinking water. Sharp differences are also observed with other nitrosamines, such as those containing a propyl group with an oxygen substituent in the 2-position. These discrepancies indicate that, in addition to alkylation of DNA, pharmacokinetics of dosing and distribution and other reactions of the carcinogen are the dominant factors in determining the development of tumors in the liver. JF - Quality assurance (San Diego, Calif.) AU - Lijinsky, W AD - Laboratory of Chemical and Physical Carcinogenesis, ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 115 EP - 119 VL - 1 IS - 2 SN - 1052-9411, 1052-9411 KW - Carcinogens KW - 0 KW - Index Medicus KW - Rats KW - Administration, Oral KW - Animals KW - Male KW - Female KW - Cricetinae KW - Carcinogens -- administration & dosage KW - Liver Neoplasms -- chemically induced KW - Carcinogens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75526542?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Quality+assurance+%28San+Diego%2C+Calif.%29&rft.atitle=Nonresponsiveness+of+the+rat+liver+to+alkylating+carcinogens+given+by+gavage.&rft.au=Lijinsky%2C+W&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1992-02-01&rft.volume=1&rft.issue=2&rft.spage=115&rft.isbn=&rft.btitle=&rft.title=Quality+assurance+%28San+Diego%2C+Calif.%29&rft.issn=10529411&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-05-05 N1 - Date created - 1994-05-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytokines as positive and negative regulators of tumor promotion and progression. AN - 73113397; 1322742 AB - Cytokines can have both negative and positive effects on cells undergoing carcinogenesis. The promotion and progression phases of carcinogenesis may be affected by autocrine loops involving cytokines with growth factor activities such as IL-1, IL-2, low molecular weight B cell growth factor, TNF, IL-3, GM-CSF, M-CSF and IL-9. Aberrations in cytokine receptors such as the truncated EGF receptor present in v-erB promotes the growth of neoplastic cells. Aberrant signaling mechanisms, as found with spleen focus-forming virus, which mimics the ligand that activates the erythropoietin receptor, can also contribute to proliferation of preneoplastic and neoplastic cells. In contrast, cytokines such as interferons, LIF, TGF-beta, TNF and leukoregulin, with antiproliferative or differentiating activities, are sometimes capable of inhibiting carcinogenesis. Transfection of tumor cells with cytokine genes, such as IL-2, IL-4 and TNF, can cause suppression of in vivo tumor cell growth by mobilizing host immune and inflammatory cell responses. Thus cytokines and their receptors may play a direct role in early stages of tumor cell development and growth. JF - Seminars in cancer biology AU - Michiel, D F AU - Oppenheim, J J AD - Laboratory of Molecular Immunoregulation, National Cancer Institute, Frederick, MD 21702-1201. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 3 EP - 15 VL - 3 IS - 1 SN - 1044-579X, 1044-579X KW - Cytokines KW - 0 KW - Receptors, Cell Surface KW - Index Medicus KW - Signal Transduction -- physiology KW - Animals KW - Cell Differentiation -- physiology KW - Humans KW - Mice KW - Receptors, Cell Surface -- physiology KW - Cell Transformation, Neoplastic -- immunology KW - Cell Transformation, Viral KW - Gene Expression Regulation, Neoplastic KW - Neoplasms -- pathology KW - Cytokines -- physiology KW - Neoplasms -- etiology KW - Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73113397?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+cancer+biology&rft.atitle=Cytokines+as+positive+and+negative+regulators+of+tumor+promotion+and+progression.&rft.au=Michiel%2C+D+F%3BOppenheim%2C+J+J&rft.aulast=Michiel&rft.aufirst=D&rft.date=1992-02-01&rft.volume=3&rft.issue=1&rft.spage=3&rft.isbn=&rft.btitle=&rft.title=Seminars+in+cancer+biology&rft.issn=1044579X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-10 N1 - Date created - 1992-09-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of tumor necrosis factor release from alveolar macrophages treated with pentamidine isethionate. AN - 73061517; 1624213 AB - Alveolar macrophages in AIDS patients have a marked increase in tumor necrosis factor release in active Pneumocystis carinii pneumonia. We have demonstrated that pentamidine, an aromatic diamidine currently used to treat AIDS-related P. carinii pneumonia, is an effective inhibitor of cellular tumor necrosis factor release from lipopolysaccharide-stimulated rat alveolar macrophages at concentrations greater than 10(-8) M. Inhibition of release is not dependent upon the continued presence of pentamidine in the culture medium during the release phase. In addition, this blockage occurs at neither the transcriptional level as determined by Northern blot analysis nor the translational level as determined by Western blot analysis. Timed addition studies suggest that pentamidine is targeting relatively early events following lipopolysaccharide administration. Pentamidine appears to alter early lipopolysaccharide-induced cellular processes associated with the release of tumor necrosis factor from macrophages. JF - International journal of immunopharmacology AU - Corsini, E AU - Craig, W A AU - Rosenthal, G J AD - Immunotoxicology Section, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 121 EP - 130 VL - 14 IS - 2 SN - 0192-0561, 0192-0561 KW - Lipopolysaccharides KW - 0 KW - Tumor Necrosis Factor-alpha KW - Pentamidine KW - 673LC5J4LQ KW - Index Medicus KW - AIDS/HIV KW - Rats KW - Protein Biosynthesis -- drug effects KW - Animals KW - Rats, Inbred F344 KW - Transcription, Genetic -- drug effects KW - Cells, Cultured KW - Acquired Immunodeficiency Syndrome -- immunology KW - Female KW - Macrophages, Alveolar -- metabolism KW - Pentamidine -- pharmacology KW - Tumor Necrosis Factor-alpha -- biosynthesis KW - Macrophages, Alveolar -- drug effects KW - Tumor Necrosis Factor-alpha -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73061517?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+immunopharmacology&rft.atitle=Modulation+of+tumor+necrosis+factor+release+from+alveolar+macrophages+treated+with+pentamidine+isethionate.&rft.au=Corsini%2C+E%3BCraig%2C+W+A%3BRosenthal%2C+G+J&rft.aulast=Corsini&rft.aufirst=E&rft.date=1992-02-01&rft.volume=14&rft.issue=2&rft.spage=121&rft.isbn=&rft.btitle=&rft.title=International+journal+of+immunopharmacology&rft.issn=01920561&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-13 N1 - Date created - 1992-08-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of chronic nicotine treatment and withdrawal on rat striatal D1 and D2 dopamine receptors. AN - 73060357; 1352822 AB - The effects on rat striatal dopamine receptors after chronic nicotine administration (3 and 12 mg kg-1 day-1), and after withdrawal from chronic nicotine (12 mg kg-1 day-1), were studied. After 21 days of continuous minipump infusion, the control (saline) and nicotine-treated rats were killed. The nicotine-withdrawal rats were killed on day 28, 7 days after pump removal. Radioligand studies were performed to determine D1 ([3H]SCH23390) and D2 ([3H]spiperone) striatal dopamine receptor affinity (Kd) and maximum binding (Bmax). Dopamine inhibition of antagonist binding at 3 concentrations and the effect of 0.3 mM GTP on binding affinity were examined. No statistically significant differences between control and nicotine treatment or withdrawal groups were noted in either D1 or D2 receptor Kd or Bmax. Although nicotine has been shown to affect nigrostriatal dopamine release, chronic treatment does not appear to alter overall striatal dopaminergic receptor binding parameters. JF - The Journal of pharmacy and pharmacology AU - Kirch, D G AU - Taylor, T R AU - Creese, I AU - Xu, S X AU - Wyatt, R J AD - Neuropsychiatry Branch, National Institute of Mental Health, Rockville, Maryland 20857. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 89 EP - 92 VL - 44 IS - 2 SN - 0022-3573, 0022-3573 KW - Benzazepines KW - 0 KW - Receptors, Dopamine KW - Receptors, Dopamine D1 KW - Receptors, Dopamine D2 KW - Spiperone KW - 4X6E73CJ0Q KW - Nicotine KW - 6M3C89ZY6R KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Spiperone -- metabolism KW - Benzazepines -- metabolism KW - Male KW - Receptors, Dopamine -- drug effects KW - Substance Withdrawal Syndrome -- metabolism KW - Nicotine -- pharmacology KW - Corpus Striatum -- metabolism KW - Nicotine -- adverse effects KW - Nicotine -- administration & dosage KW - Corpus Striatum -- drug effects KW - Receptors, Dopamine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73060357?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacy+and+pharmacology&rft.atitle=Effect+of+chronic+nicotine+treatment+and+withdrawal+on+rat+striatal+D1+and+D2+dopamine+receptors.&rft.au=Kirch%2C+D+G%3BTaylor%2C+T+R%3BCreese%2C+I%3BXu%2C+S+X%3BWyatt%2C+R+J&rft.aulast=Kirch&rft.aufirst=D&rft.date=1992-02-01&rft.volume=44&rft.issue=2&rft.spage=89&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacy+and+pharmacology&rft.issn=00223573&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-19 N1 - Date created - 1992-08-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Developmental toxicity of boric acid in mice and rats. AN - 73001937; 1601227 AB - Boric acid (BORA), an ingredient of many cosmetics, pharmaceuticals, and pesticides, was tested for developmental toxicity in timed-pregnant Swiss mice and Sprague-Dawley rats (n = 26-28/group). BORA (0, 0.1, 0.2, or 0.4% in feed) was provided throughout gestation to attain steady-state exposure as early as possible during prenatal development. Average doses (mg/kg/day) were 248, 452, or 1003 in mice, and 78, 163, or 330 in rats. To limit prenatal mortality, BORA (0.8% or 539 mg/kg/day) was provided to an additional group of rats on Gestational Days (GD) 6 to 15 only. On GD 17 (mice) or 20 (rats), fetuses were weighed and examined for malformations (external, visceral, skeletal). Mouse dams exhibited mild renal lesions (greater than or equal to 0.1%), increased water intake and relative kidney weight (0.4%), and decreased weight gain (0.4%) during treatment. There was a reduction of fetal body weight (greater than or equal to 0.2%) and an increased incidence of resorptions and malformed fetuses per litter (0.4%). Morphological changes included an increased incidence of short rib XIII (a malformation) and a decreased incidence of rudimentary or full rib(s) at lumbar I (an anatomical variation). Maternal rats exhibited increased liver and kidney weights at greater than or equal to 0.2%, altered water and/or food intake at greater than 0.2%, and decreased weight gain at greater than 0.4%. Average fetal body weight/litter was reduced at all doses. Prenatal mortality was increased only at 0.8%. The incidence of fetal malformations was significantly increased at greater than or equal to 0.2%. The most frequently observed malformations were enlarged lateral ventricles of the brain and agenesis or shortening of rib XIII. In rats, the no-observable-adverse-effect level (NOAEL) for maternal toxicity was 78 mg/kg (0.1%), while in mice the low dose of 248 mg/kg (0.1%) approached the maternal NOAEL with mild renal lesions in only 2 of 10 females. Embryo/fetal toxicity occurred in all groups of rats at greater than or equal to 78 mg/kg (greater than or equal to 0.1%) while the NOAEL for developmental toxicity in mice was 248 mg/kg (0.1%). Thus developmental toxicity occurred below maternally toxic levels in rats as well as in the presence of maternal toxicity in mice and rats. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Heindel, J J AU - Price, C J AU - Field, E A AU - Marr, M C AU - Myers, C B AU - Morrissey, R E AU - Schwetz, B A AD - Developmental and Reproductive Toxicology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 266 EP - 277 VL - 18 IS - 2 SN - 0272-0590, 0272-0590 KW - Boric Acids KW - 0 KW - boric acid KW - R57ZHV85D4 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Mice, Inbred ICR KW - Mice KW - Fetal Death -- chemically induced KW - Male KW - Female KW - Pregnancy KW - Boric Acids -- toxicity KW - Abnormalities, Drug-Induced -- etiology KW - Embryonic and Fetal Development -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73001937?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=Developmental+toxicity+of+boric+acid+in+mice+and+rats.&rft.au=Heindel%2C+J+J%3BPrice%2C+C+J%3BField%2C+E+A%3BMarr%2C+M+C%3BMyers%2C+C+B%3BMorrissey%2C+R+E%3BSchwetz%2C+B+A&rft.aulast=Heindel&rft.aufirst=J&rft.date=1992-02-01&rft.volume=18&rft.issue=2&rft.spage=266&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-15 N1 - Date created - 1992-07-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Risk assessment in immunotoxicology. I. Sensitivity and predictability of immune tests. AN - 72990458; 1534777 AB - We have previously reported on the design and content of a screening battery involving a "tier" approach for detecting potential immunotoxic compounds in mice (Luster et al., 1988, Fundam. Appl. Toxicol. 10, 2-19). This battery has now been utilized to examine a variety of compounds by the NIEHS Immunotoxicology Laboratory, the National Toxicology Program-sponsored laboratories, and by the Cell Biology Department at the Chemical Industry Institute of Toxicology. The database generated from these studies, which consists of over 50 selected compounds, has been collected and analyzed in an attempt to improve future testing strategies and provide information to aid in quantitative risk assessment for immunotoxicity. Studies presented here have established the ability of each of the tests or test combinations in the screening battery to detect immunotoxic compounds. Efforts are currently underway using this database to determine the relationships between these immune tests and susceptibility to challenge with infectious agents or transplantable tumor cells. The present analyses indicated that the performance of only two or three immune tests are sufficient to predict immunotoxic compounds in rodents (greater than 90% concordance). The tests that showed the highest association with immunotoxicity were the splenic antibody plaque forming cell response (78%) and cell surface marker analysis (83%). The relationship between immunotoxicity and carcinogenicity, as well as genotoxicity, was also determined. These analyses suggested that potential immunotoxic compounds are likely to be rodent carcinogens (p = 0.019) although for compounds that are not immunotoxic the carcinogenic status is unclear. There was no relationship observed between immunotoxicity and mutagenicity as determined using in vitro genotoxicity tests. The significance of these observations is discussed in terms of the relationship between immunotoxicity tests and biological/toxicological processes concerned with human health (e.g., infectious disease). JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Luster, M I AU - Portier, C AU - Pait, D G AU - White, K L AU - Gennings, C AU - Munson, A E AU - Rosenthal, G J AD - Systems Toxicity Branch, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27709. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 200 EP - 210 VL - 18 IS - 2 SN - 0272-0590, 0272-0590 KW - Carcinogens KW - 0 KW - Immunosuppressive Agents KW - Index Medicus KW - AIDS/HIV KW - Sensitivity and Specificity KW - Mice, Inbred Strains KW - B-Lymphocytes -- drug effects KW - Animals KW - Risk Factors KW - Carcinogens -- toxicity KW - CD4-CD8 Ratio -- drug effects KW - Predictive Value of Tests KW - Mice KW - B-Lymphocytes -- immunology KW - T-Lymphocytes -- drug effects KW - Meta-Analysis as Topic KW - T-Lymphocytes -- immunology KW - Immune System -- drug effects KW - Immunosuppressive Agents -- toxicity KW - Toxicology -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72990458?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=Risk+assessment+in+immunotoxicology.+I.+Sensitivity+and+predictability+of+immune+tests.&rft.au=Luster%2C+M+I%3BPortier%2C+C%3BPait%2C+D+G%3BWhite%2C+K+L%3BGennings%2C+C%3BMunson%2C+A+E%3BRosenthal%2C+G+J&rft.aulast=Luster&rft.aufirst=M&rft.date=1992-02-01&rft.volume=18&rft.issue=2&rft.spage=200&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-15 N1 - Date created - 1992-07-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pathology of spontaneous and oncogene transformed rat liver epithelial cells and derived tumours in nude mice. AN - 72924539; 1576082 AB - The histological and ultrastructural features of oncogene transformed rat liver epithelial (RLE) cells in culture and spontaneously transformed RLE cells were studied. The tumours produced in nude mice by all the transformed cells were either moderately well differentiated carcinomas or sarcomatous tumours. Epithelial tumours were produced in the RLE cells after transduction of both v-raf and v-myc oncogenes whereas sarcomatous tumours were produced after transduction of v-raf alone. These data suggested that transformation of RLE cells with a single oncogene, v-raf, produced malignant tumours which were consistent with sarcomas while a combination of two oncogenes, v-raf and v-myc, produced an epithelial tumour, consistent with a carcinoma. The effects of these oncogenes on RLE cells indicate that they were able to differentiate and were capable of producing two morphologically distinct tumour types. The possible role of v-myc in switching the sarcomatous lineage to an epithelial tumour lineage is considered to be significant and worthy of further studies. The epithelial tumour produced in RLE cells by combination of v-raf and v-myc is consistent with an embryonal type of hepatoblastoma. The trabecular type of liver cell carcinoma which resulted from spontaneous transformation of RLE cells illustrates the inherent potential of the RLE cell to undergo malignant change and strongly suggests that the RLE cells may be the precursor cells in the development of hepatocellular carcinoma in the rat. JF - International journal of experimental pathology AU - Williams, A O AU - Huggett, A C AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 99 EP - 114 VL - 73 IS - 1 SN - 0959-9673, 0959-9673 KW - Oncogene Protein p55(v-myc) KW - 0 KW - Retroviridae Proteins, Oncogenic KW - Oncogene Proteins v-raf KW - EC 2.7.11.1 KW - Index Medicus KW - Rats KW - Neoplasm Transplantation KW - Animals KW - Retroviridae Proteins, Oncogenic -- genetics KW - Oncogene Protein p55(v-myc) -- genetics KW - Microscopy, Electron KW - Mice, Nude KW - Mice KW - Cell Line KW - Liver Neoplasms, Experimental -- genetics KW - Carcinoma -- ultrastructure KW - Liver Neoplasms, Experimental -- ultrastructure KW - Oncogenes -- physiology KW - Cell Transformation, Neoplastic -- ultrastructure KW - Cell Transformation, Neoplastic -- genetics KW - Carcinoma -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72924539?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+experimental+pathology&rft.atitle=Pathology+of+spontaneous+and+oncogene+transformed+rat+liver+epithelial+cells+and+derived+tumours+in+nude+mice.&rft.au=Williams%2C+A+O%3BHuggett%2C+A+C%3BThorgeirsson%2C+S+S&rft.aulast=Williams&rft.aufirst=A&rft.date=1992-02-01&rft.volume=73&rft.issue=1&rft.spage=99&rft.isbn=&rft.btitle=&rft.title=International+journal+of+experimental+pathology&rft.issn=09599673&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-08 N1 - Date created - 1992-06-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer. 1976 May;37(5):2275-82 [1260715] Mol Carcinog. 1990;3(1):20-9 [2322386] Carcinogenesis. 1989 Jul;10(7):1345-8 [2472233] Mol Cell Biol. 1987 Apr;7(4):1436-44 [3037318] Cancer. 1984 Sep 1;54(5):837-42 [6331629] Ann N Y Acad Sci. 1980;349:128-37 [7013608] Cancer. 1983 Jan 1;51(1):15-9 [6185194] Mol Carcinog. 1988;1(3):189-95 [3074814] Carcinogenesis. 1987 Jan;8(1):1-4 [3100081] Nature. 1985 Dec 12-18;318(6046):533-8 [3906410] Gan. 1967 Aug;58(4):355-66 [4295056] Int J Cancer. 1983 Sep 15;32(3):373-7 [6136467] Hepatology. 1982 Jan-Feb;2(1):77-86 [6172353] Mol Carcinog. 1989;2(6):345-54 [2619882] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential effects of injection regimen on behavioral responses to cocaine. AN - 72918076; 1574527 AB - Locomotor behavior was measured in mice receiving IP cocaine at 5, 10, 20, or 40 mg/kg. then with 5, 5, 10, and 20 mg/kg at 10-min intervals. In the single-dose treatment, mice received a single dose of cocaine at a time corresponding to the equivalent cumulative dose, with saline injections at other times. The single-injection treatment was similar, but saline injections were omitted. Locomotor activity was measured across each 10-min interval. Mice were retested 6 weeks later and 1 day after that. Dose-response curves were similar for all three treatments on the first test, but diverged markedly on subsequent tests. Significant locomotor sensitization occurred at the higher doses on the second test, particularly in the treatments receiving single cocaine injections. On the third test, convulsions occurred at 40 mg/kg, but only in the singly dosed treatments. The results demonstrate that injection parameters can modify both the behavioral and toxic effects of cocaine. JF - Pharmacology, biochemistry, and behavior AU - Terry, P AD - Psychobiology Laboratory, National Institute on Drug Abuse Addiction Research Center, Baltimore, MD 21224. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 365 EP - 369 VL - 41 IS - 2 SN - 0091-3057, 0091-3057 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Injections, Intraperitoneal KW - Mice, Inbred Strains KW - Animals KW - Drug Administration Schedule KW - Dose-Response Relationship, Drug KW - Mice KW - Male KW - Locomotion -- drug effects KW - Cocaine -- pharmacology KW - Cocaine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72918076?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology%2C+biochemistry%2C+and+behavior&rft.atitle=Differential+effects+of+injection+regimen+on+behavioral+responses+to+cocaine.&rft.au=Terry%2C+P&rft.aulast=Terry&rft.aufirst=P&rft.date=1992-02-01&rft.volume=41&rft.issue=2&rft.spage=365&rft.isbn=&rft.btitle=&rft.title=Pharmacology%2C+biochemistry%2C+and+behavior&rft.issn=00913057&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-29 N1 - Date created - 1992-05-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of separate determinants on the thyrotropin receptor reactive with Graves' thyroid-stimulating antibodies and with thyroid-stimulating blocking antibodies in idiopathic myxedema: these determinants have no homologous sequence on gonadotropin receptors. AN - 72907941; 1349156 AB - Deletions, substitutions, or mutations of the rat TSH receptor extracellular domain between residues 20 and 107 (all residue numbers are determined by counting from the methionine start site) have been made by site-directed mutagenesis of receptor cDNA. After transfection in Cos-7 cells, constructs were evaluated for their ability to bind [125I]TSH or respond to TSH and thyroid-stimulating antibodies (TSAbs) from Graves' patients in assays measuring cAMP levels of the transfected cells. Assay results were compared to results from Cos-7 cells transfected with wild-type receptor constructs or vector alone. We identify threonine-40 as a TSAb-specific site whose mutation to asparagine, but not alanine, reduces TSAb activity 10-fold, but only minimally affects TSH-increased cAMP levels. We show that thyroid-stimulating blocking antibodies (TSBAbs), which block TSH or TSAb activity and are found in hypothyroid patients with idiopathic myxedema, continue to inhibit TSH-stimulated cAMP levels when threonine-40 is mutated to asparagine or alanine, suggesting that TSBAbs interact with different TSH receptor epitopes than the TSAb autoantibodies in Graves' patients. This is confirmed by the demonstration that these TSBAbs interact with high affinity TSH-binding sites previously identified at tyrosine-385 or at residues 295-306 of the extracellular domain of the TSH receptor. This is evidenced by a loss in the ability of TSBAbs to inhibit TSAb activity when these residues are mutated or deleted, respectively. Since the TSAb and TSBAb epitopes are in regions of the extracellular domain of the TSH receptor that have no homology in gonadotropin receptors, these data explain at least in part the organ-specific nature of TSH receptor autoantibodies in autoimmune thyroid disease. Data are additionally provided which indicate that residues 30-37 and 42-45, which flank the TSAb epitope at threonine-40, appear to be ligand interaction sites more important for high affinity TSH binding than for the ability of TSH to increase cAMP levels and that cysteine-41 is critical for TSH receptor conformation and expression on the surface of the cell. Thus, despite unchanged maximal values for TSH-increased cAMP levels, substitution of residues 42-45 or deletion of residues 30-37 results in receptors, which, by comparison to wild-type constructs, exhibit significantly worsened Kd values for TSH binding than EC50 values for TSH- or TSAb-increased cAMP activity.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Molecular endocrinology (Baltimore, Md.) AU - Kosugi, S AU - Ban, T AU - Akamizu, T AU - Kohn, L D AD - Cell Regulation Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 168 EP - 180 VL - 6 IS - 2 SN - 0888-8809, 0888-8809 KW - Autoantibodies KW - 0 KW - Immunoglobulins, Thyroid-Stimulating KW - Receptors, Gonadotropin KW - Receptors, Thyrotropin KW - Asparagine KW - 7006-34-0 KW - Cyclic AMP KW - E0399OZS9N KW - Alanine KW - OF5P57N2ZX KW - Index Medicus KW - Animals KW - Humans KW - Receptors, Gonadotropin -- genetics KW - Alanine -- chemistry KW - Amino Acid Sequence KW - Binding Sites KW - Rats KW - Receptors, Gonadotropin -- chemistry KW - Transfection KW - Binding, Competitive KW - Cyclic AMP -- metabolism KW - Molecular Sequence Data KW - Receptors, Gonadotropin -- metabolism KW - Mutation KW - Asparagine -- chemistry KW - Receptors, Thyrotropin -- metabolism KW - Receptors, Thyrotropin -- chemistry KW - Receptors, Thyrotropin -- immunology KW - Myxedema -- immunology KW - Autoantibodies -- immunology KW - Thyroid Gland -- immunology KW - Graves Disease -- immunology KW - Receptors, Thyrotropin -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72907941?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.atitle=Identification+of+separate+determinants+on+the+thyrotropin+receptor+reactive+with+Graves%27+thyroid-stimulating+antibodies+and+with+thyroid-stimulating+blocking+antibodies+in+idiopathic+myxedema%3A+these+determinants+have+no+homologous+sequence+on+gonadotropin+receptors.&rft.au=Kosugi%2C+S%3BBan%2C+T%3BAkamizu%2C+T%3BKohn%2C+L+D&rft.aulast=Kosugi&rft.aufirst=S&rft.date=1992-02-01&rft.volume=6&rft.issue=2&rft.spage=168&rft.isbn=&rft.btitle=&rft.title=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.issn=08888809&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-22 N1 - Date created - 1992-05-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The use of DNA heteroduplex patterns to map recombination within the HLA class II region. AN - 72892018; 1532959 AB - Differential DNA heteroduplex patterns were used to investigate inheritance of HLA class II region genes in a family where a living related kidney transplant was under consideration. Serologic typing of the family members for HLA class I (HLA-A, B, and C) and class II (HLA-DR and DQ) alleles indicated that the patient (109) and one sibling (126) had inherited the same maternal and paternal HLA alleles. However, a strong reciprocal mixed lymphocyte response implied that these two individuals were not completely HLA identical. Serologic typing for HLA-DQ was confirmed by allele-specific oligonucleotide typing family members for HLA-DQ alpha and beta genes. To assess a possible nonidentical gene(s), DNA was amplified from all family members at the second exon of the DR beta, DQ alpha, DP alpha, and DP beta genes and the products were analyzed by DNA heteroduplex formation. This method showed that individuals 109 and 126 were identical at DR and DQ but differed at DP. This difference was confirmed by allele-specific oligonucleotide hybridization and indicated that 126 had inherited a recombinant maternal chromosome with a cross-over occurring in the region between the DQ beta and DP alpha genes. These data demonstrate the applicability of DNA heteroduplex patterns in establishing identity-nonidentity of alleles in the major histocompatibility complex. JF - Human immunology AU - Carrington, M AU - White, M B AU - Dean, M AU - Mann, D AU - Ward, F E AD - Biological Carcinogenesis and Development Program, PRI/DynCorp., NCI-FCRDC, MD 21702. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 114 EP - 121 VL - 33 IS - 2 SN - 0198-8859, 0198-8859 KW - HLA-D Antigens KW - 0 KW - Nucleic Acid Heteroduplexes KW - Oligodeoxyribonucleotides KW - Index Medicus KW - Pedigree KW - Base Sequence KW - Humans KW - Lymphocyte Culture Test, Mixed KW - Molecular Sequence Data KW - Oligodeoxyribonucleotides -- genetics KW - Male KW - Female KW - Nucleic Acid Heteroduplexes -- genetics KW - Recombination, Genetic -- genetics KW - HLA-D Antigens -- genetics KW - Genes, MHC Class II -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72892018?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+immunology&rft.atitle=The+use+of+DNA+heteroduplex+patterns+to+map+recombination+within+the+HLA+class+II+region.&rft.au=Carrington%2C+M%3BWhite%2C+M+B%3BDean%2C+M%3BMann%2C+D%3BWard%2C+F+E&rft.aulast=Carrington&rft.aufirst=M&rft.date=1992-02-01&rft.volume=33&rft.issue=2&rft.spage=114&rft.isbn=&rft.btitle=&rft.title=Human+immunology&rft.issn=01988859&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-15 N1 - Date created - 1992-05-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular analysis of the chromosome 11p region in renal cell carcinomas. AN - 72876163; 1348450 AB - Comparative histological data suggest that papillary renal cell tumors in adults and Wilms' tumors in children develop from maturation-arrested cells of similar origin. Wilms' tumor is characterized by genetic changes at the chromosome 11p region. In the present study, we have analyzed 10 papillary and 10 non-papillary renal cell tumors and determined the allelic status of 6 loci on the short arm of chromosome 11. Only one papillary renal cell carcinoma among the 20 tumors showed a loss of constitutional heterozygosity for the chromosome 11p region. These data suggest that separate molecular events occur in the development of Wilms' tumor and papillary renal cell tumors, subsequent to the proliferation of maturation-arrested cells of the kidney. JF - Cellular and molecular biology AU - Kovacs, G AU - Kiechle-Schwarz, M AU - Scherer, G AU - Kung, H F AD - Biological Carcinogenesis and Development Program, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 59 EP - 62 VL - 38 IS - 1 KW - DNA, Neoplasm KW - 0 KW - Index Medicus KW - Humans KW - Heterozygote KW - Wilms Tumor -- genetics KW - Kidney Neoplasms -- genetics KW - Polymorphism, Restriction Fragment Length KW - DNA, Neoplasm -- genetics KW - Carcinoma, Renal Cell -- genetics KW - Carcinoma, Papillary -- genetics KW - Chromosomes, Human, Pair 11 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72876163?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cellular+and+molecular+biology&rft.atitle=Molecular+analysis+of+the+chromosome+11p+region+in+renal+cell+carcinomas.&rft.au=Kovacs%2C+G%3BKiechle-Schwarz%2C+M%3BScherer%2C+G%3BKung%2C+H+F&rft.aulast=Kovacs&rft.aufirst=G&rft.date=1992-02-01&rft.volume=38&rft.issue=1&rft.spage=59&rft.isbn=&rft.btitle=&rft.title=Cellular+and+molecular+biology&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-08 N1 - Date created - 1992-05-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prevalence of the proposed DSM-IV alcohol use disorders: United States, 1988. AN - 72874868; 1555008 AB - Data from a 1988 survey on United States drinking practices and related problems was used to derive the proposed DSM-IV definitions of alcohol abuse and dependence. The prevalence of DSM-IV alcohol abuse and dependence combined, incorporating the DSM-III-R duration criterion, was 6.00% in this general population sample. The majority of respondents were classified as alcohol dependent (5.93%), dependent without abuse (5.24%), and dependent with physiological dependence (5.06%). The rate for DSM-IV alcohol abuse was negligible (0.06%) while elimination of the duration criterion had little impact on the prevalence of DSM-IV alcohol use disorders. Reasons for the extremely low prevalence of DSM-IV alcohol abuse and the slight increase in the prevalence of DSM-IV alcohol use disorders as the result of eliminating the duration criterion are discussed in terms of the content of the abuse category and its relationship to the dependence definition. JF - British journal of addiction AU - Grant, B F AD - National Institute on Alcohol Abuse and Alcoholism, Division of Biometry and Epidemiology, Rockville, Maryland 20857. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 309 EP - 316 VL - 87 IS - 2 SN - 0952-0481, 0952-0481 KW - Index Medicus KW - Cross-Sectional Studies KW - Humans KW - Adult KW - Incidence KW - Aged KW - Middle Aged KW - Adolescent KW - United States -- epidemiology KW - Psychometrics KW - Male KW - Female KW - Alcoholism -- epidemiology KW - Alcoholism -- diagnosis KW - Psychiatric Status Rating Scales -- statistics & numerical data UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72874868?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+addiction&rft.atitle=Prevalence+of+the+proposed+DSM-IV+alcohol+use+disorders%3A+United+States%2C+1988.&rft.au=Grant%2C+B+F&rft.aulast=Grant&rft.aufirst=B&rft.date=1992-02-01&rft.volume=87&rft.issue=2&rft.spage=309&rft.isbn=&rft.btitle=&rft.title=British+journal+of+addiction&rft.issn=09520481&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-01 N1 - Date created - 1992-05-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Epidemiology of bladder cancer. AN - 72864665; 1556044 AB - Approximately 49,000 persons in the United States develop bladder cancer each year, and about 9700 die of it. White men face a lifetime risk of almost 3%; white women and black men face a risk of about 1%, and black women, about 0.5%. Cigarette smoking is accepted widely as a cause of bladder cancer. Smoking accounts for about half of bladder cancer diagnosed among men and about one third of that among women. Moderate to heavy smokers typically show a two to five fold risk of bladder cancer, compared with persons who never smoked. When cigarette smokers quit smoking, their bladder cancer risk falls measurably within 2 to 4 years, but probably does not continue to decline with increasing years since quitting and does not appear to return to the baseline level of nonsmokers. Occupational exposure to certain aromatic amines causes human bladder cancer. Clear evidence of bladder cancer risk also is apparent for a small number of occupational groups: dye workers, rubber workers, leather workers, painters, truck drivers, and aluminum workers. Many other occupational groups have been reported to have increased bladder cancer risk, but evidence for these is not as strong. Coffee drinking has been studied extensively as a potential risk factor, but the inconsistency of the observed associations suggests that the relationship is either quite weak, noncausal, or dependent in a complex way on unmeasured factors. Artificial sweeteners confer little or no excess bladder cancer risk. Alcohol consumption apparently does not affect risk either. Consumption of fruits, vegetables, and foods high in vitamin A have been suggested as possible protective factors; consumption of high-fat foods, pork, and beef have been suggested as possible risk factors. Further epidemiologic research is needed to elucidate the role of diet in human bladder carcinogenesis. Less common risk factors for bladder cancer include ionizing radiation, cyclophosphamide use, and abuse of phenacetin-containing analgesics. Schistosomiasis infection may contribute substantially to the bladder cancer burden in Egypt and elsewhere, though not in the United States.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Hematology/oncology clinics of North America AU - Silverman, D T AU - Hartge, P AU - Morrison, A S AU - Devesa, S S AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, Maryland. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 1 EP - 30 VL - 6 IS - 1 SN - 0889-8588, 0889-8588 KW - Index Medicus KW - Aged, 80 and over KW - Risk Factors KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Male KW - Female KW - Urinary Bladder Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72864665?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hematology%2Foncology+clinics+of+North+America&rft.atitle=Epidemiology+of+bladder+cancer.&rft.au=Silverman%2C+D+T%3BHartge%2C+P%3BMorrison%2C+A+S%3BDevesa%2C+S+S&rft.aulast=Silverman&rft.aufirst=D&rft.date=1992-02-01&rft.volume=6&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Hematology%2Foncology+clinics+of+North+America&rft.issn=08898588&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-05 N1 - Date created - 1992-05-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Endothelins belong to the assortment of mast cell-derived and mast cell-bound cytokines. AN - 72861386; 1313283 AB - Local accumulation of endothelins (ETs) as cytokine-like factors via autocrine/paracrine mechanisms seems to represent an important aspect of their pathophysiological action. This assumption prompted us to investigate mast cells as a possible source of these peptides. With the use of a combination of high-performance liquid chromatography and a radioimmunoassay specific for endothelin-1 (ET-1), 3-week-old cultures of primary murine bone marrow mast cells (BMMC) as well as various mast cell lines were shown to contain and secrete immunoreactive ET-1. The amounts of this peptide were constitutively high in cellular extracts of BMMC, while there was considerable variation in the basal cellular content among mast cell lines, ranging from high (C57) to undetectable (RBL) levels. Treatment of the cells with the combination of phorbol myristate acetate (PMA) and A23187 for 5 h led to induction of ET-1 production in all cases tested. In contrast to the rapid stimulation by PMA/A23187 of histamine release from BMMC or C57 cells, however, no ET-1 secretory response was noted as early as 30 min after this combined treatment. Moreover, stimulation of mast cells with crosslinked IgE for 30 min or 5 h did not affect ET-1 secretion, suggesting that mast cell ET-1 release is not directly related to mast cell degranulation. After exposure of the cells to crosslinked IgE for 20 h, however, there was a distinct increase in immunoreactive ET-1 in the medium, to approximate 10 times the basal level. Polymerase chain reaction (PCR) analysis of mRNA expression in mast cells revealed that the amount of ET-1 PCR product, which is low or undetectable under nonstimulated conditions, is enhanceable by both PMA/A23187 and crosslinked IgE. The IgE-mediated induction kinetics for ET-1 mRNA parallel the kinetics obtained with PMA/A23187, albeit at somewhat lower levels. With the use of fluorescent ligand binding/flow cytometry as a screening method and a radioreceptor assay as the confirming method, mast cells were found to express a single class of high affinity ET receptors with distinct selectivity for ET-1 and a pharmacological profile resembling that of the ETA type ET receptor. Stimulation of mast cell ET-1 receptors did not provoke histamine release, nor did it result in a mitogenic response of BMMC. In conclusion, mast cells synthesize and secrete ET-1 and have ET receptors, suggesting that ET-1 may participate in mediating mast cell-related long-term changes in the microenvironment, e.g., in smooth muscle tone or the proliferation rate of fibroblasts. JF - The New biologist AU - Ehrenreich, H AU - Burd, P R AU - Rottem, M AU - Hültner, L AU - Hylton, J B AU - Garfield, M AU - Coligan, J E AU - Metcalfe, D D AU - Fauci, A S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 147 EP - 156 VL - 4 IS - 2 SN - 1043-4674, 1043-4674 KW - Cytokines KW - 0 KW - Endothelins KW - Receptors, Cell Surface KW - Receptors, Endothelin KW - Calcimycin KW - 37H9VM9WZL KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Transcription, Genetic KW - Mice KW - Calcimycin -- pharmacology KW - Mice, Inbred BALB C KW - Bone Marrow Cells KW - Receptors, Cell Surface -- metabolism KW - Polymerase Chain Reaction KW - Base Sequence KW - Cells, Cultured KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mast Cells -- secretion KW - Endothelins -- metabolism KW - Mast Cells -- metabolism KW - Cytokines -- secretion KW - Endothelins -- secretion KW - Cytokines -- metabolism KW - Mast Cells -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72861386?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+New+biologist&rft.atitle=Endothelins+belong+to+the+assortment+of+mast+cell-derived+and+mast+cell-bound+cytokines.&rft.au=Ehrenreich%2C+H%3BBurd%2C+P+R%3BRottem%2C+M%3BH%C3%BCltner%2C+L%3BHylton%2C+J+B%3BGarfield%2C+M%3BColigan%2C+J+E%3BMetcalfe%2C+D+D%3BFauci%2C+A+S&rft.aulast=Ehrenreich&rft.aufirst=H&rft.date=1992-02-01&rft.volume=4&rft.issue=2&rft.spage=147&rft.isbn=&rft.btitle=&rft.title=The+New+biologist&rft.issn=10434674&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-06 N1 - Date created - 1992-05-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Biology of cancer: current issues and future prospects. AN - 72846231; 1546220 AB - The future of cancer treatment is limited only by the rate of progress made in understanding the biology of cancer. The future will present a considerable challenge to health care professionals to learn new theories, understand new terms, and expect different toxicities. The explosion of information and technology is exciting, yet frightening. The willingness of scientists, health care professionals, and consumers to deal with the ethical, financial, and political issues generated by this progress is gratifying. Because science has created such advances, the effort to deal with the outcomes is worthwhile but still difficult. The challenge to rapidly facilitate the sharing of the scientific and clinical advances has been recognized by the nation. A legislative mandate to create a way to store and analyze the vast data related to molecular biology, biochemistry, and genetics resulted in the National Center for Biotechnology Information. The development of automated systems to analyze genetic, environmental, biological, and chemistry information can only enhance future progress in the management of cancer. JF - Seminars in oncology nursing AU - Jenkins, J AD - Cancer Nursing Service, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 63 EP - 69 VL - 8 IS - 1 SN - 0749-2081, 0749-2081 KW - Antineoplastic Agents KW - 0 KW - Growth Substances KW - Immunologic Factors KW - Index Medicus KW - Nursing KW - Nursing Care -- standards KW - Growth Substances -- genetics KW - Oncogenes -- genetics KW - Immunologic Factors -- therapeutic use KW - Humans KW - Genetic Therapy -- standards KW - Ethics, Medical KW - Forecasting KW - Antineoplastic Agents -- therapeutic use KW - Research Design KW - Research -- economics KW - Neoplasms -- nursing KW - Molecular Biology -- trends KW - Research -- standards KW - Research -- trends KW - Neoplasms -- therapy KW - Molecular Biology -- standards UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72846231?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+oncology+nursing&rft.atitle=Biology+of+cancer%3A+current+issues+and+future+prospects.&rft.au=Jenkins%2C+J&rft.aulast=Jenkins&rft.aufirst=J&rft.date=1992-02-01&rft.volume=8&rft.issue=1&rft.spage=63&rft.isbn=&rft.btitle=&rft.title=Seminars+in+oncology+nursing&rft.issn=07492081&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-16 N1 - Date created - 1992-04-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Development of tolerance to 2-butoxyethanol-induced hemolytic anemia and studies to elucidate the underlying mechanisms. AN - 72830738; 1539158 AB - Early work demonstrated that a single administration of 2-butoxyethanol (BE) causes acute hemolytic anemia in rats. Current studies were undertaken to investigate the effect of repetitive daily dosing of BE on the hematologic parameters of male F344 rats. Treatment of rats with BE daily (125 mg/kg/day) for 1 to 3 consecutive days resulted in a time-dependent increase in the hemolysis of erythrocytes. However, when daily treatment with BE continued beyond 3 days, the number of erythrocytes began to rebound and approached pretreatment levels within 12 days despite continued daily exposure, suggesting development of tolerance to the hemolytic effect of BE. In vivo and in vitro studies were designed to investigate the underlying mechanism(s) of tolerance to the hematotoxicity of BE. Rats were treated with 125 mg BE/kg/day for 3 days followed by a 7-day recovery. At the end of this recovery period, rats were challenged with a single 125 or 250 mg BE/kg dose and the hematologic profiles were assessed at 2, 8, and 24 hr later. A significant decline in the sensitivity of BE-pretreated/recovered rats compared to vehicle-pretreated rats was observed. Further, in vitro incubation of blood obtained from BE-pretreated/recovered with the hematotoxic metabolite of BE, 2-butoxyacetic acid (BAA), revealed that erythrocytes obtained from these rats were significantly less sensitive to BAA than those obtained from normal rats. These studies suggested that tolerance is due, at least in part, to the lesser sensitivity of young erythrocytes formed during the regeneration process. In another study, rats were rendered anemic by bleeding followed by a 7-day recovery. BE administration to bled/recovered rats demonstrated that these rats were less sensitive than rats which were not subjected to bleeding. In vitro incubation of blood obtained from the bled/recovered animals with BAA demonstrated that erythrocytes were significantly less sensitive to BAA than those obtained from control rats. This further confirmed that young erythrocytes, formed during the regeneration process, were less sensitive to BAA than older erythrocytes. Current data also suggested that it is unlikely that tolerance is caused by modification of BE metabolism in rats repetitively exposed to this chemical. In conclusion, chronic exposure to BE would be expected to result in tolerance to BE-induced hemolytic anemia. The mechanisms responsible are likely related to the fact that older cells are more susceptible to BE and BAA and that hemolysis of these cells during the initial exposure followed by their replacement with less susceptible younger cells may account for tolerance development. JF - Toxicology and applied pharmacology AU - Ghanayem, B I AU - Sanchez, I M AU - Matthews, H B AD - National Institute of Environmental Health Sciences, Experimental Toxicology Branch, Research Triangle Park, North Carolina 27709. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 198 EP - 206 VL - 112 IS - 2 SN - 0041-008X, 0041-008X KW - Ethylene Glycols KW - 0 KW - Hemoglobins KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - n-butoxyethanol KW - I0P9XEZ9WV KW - Index Medicus KW - Rats KW - Drug Tolerance KW - Animals KW - Rats, Inbred F344 KW - Hemoglobins -- analysis KW - Erythrocyte Count -- drug effects KW - Dose-Response Relationship, Drug KW - Adenosine Triphosphate -- blood KW - Hematocrit KW - Time Factors KW - Male KW - Anemia, Hemolytic -- chemically induced KW - Ethylene Glycols -- toxicity KW - Ethylene Glycols -- blood KW - Anemia, Hemolytic -- blood KW - Ethylene Glycols -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72830738?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Development+of+tolerance+to+2-butoxyethanol-induced+hemolytic+anemia+and+studies+to+elucidate+the+underlying+mechanisms.&rft.au=Ghanayem%2C+B+I%3BSanchez%2C+I+M%3BMatthews%2C+H+B&rft.aulast=Ghanayem&rft.aufirst=B&rft.date=1992-02-01&rft.volume=112&rft.issue=2&rft.spage=198&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=0041008X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-30 N1 - Date created - 1992-03-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alcoholism and primary major depression: a family study approach to co-existing disorders. AN - 72829280; 1541771 AB - Alcoholism and major depression appear together at much higher than chance rates, but reasons for this are obscure. We used the direct diagnostic assessment of 177 probands with primary, unipolar depression and 619 of their first degree relatives to explore the significance of concomitant alcoholism. The male relatives of alcoholic probands of both sexes had substantially higher rates of alcoholism than did the male relatives of non-alcoholic probands. Among female probands, but not among male probands, alcoholism was associated with markedly higher familial rates of primary depression, particularly among female relatives. These data contained no evidence that comorbidity itself was familial. The appearance of alcoholism in depressed women may indicate depression spectrum disease, a disorder which manifests as depression in women and alcoholism in men. In contrast, men with both primary depression and alcoholism may be exhibiting two distinct illnesses. JF - Journal of affective disorders AU - Coryell, W AU - Winokur, G AU - Keller, M AU - Scheftner, W AU - Endicott, J AD - National Institute of Mental Health Collaborative Program on the Psychobiology of Depression - Clinical Studies, Bethesda, MD. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 93 EP - 99 VL - 24 IS - 2 SN - 0165-0327, 0165-0327 KW - Index Medicus KW - Sex Factors KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Comorbidity KW - Depressive Disorder -- epidemiology KW - Alcoholism -- epidemiology KW - Family KW - Alcoholism -- genetics KW - Alcoholism -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72829280?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+affective+disorders&rft.atitle=Alcoholism+and+primary+major+depression%3A+a+family+study+approach+to+co-existing+disorders.&rft.au=Coryell%2C+W%3BWinokur%2C+G%3BKeller%2C+M%3BScheftner%2C+W%3BEndicott%2C+J&rft.aulast=Coryell&rft.aufirst=W&rft.date=1992-02-01&rft.volume=24&rft.issue=2&rft.spage=93&rft.isbn=&rft.btitle=&rft.title=Journal+of+affective+disorders&rft.issn=01650327&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-08 N1 - Date created - 1992-04-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Exposure to tetrachlorodibenzo-p-dioxin (TCDD) alters fetal thymocyte maturation. AN - 72823973; 1531708 AB - We previously reported that thymic atrophy and reduced thymic cellularity associated with prenatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in mice are characterized by quantitative alerations in the number of thymocytes expressing CD4 and CD8 surface antigens. In the present study, these observations have been extended to establish the specific thymocyte maturation processes affected by TCDD through an examination of cell size distributions, alpha beta and gamma delta T cell receptor (TCR) expression, peanut agglutinin (PNA) binding, and J11d marker analysis in murine thymocytes exposed prenatally to TCDD. Pregnant mice were administered vehicle, 1.5 or 3.0 micrograms/kg body wt TCDD by gavage on gestational Days (gd) 6-14. Flow cytometry analysis of gd 18 fetal thymocytes revealed a reduction in the number of small CD4+CD8+ double positive (DP) and PNA+, small thymocytes in the TCDD-exposed groups. The large cell population was reduced by TCDD to approximately 70% of control values. There was also a significant shift in TCR expression of thymocytes with a decrease in alpha beta TCR and a concommitant increase in gamma delta TCR expression from TCDD-exposed fetuses. The CD4-CD8+J11d+ thymocytes were increased in TCDD-treated mice while the more mature CD4-CD8+J11d- thymocyte numbers were similar to controls. Taken together, these data indicate that TCDD inhibits thymocyte maturation at the transition phase between the CD4-CD8+J11d+ phenotype and the DP/J11d+ thymocytes. JF - Toxicology and applied pharmacology AU - Blaylock, B L AU - Holladay, S D AU - Comment, C E AU - Heindel, J J AU - Luster, M I AD - Immunotoxicology Group, Systems Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 207 EP - 213 VL - 112 IS - 2 SN - 0041-008X, 0041-008X KW - Antigens, CD KW - 0 KW - Antigens, CD24 KW - Antigens, CD4 KW - Antigens, CD8 KW - Antigens, Differentiation KW - Cd24a protein, mouse KW - Lectins KW - Membrane Glycoproteins KW - Peanut Agglutinin KW - Polychlorinated Dibenzodioxins KW - Receptors, Antigen, T-Cell KW - Receptors, Antigen, T-Cell, alpha-beta KW - Receptors, Antigen, T-Cell, gamma-delta KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Antigens, CD8 -- physiology KW - Antigens, Differentiation -- physiology KW - Mice KW - CD4-CD8 Ratio KW - Receptors, Antigen, T-Cell -- physiology KW - Receptors, Antigen, T-Cell, alpha-beta -- physiology KW - Pregnancy KW - Receptors, Antigen, T-Cell, gamma-delta -- drug effects KW - Antigens, CD4 -- physiology KW - Mice, Inbred C57BL KW - Receptors, Antigen, T-Cell, alpha-beta -- drug effects KW - Receptors, Antigen, T-Cell -- drug effects KW - Female KW - Lectins -- metabolism KW - Male KW - Receptors, Antigen, T-Cell, gamma-delta -- physiology KW - Thymus Gland -- cytology KW - Polychlorinated Dibenzodioxins -- pharmacology KW - Thymus Gland -- embryology KW - T-Lymphocytes -- physiology KW - T-Lymphocytes -- drug effects KW - Embryo, Mammalian -- immunology KW - Embryo, Mammalian -- drug effects KW - Thymus Gland -- drug effects KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72823973?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Exposure+to+tetrachlorodibenzo-p-dioxin+%28TCDD%29+alters+fetal+thymocyte+maturation.&rft.au=Blaylock%2C+B+L%3BHolladay%2C+S+D%3BComment%2C+C+E%3BHeindel%2C+J+J%3BLuster%2C+M+I&rft.aulast=Blaylock&rft.aufirst=B&rft.date=1992-02-01&rft.volume=112&rft.issue=2&rft.spage=207&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=0041008X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-30 N1 - Date created - 1992-03-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential sensitivity of freshly isolated and cultured murine Langerhans cells to ultraviolet B radiation and chemical fixation. AN - 72822660; 1347017 AB - Previous studies have demonstrated that low doses of ultraviolet B (UVB) radiation (100 J/m2) abrogate the accessory function of freshly isolated murine epidermal Langerhans cells (fLC) and cause a parallel decrease in the ability of LC to express increased amounts of ICAM-1 (CD54) in vitro. We have subsequently observed that the accessory cell function of cultured LC (cLC), as assessed by their ability to support anti-CD3 monoclonal antibody (mAb)-induced T cell mitogenesis, was not inhibited by levels of UVB exposure (100 J/m2) that completely inhibited the function of fLC, although exposure of cLC to UVB radiation (100 J/m2) resulted in a decrease in the level of ICAM-1 expression on most cLC and a concomitant decrease in cLC survival during a subsequent 24-h incubation. Time course studies revealed that T cells stimulated with anti-CD3 mAb in the presence of cLC became committed to proliferate 4-8 h after culture initiation, while 24-30 h of co-culture was required for irreversible T cell activation when fLC were utilized as accessory cells. In addition, paraformaldehyde (PFA)-fixed (non-viable) cLC supported anti-CD3 mAb-induced T cell proliferation, whereas PFA-fixed fLC were ineffective. We propose that cLC are functionally resistant to low doses of UVB radiation and chemical fixation because cLC express sufficient levels of the adhesion or co-stimulatory molecules [including ICAM-1 and Mac-1 (CD11b/CD18)] required to induce T cell activation. Conversely, fLC are sensitive to the effects of UVB radiation and chemical fixation because these physicochemical agents prevent acquisition of critically important surface molecules in culture. JF - European journal of immunology AU - Tang, A AU - Udey, M C AD - Dermatology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 581 EP - 586 VL - 22 IS - 2 SN - 0014-2980, 0014-2980 KW - Antigens, CD3 KW - 0 KW - Antigens, Differentiation, T-Lymphocyte KW - Cell Adhesion Molecules KW - Fixatives KW - Polymers KW - Receptors, Antigen, T-Cell KW - Intercellular Adhesion Molecule-1 KW - 126547-89-5 KW - Formaldehyde KW - 1HG84L3525 KW - paraform KW - Y19UC83H8E KW - Index Medicus KW - Animals KW - Ultraviolet Rays KW - Formaldehyde -- chemistry KW - Receptors, Antigen, T-Cell -- immunology KW - Polymers -- chemistry KW - Mice KW - Cell Separation KW - Dose-Response Relationship, Radiation KW - Mice, Inbred BALB C KW - Antigen-Presenting Cells -- drug effects KW - Cell Survival KW - Lymphocyte Activation KW - Cells, Cultured KW - In Vitro Techniques KW - Antigen-Presenting Cells -- cytology KW - Cell Adhesion Molecules -- metabolism KW - Antigen-Presenting Cells -- radiation effects KW - Antigens, Differentiation, T-Lymphocyte -- immunology KW - Time Factors KW - T-Lymphocytes -- immunology KW - Cell Adhesion KW - Langerhans Cells -- radiation effects KW - Langerhans Cells -- drug effects KW - Langerhans Cells -- cytology KW - Langerhans Cells -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72822660?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+immunology&rft.atitle=Differential+sensitivity+of+freshly+isolated+and+cultured+murine+Langerhans+cells+to+ultraviolet+B+radiation+and+chemical+fixation.&rft.au=Tang%2C+A%3BUdey%2C+M+C&rft.aulast=Tang&rft.aufirst=A&rft.date=1992-02-01&rft.volume=22&rft.issue=2&rft.spage=581&rft.isbn=&rft.btitle=&rft.title=European+journal+of+immunology&rft.issn=00142980&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-01 N1 - Date created - 1992-04-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of human mu or alpha class glutathione S-transferases in stably transfected human MCF-7 breast cancer cells: effect on cellular sensitivity to cytotoxic agents. AN - 72821198; 1538704 AB - Increased expression of certain glutathione S-transferase (GST) isoenzymes has frequently been associated with the development of resistance to alkylating agents and other classes of antineoplastic drugs in drug-selected cell lines. The question arises whether this phenomenon is causal or is a stress-induced response associated with drug resistance in these cell lines. We have constructed mammalian expression vectors containing the human GST mu and GST alpha 2 (Ha2) cDNAs and stably transfected them into the human breast cancer cell line MCF-7. Whereas the parental and pSV2neo-transfected cell lines display low GST activity, three individual transfected clones were identified in each group that expressed either GST mu or GST alpha 2. The range of GST activities was similar to those observed in cells selected for anticancer drug resistance. The GST mu specific activities were 56, 150, and 340 mlU/mg, compared with 10 mlU/mg of endogenous GST mu in control lines. Specific activities in GST alpha 2-transfected clones were 17, 28, and 52 mlU/mg, compared with no detectable alpha class GST in control lines. These clonal lines and the parental and pSV2neo-transfected control lines were tested for sensitivity to antineoplastic agents and other cytotoxic compounds. The clones with the highest activity in each group were 1.7-fold (GST alpha 2) to 2.1-fold (GST mu) resistant to the toxic effects of ethacrynic acid, a known substrate for GSTs. However, the GST-transfected cell lines were not resistant to doxorubicin, L-phenylalanine mustard, bis(2-chloroethyl)-1-nitrosourea, cisplatin, chlorambucil, or the GST substrates 1-chloro-2,4-dinitrobenzene or tert-butyl hydroperoxide. Thus, although L-phenylalanine mustard, bis(2-chloroethyl)-1-nitrosourea, chlorambucil, tert-butyl hydroperoxide, and 1-chloro-2,4-dinitrobenzene are known to be metabolized by glutathione-dependent GST-catalyzed reactions, there was no protection against any of these agents in MCF-7 cell lines overexpressing GST mu or GST alpha 2. We conclude that, at the levels of GST obtained in this transfection model system, overexpression of GST mu or GST alpha 2 is not by itself sufficient to confer resistance to these anticancer agents. These studies do not exclude the possibility that GST may be a marker of drug resistance or that other gene products not expressed in MCF-7 cells might cooperate with GST to confer drug resistance. JF - Molecular pharmacology AU - Townsend, A J AU - Tu, C P AU - Cowan, K H AD - Medicine Branch, National Cancer Institute, National Institues of Health, Bethesda, Maryland 20892. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 230 EP - 236 VL - 41 IS - 2 SN - 0026-895X, 0026-895X KW - GST&agr;2 KW - GST&mgr; KW - Antineoplastic Agents KW - 0 KW - Isoenzymes KW - DNA KW - 9007-49-2 KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Ethacrynic Acid KW - M5DP350VZV KW - Index Medicus KW - Drug Resistance -- genetics KW - Gene Expression -- genetics KW - Tumor Cells, Cultured -- drug effects KW - Transfection KW - Humans KW - DNA -- genetics KW - Ethacrynic Acid -- pharmacology KW - Breast Neoplasms -- genetics KW - Breast Neoplasms -- drug therapy KW - Glutathione Transferase -- physiology KW - Glutathione Transferase -- genetics KW - Breast Neoplasms -- enzymology KW - Isoenzymes -- genetics KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72821198?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=Expression+of+human+mu+or+alpha+class+glutathione+S-transferases+in+stably+transfected+human+MCF-7+breast+cancer+cells%3A+effect+on+cellular+sensitivity+to+cytotoxic+agents.&rft.au=Townsend%2C+A+J%3BTu%2C+C+P%3BCowan%2C+K+H&rft.aulast=Townsend&rft.aufirst=A&rft.date=1992-02-01&rft.volume=41&rft.issue=2&rft.spage=230&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=0026895X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-27 N1 - Date created - 1992-03-27 N1 - Date revised - 2017-01-13 N1 - Gene symbol - GST&agr;2; GST&mgr; N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Enhancement by nickel(II) and L-histidine of 2'-deoxyguanosine oxidation with hydrogen peroxide. AN - 72820924; 1740020 AB - Conversion of the 2'-deoxyguanosine (dG) residues in calf thymus DNA to 8-hydroxy-2'-deoxyguanosine (8-OH-dG) was achieved at physiological pH by treating the DNA with hydrogen peroxide (H2O2) in the presence of nickel(II) chloride (NiCl2). The effectiveness of this reaction was enhanced by L-histidine (His) which forms the Ni(II)-His2 complex. Similar effects of NiCl2 and His were observed on hydroxylation of pure dG with H2O2. The rate of pure dG conversion to 8-OH-dG at 37 degrees C (100 mM phosphate buffer) depended on combination and concentration of the reagents and on pH. Following 24 h incubation at pH 7.4 of 0.75 mM dG with 30 mM H2O2 and 1 mM NiCl2, dG was converted into 8-OH-dG to the extent of 0.05% in the absence of His and 0.45% in the presence of 2 mM His. After 24 h incubation at pH 7.4 of 0.5 mg/ml DNA with 7.5 mM H2O2 and 0.1 mM NiCl2, 0.18% of the dG moiety was converted into 8-OH-dG in the absence of His and 0.42% in the presence of 0.2 mM His. Interestingly, a mixture of H2O2 with His was also capable of oxidizing dG to 8-OH-dG even in the absence of NiCl2, albeit less effectively than in the presence of NiCl2. This effect was not suppressed after treatment of dG, His and the buffer with Chelex to remove divalent metal contaminants, if any. The exact chemistry of the observed phenomena remains to be determined. Since the Ni(II)-His2 complex is the major low mol. wt nickel carrier in mammalian organisms, the observed redox properties of this complex, reported here for the first time, may be crucial for the toxicity and carcinogenicity of nickel. JF - Carcinogenesis AU - Dutta, A K AU - Misra, M AU - North, S L AU - Kasprzak, K S AD - National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 283 EP - 287 VL - 13 IS - 2 SN - 0143-3334, 0143-3334 KW - Histidine KW - 4QD397987E KW - nickel chloride KW - 696BNE976J KW - Nickel KW - 7OV03QG267 KW - 8-oxo-7-hydrodeoxyguanosine KW - 88847-89-6 KW - DNA KW - 9007-49-2 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Deoxyguanosine KW - G9481N71RO KW - Index Medicus KW - Oxidation-Reduction KW - Animals KW - Cattle KW - Hydrogen-Ion Concentration KW - Chromatography, High Pressure Liquid KW - Hydroxylation KW - DNA -- drug effects KW - Deoxyguanosine -- metabolism KW - Nickel -- pharmacology KW - Thymus Gland -- metabolism KW - Hydrogen Peroxide -- pharmacology KW - Deoxyguanosine -- analysis KW - Thymus Gland -- drug effects KW - Histidine -- pharmacology KW - Deoxyguanosine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72820924?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Enhancement+by+nickel%28II%29+and+L-histidine+of+2%27-deoxyguanosine+oxidation+with+hydrogen+peroxide.&rft.au=Dutta%2C+A+K%3BMisra%2C+M%3BNorth%2C+S+L%3BKasprzak%2C+K+S&rft.aulast=Dutta&rft.aufirst=A&rft.date=1992-02-01&rft.volume=13&rft.issue=2&rft.spage=283&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-23 N1 - Date created - 1992-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA polymerase II, the probable homolog of mammalian DNA polymerase epsilon, replicates chromosomal DNA in the yeast Saccharomyces cerevisiae. AN - 72820872; 1537345 AB - Two temperature-sensitive DNA polymerase II mutants (pol2-9 and pol2-18) of the yeast Saccharomyces cerevisiae were isolated by the plasmid shuffling method. DNA polymerase II activity partially purified from both mutants was thermolabile, while DNA polymerase I and III activities remained thermotolerant. At the restrictive temperature, the pol2 mutants were defective in chromosomal DNA replication and exhibited the dumbbell terminal morphology typical of DNA replication mutants. The POL2 transcript accumulated periodically during the cell cycle, peaking at the G1/S boundary in the same manner as the transcripts of more than 10 other DNA replication genes. These results indicate that DNA polymerase II participates in nuclear DNA replication. The similarities in structure and activities between the DNA polymerases of yeast and mammals make it likely that mammalian DNA polymerase epsilon too is required for chromosomal DNA replication. JF - The EMBO journal AU - Araki, H AU - Ropp, P A AU - Johnson, A L AU - Johnston, L H AU - Morrison, A AU - Sugino, A AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 733 EP - 740 VL - 11 IS - 2 SN - 0261-4189, 0261-4189 KW - pol2 KW - pol2-18 KW - pol2-9 KW - RNA, Fungal KW - 0 KW - DNA Polymerase II KW - EC 2.7.7.- KW - DNA Polymerase III KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - Index Medicus KW - Animals KW - RNA, Fungal -- genetics KW - RNA, Fungal -- isolation & purification KW - Blotting, Northern KW - Genes, Fungal KW - Mammals KW - Sequence Homology, Nucleic Acid KW - Temperature KW - Transcription, Genetic KW - Amino Acid Sequence KW - Plasmids KW - Mutagenesis KW - Kinetics KW - Molecular Sequence Data KW - Saccharomyces cerevisiae -- genetics KW - DNA Polymerase II -- isolation & purification KW - DNA Polymerase II -- metabolism KW - Saccharomyces cerevisiae -- enzymology KW - DNA Polymerase II -- genetics KW - DNA-Directed DNA Polymerase -- genetics KW - DNA Replication KW - DNA-Directed DNA Polymerase -- metabolism KW - Chromosomes, Fungal UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72820872?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+EMBO+journal&rft.atitle=DNA+polymerase+II%2C+the+probable+homolog+of+mammalian+DNA+polymerase+epsilon%2C+replicates+chromosomal+DNA+in+the+yeast+Saccharomyces+cerevisiae.&rft.au=Araki%2C+H%3BRopp%2C+P+A%3BJohnson%2C+A+L%3BJohnston%2C+L+H%3BMorrison%2C+A%3BSugino%2C+A&rft.aulast=Araki&rft.aufirst=H&rft.date=1992-02-01&rft.volume=11&rft.issue=2&rft.spage=733&rft.isbn=&rft.btitle=&rft.title=The+EMBO+journal&rft.issn=02614189&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-31 N1 - Date created - 1992-03-31 N1 - Date revised - 2017-01-13 N1 - Gene symbol - pol2; pol2-18; pol2-9 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9473-7 [1658784] Mol Cell Biol. 1983 Jun;3(6):1000-12 [6348512] Nucleic Acids Res. 1991 Sep 25;19(18):4867-72 [1923754] Nature. 1991 Mar 21;350(6315):247-50 [2005980] Gene. 1991 Apr;100:27-38 [2055476] Cell. 1990 Sep 21;62(6):1143-51 [2169349] Proc Natl Acad Sci U S A. 1990 Dec;87(24):9712-6 [2175912] Eur J Biochem. 1990 Aug 17;191(3):617-8 [2390988] Nucleic Acids Res. 1989 Nov 25;17(22):9231-44 [2555788] EMBO J. 1989 Dec 1;8(12):3883-9 [2573521] FASEB J. 1989 Jan;3(1):14-21 [2642867] Mol Cell Biol. 1989 Feb;9(2):365-76 [2651896] EMBO J. 1989 Jun;8(6):1849-54 [2670563] Nature. 1987 Apr 2-8;326(6112):515-7 [2882423] Cell. 1988 Apr 8;53(1):117-26 [2894900] EMBO J. 1987 Jan;6(1):169-75 [3034575] Proc Natl Acad Sci U S A. 1988 Jun;85(11):3772-6 [3287376] Methods Enzymol. 1987;154:164-75 [3323810] Proc Natl Acad Sci U S A. 1987 May;84(9):2838-42 [3554248] J Biol Chem. 1986 Aug 15;261(23):10802-7 [3733734] Methods Enzymol. 1983;100:293-308 [6312261] Mol Cell Biol. 1991 May;11(5):2350-61 [1673224] J Biol Chem. 1991 Nov 25;266(33):22698-706 [1682322] Cell. 1991 Jul 26;66(2):185-7 [1855251] Nucleic Acids Res. 1990 Jan 25;18(2):261-5 [1970160] Proc Natl Acad Sci U S A. 1990 Sep;87(17):6664-8 [1975694] Proc Natl Acad Sci U S A. 1991 Jun 1;88(11):4601-5 [2052544] Nature. 1990 Aug 9;346(6284):534-9 [2165567] J Virol. 1990 Dec;64(12):5912-8 [2173773] Proc Natl Acad Sci U S A. 1990 Nov;87(22):8692-6 [2174160] Biochem Biophys Res Commun. 1990 Aug 16;170(3):1294-300 [2202298] J Biol Chem. 1990 Mar 5;265(7):4072-83 [2406268] Nature. 1989 Nov 2;342(6245):92-5 [2554144] Proc Natl Acad Sci U S A. 1989 Oct;86(19):7361-5 [2571990] Proc Natl Acad Sci U S A. 1989 Dec;86(24):9742-6 [2574863] Exp Cell Res. 1989 Feb;180(2):419-28 [2644125] Cell. 1989 Feb 24;56(4):599-605 [2645055] Yeast. 1989 Mar-Apr;5(2):117-29 [2652918] Proc Natl Acad Sci U S A. 1988 Sep;85(18):6672-6 [2842788] J Biol Chem. 1988 Dec 25;263(36):19723-33 [2848839] Nature. 1987 Apr 2-8;326(6112):517-20 [2882424] Proc Natl Acad Sci U S A. 1986 May;83(9):2869-73 [3010320] Gene. 1988 Dec 30;74(2):527-34 [3073106] J Biol Chem. 1988 Jan 5;263(1):1-4 [3275635] Nucleic Acids Res. 1987 Jul 10;15(13):5017-30 [3299263] J Biol Chem. 1988 Jan 5;263(1):501-10 [3335506] EMBO J. 1986 Jul;5(7):1705-9 [3527694] J Biol Chem. 1986 Jul 5;261(19):8888-93 [3722180] Cell. 1985 Nov;43(1):369-77 [3907855] J Mol Biol. 1983 Jun 5;166(4):557-80 [6345791] Biochim Biophys Acta. 1991 Jan 17;1088(1):11-24 [1846563] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tamoxifen prevents induction of hepatic neoplasia by zeranol, an estrogenic food contaminant. AN - 72812490; 1736291 AB - Zeranol (alpha-zearalanol) is a beta-resorcylic acid lactone (RAL) that has estrogen activity. It is synthesized by molds and is difficult to avoid in human food products. We tested the ability of this mycoestrogen to damage the liver of the Armenian hamster, a rodent that is especially sensitive to hepatotoxic effects of exogenous estrogens. Zeranol induced acute hepatotoxicity and, subsequently, hepatic carcinogenesis; both effects were blocked by tamoxifen, suggesting estrogen receptor mediation. Because zeranol is acting alone as a primary initiator of hepatic neoplasms, this model provides an unusual opportunity to study the pathogenesis of estrogen-initiated tumorigenesis. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Coe, J E AU - Ishak, K G AU - Ward, J M AU - Ross, M J AD - National Institutes of Health, National Institute of Allergy and Infectious Diseases, Hamilton, MT 59840. Y1 - 1992/02/01/ PY - 1992 DA - 1992 Feb 01 SP - 1085 EP - 1089 VL - 89 IS - 3 SN - 0027-8424, 0027-8424 KW - Estrogens KW - 0 KW - Tamoxifen KW - 094ZI81Y45 KW - Zeranol KW - 76LO2L2V39 KW - Bilirubin KW - RFM9X3LJ49 KW - Index Medicus KW - Animals KW - Cricetulus KW - Dose-Response Relationship, Drug KW - Food Contamination KW - Bilirubin -- blood KW - Male KW - Female KW - Estrogens -- toxicity KW - Cricetinae KW - Tamoxifen -- pharmacology KW - Liver Neoplasms -- pathology KW - Zeranol -- toxicity KW - Liver Neoplasms -- chemically induced KW - Zeranol -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72812490?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Tamoxifen+prevents+induction+of+hepatic+neoplasia+by+zeranol%2C+an+estrogenic+food+contaminant.&rft.au=Coe%2C+J+E%3BIshak%2C+K+G%3BWard%2C+J+M%3BRoss%2C+M+J&rft.aulast=Coe&rft.aufirst=J&rft.date=1992-02-01&rft.volume=89&rft.issue=3&rft.spage=1085&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-10 N1 - Date created - 1992-03-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Prev Med. 1991 Jan;20(1):27-37 [1672563] Br Med J (Clin Res Ed). 1986 May 24;292(6532):1355-7 [3011185] Proc Natl Acad Sci U S A. 1991 Jan 1;88(1):21-5 [1986369] Liver. 1990 Oct;10(5):264-8 [1701511] Lab Invest. 1987 Jan;56(1):4-22 [3025514] Regul Toxicol Pharmacol. 1987 Sep;7(3):253-306 [2961013] Food Chem Toxicol. 1985 Aug;23(8):767-74 [2931335] Adv Cancer Res. 1985;45:217-90 [2936065] Cancer Res. 1988 Aug 1;48(15):4135-43 [3292040] Yale J Biol Med. 1989 Sep-Oct;62(5):459-80 [2697981] Endocrinology. 1988 Jan;122(1):137-44 [3335202] Nature. 1984 Dec 6-12;312(5994):513-6 [6095109] Pharmacol Ther. 1984;25(2):127-205 [6438654] J Natl Cancer Inst. 1986 Jun;76(6):1243-6 [3458960] Am J Physiol. 1990 Aug;259(2 Pt 2):R341-9 [1696791] Prog Clin Biol Res. 1990;331:231-48 [1690432] J Exp Med. 1990 Apr 1;171(4):1257-67 [1691262] Cell. 1990 Jun 1;61(5):759-67 [2188735] Hepatology. 1990 Apr;11(4):570-7 [2328952] Gastroenterology. 1982 Jul;83(1 Pt 1):109-13 [6176493] Br J Cancer. 1983 Sep;48(3):437-40 [6311235] Biochem Biophys Res Commun. 1984 Jan 13;118(1):27-32 [6320825] Semin Liver Dis. 1984 May;4(2):147-57 [6087460] Mol Pharmacol. 1981 Jul;20(1):35-42 [6457245] Hepatology. 1983 Jul-Aug;3(4):489-96 [6602753] Cancer. 1983 Jun 15;51(12 Suppl):2426-9 [6850519] JAMA. 1979 Aug 17;242(7):644-8 [221698] J Environ Pathol Toxicol. 1979 Dec;3(1-2):329-51 [575723] Endocrinology. 1979 Jul;105(1):33-40 [446414] Endocrinology. 1978 Feb;102(2):433-42 [743966] Biochem Biophys Res Commun. 1978 Nov 14;85(1):167-73 [743272] Pediatrics. 1978 Dec;62(6 Pt 2):1138-42 [724351] J Steroid Biochem. 1977 Apr;8(4):251-8 [886856] N Engl J Med. 1971 Apr 15;284(15):878-81 [5549830] Lancet. 1973 Oct 27;2(7835):926-9 [4126557] Lab Invest. 1975 Jun;32(6):773-6 [50498] Steroids. 1975 Sep;26(3):363-71 [173045] N Engl J Med. 1976 Feb 26;294(9):470-2 [173996] J Endocrinol. 1976 Apr;69(1):167-8 [1270957] J Natl Cancer Inst. 1991 Apr 3;83(7):492-6 [2005632] J Gastroenterol Hepatol. 1990 Mar-Apr;5(2):149-59 [1966478] Science. 1989 May 12;244(4905):707-12 [2470152] Hepatology. 1987 Jul-Aug;7(4):764-72 [3038725] Br Med J (Clin Res Ed). 1986 May 24;292(6532):1357-61 [3011186] Prev Med. 1991 Jan;20(1):15-26 [1672562] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retinoic acid-dependent transactivation of major histocompatibility complex class I promoters by the nuclear hormone receptor H-2RIIBP in undifferentiated embryonal carcinoma cells. AN - 72801658; 1736309 AB - H-2RIIBP is a member of the nuclear hormone receptor superfamily that binds to the region II enhancer of major histocompatibility complex (MHC) class I genes. The binding occurs through the GG(T/A)CA motif present also in many other genes. The role of H-2RIIBP in developmental regulation of MHC class I genes has been studied in undifferentiated N-Tera2 embryonal carcinoma cells by transient cotransfection of an expressible H-2RIIBP plasmid and a chloramphenicol acetyltransferase reporter gene linked to the MHC class I promoter. Transfection of the expression plasmid led to production of H-2RIIBP transcripts and enhanced MHC class I promoter activity in cells that were treated with retinoic acid but not yet differentiated. Retinoic acid concentrations required for transactivation overlapped with those capable of inducing morphological differentiation and expression of endogenous MHC class I genes in these cells. This enhancement was mediated by region II, as a heterologous thymidine kinase promoter driven by region II also served as a target for H-2RIIBP transactivation. Deletion of the bulk of the DNA-binding domain or the ligand-binding domain of H-2RIIBP, but not of the N-terminal domain, abolished transactivation, indicating that the former two domains are critical for the enhancement. Moreover, H-2RIIBP transactivation exhibited a strict cell-type restriction. As observed in other cell lines, N-Tera2 cells that had undergone differentiation failed to elicit transactivation, suggesting that H-2RIIBP acts in concert with a cofactor expressed in undifferentiated N-Tera2 cells that requires retinoic acid for its function. These results suggest that H-2RIIBP can function as a developmentally specific transcription factor for MHC class I genes. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Nagata, T AU - Segars, J H AU - Levi, B Z AU - Ozato, K AD - Laboratory of Developmental and Molecular Immunity, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/02/01/ PY - 1992 DA - 1992 Feb 01 SP - 937 EP - 941 VL - 89 IS - 3 SN - 0027-8424, 0027-8424 KW - DNA-Binding Proteins KW - 0 KW - Nuclear Proteins KW - Tretinoin KW - 5688UTC01R KW - Index Medicus KW - Regulatory Sequences, Nucleic Acid KW - Polymerase Chain Reaction KW - Promoter Regions, Genetic KW - Base Sequence KW - Tumor Cells, Cultured KW - Humans KW - Enhancer Elements, Genetic KW - DNA Mutational Analysis KW - In Vitro Techniques KW - Molecular Sequence Data KW - Gene Expression Regulation KW - DNA-Binding Proteins -- physiology KW - Cell Differentiation -- drug effects KW - Transcriptional Activation KW - Structure-Activity Relationship KW - Tretinoin -- pharmacology KW - Teratoma -- genetics KW - Nuclear Proteins -- physiology KW - Genes, MHC Class I UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72801658?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Retinoic+acid-dependent+transactivation+of+major+histocompatibility+complex+class+I+promoters+by+the+nuclear+hormone+receptor+H-2RIIBP+in+undifferentiated+embryonal+carcinoma+cells.&rft.au=Nagata%2C+T%3BSegars%2C+J+H%3BLevi%2C+B+Z%3BOzato%2C+K&rft.aulast=Nagata&rft.aufirst=T&rft.date=1992-02-01&rft.volume=89&rft.issue=3&rft.spage=937&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-10 N1 - Date created - 1992-03-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Mol Cell Biol. 1991 Jul;11(7):3814-20 [1646397] Proc Natl Acad Sci U S A. 1986 Dec;83(24):9537-41 [3467324] Cell. 1990 Nov 16;63(4):729-38 [2171781] Mol Endocrinol. 1990 Sep;4(9):1293-301 [2172797] Proc Natl Acad Sci U S A. 1989 Nov;86(21):8289-93 [2554307] Cell. 1989 May 5;57(3):367-78 [2566383] Nature. 1989 Jul 13;340(6229):140-4 [2739735] Science. 1988 May 13;240(4854):889-95 [3283939] Genes Dev. 1989 Oct;3(10):1507-17 [2482225] Proc Natl Acad Sci U S A. 1988 Aug;85(16):5884-8 [2457903] Genes Dev. 1988 May;2(5):554-66 [2454869] Proc Natl Acad Sci U S A. 1985 Apr;82(8):2427-31 [2581247] Mol Endocrinol. 1989 Oct;3(10):1610-26 [2558297] Cell. 1989 Nov 17;59(4):697-708 [2555064] Cell. 1989 Jun 30;57(7):1131-8 [2500250] Cell. 1989 Feb 10;56(3):335-44 [2644044] Mol Endocrinol. 1989 Sep;3(9):1434-42 [2608066] Proc Natl Acad Sci U S A. 1989 May;86(10):3494-8 [2726731] J Exp Med. 1989 Apr 1;169(4):1309-21 [2926327] Nature. 1988 Jan 7;331(6151):91-4 [3267207] Cell. 1984 Dec;39(3 Pt 2):653-62 [6096017] Cell. 1986 Jan 31;44(2):261-72 [3510743] Mol Cell Biol. 1987 Dec;7(12):4542-8 [3501825] Cell. 1987 Dec 24;51(6):941-51 [3690665] Mol Cell Biol. 1987 Jan;7(1):305-13 [3561391] Science. 1987 Apr 24;236(4800):423-7 [3563519] Cell. 1987 Apr 10;49(1):39-46 [3829127] Nature. 1987 Jan 22-28;325(6102):365-8 [3808033] Nature. 1986 Aug 21-27;322(6081):743-6 [3748155] Nucleic Acids Res. 1990 Jul 25;18(14):4143-8 [2165589] Nature. 1990 Aug 23;346(6286):763-6 [1975088] Nature. 1990 Sep 20;347(6290):298-301 [2169594] Nature. 1990 May 17;345(6272):224-9 [2159111] Nature. 1990 Jun 28;345(6278):815-9 [2359458] Cell. 1990 Mar 23;60(6):953-62 [2317866] Proc Natl Acad Sci U S A. 1981 Sep;78(9):5754-8 [6170985] Nature. 1982 Mar 18;296(5854):260-2 [6174872] Dev Biol. 1984 Jun;103(2):285-93 [6144603] Science. 1980 Aug 15;209(4458):768-76 [6250214] Cell. 1978 Oct;15(2):393-403 [214238] Mol Endocrinol. 1990 Nov;4(11):1627-35 [2280769] Cell. 1988 Oct 21;55(2):361-9 [3167984] Cell. 1988 Oct 7;55(1):145-56 [3167974] Nucleic Acids Res. 1986 Nov 25;14(22):8755-70 [3466137] Mol Cell Biol. 1987 Aug;7(8):2745-52 [3670292] EMBO J. 1991 Feb;10(2):263-8 [1846802] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Duplication-targeted DNA methylation and mutagenesis in the evolution of eukaryotic chromosomes. AN - 72800625; 1736289 AB - Mammalian genomes are threatened with gene inactivation and chromosomal scrambling by recombination between repeated sequences such as mobile genetic elements and pseudogenes. We present and test a model for a defensive strategy based on the methylation and subsequent mutation of CpG dinucleotides in those DNA duplications that create uninterrupted homologous sequences longer than about 0.3 kilobases. The model helps to explain both the diversity of CpG frequencies in different genes and the persistence of gene fragmentation into exons and introns. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Kricker, M C AU - Drake, J W AU - Radman, M AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/02/01/ PY - 1992 DA - 1992 Feb 01 SP - 1075 EP - 1079 VL - 89 IS - 3 SN - 0027-8424, 0027-8424 KW - Index Medicus KW - Space life sciences KW - Pseudogenes KW - Animals KW - Genes KW - Multigene Family KW - Humans KW - Chromosomes -- ultrastructure KW - Repetitive Sequences, Nucleic Acid KW - Methylation KW - Biological Evolution KW - Eukaryotic Cells -- physiology KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72800625?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Duplication-targeted+DNA+methylation+and+mutagenesis+in+the+evolution+of+eukaryotic+chromosomes.&rft.au=Kricker%2C+M+C%3BDrake%2C+J+W%3BRadman%2C+M&rft.aulast=Kricker&rft.aufirst=M&rft.date=1992-02-01&rft.volume=89&rft.issue=3&rft.spage=1075&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-10 N1 - Date created - 1992-03-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Gene. 1990 Jul 16;91(2):179-84 [2210379] Proc Natl Acad Sci U S A. 1988 Dec;85(24):9625-9 [2849112] Science. 1990 Dec 21;250(4988):1745-8 [1980158] Annu Rev Genet. 1990;24:579-613 [2150906] Trends Genet. 1990 Dec;6(12):385-9 [2087779] Science. 1990 Dec 7;250(4986):1377-82 [2255907] Nature. 1986 May 15-21;321(6067):209-13 [2423876] Mol Gen Genet. 1989 Aug;218(2):358-60 [2550771] Genetics. 1986 Mar;112(3):441-57 [3007275] Proc Natl Acad Sci U S A. 1987 Aug;84(15):5340-4 [3037544] Annu Rev Genet. 1986;20:523-38 [2949693] Gene. 1989 Nov 15;83(1):181-3 [2574129] Annu Rev Genet. 1989;23:199-225 [2694931] Nucleic Acids Res. 1989 Jan 11;17(1):185-95 [2911464] Proc Natl Acad Sci U S A. 1988 Jul;85(13):4770-4 [3387437] Cell. 1990 Aug 10;62(3):503-14 [1974172] J Mol Biol. 1990 May 20;213(2):203-6 [2342101] Proc Natl Acad Sci U S A. 1990 Feb;87(4):1551-5 [2154751] Trends Genet. 1990 Jun;6(6):182-6 [2196721] Science. 1990 Sep 14;249(4974):1288-90 [1697983] J Biol Chem. 1984 Mar 25;259(6):3748-56 [6706976] Mol Cell Biol. 1984 May;4(5):985-8 [6374428] Nucleic Acids Res. 1984 Jan 11;12(1 Pt 1):387-95 [6546423] Nature. 1978 Aug 24;274(5673):775-80 [355893] Nature. 1978 Feb 9;271(5645):501 [622185] Nature. 1989 Nov 23;342(6248):396-401 [2555716] Cell. 1985 Jan;40(1):91-9 [2981636] Mol Cell Biol. 1985 Jul;5(7):1694-706 [4022011] Annu Rev Genet. 1988;22:147-68 [3071247] Proc Natl Acad Sci U S A. 1989 Jun;86(12):4584-8 [2734309] Genetics. 1991 Oct;129(2):327-32 [1743481] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Defective insulin response of phosphorylase phosphatase in insulin-resistant humans. AN - 72799434; 1737850 AB - Insulin-stimulated glycogen synthase activity in human muscle is reduced in insulin-resistant subjects. Insulin regulation of human muscle glycogen synthase may require activation of a type-1 protein phosphatase (PP-1). We investigated the change of phosphorylase phosphatase and glycogen synthase activities in muscle biopsies obtained during a 2-h hyperinsulinemic euglycemic clamp in 12 insulin-sensitive (group S) and 8 insulin-resistant (group R) subjects. Fasting phosphorylase phosphatase activity was lower in group R than in group S, and did not increase significantly with insulin infusion in group R until 20 min. In group S, phosphorylase phosphatase was significantly stimulated by 10 min, remaining significantly higher than in group R at all time points. The insulin-mediated changes in phosphatase activities were not decreased by 3 nM okadaic acid but were completely inhibited by 1 microM okadaic acid, thereby verifying that insulin-stimulated phosphorylase phosphatase is accounted for by a PP-1. Subcellular fractionation demonstrated reduced fasting PP-1 activities in both the glycogen and cytosolic fractions of muscle obtained from subjects in group R compared to those in group S. These results suggest that insulin activation of PP-1 could contribute to the stimulation of glycogen synthase by this hormone in human muscle. Lower fasting PP-1 activity in cytosol and glycogen fractions plus lower insulin-stimulated PP-1 activity could explain, in part, reduced insulin-stimulated glycogen synthase in skeletal muscle of insulin-resistant subjects. JF - The Journal of clinical investigation AU - Kida, Y AU - Raz, I AU - Maeda, R AU - Nyomba, B L AU - Stone, K AU - Bogardus, C AU - Sommercorn, J AU - Mott, D M AD - Clinical Diabetes & Nutrition Section, National Institutes of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Phoenix, Arizonia 85016. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 610 EP - 617 VL - 89 IS - 2 SN - 0021-9738, 0021-9738 KW - Ethers, Cyclic KW - 0 KW - Insulin KW - Okadaic Acid KW - 1W21G5Q4N2 KW - Glycogen Synthase KW - EC 2.4.1.11 KW - Phosphorylase Phosphatase KW - EC 3.1.3.17 KW - Abridged Index Medicus KW - Index Medicus KW - Glycogen Synthase -- analysis KW - Phosphorylation KW - Humans KW - Adult KW - Muscles -- enzymology KW - Ethers, Cyclic -- pharmacology KW - Male KW - Female KW - Insulin -- pharmacology KW - Phosphorylase Phosphatase -- analysis KW - Insulin Resistance UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72799434?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+clinical+investigation&rft.atitle=Defective+insulin+response+of+phosphorylase+phosphatase+in+insulin-resistant+humans.&rft.au=Kida%2C+Y%3BRaz%2C+I%3BMaeda%2C+R%3BNyomba%2C+B+L%3BStone%2C+K%3BBogardus%2C+C%3BSommercorn%2C+J%3BMott%2C+D+M&rft.aulast=Kida&rft.aufirst=Y&rft.date=1992-02-01&rft.volume=89&rft.issue=2&rft.spage=610&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+clinical+investigation&rft.issn=00219738&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-18 N1 - Date created - 1992-03-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1965 Feb;240:588-93 [14275108] J Biol Chem. 1984 Oct 10;259(19):12144-52 [6090457] Nature. 1990 Nov 22;348(6299):302-8 [2123524] J Clin Invest. 1991 Nov;88(5):1540-5 [1658044] Eur J Biochem. 1990 Dec 27;194(3):739-45 [2176604] Jpn J Cancer Res. 1990 Dec;81(12):1272-80 [2177460] Diabetes Metab Rev. 1987 Jan;3(1):127-61 [3032540] Biochem J. 1988 Nov 15;256(1):283-90 [2851982] FEBS Lett. 1989 Jul 3;250(2):596-600 [2546812] Metabolism. 1988 Dec;37(12):1171-6 [2848177] Biochem Biophys Res Commun. 1988 Feb 29;151(1):61-9 [2831896] J Clin Endocrinol Metab. 1986 May;62(5):922-7 [3514652] J Clin Invest. 1990 Feb;85(2):476-81 [2153707] Adv Enzymol Relat Areas Mol Biol. 1990;63:173-231 [2154910] Biochim Biophys Acta. 1981 Sep 18;677(1):13-22 [6794645] Philos Trans R Soc Lond B Biol Sci. 1983 Jul 5;302(1108):13-25 [6137000] J Biol Chem. 1984 Jun 10;259(11):7024-30 [6327704] Eur J Biochem. 1983 Jan 17;130(1):227-34 [6402364] J Biol Chem. 1984 May 10;259(9):5864-70 [6325452] Eur J Biochem. 1981 Oct;119(3):443-51 [6273157] Biochemistry. 1983 Jul 5;22(14):3393-9 [6311247] Biochem J. 1984 Jan 15;217(2):427-34 [6320806] Eur J Biochem. 1983 May 2;132(2):297-307 [6301829] Science. 1983 Jul 22;221(4608):331-8 [6306765] Acta Endocrinol (Copenh). 1980 Nov;95(3):427-32 [6254314] J Clin Invest. 1984 Apr;73(4):1185-90 [6423666] FEBS Lett. 1982 Dec 13;150(1):191-6 [6819160] Am J Physiol. 1980 Jul;239(1):E69-74 [6772036] Biochim Biophys Acta. 1979 Feb 19;583(1):36-46 [217447] Biochem J. 1977 Feb 15;162(2):423-33 [192224] Mol Cell Biochem. 1978 Feb 24;19(1):31-41 [25380] Eur J Biochem. 1978 Jun 15;87(2):341-51 [208844] Eur J Biochem. 1976 Nov 15;70(2):419-26 [188646] FEBS Lett. 1979 Oct 15;106(2):284-8 [115716] Anal Biochem. 1968 Oct 24;25(1):486-99 [5704765] J Biol Chem. 1976 Apr 10;251(7):1920-5 [5435] Anal Biochem. 1976 May 7;72:248-54 [942051] Biochem Biophys Res Commun. 1987 Nov 13;148(3):1174-81 [2825677] J Clin Invest. 1988 Nov;82(5):1503-9 [2846655] J Biol Chem. 1988 Oct 5;263(28):14061-6 [2844753] Eur J Biochem. 1986 Dec 15;161(3):763-9 [3024984] Diabetes. 1988 Mar;37(3):303-8 [3286330] Annu Rev Biochem. 1989;58:453-508 [2549856] Eur J Biochem. 1989 Mar 15;180(2):457-65 [2538333] J Clin Invest. 1991 Mar;87(3):1017-22 [1999482] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Flanking sequences influence the presentation of an endogenously synthesized peptide to cytotoxic T lymphocytes. AN - 72793776; 1732413 AB - Cytotoxic T lymphocytes (CTL) recognize class I major histocompatibility complex molecules complexed to peptides of eight to nine residues generated from cytosolic proteins. We find that CTL recognize, in vitro and in vivo, cells synthesizing a 10-residue peptide consisting of an initiating methionine followed by nine residues corresponding to a naturally processed determinant from influenza virus nucleoprotein (NP) (residues 147-155). Addition of two COOH-terminal residues corresponding to NP residues 157 and 158 severely reduced presentation of the endogenously produced peptide to CTL in vitro and in vivo. Extension of NH2 and COOH terminal flanking residues to include residues corresponding to NP residues 137-146 and 159-168 failed to increase the antigenicity of this peptide. Its presentation was greatly enhanced, however, by further extending the NH2 and COOH termini to include all of the additional residues of NP. These findings indicate first, that a naturally processed viral ligand (with an NH2-terminal Met) of a class I molecule contains sufficient information to access intracellular class I molecules, and second, that flanking residues can influence the processing and presentation of antigens to CTL. JF - The Journal of experimental medicine AU - Eisenlohr, L C AU - Yewdell, J W AU - Bennink, J R AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1992/02/01/ PY - 1992 DA - 1992 Feb 01 SP - 481 EP - 487 VL - 175 IS - 2 SN - 0022-1007, 0022-1007 KW - Histocompatibility Antigens Class I KW - 0 KW - Ligands KW - NP protein, Influenza A virus KW - Nucleoproteins KW - Oligopeptides KW - RNA-Binding Proteins KW - Viral Core Proteins KW - Viral Structural Proteins KW - Index Medicus KW - Animals KW - Blotting, Northern KW - Histocompatibility Antigens Class I -- immunology KW - Oligopeptides -- immunology KW - Oligopeptides -- genetics KW - Amino Acid Sequence KW - Mice KW - Mice, Inbred BALB C KW - Oligopeptides -- chemical synthesis KW - Polymerase Chain Reaction KW - Base Sequence KW - Molecular Sequence Data KW - Cytotoxicity Tests, Immunologic KW - Influenza A virus -- immunology KW - Genes, Viral KW - Influenza A virus -- genetics KW - Viral Structural Proteins -- genetics KW - Nucleoproteins -- genetics KW - Viral Core Proteins -- immunology KW - Viral Core Proteins -- genetics KW - T-Lymphocytes, Cytotoxic -- immunology KW - Nucleoproteins -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72793776?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+experimental+medicine&rft.atitle=Flanking+sequences+influence+the+presentation+of+an+endogenously+synthesized+peptide+to+cytotoxic+T+lymphocytes.&rft.au=Eisenlohr%2C+L+C%3BYewdell%2C+J+W%3BBennink%2C+J+R&rft.aulast=Eisenlohr&rft.aufirst=L&rft.date=1992-02-01&rft.volume=175&rft.issue=2&rft.spage=481&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+experimental+medicine&rft.issn=00221007&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-27 N1 - Date created - 1992-02-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Exp Med. 1989 Sep 1;170(3):1033-8 [2475568] Nature. 1989 May 18;339(6221):223-6 [2785645] J Exp Med. 1989 Mar 1;169(3):603-12 [2784478] Cell. 1985 Sep;42(2):457-67 [2411422] Nature. 1989 Nov 9;342(6246):180-2 [2478887] J Exp Med. 1989 Sep 1;170(3):1051-6 [2475569] Eur J Immunol. 1986 Dec;16(12):1479-87 [3493144] Cell. 1988 Jan 29;52(2):253-8 [2449284] J Virol. 1986 Mar;57(3):786-91 [3485199] J Immunol. 1989 Feb 15;142(4):1079-83 [2492575] Proc Natl Acad Sci U S A. 1985 Mar;82(6):1785-9 [3872457] J Exp Med. 1989 Jan 1;169(1):297-302 [2462610] Cell. 1986 Mar 28;44(6):959-68 [2420472] Nature. 1989 Feb 16;337(6208):653-5 [2537466] J Cell Biol. 1989 Feb;108(2):229-41 [2645293] Nature. 1989 Aug 10;340(6233):443-8 [2666863] J Biol Chem. 1990 Nov 15;265(32):19638-43 [2174047] J Exp Med. 1988 Nov 1;168(5):1935-9 [3263469] Mol Cell Biol. 1985 Dec;5(12):3403-9 [3939316] Science. 1990 Feb 9;247(4943):715-8 [2137259] Virology. 1983 Jul 30;128(2):319-30 [6310860] J Exp Med. 1966 Sep 1;124(3):331-45 [5922742] Nature. 1990 Nov 15;348(6298):213-6 [1700303] Science. 1990 Dec 21;250(4988):1723-6 [2270487] Nature. 1991 Apr 25;350(6320):703-6 [1708852] Nature. 1990 Nov 15;348(6298):252-4 [1700304] Cell. 1991 Sep 20;66(6):1145-53 [1913805] J Exp Med. 1991 Sep 1;174(3):733-6 [1875170] Nature. 1990 Dec 20-27;348(6303):738-41 [1979660] Nature. 1990 Dec 20-27;348(6303):744-7 [2259384] Nature. 1990 Dec 20-27;348(6303):741-4 [2259383] Nature. 1990 Nov 15;348(6298):248-51 [2234092] J Exp Med. 1988 Oct 1;168(4):1211-24 [2459295] Science. 1989 Jun 2;244(4908):1072-5 [2471266] Annu Rev Immunol. 1989;7:601-24 [2469442] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Extensive sequence-specific information throughout the CAR/RRE, the target sequence of the human immunodeficiency virus type 1 Rev protein. AN - 72786615; 1731093 AB - The significance and location of sequence-specific information in the CAR/RRE, the target sequence for the Rev protein of the human immunodeficiency virus type 1 (HIV-1), have been controversial. We present here a comprehensive experimental and computational approach combining mutational analysis, phylogenetic comparison, and thermodynamic structure calculations with a systematic strategy for distinguishing sequence-specific information from secondary structural information. A target sequence analog was designed to have a secondary structure identical to that of the wild type but a sequence that differs from that of the wild type at every position. This analog was inactive. By exchanging fragments between the wild-type sequence and the inactive analog, we were able to detect an unexpectedly extensive distribution of sequence specificity throughout the CAR/RRE. The analysis enabled us to identify a critically important sequence-specific region, region IIb in the Rev-binding domain, strongly supports a proposed base-pairing interaction in this location, and places forceful constraints on mechanisms of Rev action. The generalized approach presented can be applied to other systems. JF - Journal of virology AU - Dayton, E T AU - Konings, D A AU - Powell, D M AU - Shapiro, B A AU - Butini, L AU - Maizel, J V AU - Dayton, A I AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 1139 EP - 1151 VL - 66 IS - 2 SN - 0022-538X, 0022-538X KW - gag KW - rev KW - Gene Products, rev KW - 0 KW - RNA, Viral KW - rev Gene Products, Human Immunodeficiency Virus KW - Index Medicus KW - AIDS/HIV KW - Phylogeny KW - Models, Structural KW - Plasmids KW - Nucleic Acid Conformation KW - Mutagenesis, Site-Directed KW - HIV Long Terminal Repeat KW - Polymerase Chain Reaction KW - Virus Replication -- genetics KW - Base Sequence KW - Models, Genetic KW - Molecular Sequence Data KW - RNA, Viral -- genetics KW - RNA, Viral -- metabolism KW - Genes, gag KW - Protein Conformation KW - HIV-1 -- genetics KW - Gene Products, rev -- genetics KW - Genes, rev KW - HIV-1 -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72786615?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Extensive+sequence-specific+information+throughout+the+CAR%2FRRE%2C+the+target+sequence+of+the+human+immunodeficiency+virus+type+1+Rev+protein.&rft.au=Dayton%2C+E+T%3BKonings%2C+D+A%3BPowell%2C+D+M%3BShapiro%2C+B+A%3BButini%2C+L%3BMaizel%2C+J+V%3BDayton%2C+A+I&rft.aulast=Dayton&rft.aufirst=E&rft.date=1992-02-01&rft.volume=66&rft.issue=2&rft.spage=1139&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-14 N1 - Date created - 1992-02-14 N1 - Date revised - 2017-01-13 N1 - Gene symbol - gag; rev N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1989 Oct;86(20):7706-10 [2479010] Science. 1989 Apr 7;244(4900):48-52 [2468181] Nature. 1985 Oct 3-9;317(6036):395-403 [2413364] Cell. 1989 Aug 11;58(3):423-6 [2569361] Nature. 1989 Dec 7;342(6250):714-6 [2556643] AIDS. 1989 Dec;3(12):859-61 [2517208] Science. 1989 Dec 22;246(4937):1625-9 [2688093] J Acquir Immune Defic Syndr. 1989;2(5):431-40 [2677310] Oncogene. 1989 Nov;4(11):1275-9 [2682457] J Acquir Immune Defic Syndr. 1989;2(3):256-63 [2656990] J Virol. 1989 Mar;63(3):1265-74 [2783738] Proc Natl Acad Sci U S A. 1989 Mar;86(5):1495-9 [2784208] Nature. 1989 Mar 16;338(6212):254-7 [2784194] J Virol. 1989 Sep;63(9):3708-13 [2760980] Cell. 1989 Jul 14;58(1):205-14 [2752419] Cell. 1989 Jun 30;57(7):1155-65 [2736624] J Virol. 1989 May;63(5):1959-66 [2704072] Science. 1988 Feb 5;239(4840):617-22 [3277274] Nature. 1988 Oct 20;335(6192):738-40 [3262832] J Virol. 1988 Feb;62(2):655-8 [3257271] Nucleic Acids Res. 1988;16 Suppl:r175-269 [3368328] J Mol Evol. 1984-1985;21(4):323-33 [6443312] Biochemistry. 1987 Jul 14;26(14):4559-62 [3663607] Cell. 1986 Sep 12;46(6):807-17 [3638988] Proc Natl Acad Sci U S A. 1990 Feb;87(3):1198-202 [2405396] Cell. 1990 Jun 29;61(7):1271-6 [2364429] J Virol. 1990 Jun;64(6):2519-29 [2335812] Nucleic Acids Res. 1990 Mar 25;18(6):1613-23 [2326200] Microbiol Rev. 1983 Dec;47(4):621-69 [6363901] Nucleic Acids Res. 1982 Apr 24;10(8):2701-8 [7043400] New Biol. 1989 Dec;1(3):318-28 [2562124] Biochemistry. 1990 Sep 18;29(37):8813-9 [2271557] Cell. 1991 Apr 19;65(2):241-8 [2015625] Biochimie. 1991 Jan;73(1):9-16 [1903308] Biochemistry. 1991 Jul 30;30(30):7527-34 [1854752] New Biol. 1991 Feb;3(2):142-50 [2065010] Nucleic Acids Res. 1991 Apr 11;19(7):1577-83 [2027765] Virology. 1991 Apr;181(2):433-44 [2014632] J Virol. 1991 Apr;65(4):2131-4 [2002556] Proc Natl Acad Sci U S A. 1991 Feb 1;88(3):683-7 [1992459] Biochemistry. 1990 Oct 23;29(42):9791-5 [2125482] New Biol. 1990 Dec;2(12):1111-22 [2088501] Virology. 1990 May;176(1):39-47 [2109912] Cell. 1990 Feb 23;60(4):685-93 [1689218] J Virol. 1990 Apr;64(4):1690-7 [2157051] Genes Dev. 1990 Jun;4(6):1014-22 [2116986] J Virol. 1990 May;64(5):2202-7 [2182909] Cell. 1990 Feb 23;60(4):675-83 [2406030] Science. 1990 Feb 16;247(4944):845-8 [2406903] J Virol. 1990 Dec;64(12):6010-7 [2243384] J Virol. 1990 Dec;64(12):5966-75 [2243382] Genes Dev. 1990 Aug;4(8):1357-64 [2227413] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7593-7 [2217189] Cell. 1989 Dec 1;59(5):789-95 [2686839] J Acquir Immune Defic Syndr. 1988;1(5):441-52 [2851651] J Virol. 1989 Nov;63(11):4875-81 [2677405] J Virol. 1988 Apr;62(4):1115-9 [2831374] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2071-5 [2832844] J Virol. 1988 Jul;62(7):2498-501 [2836628] Nature. 1986 May 22-28;321(6068):412-7 [3012355] FEBS Lett. 1986 Dec 15;209(2):187-90 [3025015] Proc Natl Acad Sci U S A. 1985 Dec;82(24):8359-63 [3001699] Science. 1987 May 15;236(4803):837-40 [3033827] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3653-7 [3035544] Nature. 1985 Feb 7-13;313(6002):450-8 [2982104] Mol Cell Biol. 1987 Aug;7(8):2899-913 [2959855] Cell. 1988 Oct 21;55(2):197-209 [3048703] Nature. 1989 Dec 14;342(6251):816-9 [2481237] Genes Dev. 1989 Oct;3(10):1534-44 [2482226] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pediatric phase I trial, pharmacokinetic study, and limited sampling strategy for piritrexim administered on a low-dose, intermittent schedule. AN - 72784553; 1732038 AB - Piritrexim, an orally administered, lipid-soluble antifolate, was evaluated in a multi-institutional phase I trial in children. The starting dose was 10 mg/m2/dose administered every 8 h daily for 5 days for 3 consecutive weeks, with dose escalations in increments of 5 mg/m2/dose. Eighteen patients (16 with metastatic sarcoma, 1 with acute lymphoblastic leukemia, and 1 with a brainstem glioma), 3.5-20 years of age, with malignancy refractory to therapy, were entered into the study. The dose-limiting toxicities (DLTs), which were myelosuppression and mucositis, occurred in 4 of 4 patients treated at the 25-mg/m2/dose level but in none of the patients treated at the 15- and 20-mg/m2/dose levels. The recommended dose for phase II trials is 20 mg/m2/dose. Pharmacokinetic monitoring was performed in 15 of the 18 children. The area under the concentration-time curve (AUC) was linearly related to the dose administered. Piritrexim was rapidly absorbed, with the median time to peak level occurring 1.5 h after an oral dose. The terminal half-life of piritrexim ranged from 1.5 to 4.5 h. A limited sampling strategy developed earlier, capable of predicting the AUC based on the plasma concentrations at 3 and 6 h after an oral dose, was prospectively tested in this trial and proved to be highly predictive of the AUC (r = 0.98, P = 0.0001). Pharmacodynamic-pharmacokinetic correlations were obtained after combining data from this and the prior phase I pediatric trial. Trough plasma piritrexim concentration strongly correlated with DLT (P = 0.0016). A trough plasma piritrexim concentration greater than 0.5 microM appeared to be predictive of toxicity. Eleven of 15 patients with trough concentrations exceeding this threshold experienced DLTs. Therapeutic drug monitoring may thus play an important role in adjusting the dose and schedule of piritrexim in future trials. JF - Cancer research AU - Adamson, P C AU - Balis, F M AU - Miser, J AU - Arndt, C AU - Wells, R J AU - Gillespie, A AU - Aronson, L AU - Penta, J S AU - Clendeninn, N J AU - Poplack, D G AD - Pediatric Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/02/01/ PY - 1992 DA - 1992 Feb 01 SP - 521 EP - 524 VL - 52 IS - 3 SN - 0008-5472, 0008-5472 KW - Antineoplastic Agents KW - 0 KW - Pyrimidines KW - piritrexim KW - MK2A783ZUT KW - Index Medicus KW - Drug Administration Schedule KW - Humans KW - Platelet Count -- drug effects KW - Child KW - Sarcoma -- drug therapy KW - Child, Preschool KW - Drug Evaluation KW - Leukocyte Count -- drug effects KW - Brain Neoplasms -- drug therapy KW - Glioma -- drug therapy KW - Adult KW - Adolescent KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- drug therapy KW - Female KW - Male KW - Neoplasms -- drug therapy KW - Pyrimidines -- therapeutic use KW - Pyrimidines -- toxicity KW - Antineoplastic Agents -- toxicity KW - Pyrimidines -- pharmacokinetics KW - Pyrimidines -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72784553?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Pediatric+phase+I+trial%2C+pharmacokinetic+study%2C+and+limited+sampling+strategy+for+piritrexim+administered+on+a+low-dose%2C+intermittent+schedule.&rft.au=Adamson%2C+P+C%3BBalis%2C+F+M%3BMiser%2C+J%3BArndt%2C+C%3BWells%2C+R+J%3BGillespie%2C+A%3BAronson%2C+L%3BPenta%2C+J+S%3BClendeninn%2C+N+J%3BPoplack%2C+D+G&rft.aulast=Adamson&rft.aufirst=P&rft.date=1992-02-01&rft.volume=52&rft.issue=3&rft.spage=521&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-25 N1 - Date created - 1992-02-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cassette mutagenesis of the reverse transcriptase of human immunodeficiency virus type 1. AN - 72781978; 1370546 AB - We constructed a series of BspMI cassettes that simplify the introduction of specific point mutations in the polymerase domain of human immunodeficiency virus type 1 reverse transcriptase. A series of point mutants were constructed by using these cassette vectors. The RNA-dependent DNA polymerase and RNase H activities of 20 point mutations in the conserved portion of the polymerase domain were assayed. All the mutations analyzed are conservative substitutions of evolutionarily conserved amino acids. The mutations were divided into four classes. The first class has little effect on either polymerase or RNase H activity. The second class affects RNase H but not polymerase activity, while the third class has a normal RNase H activity with diminished polymerase activity. The fourth class affects both activities. JF - Journal of virology AU - Boyer, P L AU - Ferris, A L AU - Hughes, S H AD - ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 1031 EP - 1039 VL - 66 IS - 2 SN - 0022-538X, 0022-538X KW - Macromolecular Substances KW - 0 KW - Oligodeoxyribonucleotides KW - RNA-Directed DNA Polymerase KW - EC 2.7.7.49 KW - Ribonucleases KW - EC 3.1.- KW - Index Medicus KW - AIDS/HIV KW - Base Sequence KW - Sequence Homology, Nucleic Acid KW - Electrophoresis, Polyacrylamide Gel KW - Restriction Mapping KW - Polymerase Chain Reaction -- methods KW - Ribonucleases -- genetics KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Ribonucleases -- metabolism KW - Cloning, Molecular KW - HIV-1 -- genetics KW - RNA-Directed DNA Polymerase -- isolation & purification KW - HIV-1 -- enzymology KW - RNA-Directed DNA Polymerase -- metabolism KW - RNA-Directed DNA Polymerase -- genetics KW - Mutagenesis, Insertional UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72781978?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Cassette+mutagenesis+of+the+reverse+transcriptase+of+human+immunodeficiency+virus+type+1.&rft.au=Boyer%2C+P+L%3BFerris%2C+A+L%3BHughes%2C+S+H&rft.aulast=Boyer&rft.aufirst=P&rft.date=1992-02-01&rft.volume=66&rft.issue=2&rft.spage=1031&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-14 N1 - Date created - 1992-02-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Virology. 1990 Apr;175(2):575-80 [1691564] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1777-81 [2450347] Nucleic Acids Res. 1990 Sep 25;18(18):5359-63 [1699202] FEBS Lett. 1990 Sep 17;270(1-2):76-80 [1699794] Virology. 1979 Aug;97(1):221-3 [89754] AIDS Res Hum Retroviruses. 1990 Jun;6(6):753-64 [1694680] Virology. 1991 Jan;180(1):339-46 [1701948] FEBS Lett. 1989 Nov 6;257(2):311-4 [2479577] Mol Cell Biol. 1988 Aug;8(8):3565-9 [3062384] AIDS Res Hum Retroviruses. 1990 Sep;6(9):1061-72 [1702298] FEBS Lett. 1991 May 6;282(2):231-4 [1709876] J Biol Chem. 1988 Apr 15;263(11):5132-4 [2451663] Proc Natl Acad Sci U S A. 1988 Apr;85(8):2469-73 [2451824] EMBO J. 1988 Jan;7(1):239-43 [2452083] J Virol. 1988 Jul;62(7):2525-9 [2453682] J Virol. 1988 Oct;62(10):3662-7 [2458486] J Virol. 1988 Nov;62(11):4376-80 [2459414] Biochemistry. 1988 Dec 13;27(25):8884-9 [2466481] Proc Natl Acad Sci U S A. 1989 May;86(9):3104-8 [2470090] Virology. 1989 May;170(1):326-9 [2470195] Proc Natl Acad Sci U S A. 1989 Jul;86(13):4803-7 [2472634] J Biol Chem. 1989 Aug 25;264(24):13975-8 [2474539] Proc Natl Acad Sci U S A. 1989 Nov;86(22):8650-4 [2682655] Science. 1988 Jun 10;240(4858):1427-35 [3287617] Nucleic Acids Res. 1981 Apr 24;9(8):1825-39 [6264395] Science. 1991 Apr 5;252(5002):88-95 [1707186] Proc Natl Acad Sci U S A. 1991 Feb 15;88(4):1148-52 [1705027] FEBS Lett. 1991 Jun 3;283(2):298-302 [1710580] Proc Natl Acad Sci U S A. 1991 Jun 1;88(11):4596-600 [1711203] Proc Natl Acad Sci U S A. 1991 Jun 15;88(12):5262-66 [1711222] AIDS Res Hum Retroviruses. 1991 Nov;7(11):883-8 [1722105] Nucleic Acids Res. 1990 Mar 25;18(6):1656 [2158085] Science. 1986 Mar 14;231(4743):1289-91 [2418504] Nature. 1987 Jun 25-Jul 1;327(6124):716-7 [2439916] EMBO J. 1987 Oct;6(10):3133-7 [2446866] Nucleic Acids Res. 1988 Jan 11;16(1):265-77 [2448747] Proc Natl Acad Sci U S A. 1988 Feb;85(4):1218-22 [2448794] J Biol Chem. 1990 Jun 5;265(16):8986-8 [1693146] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutations in both the 2B and 2C genes of hepatitis A virus are involved in adaptation to growth in cell culture. AN - 72777853; 1309907 AB - Oligonucleotide-directed mutagenesis of an infectious cDNA clone of wild-type hepatitis A virus was performed to determine which mutations acquired in the nonstructural 2B and 2C genes during adaptation to growth in cell culture were effective in enhancing virus growth in vitro. Results of transfection assays demonstrated that one mutation in the 2B gene and two mutations in the 2C gene were responsible for an increased efficiency in growth, but growth enhancement required the participation of at least two of the three mutations. JF - Journal of virology AU - Emerson, S U AU - Huang, Y K AU - McRill, C AU - Lewis, M AU - Purcell, R H AD - Hepatitis Viruses Section, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 650 EP - 654 VL - 66 IS - 2 SN - 0022-538X, 0022-538X KW - Codon KW - 0 KW - DNA, Viral KW - Index Medicus KW - Animals KW - Codon -- genetics KW - Transfection KW - Humans KW - Restriction Mapping KW - Transcription, Genetic KW - DNA, Viral -- genetics KW - Cell Line KW - Cloning, Molecular KW - Mutagenesis, Site-Directed KW - Hepatovirus -- growth & development KW - Genes, Viral KW - Hepatovirus -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72777853?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Mutations+in+both+the+2B+and+2C+genes+of+hepatitis+A+virus+are+involved+in+adaptation+to+growth+in+cell+culture.&rft.au=Emerson%2C+S+U%3BHuang%2C+Y+K%3BMcRill%2C+C%3BLewis%2C+M%3BPurcell%2C+R+H&rft.aulast=Emerson&rft.aufirst=S&rft.date=1992-02-01&rft.volume=66&rft.issue=2&rft.spage=650&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-14 N1 - Date created - 1992-02-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Virol. 1991 Apr;65(4):2056-65 [1705995] Virus Res. 1989 Apr;12(4):361-9 [2543159] Nucleic Acids Res. 1989 Nov 11;17(21):8413-40 [2555771] Virus Res. 1987 Aug;8(2):153-71 [2823500] J Virol. 1988 Nov;62(11):4016-21 [2845120] J Virol. 1987 Jan;61(1):50-9 [3023706] Infect Immun. 1981 Apr;32(1):388-93 [6260685] J Virol. 1991 Aug;65(8):4341-9 [1649334] J Virol. 1991 Sep;65(9):4882-6 [1651411] Infect Immun. 1977 Nov;18(2):524-30 [200565] J Virol. 1990 Mar;64(3):1156-63 [2154600] J Gen Virol. 1989 Oct;70 ( Pt 10):2805-10 [2552009] Virology. 1987 Sep;160(1):220-6 [2820130] Proc Natl Acad Sci U S A. 1985 May;82(9):2627-31 [2986127] Proc Natl Acad Sci U S A. 1987 Apr;84(8):2497-501 [3031686] J Virol. 1983 Nov;48(2):410-8 [6312099] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vitro resolution of adeno-associated virus DNA hairpin termini by wild-type Rep protein is inhibited by a dominant-negative mutant of rep. AN - 72777360; 1309900 AB - An adeno-associated virus (AAV) genome with a Lys-to-His (K340H) mutation in the consensus nucleotide triphosphate binding site of the rep gene has a dominant-negative DNA replication phenotype in vivo. We expressed both wild-type (Rep78) and mutant (Rep78NTP) proteins in two helper-free expression systems consisting of either recombinant baculoviruses in insect cells or the human immunodeficiency virus type 1 long terminal repeat promoter in human 293 cell transient transfections. We analyzed nuclear extracts from both expression systems for the ability to complement uninfected HeLa cell cytoplasmic extracts in an in vitro terminal resolution assay in which a covalently closed AAV terminal hairpin structure is converted to an extended linear duplex. Although both Rep78 and Rep78NTP bound to AAV terminal hairpin DNA in vitro, Rep78 but not Rep78NTP complemented the terminal resolution assay. Furthermore, Rep78NTP was trans dominant for AAV terminal resolution in vitro. We propose that the dominant-negative replication phenotype of AAV genomes carrying the K340H mutation is mediated by mutant Rep proteins binding to the terminal repeat hairpin. JF - Journal of virology AU - Owens, R A AU - Carter, B J AD - Laboratory of Molecular and Cellular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1992/02// PY - 1992 DA - February 1992 SP - 1236 EP - 1240 VL - 66 IS - 2 SN - 0022-538X, 0022-538X KW - DNA, Viral KW - 0 KW - DNA-Binding Proteins KW - Viral Proteins KW - rep proteins, Adeno-associated virus 2 KW - 137750-19-7 KW - Index Medicus KW - AIDS/HIV KW - Mutagenesis, Site-Directed KW - HIV Long Terminal Repeat KW - Genes, Dominant KW - Transfection KW - HeLa Cells KW - Humans KW - Restriction Mapping KW - Genes, Viral KW - Nucleic Acid Conformation KW - Cell Line KW - Binding Sites KW - Viral Proteins -- genetics KW - Dependovirus -- metabolism KW - Dependovirus -- genetics KW - Viral Proteins -- metabolism KW - DNA, Viral -- genetics KW - DNA, Viral -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72777360?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=In+vitro+resolution+of+adeno-associated+virus+DNA+hairpin+termini+by+wild-type+Rep+protein+is+inhibited+by+a+dominant-negative+mutant+of+rep.&rft.au=Owens%2C+R+A%3BCarter%2C+B+J&rft.aulast=Owens&rft.aufirst=R&rft.date=1992-02-01&rft.volume=66&rft.issue=2&rft.spage=1236&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-14 N1 - Date created - 1992-02-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Virol. 1990 Apr;64(4):1764-70 [2157057] J Virol. 1983 Feb;45(2):555-64 [6300419] Virology. 1989 Jul;171(1):239-47 [2545030] Virology. 1989 Nov;173(1):120-8 [2554565] Cell. 1983 May;33(1):135-43 [6088052] J Gen Virol. 1987 Mar;68 ( Pt 3):885-93 [3819702] Proc Natl Acad Sci U S A. 1976 Mar;73(3):742-6 [1062784] Virology. 1991 Sep;184(1):14-22 [1651588] Cell. 1990 Jan 12;60(1):105-13 [2153052] Cell. 1990 May 4;61(3):447-57 [2159383] J Virol. 1989 Jul;63(7):3034-9 [2542611] J Virol. 1989 Jul;63(7):3095-104 [2542617] J Virol. 1989 Oct;63(10):4450-4 [2550677] Virology. 1987 Nov;161(1):18-28 [2823460] Virology. 1986 Jul 15;152(1):110-7 [3012864] J Virol. 1986 Dec;60(3):823-32 [3023672] J Virol. 1987 Apr;61(4):972-81 [3029431] J Virol. 1984 Aug;51(2):329-39 [6086948] J Virol. 1984 Sep;51(3):611-9 [6088786] Virology. 1977 May 15;78(2):488-99 [867815] J Virol. 1991 Jan;65(1):396-404 [1845899] J Virol. 1988 Sep;62(9):3356-63 [2841488] Mol Cell Biol. 1985 Aug;5(8):2051-60 [3018548] J Virol. 1990 Dec;64(12):6204-13 [2173787] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A single amino acid mutation (Ser180----Cys) determines the polymorphism in cytochrome P450g (P4502C13) by altering protein stability. AN - 72779660; 1730734 AB - Cytochrome P450g is polymorphic in the male rat. This polymorphism is characterized by a 20-40-fold difference in the hepatic content of P450g in the two phenotypes. Sequencing of cDNAs from high (+g) and low (-g) phenotype rats has shown that the low phenotype is due to a defective mRNA containing nine base mutations encoding 7 amino acid substitutions. To determine the role of these structural changes in the phenotypic expression of P450g, we altered each of these residues by site-directed mutagenesis in the present studies and expressed the normal and mutant cDNAs in Saccharomyces cerevisiae. P450+g protein was expressed at a level 4-6-fold higher than that of P450-g in yeast cells, despite the presence of identical mRNA levels. This difference in protein expression approaches the difference seen in the rat. A single amino acid change from Ser180 in P450+g to Cys in P450-g, in a highly conserved region in the P4502C subfamily, was found to be solely responsible for the phenotypic differences in expression of P450g. Protein half-life studies demonstrated that this mutation increases the degradation of P450g. This is the first example of a single amino acid substitution which alters the phenotypic expression of a P450 protein by affecting its stability. JF - The Journal of biological chemistry AU - Faletto, M B AU - Linko, P AU - Goldstein, J A AD - Laboratory of Biochemical Risk Analysis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1992/01/25/ PY - 1992 DA - 1992 Jan 25 SP - 2032 EP - 2037 VL - 267 IS - 3 SN - 0021-9258, 0021-9258 KW - Oligodeoxyribonucleotides KW - 0 KW - Recombinant Proteins KW - Serine KW - 452VLY9402 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Cysteine KW - K848JZ4886 KW - Index Medicus KW - Animals KW - Amino Acid Sequence KW - Plasmids KW - Cloning, Molecular KW - Saccharomyces cerevisiae -- genetics KW - Rats KW - Phenotype KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Blotting, Western KW - Recombinant Proteins -- metabolism KW - Enzyme Stability KW - Kinetics KW - Restriction Mapping KW - DNA -- genetics KW - Molecular Sequence Data KW - Recombinant Proteins -- chemistry KW - Polymorphism, Genetic KW - Cytochrome P-450 Enzyme System -- genetics KW - Cytochrome P-450 Enzyme System -- chemistry KW - Cytochrome P-450 Enzyme System -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72779660?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=A+single+amino+acid+mutation+%28Ser180----Cys%29+determines+the+polymorphism+in+cytochrome+P450g+%28P4502C13%29+by+altering+protein+stability.&rft.au=Faletto%2C+M+B%3BLinko%2C+P%3BGoldstein%2C+J+A&rft.aulast=Faletto&rft.aufirst=M&rft.date=1992-01-25&rft.volume=267&rft.issue=3&rft.spage=2032&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-18 N1 - Date created - 1992-02-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression and chromosomal localization of the gene for the human transcriptional repressor GCF. AN - 72778890; 1370479 AB - GCF is a human transcriptional regulator that represses transcription of certain genes and is encoded by a 3-kilobase (kb) mRNA (Kageyama, R., and Pastan, I. (1989) Cell 59, 815-825). The expression of GCF was examined in a variety of clonal cell lines. The 3.0-kb GCF mRNA was found to be expressed at the highest level in HUT 102 cells (derived from a T-cell lymphoma). Elevated levels of the GCF mRNA were also noted in KATO III and AGS (gastric carcinomas), FEM-X (melanoma), and U266B1 (myeloma) cell lines. A human fibroblast cell line (WI38) did not express GCF mRNA, and no cross-hybridization to a mouse cell line (NIH 3T3) or monkey cell line (CV-1) could be detected. The GCF cDNA also hybridizes to RNA species of 4.5 and 1.2 kb. The 4.5-kb RNA has the same general expression pattern as the GCF mRNA. Hybridization of cellular RNA with various probes derived from the 3-kb cDNA revealed that the 4.5-kb RNA species only hybridizes to GCF cDNA probes from the extreme 5' end. By using single-stranded RNA probes, hybridization to the three RNA species was detected with the antisense probe for the 5' end (nucleotides 1-561). The single-stranded antisense probe for the region encompassing nucleotides 561-1692 hybridized to the 3.0- and 1.2-kb RNA species. The sense probes for these regions did not hybridize to these RNAs. The GCF gene was localized to a single locus, the chromosome 2 p11.1-11.2 region, by in situ hybridization. Treatment of human KB epidermoid carcinoma cells with phorbol 12-myristate 13-acetate (PMA) lead to a rapid induction of GCF RNA after 1 h and a decline to lower than control levels after 6 h. Epidermal growth factor receptor mRNAs were not increased by PMA until 2 h after treatment and were at their highest level only after GCF mRNAs were decreased. The 4.5- and 1.2-kb RNAs were also induced by PMA with the same kinetics as the GCF mRNA. These results show that the GCF gene is widely expressed in human tissues and cell lines and that the 4.5- and 1.2-kb RNAs have similar expression patterns. JF - The Journal of biological chemistry AU - Johnson, A C AU - Kageyama, R AU - Popescu, N C AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/01/25/ PY - 1992 DA - 1992 Jan 25 SP - 1689 EP - 1694 VL - 267 IS - 3 SN - 0021-9258, 0021-9258 KW - GCFC2 protein, human KW - 0 KW - RNA Probes KW - RNA, Messenger KW - RNA, Neoplasm KW - Repressor Proteins KW - RNA KW - 63231-63-0 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Clone Cells KW - Karyotyping KW - Animals KW - KB Cells KW - Blotting, Northern KW - Chromosome Banding KW - Humans KW - RNA, Neoplasm -- genetics KW - Chromosome Mapping KW - Plasmacytoma -- genetics KW - RNA, Neoplasm -- isolation & purification KW - Melanoma -- genetics KW - Stomach Neoplasms -- genetics KW - Restriction Mapping KW - RNA -- isolation & purification KW - Tetradecanoylphorbol Acetate -- pharmacology KW - RNA -- genetics KW - Chromosomes, Human, Pair 1 KW - RNA, Messenger -- metabolism KW - RNA, Messenger -- genetics KW - Repressor Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72778890?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Expression+and+chromosomal+localization+of+the+gene+for+the+human+transcriptional+repressor+GCF.&rft.au=Johnson%2C+A+C%3BKageyama%2C+R%3BPopescu%2C+N+C%3BPastan%2C+I&rft.aulast=Johnson&rft.aufirst=A&rft.date=1992-01-25&rft.volume=267&rft.issue=3&rft.spage=1689&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-18 N1 - Date created - 1992-02-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of CD3-linked phospholipase C by phorbol ester and by cAMP is associated with decreased phosphotyrosine and increased phosphoserine contents of PLC-gamma 1. AN - 72772161; 1370476 AB - The mechanisms by which phorbol 12-myristate 13-acetate (PMA) and cAMP attenuate the hydrolysis of phosphatidylinositol 4,5-bisphosphate (PtdIns 4,5-P2) induced by ligation of the T-cell antigen receptor complex (TCR) was studied in the human Jurkat T-cell line. It has previously been shown that stimulation of Jurkat cells with antibodies to CD3, components of the TCR, elicits a rapid and transient phosphorylation of phospholipase C (PLC)-gamma 1, the predominant PLC isozyme in Jurkat cells, at multiple tyrosine residues and that such tyrosine phosphorylation leads to activation of PLC-gamma 1. Prior incubation of Jurkat cells with PMA or forskolin, which increases intracellular cAMP concentrations, prevented tyrosine phosphorylation of PLC-gamma 1 as well as the hydrolysis of PtdIns 4,5-P2 induced by ligation of CD3. Dose-response curves of PMA and of forskolin for the inhibition of PLC-gamma 1 tyrosine phosphorylation and of PtdIns 4,5-P2 hydrolysis were similar. These results suggest that the inhibition of PtdIns 4,5-P2 hydrolysis by PMA and cAMP is attributable to reduced tyrosine phosphorylation of PLC-gamma 1. Treatment of Jurkat cells with PMA or forskolin stimulated the phosphorylation of PLC-gamma 1 at serine 1248. PMA treatment also elicited the phosphorylation of PLC-gamma 1 at an unidentified serine site. Phosphopeptide map analysis indicated that the sites of PLC-gamma 1 phosphorylated in Jurkat cells treated with PMA and forskolin are the same as those phosphorylated in vitro by protein kinase C (PKC) and cAMP-dependent protein kinase (PKA), respectively. Stimulation of Jurkat cells with antibodies to CD3 also elicited phosphorylation of PLC-gamma 1 at serine 1248 and at the unidentified serine site phosphorylated in PLC-gamma 1 from PMA-treated cells. Thus, phosphorylation of PLC-gamma 1 by PKC or PKA at serine 1248 may modulate the interaction of PLC-gamma 1 with the protein tyrosine kinase or the protein tyrosine phosphatase; this altered interaction may, at least in part, be responsible for the decreased tyrosine phosphorylation of PLC-gamma 1 seen in PMA- and forskolin-treated Jurkat cells. Furthermore, in the absence of PMA, activation of PKC by diacylglycerol provides a negative feedback signal responsible for reducing the phosphotyrosine contents of PLC-gamma 1. JF - The Journal of biological chemistry AU - Park, D J AU - Min, H K AU - Rhee, S G AD - Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/01/25/ PY - 1992 DA - 1992 Jan 25 SP - 1496 EP - 1501 VL - 267 IS - 3 SN - 0021-9258, 0021-9258 KW - Antigens, CD KW - 0 KW - Antigens, CD3 KW - Antigens, Differentiation, T-Lymphocyte KW - Inositol Phosphates KW - Muromonab-CD3 KW - Phosphates KW - Phosphopeptides KW - Phosphoproteins KW - Receptors, Antigen, T-Cell KW - Phosphoserine KW - 17885-08-4 KW - Colforsin KW - 1F7A44V6OU KW - Phosphotyrosine KW - 21820-51-9 KW - Tyrosine KW - 42HK56048U KW - Cyclic AMP KW - E0399OZS9N KW - Type C Phospholipases KW - EC 3.1.4.- KW - Trypsin KW - EC 3.4.21.4 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Peptide Mapping KW - Dose-Response Relationship, Drug KW - Humans KW - Phosphates -- metabolism KW - Phosphopeptides -- isolation & purification KW - Phosphorylation KW - Kinetics KW - Antigens, CD -- metabolism KW - Phosphoproteins -- isolation & purification KW - Cell Line KW - Phosphoproteins -- metabolism KW - Colforsin -- pharmacology KW - Type C Phospholipases -- antagonists & inhibitors KW - Antigens, Differentiation, T-Lymphocyte -- metabolism KW - Inositol Phosphates -- metabolism KW - Receptors, Antigen, T-Cell -- metabolism KW - Cyclic AMP -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Tyrosine -- analogs & derivatives KW - Type C Phospholipases -- chemistry KW - Phosphoserine -- analysis KW - Tyrosine -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72772161?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Inhibition+of+CD3-linked+phospholipase+C+by+phorbol+ester+and+by+cAMP+is+associated+with+decreased+phosphotyrosine+and+increased+phosphoserine+contents+of+PLC-gamma+1.&rft.au=Park%2C+D+J%3BMin%2C+H+K%3BRhee%2C+S+G&rft.aulast=Park&rft.aufirst=D&rft.date=1992-01-25&rft.volume=267&rft.issue=3&rft.spage=1496&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-18 N1 - Date created - 1992-02-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selective modulation of glutathione in mouse brain regions and its effect on acrylamide-induced neurotoxicity. AN - 72814160; 1739414 AB - Selective modulation of brain glutathione (GSH) may assist the elucidation of the role of GSH in the central nervous system. Subcutaneous administration of diethyl maleate (DEM) depleted both cerebral and hepatic GSH in a dose- and time-dependent manner. While hepatic GSH levels returned to control levels 6 hr after DEM administration, brain GSH levels remained significantly lowered for up to 12 hr after administration of DEM. However, intrathecal administration of DEM resulted in a selective lowering of brain GSH without altering hepatic levels. Intrathecal administration of L-buthionine sulfoximine (L-BSO; 1.0 mmol/kg body wt) also depleted the GSH content of the brain and the levels remained low 24 hr after L-BSO administration. The extent of GSH depletion varied in different regions of the brain; maximal depletion was observed in the brainstem, followed by the cerebellum, striatum, cortex and hippocampus. Intrathecal administration of L-2-oxothiazolidine 4-carboxylate (OTC) resulted in a marginal elevation of GSH levels in the brain. There was considerable regional variation. A maximal elevation of 134% was seen in the hippocampus, 6 hr following the intrathecal administration of 8.0 mmol of OTC/kg body wt. The effect of the modulation of brain GSH levels on acrylamide (ACR)-induced neurotoxicity was examined. Depletion of GSH by pretreatment of mice with L-BSO or DEM (administered intrathecally) enhanced the toxicity of ACR as measured by the inhibition of brain glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity. The inhibition of GAPDH by ACR was attenuated by pretreatment of animals with OTC. Thus, brain GSH may play an important role in the detoxification of xenobiotics, in situ within the central nervous system. JF - Biochemical pharmacology AU - Shivakumar, B R AU - Ravindranath, V AD - Department of Neurochemistry, National Institute of Mental Health and Neuro Sciences, Bangalore, India. Y1 - 1992/01/22/ PY - 1992 DA - 1992 Jan 22 SP - 263 EP - 269 VL - 43 IS - 2 SN - 0006-2952, 0006-2952 KW - Acrylamides KW - 0 KW - Maleates KW - Thiazoles KW - Thiazolidines KW - Methionine Sulfoximine KW - 1982-67-8 KW - Buthionine Sulfoximine KW - 5072-26-4 KW - diethyl maleate KW - AK5N1DQX7U KW - Glyceraldehyde-3-Phosphate Dehydrogenases KW - EC 1.2.1.- KW - Glutathione KW - GAN16C9B8O KW - Pyrrolidonecarboxylic Acid KW - SZB83O1W42 KW - 2-oxothiazolidine-4-carboxylic acid KW - X7063P804E KW - Index Medicus KW - Animals KW - Drug Interactions KW - Mice KW - Methionine Sulfoximine -- analogs & derivatives KW - Thiazoles -- pharmacology KW - Maleates -- pharmacology KW - Liver -- drug effects KW - Injections, Spinal KW - Maleates -- administration & dosage KW - Methionine Sulfoximine -- pharmacology KW - Female KW - Glutathione -- metabolism KW - Brain -- drug effects KW - Acrylamides -- toxicity KW - Brain -- metabolism KW - Glyceraldehyde-3-Phosphate Dehydrogenases -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72814160?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+pharmacology&rft.atitle=Selective+modulation+of+glutathione+in+mouse+brain+regions+and+its+effect+on+acrylamide-induced+neurotoxicity.&rft.au=Shivakumar%2C+B+R%3BRavindranath%2C+V&rft.aulast=Shivakumar&rft.aufirst=B&rft.date=1992-01-22&rft.volume=43&rft.issue=2&rft.spage=263&rft.isbn=&rft.btitle=&rft.title=Biochemical+pharmacology&rft.issn=00062952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-17 N1 - Date created - 1992-03-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of nerve growth factor on TTX- and capsaicin-sensitivity in adult rat sensory neurons. AN - 73034886; 1617430 AB - We have investigated the effects of nerve growth factor (NGF, 2.5 ng/ml for 1-2 weeks) on enriched adult rat dorsal root ganglion (DRG) neurons maintained in cell culture in defined media. Whole-cell recordings in cells cultured in the absence and presence of NGF revealed no significant difference in resting membrane potential and input resistance. However, the threshold for spike generation was significantly lower in untreated cells than in treated cells; -25 +/- 1.1 mV vs -19 +/- 2.2 mV, respectively. The sensitivity of the Na+ spike to tetrodotoxin (TTX, 1 microM) was different in cells cultured in the absence or presence of NGF. For example, spikes were abolished by TTX in 100% of untreated cells, while in NGF-treated cells the spike was abolished in only 41% of the neurons. Chemosensitivity of DRG neurons was also different in the absence and presence of NGF. For example, the percent of neurons in which a current activated by 8-methyl-N-vanillyl-6-nonenamide (capsaicin, 500 nM) was detected, increased from 18% in untreated cells to 55% in NGF-treated cells. NGF did not influence the number of cells surviving. The results indicate that NGF can regulate TTX and capsaicin sensitivity in these adult rat sensory neurons. Our experimental protocol indicates that this effect is not mediated by a factor in the serum or released from non-neuronal cells. JF - Brain research AU - Aguayo, L G AU - White, G AD - Section of Electrophysiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852. Y1 - 1992/01/20/ PY - 1992 DA - 1992 Jan 20 SP - 61 EP - 67 VL - 570 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Nerve Growth Factors KW - 0 KW - Tetrodotoxin KW - 4368-28-9 KW - gamma-Aminobutyric Acid KW - 56-12-2 KW - Capsaicin KW - S07O44R1ZM KW - Index Medicus KW - Rats KW - Animals KW - Action Potentials -- physiology KW - Membrane Potentials -- physiology KW - Male KW - Cell Survival -- physiology KW - Nerve Growth Factors -- pharmacology KW - gamma-Aminobutyric Acid -- pharmacology KW - Neurons, Afferent -- drug effects KW - Tetrodotoxin -- pharmacology KW - Capsaicin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73034886?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Effects+of+nerve+growth+factor+on+TTX-+and+capsaicin-sensitivity+in+adult+rat+sensory+neurons.&rft.au=Aguayo%2C+L+G%3BWhite%2C+G&rft.aulast=Aguayo&rft.aufirst=L&rft.date=1992-01-20&rft.volume=570&rft.issue=1-2&rft.spage=61&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-31 N1 - Date created - 1992-07-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Learning impairment following intracerebral administration of the HIV envelope protein gp120 or a VIP antagonist. AN - 73028176; 1617429 AB - The external envelope glycoprotein (gp120) of the human immunodeficiency virus (HIV) has been shown to be toxic to neurons in culture. To further investigate the neurological effects of gp120, the involvement of this protein with the acquisition of spatial discrimination was assessed. Both native and recombinant gp120 were administered into the cerebral ventricles of adult rats and performance was evaluated in the Morris swim maze. Gp120 treatment retarded acquisition after daily administration of 12 ng. The specificity of this impairment was demonstrated in that the performance of animals given the same amount of gp160 from recombinant baculovirus was not different from animals given saline. Vasoactive intestinal peptide (VIP) has been shown to block gp120-induced neurotoxicity in culture and a VIP receptor antagonist has displayed toxic properties to neurons in culture. We show here that this antagonist, which competitively inhibits VIP binding and blocks VIP-mediated functions in cell cultures from the CNS, also produced an impairment of performance. This retardation was attenuated by cotreatment with VIP, supporting the specificity of the observed impairment. Thus, gp120 and the VIP antagonist produced similar retardation of spatial discrimination, suggesting that both may impair memory for spatially related stimulus control. JF - Brain research AU - Glowa, J R AU - Panlilio, L V AU - Brenneman, D E AU - Gozes, I AU - Fridkin, M AU - Hill, J M AD - Biopsychology Unit, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/01/20/ PY - 1992 DA - 1992 Jan 20 SP - 49 EP - 53 VL - 570 IS - 1-2 SN - 0006-8993, 0006-8993 KW - HIV Envelope Protein gp120 KW - 0 KW - Vasoactive Intestinal Peptide KW - 37221-79-7 KW - Index Medicus KW - AIDS/HIV KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Male KW - Injections, Intraventricular KW - Vasoactive Intestinal Peptide -- antagonists & inhibitors KW - Learning -- drug effects KW - HIV Envelope Protein gp120 -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73028176?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Learning+impairment+following+intracerebral+administration+of+the+HIV+envelope+protein+gp120+or+a+VIP+antagonist.&rft.au=Glowa%2C+J+R%3BPanlilio%2C+L+V%3BBrenneman%2C+D+E%3BGozes%2C+I%3BFridkin%2C+M%3BHill%2C+J+M&rft.aulast=Glowa&rft.aufirst=J&rft.date=1992-01-20&rft.volume=570&rft.issue=1-2&rft.spage=49&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-31 N1 - Date created - 1992-07-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The guanine nucleotide-binding protein Gs activates a novel calcium transporter in Xenopus oocytes. AN - 72783378; 1309778 AB - Calcium influx is an important aspect of receptor-mediated signal transduction, yet limited information is available regarding the pathways of calcium influx into nonexcitable cells. We show that treatment of oocytes from Xenopus laevis with cholera toxin, a potent activator of the guanine nucleotide-binding protein Gs, specifically stimulates a sustained inward whole cell flux of calcium through a novel membrane transporter. The calcium is distributed into a mobilizable pool. The flux is voltage-independent and is completely and specifically blocked by microinjection of oocytes with an antiserum directed against Gs alpha. The flux is not activated by treatment of the cells with forskolin or 8-bromo-cyclic adenosine monophosphate indicating that the effect of Gs alpha on the transporter occurs independently of adenylylcyclase activation. Transporter activity is insensitive to benzyl amiloride, does not require a sodium gradient, and is not stimulated by external calcium, indicating that it is not a sodium-calcium exchanger. The Gs-activated flux is dramatically potentiated by lanthanum ion and other trivalent cations but not by any of six divalent cations that were tested; all other known calcium channels and exchangers are, in contrast, potently blocked by lanthanum. The divalent cation cadmium inhibited transporter activity in a concentration-dependent manner. This novel calcium transporter may be important for receptor-mediated calcium influx in the oocyte and perhaps other cell types. JF - The Journal of biological chemistry AU - Murphy, P M AU - McDermott, D AD - Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/01/15/ PY - 1992 DA - 1992 Jan 15 SP - 883 EP - 888 VL - 267 IS - 2 SN - 0021-9258, 0021-9258 KW - Calcium Channels KW - 0 KW - Cations, Divalent KW - Lanthanum KW - 6I3K30563S KW - Cholera Toxin KW - 9012-63-9 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Calcium -- metabolism KW - Xenopus laevis KW - Animals KW - Lanthanum -- pharmacology KW - Cholera Toxin -- pharmacology KW - Membrane Potentials KW - Calcium Channels -- physiology KW - GTP-Binding Proteins -- metabolism KW - Calcium Channels -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72783378?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=The+guanine+nucleotide-binding+protein+Gs+activates+a+novel+calcium+transporter+in+Xenopus+oocytes.&rft.au=Murphy%2C+P+M%3BMcDermott%2C+D&rft.aulast=Murphy&rft.aufirst=P&rft.date=1992-01-15&rft.volume=267&rft.issue=2&rft.spage=883&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-14 N1 - Date created - 1992-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Muscarinic receptor-operated Ca2+ influx in transfected fibroblast cells is independent of inositol phosphates and release of intracellular Ca2+. AN - 72777189; 1731321 AB - Receptor-mediated changes in cytoplasmic calcium concentrations occur either through release from intracellular calcium stores or by the opening of channels in the plasma membrane, allowing influx of calcium from the extracellular fluid. Carbachol, a muscarinic receptor agonist, stimulated both calcium influx and inositol 1,4,5-trisphosphate (InsP3)-mediated intracellular calcium release in A9 fibroblast cells expressing a m3 muscarinic receptor clone. The calcium influx persisted even after pretreatment of cells with phorbol 12-myristate 13-acetate, which completely prevented the rise in inositol phosphates and intracellular calcium levels. The calcium influx was blocked by divalent cations but was not affected by inhibitors of voltage-dependent calcium channels or high potassium depolarization, indicating the presence of a receptor-operated and voltage-insensitive calcium channel in these cells. Calcium influx was not stimulated by the addition of cAMP analogs or arachidonic acid. To examine the possible involvement of G proteins in m3 receptor-activated calcium influx, two chimeric m2 and m3 muscarinic receptors were expressed in A9 cells in which the third cytoplasmic loop (the primary structural determinant in G protein coupling selectivity of muscarinic receptors) had been exchanged between the m2 receptor, which has no effect on calcium influx, and the m3 receptor. Calcium influx was found to be associated with a structural component of the m3 muscarinic receptor other than the third cytoplasmic loop. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Felder, C C AU - Poulter, M O AU - Wess, J AD - Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1992/01/15/ PY - 1992 DA - 1992 Jan 15 SP - 509 EP - 513 VL - 89 IS - 2 SN - 0027-8424, 0027-8424 KW - Inositol Phosphates KW - 0 KW - Potassium Channels KW - Receptors, Muscarinic KW - Carbachol KW - 8Y164V895Y KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Molecular Structure KW - Animals KW - Second Messenger Systems KW - Transfection KW - In Vitro Techniques KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Potassium Channels -- physiology KW - Mice KW - GTP-Binding Proteins -- physiology KW - Inositol Phosphates -- physiology KW - Carbachol -- pharmacology KW - Signal Transduction KW - Structure-Activity Relationship KW - Calcium -- physiology KW - Receptors, Muscarinic -- chemistry KW - Receptors, Muscarinic -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72777189?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Muscarinic+receptor-operated+Ca2%2B+influx+in+transfected+fibroblast+cells+is+independent+of+inositol+phosphates+and+release+of+intracellular+Ca2%2B.&rft.au=Felder%2C+C+C%3BPoulter%2C+M+O%3BWess%2C+J&rft.aulast=Felder&rft.aufirst=C&rft.date=1992-01-15&rft.volume=89&rft.issue=2&rft.spage=509&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-18 N1 - Date created - 1992-02-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1986 Mar 15;261(8):3501-11 [3081507] Science. 1987 Jul 31;237(4814):527-32 [3037705] Nature. 1987 Jul 16-22;328(6127):275-8 [2439921] Nature. 1986 Nov 27-Dec 3;324(6095):369-72 [2431318] Nature. 1987 Mar 19-25;326(6110):301-4 [2434867] Cell Calcium. 1986 Feb;7(1):1-12 [2420465] Nature. 1989 Sep 21;341(6239):197-205 [2550825] FEBS Lett. 1988 Dec 5;241(1-2):119-25 [3197827] J Biol Chem. 1987 Feb 5;262(4):1638-43 [3543007] Biochem J. 1986 Dec 15;240(3):917-20 [3827881] J Biol Chem. 1985 Mar 25;260(6):3440-50 [3838314] Nature. 1991 Jul 11;352(6331):162-5 [1648669] Mol Pharmacol. 1990 Oct;38(4):517-23 [2172767] J Physiol. 1990 Feb;421:499-519 [1693402] Biochem Biophys Res Commun. 1991 May 31;177(1):551-8 [1645964] Trends Pharmacol Sci. 1991 Aug;12(8):289-92 [1658997] J Pharmacol Exp Ther. 1990 Dec;255(3):1140-7 [2124620] J Physiol. 1987 Dec;394:173-200 [2451017] J Biol Chem. 1987 May 5;262(13):6121-7 [3032956] Neurosci Res. 1987 Feb;4(3):228-35 [2437502] Science. 1988 Jun 3;240(4857):1310-6 [2836950] J Biol Chem. 1989 Dec 5;264(34):20356-62 [2555356] FEBS Lett. 1989 Nov 20;258(1):133-6 [2556294] Proc Natl Acad Sci U S A. 1988 Nov;85(22):8698-702 [2847172] J Biol Chem. 1988 Sep 5;263(25):12454-60 [2900837] Proc Natl Acad Sci U S A. 1988 Jun;85(11):4056-60 [2453885] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The multichain interleukin-2 receptor: a target for immunotherapy. AN - 72758856; 1727619 AB - Activation of resting T-lymphocytes induces synthesis of interleukin-2 (IL-2) and expression of cell surface receptors for this lymphokine. In contrast to resting normal T-cells that do not express high-affinity IL-2 receptors (IL-2R), abnormal T-cells of patients with leukemia-lymphoma, certain autoimmune disorders, and individuals rejecting allografts express this receptor. Exploiting this difference in receptor expression, antibodies to the IL-2 receptor have been used effectively to treat patients with leukemia and lymphoma. One approach is to use monoclonal antibodies produced in mice; the disadvantage is that they are highly immunogenic. In an effort to reduce the immunogenicity of the mouse monoclonal antibodies, monoclonal-antibody-mediated therapy has been revolutionized by generating humanized antibodies produced by genetic engineering in which the molecule is human except for the antigen-combining regions, which are retained from the mouse. Further, to increase its cytotoxic effectiveness, the monoclonal antibody has been armed with toxins or radionuclides. Alternatively, IL-2 itself has been linked to a toxin to kill IL-2 receptor-bearing cells. Thus, IL-2 receptor-directed therapy provides a new method for treating certain neoplastic diseases and autoimmune disorders and for preventing allograft rejection. JF - Annals of internal medicine AU - Waldmann, T A AU - Pastan, I H AU - Gansow, O A AU - Junghans, R P AD - National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/01/15/ PY - 1992 DA - 1992 Jan 15 SP - 148 EP - 160 VL - 116 IS - 2 SN - 0003-4819, 0003-4819 KW - Antibodies, Monoclonal KW - 0 KW - Bacterial Toxins KW - Exotoxins KW - Immunotoxins KW - Receptors, Interleukin-2 KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Radioimmunotherapy KW - Leukemia-Lymphoma, Adult T-Cell -- therapy KW - Genetic Engineering KW - Humans KW - Radioimmunodetection KW - Leukemia-Lymphoma, Adult T-Cell -- immunology KW - Immunotoxins -- therapeutic use KW - Autoimmune Diseases -- immunology KW - Receptors, Interleukin-2 -- physiology KW - Antibodies, Monoclonal -- chemistry KW - Receptors, Interleukin-2 -- chemistry KW - Receptors, Interleukin-2 -- immunology KW - Antibodies, Monoclonal -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72758856?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+internal+medicine&rft.atitle=The+multichain+interleukin-2+receptor%3A+a+target+for+immunotherapy.&rft.au=Waldmann%2C+T+A%3BPastan%2C+I+H%3BGansow%2C+O+A%3BJunghans%2C+R+P&rft.aulast=Waldmann&rft.aufirst=T&rft.date=1992-01-15&rft.volume=116&rft.issue=2&rft.spage=148&rft.isbn=&rft.btitle=&rft.title=Annals+of+internal+medicine&rft.issn=00034819&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-21 N1 - Date created - 1992-01-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retinal toxicity in human immunodeficiency virus-infected children treated with 2',3'-dideoxyinosine. AN - 72742179; 1728133 AB - To assess the safety and antiretroviral activity of 2',3'-dideoxyinosine, we enrolled 43 children with symptomatic (Centers for Disease Control class P-2) human immunodeficiency virus infection in a Phase I-II study and monitored them prospectively for the development of ocular complications secondary to HIV infection or drug toxicity. Follow-up ranged from 12 to 103 weeks with a median follow-up of 71 weeks. Three of 43 children (7.0%) developed peripheral atrophy of the retinal pigment epithelium during treatment with 2',3'-dideoxyinosine. The two children with the most severe retinal atrophy were enrolled in the study at the highest dosage studied (540 mg/m2/day). In contrast to findings in children, no retinal atrophy in HIV-infected adults treated with 2',3'-dideoxyinosine has been evident to date. JF - American journal of ophthalmology AU - Whitcup, S M AU - Butler, K M AU - Caruso, R AU - de Smet, M D AU - Rubin, B AU - Husson, R N AU - Lopez, J S AU - Belfort, R AU - Pizzo, P A AU - Nussenblatt, R B AD - Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/01/15/ PY - 1992 DA - 1992 Jan 15 SP - 1 EP - 7 VL - 113 IS - 1 SN - 0002-9394, 0002-9394 KW - Zidovudine KW - 4B9XT59T7S KW - Didanosine KW - K3GDH6OH08 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Zidovudine -- therapeutic use KW - Humans KW - Child KW - HIV-1 KW - Child, Preschool KW - Drug Evaluation KW - Fundus Oculi KW - Prospective Studies KW - Electrooculography KW - Atrophy KW - Follow-Up Studies KW - Retina -- pathology KW - Pigment Epithelium of Eye -- pathology KW - Female KW - Male KW - Electroretinography KW - Didanosine -- therapeutic use KW - HIV Infections -- complications KW - HIV Infections -- drug therapy KW - Retinal Diseases -- etiology KW - Retinal Diseases -- chemically induced KW - Didanosine -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72742179?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+ophthalmology&rft.atitle=Retinal+toxicity+in+human+immunodeficiency+virus-infected+children+treated+with+2%27%2C3%27-dideoxyinosine.&rft.au=Whitcup%2C+S+M%3BButler%2C+K+M%3BCaruso%2C+R%3Bde+Smet%2C+M+D%3BRubin%2C+B%3BHusson%2C+R+N%3BLopez%2C+J+S%3BBelfort%2C+R%3BPizzo%2C+P+A%3BNussenblatt%2C+R+B&rft.aulast=Whitcup&rft.aufirst=S&rft.date=1992-01-15&rft.volume=113&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=American+journal+of+ophthalmology&rft.issn=00029394&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-30 N1 - Date created - 1992-01-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Experimental analysis by site-directed mutagenesis of somatic mutation effects on affinity and fine specificity in antibodies specific for lysozyme. AN - 72739205; 1729369 AB - To experimentally examine the functional roles of somatically derived structural variation in the lysozyme-binding mAb HyHEL-10, we have introduced three different point mutations and one insertion at two different sites in HyHEL-10 by site-directed mutagenesis and expression of the mutant antibodies. Mutation of Asp----Ala at position 101 of the H chain returns a somatically mutated residue to its germline sequence for HyHEL-10, and reduces affinity for chicken lysozyme by approximately 9000-fold. Lengthening the third H chain hypervariable region by two amino acids reduces affinity by about 2000-fold. Two mutations, Asp----Thr at position 101 in the H chain and Lys----Thr at position 49 in the L chain, model somatic differences found in another structurally related but functionally distinguishable mAb and minimally decrease affinity for chicken lysozyme. The H chain mutation Asp101VVH----Thr has little effect on affinity for other avian lysozymes but does alter relative fine specificity for these lysozymes. The L chain mutation Lys49VK----Thr increases affinity for duck lysozyme by approximately fivefold. Neither of the positions mutated, 101 in the H chain nor 49 in the L chain, nor the residues near the insertion contact lysozyme in the x-ray structure of the HyHEL-10 F(ab)-HEL complex. The results suggest that these mutations, which model observed somatic mutations, produce functional variation by indirect or long-range effects. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Lavoie, T B AU - Drohan, W N AU - Smith-Gill, S J AD - Laboratory of Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/01/15/ PY - 1992 DA - 1992 Jan 15 SP - 503 EP - 513 VL - 148 IS - 2 SN - 0022-1767, 0022-1767 KW - Muramidase KW - EC 3.2.1.17 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Base Sequence KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Structure-Activity Relationship KW - Antibody Affinity -- genetics KW - Muramidase -- immunology KW - Antibody Specificity -- genetics KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72739205?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Experimental+analysis+by+site-directed+mutagenesis+of+somatic+mutation+effects+on+affinity+and+fine+specificity+in+antibodies+specific+for+lysozyme.&rft.au=Lavoie%2C+T+B%3BDrohan%2C+W+N%3BSmith-Gill%2C+S+J&rft.aulast=Lavoie&rft.aufirst=T&rft.date=1992-01-15&rft.volume=148&rft.issue=2&rft.spage=503&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-11 N1 - Date created - 1992-02-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A health survey of radiologic technologists. AN - 72734491; 1728391 AB - A health survey of more than 143,000 radiologic technologists is described. The population was identified from the 1982 computerized files of the American Registry of Radiologic Technologists, which was established in 1926. Inactive members were traced to obtain current addresses or death notifications. More than 6000 technologists were reported to have died. For all registrants who were alive when located, a detailed 16-page questionnaire was sent, covering occupational histories, medical conditions, and other personal and lifestyle characteristics. Nonrespondents were contacted by telephone to complete an abbreviated questionnaire. More than 104,000 responses were obtained. The overall response rate was 79%. Most technologists were female (76%), white (93%), and employed for an average of 12 years; 37% attended college, and approximately 50% never smoked cigarettes. Radiation exposure information was sought from employer records and commercial dosimetry companies. Technologists employed for the longest times had the highest estimated cumulative exposures, with approximately 9% with exposures greater than 5 cGy. There was a high correlation between cumulative occupational exposure and personal exposure to medical radiographs, related, in part, to the association of both factors with attained age. It is interesting that 10% of all technologists allowed others to practice taking radiographs on them during their training. Nearly 4% of the respondents reported having some type of cancer, mainly of the skin (1517), breast (665), and cervix (726). Prospective surveys will monitor cancer mortality rates through use of the National Death Index and cancer incidence through periodic mailings of questionnaires. This is the only occupational study of radiation employees who are primarily women and should provide new information on the possible risks associated with relatively low levels of exposure. JF - Cancer AU - Boice, J D AU - Mandel, J S AU - Doody, M M AU - Yoder, R C AU - McGowan, R AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/01/15/ PY - 1992 DA - 1992 Jan 15 SP - 586 EP - 598 VL - 69 IS - 2 SN - 0008-543X, 0008-543X KW - Abridged Index Medicus KW - Index Medicus KW - Employment -- statistics & numerical data KW - Radiation Dosage KW - Neoplasms, Radiation-Induced -- epidemiology KW - Humans KW - Adult KW - Surveys and Questionnaires KW - Occupational Diseases -- epidemiology KW - Middle Aged KW - United States -- epidemiology KW - Male KW - Female KW - Occupational Exposure -- statistics & numerical data KW - Health Surveys KW - Technology, Radiologic -- manpower KW - Allied Health Personnel -- statistics & numerical data UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72734491?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=A+health+survey+of+radiologic+technologists.&rft.au=Boice%2C+J+D%3BMandel%2C+J+S%3BDoody%2C+M+M%3BYoder%2C+R+C%3BMcGowan%2C+R&rft.aulast=Boice&rft.aufirst=J&rft.date=1992-01-15&rft.volume=69&rft.issue=2&rft.spage=586&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-04 N1 - Date created - 1992-02-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of colorectal cancer in rats by 20-methylcholanthrene. AN - 72779931; 1730142 AB - Colorectal carcinoma was induced in Sprague-Dawley rats by 20-methylcholanthrene. Macroscopical studies revealed that the tumors, either sessile type or semi-pedunculated polyp, were generally observed after 32 weeks of the carcinogen treatment. In the distal colon 46.9% tumors appeared, whereas 20.4% and 32.6% tumors were found in the rectum and proximal colon, respectively. Sequential histopathological studies indicated that hyperplasia of goblet cells was common in early stages, which was reduced thereafter. Carcinogenesis progressed with the appearance of the different grades of dysplasia in colorectal mucosa with first incidence of the severe dysplasia in rats at the 20th week and in situ carcinoma at the close of 28th week. Most of the carcinomas were multifocal in origin and were well differentiated adenocarcinoma with primary invasion at the submucosa. In immunohistological studies, this carcinoma was also reactive with monoclonal antibody 660, prepared against a colorectal carcinoma associated mucin antigen. JF - Cancer letters AU - Baral, R N AU - Maity, P AD - Department of Cell Biology, Chittaranjan National Cancer Institute, Calcutta, India. Y1 - 1992/01/10/ PY - 1992 DA - 1992 Jan 10 SP - 177 EP - 183 VL - 61 IS - 2 SN - 0304-3835, 0304-3835 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Neoplasm KW - Methylcholanthrene KW - 56-49-5 KW - Index Medicus KW - Rats KW - Hyperplasia -- pathology KW - Animals KW - Antigens, Neoplasm -- analysis KW - Time Factors KW - Administration, Topical KW - Antibodies, Monoclonal -- immunology KW - Methylcholanthrene -- administration & dosage KW - Carcinoma -- pathology KW - Colorectal Neoplasms -- pathology KW - Colorectal Neoplasms -- immunology KW - Carcinoma -- immunology KW - Colorectal Neoplasms -- chemically induced KW - Carcinoma -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72779931?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+letters&rft.atitle=Induction+of+colorectal+cancer+in+rats+by+20-methylcholanthrene.&rft.au=Baral%2C+R+N%3BMaity%2C+P&rft.aulast=Baral&rft.aufirst=R&rft.date=1992-01-10&rft.volume=61&rft.issue=2&rft.spage=177&rft.isbn=&rft.btitle=&rft.title=Cancer+letters&rft.issn=03043835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-20 N1 - Date created - 1992-02-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - From the National Institutes of Health. AN - 72732174; 1309267 JF - JAMA AU - Healy, B AD - National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/01/08/ PY - 1992 DA - 1992 Jan 08 SP - 209 VL - 267 IS - 2 SN - 0098-7484, 0098-7484 KW - Anti-Inflammatory Agents, Non-Steroidal KW - 0 KW - Antiviral Agents KW - Foscarnet KW - 364P9RVW4X KW - Phosphonoacetic Acid KW - N919E46723 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - United States KW - Exercise Test KW - Arthritis, Rheumatoid -- drug therapy KW - Antiviral Agents -- therapeutic use KW - Humans KW - Phosphonoacetic Acid -- analogs & derivatives KW - National Institutes of Health (U.S.) KW - Phosphonoacetic Acid -- therapeutic use KW - Radionuclide Imaging KW - Cytomegalovirus Infections -- drug therapy KW - Retinitis -- drug therapy KW - Anti-Inflammatory Agents, Non-Steroidal -- adverse effects KW - Acquired Immunodeficiency Syndrome KW - Death, Sudden, Cardiac KW - Coronary Disease -- diagnostic imaging KW - Eye Infections, Viral -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72732174?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=JAMA&rft.atitle=From+the+National+Institutes+of+Health.&rft.au=Healy%2C+B&rft.aulast=Healy&rft.aufirst=B&rft.date=1992-01-08&rft.volume=267&rft.issue=2&rft.spage=209&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-23 N1 - Date created - 1992-01-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of T cells by a tyrosine kinase activation domain in the cytoplasmic tail of CD3 epsilon. AN - 72861944; 1532456 AB - The multichain T cell antigen receptor functions by interacting with and activating one or more nonreceptor tyrosine kinases. The cytoplasmic tail of the zeta chain can activate T cells independently of the rest of the receptor complex. The function of the remaining invariant CD3 chains remains unknown. A 22-amino acid region of the cytoplasmic tail of CD3 epsilon was also able to independently activate T cells. Stimulation of T cells by means of the cytoplasmic tails of either zeta or CD3 epsilon resulted in quantitatively distinct patterns of tyrosine phosphorylation, suggesting activation of different biochemical pathways. JF - Science (New York, N.Y.) AU - Letourneur, F AU - Klausner, R D AD - Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/01/03/ PY - 1992 DA - 1992 Jan 03 SP - 79 EP - 82 VL - 255 IS - 5040 SN - 0036-8075, 0036-8075 KW - Antigens, CD3 KW - 0 KW - Antigens, Differentiation, T-Lymphocyte KW - Interleukin-2 KW - Macromolecular Substances KW - Receptors, Antigen, T-Cell KW - Receptors, Interleukin-2 KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Index Medicus KW - Clone Cells KW - Animals KW - Humans KW - Interleukin-2 -- biosynthesis KW - Mice KW - Amino Acid Sequence KW - Receptors, Interleukin-2 -- genetics KW - Mutagenesis, Site-Directed KW - Polymerase Chain Reaction KW - Receptors, Interleukin-2 -- metabolism KW - Cell Membrane -- immunology KW - Chimera KW - Phosphorylation KW - Transfection KW - Kinetics KW - Molecular Sequence Data KW - Cell Membrane -- metabolism KW - Cell Line KW - Lymphocyte Activation KW - Protein-Tyrosine Kinases -- genetics KW - Antigens, Differentiation, T-Lymphocyte -- genetics KW - Antigens, Differentiation, T-Lymphocyte -- metabolism KW - Receptors, Antigen, T-Cell -- metabolism KW - Protein-Tyrosine Kinases -- metabolism KW - Receptors, Antigen, T-Cell -- genetics KW - T-Lymphocytes -- immunology KW - T-Lymphocytes -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72861944?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft.atitle=Activation+of+T+cells+by+a+tyrosine+kinase+activation+domain+in+the+cytoplasmic+tail+of+CD3+epsilon.&rft.au=Letourneur%2C+F%3BKlausner%2C+R+D&rft.aulast=Letourneur&rft.aufirst=F&rft.date=1992-01-03&rft.volume=255&rft.issue=5040&rft.spage=79&rft.isbn=&rft.btitle=&rft.title=Science+%28New+York%2C+N.Y.%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-24 N1 - Date created - 1992-04-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Clinical Pathology in the National Toxicology Program AN - 856755580; 13645509 AB - The National Toxicology Program (NTP) developed a standard approach for clinical pathology investigations that was integrated into most toxicity studies designed and conducted after 1986. Protocols for these studies include specific hematology and clinical chemistry analyses at 3 selected time points in 13-wk studies. Requirements concerning the anesthetization of animals, collection and analysis of samples, and reporting of results have been established to control sources of variability within and between contract laboratories that perform these studies for the NTP. Laboratories must meet minimum standards to be approved for participation in the Program. Important areas of consideration for these laboratories to perform clinical pathology investigations include the facility, equipment, personnel, performance, and quality control procedures. Clinical pathology results from approximately 60 13-wk studies that have been conducted by the NTP in 7 laboratories since 1987 are being analyzed to generate a database of control values for the Fischer rat and B6C3F, mouse and to identify sources of variability. Experimental data from these studies are being analyzed and correlated with histopathologic findings to evaluate the contribution of clinical pathology to the characterization of toxicity and to examine the appropriateness of the current approach. Efforts such as these will provide for the evolution and continued relevance of clinical pathology in toxicity testing. JF - Toxicologic Pathology AU - Thompson, Morrow B AD - National Institute of Environmental Health Sciences, P.O. Box 12233, Mail Drop C2-08, Research Triangle Park, North Carolina 27709 Y1 - 1992 PY - 1992 DA - 1992 SP - 484 EP - 489 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU UK VL - 20 IS - 3-2 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts KW - Databases KW - Computer programs KW - Data processing KW - Personnel KW - Quality control KW - Toxicity KW - Toxicity testing KW - Evolution KW - X 24310:Pharmaceuticals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/856755580?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Clinical+Pathology+in+the+National+Toxicology+Program&rft.au=Thompson%2C+Morrow+B&rft.aulast=Thompson&rft.aufirst=Morrow&rft.date=1992-01-01&rft.volume=20&rft.issue=3-2&rft.spage=484&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F019262339202000305 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2010-10-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - Computer programs; Databases; Data processing; Personnel; Quality control; Toxicity; Toxicity testing; Evolution DO - http://dx.doi.org/10.1177/019262339202000305 ER - TY - JOUR T1 - Metabolic brain pattern of sustained auditory discrimination. AN - 85235285; pmid-1486951 AB - Positron emission tomography of [18F]-2-fluorodeoxyglucose was used to assess the functional brain activity of normal subjects while performing auditory discrimination (CPT), while receiving an identical set of tones as in CPT, but with the instructions that they were background noise, or while at rest. The present study: (1) confirms earlier findings of an association between the functional activity of the right midprefrontal cortex and the performance of auditory discrimination, (2) localizes this increase in right prefrontal cortex activity to the middle prefrontal gyrus; and (3) provides a framework of specific testable hypotheses for the evaluation of the importance of certain limbic and paralimbic areas in the biological determination of sustained attention to be addressed in future studies. The framework accounts for the now confirmed finding that the middle cingulate has lower metabolic activity in CPT than at rest, and new findings of alterations in temporal lobe processing of tones in response to attention. JF - Experimental Brain Research AU - Cohen, R M AU - Semple, W E AU - Gross, M AU - King, A C AU - Nordahl, T E AD - Section on Clinical Brain Imaging, NIMH, Bethesda, MD 20892-1000. PY - 1992 SP - 165 EP - 172 VL - 92 IS - 1 SN - 0014-4819, 0014-4819 KW - Brain Chemistry KW - Human KW - Brain KW - Exploratory Behavior KW - Discrimination (Psychology) KW - Fludeoxyglucose F 18 KW - Adult KW - Tomography, Emission-Computed KW - Deoxyglucose KW - Middle Age KW - Psychomotor Performance KW - Adolescent KW - Male KW - Female KW - Acoustic Stimulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85235285?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Experimental+Brain+Research&rft.atitle=Metabolic+brain+pattern+of+sustained+auditory+discrimination.&rft.au=Cohen%2C+R+M%3BSemple%2C+W+E%3BGross%2C+M%3BKing%2C+A+C%3BNordahl%2C+T+E&rft.aulast=Cohen&rft.aufirst=R&rft.date=1992-01-01&rft.volume=92&rft.issue=1&rft.spage=165&rft.isbn=&rft.btitle=&rft.title=Experimental+Brain+Research&rft.issn=00144819&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - NCI reaffirms commitment to prevention AN - 839265426; 1153822 JF - International journal of health services Y1 - 1992 PY - 1992 DA - 1992 SP - 464 VL - 22 IS - 3 SN - 0020-7314, 0020-7314 KW - Sociology KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/839265426?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+health+services&rft.atitle=NCI+reaffirms+commitment+to+prevention&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1992-01-01&rft.volume=22&rft.issue=3&rft.spage=464&rft.isbn=&rft.btitle=&rft.title=International+journal+of+health+services&rft.issn=00207314&rft_id=info:doi/ LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2013-06-12 N1 - Last updated - 2013-09-16 N1 - SubjectsTermNotLitGenreText - 1939 3617 6220 ER - TY - JOUR T1 - Safe disposal of diaminobenzidine. AN - 75547011; 1369737 JF - Trends in genetics : TIG AU - Lunn, G AU - Sansone, E B AD - Program Resources Inc., Environmental Control and Research Program, NCI-Frederick Cancer Research and Development Center, MD 21702-1201, USA. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 7 VL - 8 IS - 1 SN - 0168-9525, 0168-9525 KW - Carcinogens KW - 0 KW - Hazardous Waste KW - Mutagens KW - Potassium Permanganate KW - 00OT1QX5U4 KW - 3,3'-Diaminobenzidine KW - 2RV4T6KHQI KW - Hydrogen Peroxide KW - BBX060AN9V KW - Horseradish Peroxidase KW - EC 1.11.1.- KW - Ascorbic Acid KW - PQ6CK8PD0R KW - Index Medicus KW - Oxidation-Reduction KW - Safety KW - 3,3'-Diaminobenzidine -- toxicity KW - Carcinogens -- chemistry KW - Carcinogens -- toxicity KW - Waste Disposal, Fluid -- methods KW - Mutagens -- toxicity KW - 3,3'-Diaminobenzidine -- chemistry KW - Mutagens -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75547011?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Trends+in+genetics+%3A+TIG&rft.atitle=Safe+disposal+of+diaminobenzidine.&rft.au=Lunn%2C+G%3BSansone%2C+E+B&rft.aulast=Lunn&rft.aufirst=G&rft.date=1992-01-01&rft.volume=8&rft.issue=1&rft.spage=7&rft.isbn=&rft.btitle=&rft.title=Trends+in+genetics+%3A+TIG&rft.issn=01689525&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1995-08-14 N1 - Date created - 1995-08-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A pilot study of a new ELISA test for ciguatoxin in humans. AN - 75524073; 1340355 AB - The major impediment to the thorough study of Ciguatera in human populations has been the lack of definitive diagnostic ability. However, recently an ELISA test was developed which can diagnose Ciguatera qualitatively and quantitatively in human fluids, as well as in contaminated fish tissue. This study proposes to evaluate this new ELISA test in human subjects with the clinical diagnoses of acute and chronic Ciguatera Poisoning. The contaminated fish from exposed subjects, and the blood and urine of exposed and controls, will be examined using the new ELISA. The ELISA performance will be compared to traditional bioassays for the fish testing. In addition, a distinct diagnostic profile will be developed using serial questionnaires, physical examinations, and nerve conduction tests. Ultimately this ELISA test can be used not only in establishing the correct diagnosis of Ciguatera Poisoning, but also in the treatment and clinical prognosis, and in epidemiologic studies of Ciguatera Poisoning in human populations. We hope that this protocol will serve as a model for the study of the effects of other marine toxins on human populations. JF - Bulletin de la Societe de pathologie exotique (1990) AU - Fleming, L E AU - Baden, D G AU - Ayyar, R A AU - Bean, J A AU - Blythe, D G AU - Shrank, K AU - De Sylva, D P AD - NIEHS Marine and Freshwater Biomedical Sciences Center, University of Miami. Y1 - 1992 PY - 1992 DA - 1992 SP - 508 EP - 509 VL - 85 IS - 5 Pt 2 SN - 0037-9085, 0037-9085 KW - Ciguatoxins KW - 11050-21-8 KW - Index Medicus KW - Animals KW - Vomiting KW - Humans KW - Fishes KW - Adult KW - Body Fluids -- chemistry KW - Male KW - Female KW - Enzyme-Linked Immunosorbent Assay KW - Ciguatoxins -- analysis KW - Ciguatera Poisoning UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75524073?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bulletin+de+la+Societe+de+pathologie+exotique+%281990%29&rft.atitle=A+pilot+study+of+a+new+ELISA+test+for+ciguatoxin+in+humans.&rft.au=Fleming%2C+L+E%3BBaden%2C+D+G%3BAyyar%2C+R+A%3BBean%2C+J+A%3BBlythe%2C+D+G%3BShrank%2C+K%3BDe+Sylva%2C+D+P&rft.aulast=Fleming&rft.aufirst=L&rft.date=1992-01-01&rft.volume=85&rft.issue=5+Pt+2&rft.spage=508&rft.isbn=&rft.btitle=&rft.title=Bulletin+de+la+Societe+de+pathologie+exotique+%281990%29&rft.issn=00379085&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-17 N1 - Date created - 1993-12-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - ADP-ribosylation factor, a guanine nucleotide-binding protein activator of cholera toxin, is isolated in an activated state when expressed as a fusion protein in Escherichia coli. AN - 75513100; 1308993 JF - Transactions of the Association of American Physicians AU - Welsh, C F AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 172 EP - 176 VL - 105 SN - 0066-9458, 0066-9458 KW - Carrier Proteins KW - 0 KW - Escherichia coli Proteins KW - Maltose-Binding Proteins KW - Monosaccharide Transport Proteins KW - Recombinant Fusion Proteins KW - maltose transport system, E coli KW - Guanosine Triphosphate KW - 86-01-1 KW - Cholera Toxin KW - 9012-63-9 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - ADP-Ribosylation Factors KW - EC 3.6.5.2 KW - Index Medicus KW - Recombinant Fusion Proteins -- metabolism KW - Carrier Proteins -- metabolism KW - Humans KW - Carrier Proteins -- genetics KW - Recombinant Fusion Proteins -- isolation & purification KW - Recombinant Fusion Proteins -- genetics KW - Gene Expression KW - Escherichia coli -- genetics KW - Hydrolysis KW - Guanosine Triphosphate -- metabolism KW - Carrier Proteins -- isolation & purification KW - GTP-Binding Proteins -- metabolism KW - GTP-Binding Proteins -- isolation & purification KW - ATP-Binding Cassette Transporters KW - GTP-Binding Proteins -- genetics KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75513100?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Transactions+of+the+Association+of+American+Physicians&rft.atitle=ADP-ribosylation+factor%2C+a+guanine+nucleotide-binding+protein+activator+of+cholera+toxin%2C+is+isolated+in+an+activated+state+when+expressed+as+a+fusion+protein+in+Escherichia+coli.&rft.au=Welsh%2C+C+F%3BMoss%2C+J%3BVaughan%2C+M&rft.aulast=Welsh&rft.aufirst=C&rft.date=1992-01-01&rft.volume=105&rft.issue=&rft.spage=172&rft.isbn=&rft.btitle=&rft.title=Transactions+of+the+Association+of+American+Physicians&rft.issn=00669458&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-21 N1 - Date created - 1993-10-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The N-myc proto-oncogene: developmental expression and in vivo site-directed mutagenesis. AN - 75503148; 1341949 AB - The N-myc proto-oncogene is a member of the superfamily of transcription factors. In mammals, expression of this gene is predominantly restricted to the developing embryo. Specifically, the level of expression is highest in differentiating epithelial components of the embryo including those of the developing brain, kidney and lung. The observation that N-myc is expressed in differentiating but not terminally differentiated structures suggests that these genes may function in the maintenance of cells in a determined or proliferative state. Available evidence suggests that when N-myc expression is down-regulated, cells progress through differentiation and acquire their terminal phenotype. N-myc expression is also correlated with poor prognosis in a number of tumor systems. Since malignant tumors are usually poorly differentiated, this may reflect the role that N-myc plays in preventing differentiation of otherwise determined cells. In vivo site-directed mutagenesis by homologous recombination has made it possible to introduce a variety of mutations into mice. This review summarizes this technology and describes our initial results in the characterization of mice that lack a functional N-myc gene. Specifically, we have observed that in the absence of a functional N-myc gene, embryos arrest in midgestation. This body of work demonstrates that this gene is not required for normal development until the onset of organogenesis. JF - Brain pathology (Zurich, Switzerland) AU - Stanton, B R AU - Parada, L F AD - Molecular Embryology Section, NCI-Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 71 EP - 83 VL - 2 IS - 1 SN - 1015-6305, 1015-6305 KW - N-myc KW - c-myc KW - Proto-Oncogene Proteins c-myc KW - 0 KW - Index Medicus KW - Proto-Oncogene Proteins c-myc -- biosynthesis KW - Mutagenesis, Site-Directed KW - Animals KW - Mammals KW - Cerebral Cortex -- metabolism KW - Humans KW - Gene Expression KW - Proto-Oncogene Proteins c-myc -- metabolism KW - Proto-Oncogenes KW - Embryo, Mammalian KW - Mutagenesis, Insertional KW - Brain Neoplasms -- pathology KW - Genes, myc KW - Brain Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75503148?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+pathology+%28Zurich%2C+Switzerland%29&rft.atitle=The+N-myc+proto-oncogene%3A+developmental+expression+and+in+vivo+site-directed+mutagenesis.&rft.au=Stanton%2C+B+R%3BParada%2C+L+F&rft.aulast=Stanton&rft.aufirst=B&rft.date=1992-01-01&rft.volume=2&rft.issue=1&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=Brain+pathology+%28Zurich%2C+Switzerland%29&rft.issn=10156305&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-02-03 N1 - Date created - 1994-02-03 N1 - Date revised - 2017-01-13 N1 - Gene symbol - N-myc; c-myc N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Risk factors for stomach cancer in sixty-five Chinese counties. AN - 75502362; 1306092 AB - Stomach cancer mortality data were compared with dietary and biochemical data from 65 Chinese counties to provide clues to reasons for the marked geographic variation of stomach cancer mortality rates in China. Sex-specific correlation and multivariate regression analyses showed significant positive associations with consumption of salted vegetables and eggs, prevalence of antibodies to Helicobacter pylori, and levels of plasma albumin; and significant negative associations with intake of green vegetables and levels of plasma selenium and beta-carotene. Limitations of ecological data preclude causal inferences, but these findings suggest factors that may contribute to making stomach cancer the leading cause of cancer death in China and other countries. JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology AU - Kneller, R W AU - Guo, W D AU - Hsing, A W AU - Chen, J S AU - Blot, W J AU - Li, J Y AU - Forman, D AU - Fraumeni, J F AD - National Cancer Institute, Bethesda, Maryland 20892. PY - 1992 SP - 113 EP - 118 VL - 1 IS - 2 SN - 1055-9965, 1055-9965 KW - Antibodies, Bacterial KW - 0 KW - Serum Albumin KW - Sodium, Dietary KW - beta Carotene KW - 01YAE03M7J KW - Carotenoids KW - 36-88-4 KW - Selenium KW - H6241UJ22B KW - Index Medicus KW - Helicobacter pylori KW - Vegetables KW - Serum Albumin -- analysis KW - Sodium, Dietary -- adverse effects KW - Humans KW - Helicobacter Infections -- complications KW - Diet Surveys KW - Helicobacter Infections -- epidemiology KW - Cross-Sectional Studies KW - Selenium -- blood KW - Carotenoids -- blood KW - Risk Factors KW - China -- epidemiology KW - Eggs -- adverse effects KW - Adult KW - Antibodies, Bacterial -- blood KW - Helicobacter Infections -- blood KW - Middle Aged KW - Residence Characteristics KW - Male KW - Female KW - Stomach Neoplasms -- mortality KW - Stomach Neoplasms -- blood KW - Stomach Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75502362?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.atitle=Risk+factors+for+stomach+cancer+in+sixty-five+Chinese+counties.&rft.au=Kneller%2C+R+W%3BGuo%2C+W+D%3BHsing%2C+A+W%3BChen%2C+J+S%3BBlot%2C+W+J%3BLi%2C+J+Y%3BForman%2C+D%3BFraumeni%2C+J+F&rft.aulast=Kneller&rft.aufirst=R&rft.date=1992-01-01&rft.volume=1&rft.issue=2&rft.spage=113&rft.isbn=&rft.btitle=&rft.title=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.issn=10559965&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-03 N1 - Date created - 1993-08-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - N-acetyl-cysteine is a potent suppressor of human immunodeficiency virus transcription in persistently infected cells. AN - 75498333; 1285017 JF - Transactions of the Association of American Physicians AU - Kinter, A L AU - Poli, G AU - Fauci, A S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 36 EP - 43 VL - 105 SN - 0066-9458, 0066-9458 KW - Reverse Transcriptase Inhibitors KW - 0 KW - Tumor Necrosis Factor-alpha KW - HIV Reverse Transcriptase KW - EC 2.7.7.49 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Acetylcysteine KW - WYQ7N0BPYC KW - Index Medicus KW - AIDS/HIV KW - Transcription, Genetic -- drug effects KW - Virus Replication -- drug effects KW - Transfection KW - Humans KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - HIV Long Terminal Repeat -- drug effects KW - Cell Line KW - HIV-1 -- genetics KW - Acetylcysteine -- pharmacology KW - HIV-1 -- physiology KW - HIV-1 -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75498333?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Transactions+of+the+Association+of+American+Physicians&rft.atitle=N-acetyl-cysteine+is+a+potent+suppressor+of+human+immunodeficiency+virus+transcription+in+persistently+infected+cells.&rft.au=Kinter%2C+A+L%3BPoli%2C+G%3BFauci%2C+A+S&rft.aulast=Kinter&rft.aufirst=A&rft.date=1992-01-01&rft.volume=105&rft.issue=&rft.spage=36&rft.isbn=&rft.btitle=&rft.title=Transactions+of+the+Association+of+American+Physicians&rft.issn=00669458&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-21 N1 - Date created - 1993-10-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comorbidity: meaning and uses in cross-cultural clinical research. AN - 73600366; 1305523 AB - American Indians and Alaska Natives were the subject of a workshop sponsored by the National Institute of Mental Health and the Indian Health Service. Comorbidity of anxiety, depression, and substance abuse is highly prevalent in these two populations, and this was the focus of the meeting. This paper introduces the topic of psychiatric comorbidity, and considers the topics of culture, psychiatric diagnosis, and assessment. Future research directions and a brief summary of the papers presented at the workshop, which are included in this issue, are provided. JF - Culture, medicine and psychiatry AU - Maser, J D AU - Dinges, N AD - National Institute of Mental Health, Rockville, MD 20857. PY - 1992 SP - 409 EP - 425 VL - 16 IS - 4 SN - 0165-005X, 0165-005X KW - Index Medicus KW - Cross-Sectional Studies KW - Psychiatric Status Rating Scales KW - Humans KW - Alaska -- epidemiology KW - Incidence KW - United States -- epidemiology KW - Comorbidity KW - Anxiety Disorders -- psychology KW - Depressive Disorder -- psychology KW - Anxiety Disorders -- diagnosis KW - Cross-Cultural Comparison KW - Indians, North American -- psychology KW - Inuits -- psychology KW - Inuits -- statistics & numerical data KW - Substance-Related Disorders -- psychology KW - Indians, North American -- statistics & numerical data KW - Depressive Disorder -- epidemiology KW - Substance-Related Disorders -- diagnosis KW - Depressive Disorder -- diagnosis KW - Anxiety Disorders -- epidemiology KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73600366?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Culture%2C+medicine+and+psychiatry&rft.atitle=Comorbidity%3A+meaning+and+uses+in+cross-cultural+clinical+research.&rft.au=Maser%2C+J+D%3BDinges%2C+N&rft.aulast=Maser&rft.aufirst=J&rft.date=1992-01-01&rft.volume=16&rft.issue=4&rft.spage=409&rft.isbn=&rft.btitle=&rft.title=Culture%2C+medicine+and+psychiatry&rft.issn=0165005X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-20 N1 - Date created - 1993-07-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Development of chemopreventive agents for bladder cancer. AN - 73537614; 1305671 AB - The term cancer chemoprevention refers to the prevention or prolongation of carcinogenesis by intervention with drugs prior to the malignant (i.e., invasive) stage. The development of chemopreventive drugs is the major objective of the Chemoprevention Branch of the National Cancer Institute. Neoplastic lesions of the urinary bladder present a unique opportunity for evaluating chemopreventive agents because of (1) the accessibility of the lesions to observation and biopsy, and (2) those patients who have been successfully treated for a primary lesion represent a population at unusually high risk for recurrence and/or progression. Although 70-80% of bladder cancers initially present as superficial, papillary transitional cell neoplasms with limited potential for invasion, the incidence of recurrence is high after resection (60-75%). Recurrent tumors are highly unpredictable, and may be of higher grade or stage (progression). Although recurrence is responsible for high treatment-related morbidity, progression represents the greatest potential for mortality. Thus, potential chemopreventive agents considered here would modulate bladder carcinogenesis from initiation of normal-appearing tissue through progression of superficial tumors. Clinical trials of chemopreventive drugs involve healthy target populations, and the endpoints are reduced cancer incidence or mortality, reduced/eliminated precancerous lesions or increased latency, with none to minimal toxicity. Since cancers may not appear for 20-30 years, two of the most difficult aspects of testing these drugs in intervention trials are the long observation periods and large study populations required to measure cancer incidence reduction. However, observing the regression or recurrence of superficial bladder lesions (TIS, T1, Ta) requires relatively short time periods. Thus, these lesions lend themselves to the investigation of intermediate biomarkers, defined as morphologic and/or molecular alterations in tissue between initiation and tumor invasion. It is hypothesized that modulation of one or more biomarkers would interrupt carcinogenesis and result in a decrease in cancer incidence. Thus, evaluation of biomarkers as surrogate endpoints would allow bladder trials to be of even shorter duration, use fewer subjects and be lower in cost. In addition, intermediate biomarkers could predict which superficial lesions (or normal-appearing tissue) have the greatest potential for neoplastic progression. Development of strategies for the design of intervention trials for bladder cancer and review of the current status of intermediate biomarkers in the bladder, and methods for their validation, are major objectives of this workshop. JF - Journal of cellular biochemistry. Supplement AU - Kelloff, G J AU - Boone, C W AU - Malone, W F AU - Steele, V E AU - Doody, L A AD - Chemoprevention Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 1 EP - 12 VL - 16I SN - 0733-1959, 0733-1959 KW - Antineoplastic Agents KW - 0 KW - Biomarkers KW - Index Medicus KW - United States KW - Biomarkers -- chemistry KW - Animals KW - Humans KW - National Institutes of Health (U.S.) KW - Clinical Trials as Topic KW - Urinary Bladder Neoplasms -- prevention & control KW - Antineoplastic Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73537614?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cellular+biochemistry.+Supplement&rft.atitle=Development+of+chemopreventive+agents+for+bladder+cancer.&rft.au=Kelloff%2C+G+J%3BBoone%2C+C+W%3BMalone%2C+W+F%3BSteele%2C+V+E%3BDoody%2C+L+A&rft.aulast=Kelloff&rft.aufirst=G&rft.date=1992-01-01&rft.volume=16I&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+biochemistry.+Supplement&rft.issn=07331959&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-22 N1 - Date created - 1993-07-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment and developmental therapeutics in aspergillosis. 1. Amphotericin B and its derivatives. AN - 73523500; 1488564 AB - In recent years, the frequency of infections caused by Aspergillus sp. has been on the rise. Immunocompromised patients are especially vulnerable to such infections. The polyene antibiotic amphotericin B is currently considered to be therapeutically the most effective drug against Aspergillus-induced infections. In the present review, the clinical efficacy of amphotericin B, its toxicities and various routes of applications, are discussed. Different combinations of amphotericin B with other drugs have also been reviewed, along with the anti-Aspergillus activity of various other antibiotics and some ester derivatives of amphotericin B. JF - Respiration; international review of thoracic diseases AU - Georgiev, V S AD - National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 291 EP - 302 VL - 59 IS - 5 SN - 0025-7931, 0025-7931 KW - Anti-Bacterial Agents KW - 0 KW - Amphotericin B KW - 7XU7A7DROE KW - Index Medicus KW - Drug Therapy, Combination KW - Anti-Bacterial Agents -- therapeutic use KW - Animals KW - Lung Diseases, Fungal -- drug therapy KW - Humans KW - Aspergillosis, Allergic Bronchopulmonary -- immunology KW - Anti-Bacterial Agents -- pharmacology KW - Disease Models, Animal KW - Immunocompromised Host KW - Anti-Bacterial Agents -- pharmacokinetics KW - Amphotericin B -- analogs & derivatives KW - Aspergillosis -- drug therapy KW - Amphotericin B -- administration & dosage KW - Amphotericin B -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73523500?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Respiration%3B+international+review+of+thoracic+diseases&rft.atitle=Treatment+and+developmental+therapeutics+in+aspergillosis.+1.+Amphotericin+B+and+its+derivatives.&rft.au=Georgiev%2C+V+S&rft.aulast=Georgiev&rft.aufirst=V&rft.date=1992-01-01&rft.volume=59&rft.issue=5&rft.spage=291&rft.isbn=&rft.btitle=&rft.title=Respiration%3B+international+review+of+thoracic+diseases&rft.issn=00257931&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-25 N1 - Date created - 1993-02-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alcoholism and substance abuse among selected southern Cheyenne Indians. AN - 73519557; 1305531 AB - This family and small community-based study reports the occurrence of alcoholism and co-occurring substance abuse in Southern Cheyenne Indians living in western Oklahoma. Sociocultural factors complicate operationalization of clinical data into standard (DSM-III-R) psychiatric disorder terminology; understanding sociocultural factors is essential for assessing the high rate of addictive disorders in this group. To obtain reliable and valid clinical diagnoses, data from several sources were utilized within a blind rating system: 1) SADS-L, a clinician-administered research diagnostic instrument; 2) MAST; 3) relatives; 4) medical records; 5) other official documents. The sample consisted of 69 males (45 alcoholics) and 97 females (36 alcoholics). Among clinically significant substance abusers (moderate impairment of function), 22 of 24 were alcoholics. In non-alcoholics, mean MAST scores were 8.8 (males) and 5.1 (females); in alcoholics, 32.0 (males) and 38.7 (females). Mean age of onset on heavy use of alcohol was 20.1 yrs. (males) and 22.8 (females) (p = 0.047); among all alcoholics, 86% (males) and 64% (females) had early onset (< 25 yrs. old). When data from 98 unrelated subjects were analyzed separately, similar findings were observed except that mean age of onset of heavy use of alcohol was more discrepant between males and females, viz. 20.1 versus 22.8 yrs. (p = 0.02). Among those with substance abuse disorders, early age of onset was present in all but one female. In these Cheyenne, alcoholism is usually clinically severe and early in onset; it often co-occurs with substance abuse, also early in onset. JF - Culture, medicine and psychiatry AU - Brown, G L AU - Albaugh, B J AU - Robin, R W AU - Goodson, S G AU - Trunzo, M AU - Wynne, D K AU - Goldman, D AD - Division of Intramural Clinical and Biological Research (DICBR), National Institute on Alcohol Abuse and Alcoholism (NIAAA), Rockville, MD 2087. PY - 1992 SP - 531 EP - 542 VL - 16 IS - 4 SN - 0165-005X, 0165-005X KW - Psychotropic Drugs KW - 0 KW - Street Drugs KW - Index Medicus KW - Cross-Sectional Studies KW - Humans KW - Adult KW - Incidence KW - Sex Ratio KW - Adolescent KW - Oklahoma -- epidemiology KW - Male KW - Female KW - Comorbidity KW - Alcoholism -- epidemiology KW - Cross-Cultural Comparison KW - Indians, North American -- psychology KW - Substance-Related Disorders -- psychology KW - Indians, North American -- statistics & numerical data KW - Alcoholism -- genetics KW - Alcoholism -- psychology KW - Substance-Related Disorders -- genetics KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73519557?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Culture%2C+medicine+and+psychiatry&rft.atitle=Alcoholism+and+substance+abuse+among+selected+southern+Cheyenne+Indians.&rft.au=Brown%2C+G+L%3BAlbaugh%2C+B+J%3BRobin%2C+R+W%3BGoodson%2C+S+G%3BTrunzo%2C+M%3BWynne%2C+D+K%3BGoldman%2C+D&rft.aulast=Brown&rft.aufirst=G&rft.date=1992-01-01&rft.volume=16&rft.issue=4&rft.spage=531&rft.isbn=&rft.btitle=&rft.title=Culture%2C+medicine+and+psychiatry&rft.issn=0165005X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-20 N1 - Date created - 1993-07-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Exploratory data analytic techniques to evaluate anticancer agents screened in a cell culture panel. AN - 73513901; 1300204 AB - Information theory is used to provide a measure of selectivity, i.e., the degree to which a drug has preferential toxicity or growth inhibition for one or a few cell lines from a large panel. The selectivity measure is intended to complement a measure of differential growth inhibition in evaluating the drug development potential of a new compound. Also, a similarity measure obtained from information theory is used to classify drugs according to their pattern of responses on the panel. Some structure-activity relations emerge. This work is applied to 176 agents selected to be tested by the National Cancer Institute in about 50 cell lines. JF - Journal of biopharmaceutical statistics AU - Hodes, L AU - Paull, K AU - Koutsoukos, A AU - Rubinstein, L AD - National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 31 EP - 48 VL - 2 IS - 1 SN - 1054-3406, 1054-3406 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Animals KW - Information Theory KW - Humans KW - Structure-Activity Relationship KW - Drug Screening Assays, Antitumor -- statistics & numerical data KW - Tumor Cells, Cultured -- drug effects KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73513901?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+biopharmaceutical+statistics&rft.atitle=Exploratory+data+analytic+techniques+to+evaluate+anticancer+agents+screened+in+a+cell+culture+panel.&rft.au=Hodes%2C+L%3BPaull%2C+K%3BKoutsoukos%2C+A%3BRubinstein%2C+L&rft.aulast=Hodes&rft.aufirst=L&rft.date=1992-01-01&rft.volume=2&rft.issue=1&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=Journal+of+biopharmaceutical+statistics&rft.issn=10543406&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-26 N1 - Date created - 1993-05-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effect of parental alcohol dependence on perceived children's behavior. AN - 73506654; 1294276 AB - The effect of past-year parental alcohol dependence on perceived children's behavioral problems was assessed using data from a general population sample of 3,409 father-child pairs and 5,892 mother-child pairs. Eight percent of the children living in households containing fathers had an alcoholic father; 2% of those living with mothers had an alcoholic mother. Behavioral problems in the 3 months preceding the interview were assessed using a list of 32 indicators and were evaluated by an adult household member, usually the child's mother. The unadjusted odds of a child's being in the top 10th percentile of the behavioral problem distribution were increased by a factor of 1.7 for paternal alcoholism and 2.2 for maternal alcoholism. After adjustment for social and demographic characteristics of the child and family, the odds ratio for alcohol dependence in the mother dropped to 1.6; the odds ratio for paternal alcohol dependence remained at 1.7. Parental alcohol dependence did not interact with social and demographic factors in its association with children's behavioral problems. JF - Journal of substance abuse AU - Dawson, D A AD - Division of Biometry and Epidemiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 329 EP - 340 VL - 4 IS - 4 SN - 0899-3289, 0899-3289 KW - Index Medicus KW - Humans KW - Child KW - Child, Preschool KW - Socioeconomic Factors KW - Cross-Sectional Studies KW - Risk Factors KW - Adult KW - Incidence KW - Adolescent KW - Personality Assessment KW - United States -- epidemiology KW - Female KW - Male KW - Father-Child Relations KW - Alcoholism -- epidemiology KW - Mother-Child Relations KW - Child of Impaired Parents -- psychology KW - Child Behavior Disorders -- psychology KW - Child of Impaired Parents -- statistics & numerical data KW - Child Behavior Disorders -- diagnosis KW - Alcoholism -- psychology KW - Alcoholism -- complications KW - Child Behavior Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73506654?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+substance+abuse&rft.atitle=The+effect+of+parental+alcohol+dependence+on+perceived+children%27s+behavior.&rft.au=Dawson%2C+D+A&rft.aulast=Dawson&rft.aufirst=D&rft.date=1992-01-01&rft.volume=4&rft.issue=4&rft.spage=329&rft.isbn=&rft.btitle=&rft.title=Journal+of+substance+abuse&rft.issn=08993289&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-12 N1 - Date created - 1993-04-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The interleukin-2 receptor: a target for immunotherapy. AN - 73504137; 1485565 JF - Advances in experimental medicine and biology AU - Waldmann, T A AU - Goldman, C AU - Top, L AU - Grant, A AU - Burton, J AU - Bamford, R AU - Roessler, E AU - Horak, I AU - Zaknoen, S AU - Kasten-Sportes, C AD - Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 57 EP - 66 VL - 323 SN - 0065-2598, 0065-2598 KW - Antibodies, Monoclonal KW - 0 KW - Bacterial Toxins KW - Exotoxins KW - Immunotoxins KW - Receptors, Interleukin-2 KW - Recombinant Fusion Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Exotoxins -- administration & dosage KW - Macaca fascicularis KW - Recombinant Fusion Proteins -- immunology KW - Heart Transplantation KW - Leukemia-Lymphoma, Adult T-Cell -- therapy KW - Humans KW - Mice KW - Graft Rejection -- prevention & control KW - Lymphocyte Activation KW - Protein Engineering KW - Immunotoxins -- therapeutic use KW - Leukemia-Lymphoma, Adult T-Cell -- immunology KW - Gene Expression Regulation KW - Exotoxins -- therapeutic use KW - Species Specificity KW - Recombinant Fusion Proteins -- therapeutic use KW - Receptors, Interleukin-2 -- biosynthesis KW - Receptors, Interleukin-2 -- antagonists & inhibitors KW - Autoimmune Diseases -- therapy KW - Neoplasms -- therapy KW - Antibodies, Monoclonal -- immunology KW - Antibodies, Monoclonal -- therapeutic use KW - Immunotherapy -- methods KW - Receptors, Interleukin-2 -- physiology KW - Receptors, Interleukin-2 -- chemistry KW - Autoimmune Diseases -- immunology KW - Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73504137?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+experimental+medicine+and+biology&rft.atitle=The+interleukin-2+receptor%3A+a+target+for+immunotherapy.&rft.au=Waldmann%2C+T+A%3BGoldman%2C+C%3BTop%2C+L%3BGrant%2C+A%3BBurton%2C+J%3BBamford%2C+R%3BRoessler%2C+E%3BHorak%2C+I%3BZaknoen%2C+S%3BKasten-Sportes%2C+C&rft.aulast=Waldmann&rft.aufirst=T&rft.date=1992-01-01&rft.volume=323&rft.issue=&rft.spage=57&rft.isbn=&rft.btitle=&rft.title=Advances+in+experimental+medicine+and+biology&rft.issn=00652598&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-12 N1 - Date created - 1993-02-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synergistic antiproliferative effects of the combination of interleukin-1 alpha and doxorubicin against human melanoma cells. AN - 73503595; 1292755 AB - We have investigated the antiproliferative effects of recombinant human interleukin-1 alpha (IL-1) combined with the cytotoxic antitumor drug doxorubicin against A375 human melanoma IL-1-sensitive (C6) and IL-1-resistant (C5) clonal cell lines. Growth inhibition was assessed by the MTT assay, and C5 cells were 10-fold less sensitive to IL-1 than the C6 cells, but both cell lines were equally sensitive to doxorubicin. Synergistic antitumor activity between the two agents was evaluated by median effects/combination index analysis, and IL-1 and doxorubicin were strongly synergistic over a broad range of drug concentrations. The strongest synergism occurred when C6 cells were exposed to IL-1 prior to doxorubicin, and when C5 cells were pretreated with doxorubicin for 6 hr prior to IL-1 additions. An examination of various ratios of the two agents revealed a maximum 20-fold potentiation of doxorubicin, and a 30-fold potentiation of IL-1 median dose values in the combination compared to the median dose values obtained with doxorubicin or IL-1 alone. Doxorubicin treatment enhanced the binding and internalization of [125I]IL-1 after 24 and 48 hr at 37 degrees C, but IL-1 binding to cells incubated on ice was increased only marginally by doxorubicin pretreatment. Treatment of C6 cells with IL-1 for 24 hr did not alter the cellular accumulation of doxorubicin. A recombinant protein IL-1 receptor antagonist that binds to both the 80 kDa type I and the 65 kDa type II IL-1 receptors, blocked the cytostatic effects of IL-1 and abrogated the synergism with doxorubicin. In cells synchronized following release from aphidicolin block, doxorubicin caused a G2 + M accumulation, IL-1 alone had no effect, and the combination of both agents resulted in a G2 + M block similar in magnitude to that caused by doxorubicin alone. These results provide preclinical evidence that doxorubicin combined with IL-1 may be beneficial in the clinical treatment of malignant melanoma and possibly other types of solid tumors. JF - Oncology research AU - Mimnaugh, E G AU - Monti, E AU - Sebers, S AU - Stetler-Stevenson, M AU - Sinha, B K AD - Division of Cancer Treatment, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 401 EP - 412 VL - 4 IS - 10 SN - 0965-0407, 0965-0407 KW - Interleukin-1 KW - 0 KW - Receptors, Interleukin-1 KW - Recombinant Proteins KW - Doxorubicin KW - 80168379AG KW - Index Medicus KW - Drug Screening Assays, Antitumor KW - Recombinant Proteins -- pharmacology KW - Tumor Cells, Cultured KW - Humans KW - Receptors, Interleukin-1 -- metabolism KW - Drug Synergism KW - Cell Cycle -- drug effects KW - Interleukin-1 -- pharmacology KW - Melanoma -- pathology KW - Interleukin-1 -- metabolism KW - Doxorubicin -- pharmacology KW - Doxorubicin -- metabolism KW - Melanoma -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- pharmacology KW - Melanoma -- therapy KW - Melanoma -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73503595?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncology+research&rft.atitle=Synergistic+antiproliferative+effects+of+the+combination+of+interleukin-1+alpha+and+doxorubicin+against+human+melanoma+cells.&rft.au=Mimnaugh%2C+E+G%3BMonti%2C+E%3BSebers%2C+S%3BStetler-Stevenson%2C+M%3BSinha%2C+B+K&rft.aulast=Mimnaugh&rft.aufirst=E&rft.date=1992-01-01&rft.volume=4&rft.issue=10&rft.spage=401&rft.isbn=&rft.btitle=&rft.title=Oncology+research&rft.issn=09650407&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-08 N1 - Date created - 1993-04-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Measurement and interpretation of changes in memory in response to drug treatments. AN - 73490308; 1296214 AB - Drug-induced changes in cognitive functions such as memory are generally domain specific rather than general effects, that is, only some components of memory are altered. Changes in memory can be secondary to alterations in other cognitive domains such as attention, or non-cognitive domains (mood and arousal), or the direct result of alterations on those neurobiological systems that determine memory functions. The selective memory impairing effects of benzodiazepines are used to illustrate how cognitive neuroscience methods and theory can be useful in assessing the memory changes produced by psychoactive drugs. JF - Psychopharmacology bulletin AU - Weingartner, H AU - Eckardt, M AU - Molchan, S AU - Sunderland, T AU - Wolkowitz, O AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 331 EP - 340 VL - 28 IS - 4 SN - 0048-5764, 0048-5764 KW - Psychotropic Drugs KW - 0 KW - Index Medicus KW - Animals KW - Cognition -- drug effects KW - Humans KW - Memory -- drug effects KW - Psychotropic Drugs -- therapeutic use KW - Psychotropic Drugs -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73490308?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychopharmacology+bulletin&rft.atitle=Measurement+and+interpretation+of+changes+in+memory+in+response+to+drug+treatments.&rft.au=Weingartner%2C+H%3BEckardt%2C+M%3BMolchan%2C+S%3BSunderland%2C+T%3BWolkowitz%2C+O&rft.aulast=Weingartner&rft.aufirst=H&rft.date=1992-01-01&rft.volume=28&rft.issue=4&rft.spage=331&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology+bulletin&rft.issn=00485764&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-21 N1 - Date created - 1993-04-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Natural products which interact with tubulin in the vinca domain: maytansine, rhizoxin, phomopsin A, dolastatins 10 and 15 and halichondrin B. AN - 73483857; 1287674 AB - This paper summarizes published data on the interactions of tubulin with antimitotic compounds that inhibit the binding of vinca alkaloids to the protein. These are all relatively complex natural products isolated from higher plants, fungi and marine invertebrate animals. These agents are maytansine, rhizoxin, phomopsin A, dolastatins 10 and 15 and halichondrin B and their congeners. Effects on tubulin polymerization, ligand binding interactions and structure-activity relationships are emphasized. JF - Pharmacology & therapeutics AU - Hamel, E AD - Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 31 EP - 51 VL - 55 IS - 1 SN - 0163-7258, 0163-7258 KW - Antibiotics, Antineoplastic KW - 0 KW - Antineoplastic Agents KW - Depsipeptides KW - Ethers, Cyclic KW - Lactones KW - Macrolides KW - Mycotoxins KW - Oligopeptides KW - Tubulin KW - Vinca Alkaloids KW - halichondrin B KW - 103614-76-2 KW - dolastatin 10 KW - 110417-88-4 KW - dolastatin 15 KW - 123884-00-4 KW - Maytansine KW - 14083FR882 KW - phomopsin KW - 64925-80-0 KW - rhizoxin KW - C1V1Y784E4 KW - Index Medicus KW - Animals KW - Mycotoxins -- pharmacology KW - Antibiotics, Antineoplastic -- pharmacology KW - Maytansine -- pharmacology KW - Oligopeptides -- pharmacology KW - Ethers, Cyclic -- pharmacology KW - Lactones -- pharmacology KW - Tubulin -- drug effects KW - Vinca Alkaloids -- pharmacology KW - Vinca Alkaloids -- metabolism KW - Tubulin -- metabolism KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73483857?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology+%26+therapeutics&rft.atitle=Natural+products+which+interact+with+tubulin+in+the+vinca+domain%3A+maytansine%2C+rhizoxin%2C+phomopsin+A%2C+dolastatins+10+and+15+and+halichondrin+B.&rft.au=Hamel%2C+E&rft.aulast=Hamel&rft.aufirst=E&rft.date=1992-01-01&rft.volume=55&rft.issue=1&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=Pharmacology+%26+therapeutics&rft.issn=01637258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-18 N1 - Date created - 1993-03-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The modulatory effects of tryptamine and tyramine on the S9-mediated mutagenesis of IQ and MeIQ in Salmonella strain TA98. AN - 73481420; 1363160 AB - The S9-mediated mutagenesis of IQ and MeIQ in Salmonella strain TA98 was modulated by introduction to the assay of tryptamine or tyramine. Both biogenic amines inhibited or enhanced the mutagenic response as a function of amine concentration, strain of rat used as the S9 source, and the IQ-type mutagen tested. Enhancement of IQ mutagenesis by tryptamine (10-80 microM) was observed in the presence of S9 preparations derived from Aroclor 1254-pretreated Fischer rats; the enhancing effect ceased at tryptamine concentrations > 160 microM. When Sprague-Dawley-S9 or Wistar-S9 were used for activation, the enhancement of IQ mutagenesis by tryptamine shifted to inhibition at tryptamine concentrations > 40 microM, with Sprague-Dawley-S9, and > 20 microM, with Wistar-S9. By contrast, MeIQ-mutagenesis was enhanced by tryptamine (10-160 microM), regardless of the rat strain used as S9 source. Tyramine was a weaker enhancer of MeIQ mutagenesis than was tryptamine and, unlike tryptamine, its inhibitory effects on IQ mutagenesis were observed only with Wistar-S9. Tryptamine (10-80 microM) inhibited cytochromes P450IA1 and P450IA2 activities, monitored by the O-deethylation of ethoxyresorufin and Glu-P-1 mutagenesis in TA98, respectively. These data suggest that the effects of biogenic amines on IQ and MeIQ bioactivation are complex. Furthermore, this study demonstrates that tryptamine and tyramine act both as enhancers (comutagens) and as inhibitors (antimutagens) of IQ and MeIQ mutagenesis, depending on the testing conditions. JF - Teratogenesis, carcinogenesis, and mutagenesis AU - Abu-Shakra, A AD - Experimental Carcinogenesis and Mutagenesis Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27711. Y1 - 1992 PY - 1992 DA - 1992 SP - 187 EP - 196 VL - 12 IS - 4 SN - 0270-3211, 0270-3211 KW - Cytochrome P-450 Enzyme Inhibitors KW - 0 KW - Imidazoles KW - Oxazines KW - Quinolines KW - Tryptamines KW - 2-amino-3-methylimidazo(4,5-f)quinoline KW - 30GL3D3T0G KW - tryptamine KW - 422ZU9N5TV KW - ethoxyresorufin KW - 5725-91-7 KW - 2-amino-6-methyldipyrido(1,2-a-3',2'-d)imidazole KW - 67730-11-4 KW - 2-amino-3,4-dimethylimidazo(4,5-f)quinoline KW - G2Q7M1P33X KW - Tyramine KW - X8ZC7V0OX3 KW - Index Medicus KW - Animals KW - Imidazoles -- metabolism KW - Microsomes, Liver -- metabolism KW - Salmonella typhimurium -- drug effects KW - Rats, Inbred F344 -- metabolism KW - Rats KW - Rats, Sprague-Dawley -- metabolism KW - Mutagenicity Tests KW - In Vitro Techniques KW - Rats, Wistar KW - Species Specificity KW - Oxazines -- metabolism KW - Tryptamines -- administration & dosage KW - Tyramine -- administration & dosage KW - Quinolines -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73481420?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Teratogenesis%2C+carcinogenesis%2C+and+mutagenesis&rft.atitle=The+modulatory+effects+of+tryptamine+and+tyramine+on+the+S9-mediated+mutagenesis+of+IQ+and+MeIQ+in+Salmonella+strain+TA98.&rft.au=Abu-Shakra%2C+A&rft.aulast=Abu-Shakra&rft.aufirst=A&rft.date=1992-01-01&rft.volume=12&rft.issue=4&rft.spage=187&rft.isbn=&rft.btitle=&rft.title=Teratogenesis%2C+carcinogenesis%2C+and+mutagenesis&rft.issn=02703211&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-17 N1 - Date created - 1993-03-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of phorbol ester and cytokines on matrix metalloproteinase and tissue inhibitor of metalloproteinase expression in tumor and normal cell lines. AN - 73480969; 1284126 AB - The effect of the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) and the cytokines interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) on matrix metalloproteinases (MMP) and metalloproteinase inhibitors was studied in a variety of human cell lines. Expression of the mammalian collagenase (MMP-1), 72-kD gelatinase/type IV collagenase (MMP-2), stromelysin (MMP-3), 92-kD gelatinase/type IV collagenase (MMP-9), and tissue inhibitors of metalloproteinases (TIMP-1 and TIMP-2) was assessed by zymography and Northern blot analysis. MMP-2 and TIMP-2 activities were refractory to TPA, IL-1 and TNF-alpha treatment in most of the cell lines. In contrast, MMP-3, MMP-9 and TIMP-1 activities were markedly stimulated by TPA in most of the tumor cell lines and human umbilical vein endothelial cells (HUVEC), whereas the fibroblast lines were minimally stimulated or unresponsive to TPA. The MMP-3, MMP-9 and TIMP-1 stimulation in response to IL-1 and TNF-alpha treatment was detected in some of the tumor cell lines and HUVEC. The increase in activity was less marked than in TPA. A breast carcinoma cell line, MDA-MB-231, which did not express MMP-2, had high expression of MMP-3 and MMP-9 which were unaffected by TPA and cytokine treatment. Northern blot analysis of MMP and TIMP mRNA expression reflected the zymogram findings for most of the cell lines. TPA-mediated stimulation of MMP-1 was similar to that of MMP-3 and MMP-9. Exceptions were the fibroblast cell lines which showed either a much more marked mRNA response of MMP-9 to TPA than observed at protein level, or a high constitutive MMP-9 mRNA when MMP-9 activity was not detectable by zymography. TPA-mediated stimulation of MMP-9 and TIMP-1 activity was blocked by staurosporine, an inhibitor of protein kinase C (PKC). A non-PKC-activating phorbol ester, 4 alpha-phorbol-12,13-didecanoate, did not stimulate MMP-9 and TIMP-1 activity. TPA treatment caused the increased expression of c-fos containing AP-1-specific binding activity in selected tumor cell lines. This activity was maximal at 6 h. An association was observed between AP-1 binding activity and increased expression of MMP-1, MMP-3 and MMP-9, which possess TPA-responsive elements (TRE). TPA-sensitive MMPs and TIMP-1 were variably stimulated by biologically relevant cytokines, such as IL-1 and TNF-alpha.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Invasion & metastasis AU - Mackay, A R AU - Ballin, M AU - Pelina, M D AU - Farina, A R AU - Nason, A M AU - Hartzler, J L AU - Thorgeirsson, U P AD - Division of Cancer Etiology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 168 EP - 184 VL - 12 IS - 3-4 SN - 0251-1789, 0251-1789 KW - Glycoproteins KW - 0 KW - Interleukin-1 KW - Neoplasm Proteins KW - Proto-Oncogene Proteins c-jun KW - Tissue Inhibitor of Metalloproteinases KW - Tumor Necrosis Factor-alpha KW - Tissue Inhibitor of Metalloproteinase-2 KW - 127497-59-0 KW - RNA KW - 63231-63-0 KW - Cycloheximide KW - 98600C0908 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Collagenases KW - EC 3.4.24.- KW - Metalloendopeptidases KW - Matrix Metalloproteinase 3 KW - EC 3.4.24.17 KW - Matrix Metalloproteinase 2 KW - EC 3.4.24.24 KW - Matrix Metalloproteinase 9 KW - EC 3.4.24.35 KW - Matrix Metalloproteinase 1 KW - EC 3.4.24.7 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Sensitivity and Specificity KW - Fibroblasts -- drug effects KW - Fibroblasts -- enzymology KW - Neoplasms -- enzymology KW - Blotting, Northern KW - Endothelium, Vascular -- enzymology KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Transcription, Genetic KW - Proto-Oncogene Proteins c-jun -- metabolism KW - Collagenases -- metabolism KW - Protein Kinase C -- antagonists & inhibitors KW - Base Sequence KW - Collagenases -- drug effects KW - Endothelium, Vascular -- drug effects KW - RNA -- metabolism KW - Cycloheximide -- pharmacology KW - Molecular Sequence Data KW - Neoplasm Proteins -- drug effects KW - Glycoproteins -- drug effects KW - Interleukin-1 -- pharmacology KW - Glycoproteins -- metabolism KW - Metalloendopeptidases -- drug effects KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Metalloendopeptidases -- metabolism KW - Neoplasm Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73480969?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Invasion+%26+metastasis&rft.atitle=Effect+of+phorbol+ester+and+cytokines+on+matrix+metalloproteinase+and+tissue+inhibitor+of+metalloproteinase+expression+in+tumor+and+normal+cell+lines.&rft.au=Mackay%2C+A+R%3BBallin%2C+M%3BPelina%2C+M+D%3BFarina%2C+A+R%3BNason%2C+A+M%3BHartzler%2C+J+L%3BThorgeirsson%2C+U+P&rft.aulast=Mackay&rft.aufirst=A&rft.date=1992-01-01&rft.volume=12&rft.issue=3-4&rft.spage=168&rft.isbn=&rft.btitle=&rft.title=Invasion+%26+metastasis&rft.issn=02511789&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-12 N1 - Date created - 1993-04-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pharmacokinetics of propetamphos following intravenous administration in the F344 rat. AN - 73476247; 1293308 AB - Propetamphos [(E)-1-methylethyl 3-[[(ethylamino)methoxyphosphinothioyl]oxy]-2-butenoate], the active ingredient in Safrotin, is an organophosphate developed by Sandoz, Ltd. (Switzerland) as an insecticide (1). Although metabolism of propetamphos has been previously investigated (2,3), there is no pharmacokinetic data available in the literature. The current studies were undertaken to investigate the pharmacokinetics of propetamphos following intravenous administration in male and female Fischer 344 (F344) rats. Rats were dosed via an indwelling jugular cannula at a dose of 12 mg/kg (one-tenth the oral LD-50). Blood samples were withdrawn via the cannula at predetermined timepoints to quantitate plasma concentrations of propetamphos over time. Propetamphos is highly bound to plasma proteins (free fraction = 0.06). Free propetamphos concentration in plasma vs. time data were analyzed by noncompartmental methods. The terminal elimination rate constant, lambda, was significantly different for males versus females (0.015 min-1 for males and 0.037 min-1 for females, p = 0.001). Plasma was cleared of unbound propetamphos at rates of 0.559 +/- 0.069 and 0.828 +/- 0.181 L/min/kg for males and females (mean +/- standard error). Mean residence times (MRTs) for propetamphos in the body for males and females were 28.3 +/- 5.7 and 14.4 +/- 3.5 min, and the volume of distribution at steady state (Vss) was 14.7 +/- 2.6 and 12.3 +/- 4.5 L/kg. The differences in these parameters, clearance (CI), MRT, and Vss, were not statistically significant at the p < 0.05 level for males versus females, but MRT was nearly significantly different (p = 0.08).(ABSTRACT TRUNCATED AT 250 WORDS) JF - Journal of biochemical toxicology AU - Dix, K AU - Burka, L T AU - Dauterman, W C AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 199 EP - 204 VL - 7 IS - 4 SN - 0887-2082, 0887-2082 KW - Blood Proteins KW - 0 KW - Insecticides KW - Organothiophosphorus Compounds KW - propetamphos KW - G4A07F635U KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Sex Factors KW - Injections, Intravenous KW - Blood Proteins -- metabolism KW - Protein Binding KW - Male KW - Female KW - Blood Proteins -- drug effects KW - Insecticides -- administration & dosage KW - Insecticides -- pharmacokinetics KW - Organothiophosphorus Compounds -- administration & dosage KW - Organothiophosphorus Compounds -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73476247?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+biochemical+toxicology&rft.atitle=Pharmacokinetics+of+propetamphos+following+intravenous+administration+in+the+F344+rat.&rft.au=Dix%2C+K%3BBurka%2C+L+T%3BDauterman%2C+W+C&rft.aulast=Dix&rft.aufirst=K&rft.date=1992-01-01&rft.volume=7&rft.issue=4&rft.spage=199&rft.isbn=&rft.btitle=&rft.title=Journal+of+biochemical+toxicology&rft.issn=08872082&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-06 N1 - Date created - 1993-04-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A strategy of "combination chemotherapy" in Alzheimer's disease: rationale and preliminary results with physostigmine plus deprenyl. AN - 73465782; 1288668 AB - Although the central cholinergic deficits are still considered to be of primary importance in Alzheimer's disease, there is great need for an expansion of the pharmacological approach in this illness beyond the simple cholinergic replacement hypothesis. This report focuses on the concept of "combination chemotherapy" in Alzheimer's disease as the next generation of therapeutic strategies. Based on earlier positive findings in Alzheimer patients with the monoamine oxidase B inhibitor, 1-deprenyl, the authors speculate that a combination of physostigmine, the short-acting cholinesterase inhibitor, and 1-deprenyl might be more beneficial than either agent alone. The authors outline a sample paradigm for such combination studies, report preliminary data on the first 16 Alzheimer subjects to have received an initial combination of physostigmine and deprenyl, and point to other possible "combination chemotherapy" strategies for future study. JF - International psychogeriatrics AU - Sunderland, T AU - Molchan, S AU - Lawlor, B AU - Martinez, R AU - Mellow, A AU - Martinson, H AU - Putnam, K AU - Lalonde, F AD - Section on Geriatric Psychiatry, National Institute of Mental Health, Bethesda, Maryland. Y1 - 1992 PY - 1992 DA - 1992 SP - 291 EP - 309 VL - 4 Suppl 2 SN - 1041-6102, 1041-6102 KW - Selegiline KW - 2K1V7GP655 KW - Physostigmine KW - 9U1VM840SP KW - Index Medicus KW - Drug Therapy, Combination KW - Double-Blind Method KW - Dose-Response Relationship, Drug KW - Humans KW - Aged KW - Neuropsychological Tests KW - Male KW - Female KW - Selegiline -- adverse effects KW - Selegiline -- administration & dosage KW - Physostigmine -- administration & dosage KW - Alzheimer Disease -- drug therapy KW - Alzheimer Disease -- psychology KW - Physostigmine -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73465782?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+psychogeriatrics&rft.atitle=A+strategy+of+%22combination+chemotherapy%22+in+Alzheimer%27s+disease%3A+rationale+and+preliminary+results+with+physostigmine+plus+deprenyl.&rft.au=Sunderland%2C+T%3BMolchan%2C+S%3BLawlor%2C+B%3BMartinez%2C+R%3BMellow%2C+A%3BMartinson%2C+H%3BPutnam%2C+K%3BLalonde%2C+F&rft.aulast=Sunderland&rft.aufirst=T&rft.date=1992-01-01&rft.volume=4+Suppl+2&rft.issue=&rft.spage=291&rft.isbn=&rft.btitle=&rft.title=International+psychogeriatrics&rft.issn=10416102&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-25 N1 - Date created - 1993-03-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment and developmental therapeutics in aspergillosis. 2. Azoles and other antifungal drugs. AN - 73460335; 1488565 AB - The present article surveys the anti-Aspergillus activity of various azole derivatives as well as a number of miscellaneous other antifungal agents. The drawbacks of sodium (potassium) iodide therapy in the management of pulmonary aspergilloma are discussed along with current efforts at treatment of allergic bronchopulmonary aspergillosis and Aspergillus-induced otomycosis. JF - Respiration; international review of thoracic diseases AU - Georgiev, V S AD - National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 303 EP - 313 VL - 59 IS - 5 SN - 0025-7931, 0025-7931 KW - Antifungal Agents KW - 0 KW - Azoles KW - Imidazoles KW - Miconazole KW - 7NNO0D7S5M KW - Fluconazole KW - 8VZV102JFY KW - Clotrimazole KW - G07GZ97H65 KW - Ketoconazole KW - R9400W927I KW - Index Medicus KW - Miconazole -- therapeutic use KW - Clotrimazole -- therapeutic use KW - Animals KW - Fluconazole -- therapeutic use KW - Ketoconazole -- therapeutic use KW - Humans KW - Aspergillosis, Allergic Bronchopulmonary -- drug therapy KW - Disease Models, Animal KW - Otitis Externa -- drug therapy KW - Antifungal Agents -- therapeutic use KW - Azoles -- adverse effects KW - Lung Diseases, Fungal -- drug therapy KW - Azoles -- therapeutic use KW - Aspergillosis -- drug therapy KW - Imidazoles -- therapeutic use KW - Azoles -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73460335?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Respiration%3B+international+review+of+thoracic+diseases&rft.atitle=Treatment+and+developmental+therapeutics+in+aspergillosis.+2.+Azoles+and+other+antifungal+drugs.&rft.au=Georgiev%2C+V+S&rft.aulast=Georgiev&rft.aufirst=V&rft.date=1992-01-01&rft.volume=59&rft.issue=5&rft.spage=303&rft.isbn=&rft.btitle=&rft.title=Respiration%3B+international+review+of+thoracic+diseases&rft.issn=00257931&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-25 N1 - Date created - 1993-02-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - v-Raf/v-Myc synergism in abrogation of IL-3 dependence: v-Raf suppresses apoptosis. AN - 73454388; 1490385 JF - Current topics in microbiology and immunology AU - Troppmair, J AU - Cleveland, J L AU - Askew, D S AU - Rapp, U R AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, MD 21702-1201. Y1 - 1992 PY - 1992 DA - 1992 SP - 453 EP - 460 VL - 182 SN - 0070-217X, 0070-217X KW - v-myc KW - v-raf KW - Interleukin-3 KW - 0 KW - Proto-Oncogene Proteins KW - Proto-Oncogene Proteins c-myc KW - Proto-Oncogene Proteins c-raf KW - EC 2.7.11.1 KW - Index Medicus KW - Animals KW - Apoptosis KW - Mice KW - Cell Line KW - Cell Division KW - Interleukin-3 -- physiology KW - Proto-Oncogene Proteins c-myc -- physiology KW - Proto-Oncogene Proteins c-myc -- genetics KW - Proto-Oncogene Proteins -- genetics KW - Proto-Oncogene Proteins -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73454388?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+topics+in+microbiology+and+immunology&rft.atitle=v-Raf%2Fv-Myc+synergism+in+abrogation+of+IL-3+dependence%3A+v-Raf+suppresses+apoptosis.&rft.au=Troppmair%2C+J%3BCleveland%2C+J+L%3BAskew%2C+D+S%3BRapp%2C+U+R&rft.aulast=Troppmair&rft.aufirst=J&rft.date=1992-01-01&rft.volume=182&rft.issue=&rft.spage=453&rft.isbn=&rft.btitle=&rft.title=Current+topics+in+microbiology+and+immunology&rft.issn=0070217X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-03 N1 - Date created - 1993-03-03 N1 - Date revised - 2017-01-13 N1 - Gene symbol - v-myc; v-raf N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Monitoring of patients with non-seminomatous germ cell tumors of the testis by determination of alpha-fetoprotein and beta-human chorionic gonadotropin levels and by computed tomography. AN - 73452336; 1283444 AB - The results of a 7-year monitoring of 230 patients with non-seminomatous testicular tumors are reported with respect to the employment of radioimmunoanalysis of alpha-fetoprotein and beta-human chorionic gonadotropin levels and CT examinations of retroperitoneum and lungs. Prior to orchiectomy, elevated levels of at least one of these markers were found in 79% of patients. After orchiectomy, tumor marker levels were in 70.4% of patients in agreement with the results of CT examinations. After the completion of chemotherapy, in more than a half of patients normal tumor marker levels and positive CT findings were observed. These results were most often due to the presence of mature teratoma. In Stage I patients the advantages of tumor marker determinations and CT examinations in the early detection of tumor progression have fully been confirmed. JF - Neoplasma AU - Kausitz, J AU - Ondrus, D AU - Belan, V AU - Matoska, J AD - National Cancer Institute, Bratislava, Czechoslovakia. Y1 - 1992 PY - 1992 DA - 1992 SP - 357 EP - 361 VL - 39 IS - 6 SN - 0028-2685, 0028-2685 KW - Biomarkers, Tumor KW - 0 KW - Chorionic Gonadotropin KW - alpha-Fetoproteins KW - Index Medicus KW - Lung -- diagnostic imaging KW - Humans KW - Tomography, X-Ray Computed KW - Retroperitoneal Space -- diagnostic imaging KW - Male KW - Orchiectomy KW - Testicular Neoplasms -- therapy KW - Testicular Neoplasms -- chemistry KW - Chorionic Gonadotropin -- analysis KW - Biomarkers, Tumor -- metabolism KW - Chorionic Gonadotropin -- blood KW - Dysgerminoma -- chemistry KW - Neoplasms, Germ Cell and Embryonal -- metabolism KW - Neoplasms, Germ Cell and Embryonal -- therapy KW - Biomarkers, Tumor -- analysis KW - Dysgerminoma -- metabolism KW - Neoplasms, Germ Cell and Embryonal -- chemistry KW - Dysgerminoma -- therapy KW - Biomarkers, Tumor -- blood KW - alpha-Fetoproteins -- metabolism KW - alpha-Fetoproteins -- analysis KW - Testicular Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73452336?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neoplasma&rft.atitle=Monitoring+of+patients+with+non-seminomatous+germ+cell+tumors+of+the+testis+by+determination+of+alpha-fetoprotein+and+beta-human+chorionic+gonadotropin+levels+and+by+computed+tomography.&rft.au=Kausitz%2C+J%3BOndrus%2C+D%3BBelan%2C+V%3BMatoska%2C+J&rft.aulast=Kausitz&rft.aufirst=J&rft.date=1992-01-01&rft.volume=39&rft.issue=6&rft.spage=357&rft.isbn=&rft.btitle=&rft.title=Neoplasma&rft.issn=00282685&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-01 N1 - Date created - 1993-03-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pathophysiological effects of cocaine in humans: review of scientific issues. AN - 73439349; 1486097 AB - Almost all data on pathophysiological abnormalities associated with human cocaine use comes from clinical observation and testing of cocaine abusers seeking treatment. Such data are subject to several confounding factors which preclude drawing definitive conclusions about the pathophysiological mechanism for the observed abnormality, its prevalence and prognosis, and individual differences in susceptibility. Confounding factors include the unknown purity of cocaine used, uncertainty as to quantity and duration of cocaine exposure, effects of other substances frequently used by cocaine users, abnormalities associated with drug route of administration and the drug abuse lifestyle, and selection bias. Future studies can address these issues by employing more sophisticated research designs, such as prospective, longitudinal follow-up of large, representative samples of cocaine users, case-control comparisons of well characterized cocaine users with appropriately matched groups, and experimental administration of cocaine under safe, controlled conditions. JF - Journal of addictive diseases AU - Gorelick, D A AD - Treatment Branch, National Institute on Drug Abuse, Baltimore, MD. Y1 - 1992 PY - 1992 DA - 1992 SP - 97 EP - 110 VL - 11 IS - 4 SN - 1055-0887, 1055-0887 KW - Catecholamines KW - 0 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Catecholamines -- pharmacokinetics KW - Liver -- physiopathology KW - Risk-Taking KW - Liver -- drug effects KW - Humans KW - Male KW - Female KW - Substance-Related Disorders -- therapy KW - Substance-Related Disorders -- mortality KW - Cocaine -- pharmacokinetics KW - Cocaine -- metabolism KW - Cocaine -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73439349?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+addictive+diseases&rft.atitle=Pathophysiological+effects+of+cocaine+in+humans%3A+review+of+scientific+issues.&rft.au=Gorelick%2C+D+A&rft.aulast=Gorelick&rft.aufirst=D&rft.date=1992-01-01&rft.volume=11&rft.issue=4&rft.spage=97&rft.isbn=&rft.btitle=&rft.title=Journal+of+addictive+diseases&rft.issn=10550887&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-25 N1 - Date created - 1993-02-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Growth and transformation suppressor genes for BHK Syrian hamster cells on human chromosomes 1 and 11. AN - 73435798; 1485918 AB - To map putative tumor suppressor genes for the near-diploid baby hamster kidney fibrosarcoma cell line BHK, we transferred five different normal human chromosomes (1, 3, 7, 11, and 12) into these tumor cells by microcell-mediated chromosome transfer. Transfer of human chromosome 1 into BHK cells resulted in suppression of cell growth both on plastic and in soft agar, indicating that chromosome 1 has a generalized effect on cell growth and thereby suppresses anchorage-independent growth. Selection against cells with an intact chromosome 1 was observed. In contrast, the introduction of chromosome 11 into BHK cells resulted in suppression of anchorage independence but not growth on plastic. Most chromosome-11 growth-suppressed BHK hybrids retained intact copies of human chromosome 11. Tumorigenic derivatives of chromosome 11 hybrids had lost this chromosome. Transfer of human chromosome 3, 7, or 12 into BHK cells did not correlate with growth suppression of BHK cells on plastic or in soft agar. Thus, we conclude that genes that suppress BHK-cell growth in general or in agar reside on human chromosomes 1 and 11, respectively. JF - Molecular carcinogenesis AU - Annab, L A AU - Dong, J T AU - Futreal, P A AU - Satoh, H AU - Oshimura, M AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 280 EP - 288 VL - 6 IS - 4 SN - 0899-1987, 0899-1987 KW - CAT KW - CLG KW - H19 KW - HRAS KW - SS6 KW - Index Medicus KW - Karyotyping KW - Animals KW - Fibrosarcoma KW - Humans KW - Mice KW - Chromosome Mapping KW - Chromosomes, Human, Pair 7 KW - Chromosomes, Human, Pair 12 KW - Gene Deletion KW - Polymerase Chain Reaction KW - Chromosomes, Human, Pair 3 KW - Tumor Cells, Cultured KW - Cell Fusion KW - Kidney Neoplasms KW - Blotting, Southern KW - Hybrid Cells KW - Mesocricetus KW - Cell Line KW - Cricetinae KW - Chromosomes, Human, Pair 1 KW - Transfection KW - Genes, Tumor Suppressor KW - Cell Transformation, Neoplastic -- genetics KW - Cell Division -- genetics KW - Chromosomes, Human, Pair 11 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73435798?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Growth+and+transformation+suppressor+genes+for+BHK+Syrian+hamster+cells+on+human+chromosomes+1+and+11.&rft.au=Annab%2C+L+A%3BDong%2C+J+T%3BFutreal%2C+P+A%3BSatoh%2C+H%3BOshimura%2C+M%3BBarrett%2C+J+C&rft.aulast=Annab&rft.aufirst=L&rft.date=1992-01-01&rft.volume=6&rft.issue=4&rft.spage=280&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-25 N1 - Date created - 1993-02-25 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CAT; CLG; H19; HRAS; SS6 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immunohistochemical evidence of high concentrations of metallothionein in pancreatic hepatocytes induced by cadmium in rats. AN - 73425150; 1295063 AB - A recent study from our laboratory has shown that cadmium, a toxic heavy metal, is one of the most effective agents known for inducing hepatocytic transdifferentiation of the rat pancreas. With repeated injections of cadmium, the incidence of rats with pancreatic hepatocytic foci can be as high as 93%. Cadmium is also well known as a very potent inducer of metallothionein, a metal-binding protein that appears to be important in the biologic response to several toxic heavy metals in most tissues, including the pancreas. Therefore, the present study sought to determine if metallothionein was associated with cadmium-induced transdifferentiation of pancreatic cells. Expression of metallothionein was studied immunohistochemically by the peroxidase-antiperoxidase method in tissue sections of the pancreas of rats with pancreatic hepatocytes. High levels of metallothionein were localized primarily within the pancreatic hepatocytes. Surrounding normal pancreatic islet and acinar cells were not immunoreactive. Thus, metallothionein is expressed actively in cells transdifferentiated to hepatocytes by cadmium within the pancreas. JF - Toxicologic pathology AU - Waalkes, M P AU - Cherian, M G AU - Ward, J M AU - Goyer, R A AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, Maryland 21702-1201. Y1 - 1992 PY - 1992 DA - 1992 SP - 323 EP - 326 VL - 20 IS - 3 Pt 1 SN - 0192-6233, 0192-6233 KW - Cadmium KW - 00BH33GNGH KW - Metallothionein KW - 9038-94-2 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Rats, Wistar KW - Cell Differentiation -- drug effects KW - Immunohistochemistry KW - Male KW - Immunoenzyme Techniques KW - Liver -- cytology KW - Pancreas -- cytology KW - Liver -- drug effects KW - Pancreas -- metabolism KW - Cadmium -- toxicity KW - Liver -- metabolism KW - Pancreas -- drug effects KW - Metallothionein -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73425150?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Immunohistochemical+evidence+of+high+concentrations+of+metallothionein+in+pancreatic+hepatocytes+induced+by+cadmium+in+rats.&rft.au=Waalkes%2C+M+P%3BCherian%2C+M+G%3BWard%2C+J+M%3BGoyer%2C+R+A&rft.aulast=Waalkes&rft.aufirst=M&rft.date=1992-01-01&rft.volume=20&rft.issue=3+Pt+1&rft.spage=323&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=01926233&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-14 N1 - Date created - 1993-04-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effects of iodinated glycerol, trichlorfon, and acetaminophen on tumor progression in a Fischer rat leukemia transplant model. AN - 73423466; 1458507 AB - Sixty-day bioassays of iodinated glycerol, trichlorfon, and acetaminophen were conducted using a leukemia transplant model in 6- to 8-week-old F344 rats to investigate the potential of these chemicals to affect tumor progression. The chemicals were administered in the drinking water at doses that approximated those used in previously conducted 2-year carcinogenesis studies. Simultaneous with dose administration, half of a group of young, healthy, syngeneic rats were given subcutaneous transplants of mononuclear cells derived from spleens of leukemic donors. Variables used to quantitate tumor progression included body weight, spleen weight, white blood cell (WBC) and red blood cell (RBC) counts, packed cell volume, hemoglobin concentration, and platelet counts. Iodinated glycerol at 1.25 or 2.5 mg/ml caused a greater increase in leukocytosis in dosed transplant recipients in comparison to that experienced by undosed recipients: trichlorfon at 2.5 or 5.0 mg/ml enhanced splenomegaly and induced greater reductions in RBC parameters in dosed recipients in comparison to that experienced by undosed recipients. Acetaminophen at 3.0 and 6.0 mg/ml resulted in insignificant but dose-related increases in spleen weight and leukocytosis only in the female rat transplant recipients, as was observed in 2-year studies. Based on results from the short-term leukemia transplant model, data from 2-year carcinogenicity studies, and structure-activity considerations, exposure to iodinated glycerol and trichlorfon was more strongly associated with the expression of leukemia than exposure to acetaminophen. The potential carcinogenicity of each of these chemicals should be taken into consideration when calculating estimates of risk and decisions for their use. JF - Cancer detection and prevention AU - Dieter, M P AU - Maronpot, R R AU - Jameson, C W AU - Ward, S M AD - National Institutes of Health, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 173 EP - 183 VL - 16 IS - 3 SN - 0361-090X, 0361-090X KW - Expectorants KW - 0 KW - Acetaminophen KW - 362O9ITL9D KW - iodinated glycerol KW - 8C0LU36AR9 KW - Trichlorfon KW - DBF2DG4G2K KW - Glycerol KW - PDC6A3C0OX KW - Index Medicus KW - Rats KW - Neoplasm Transplantation KW - Animals KW - Rats, Inbred F344 KW - Body Weight -- drug effects KW - Carcinogenicity Tests KW - Disease Models, Animal KW - Male KW - Female KW - Glycerol -- analogs & derivatives KW - Expectorants -- toxicity KW - Leukemia, Experimental -- chemically induced KW - Glycerol -- toxicity KW - Trichlorfon -- toxicity KW - Leukemia, Experimental -- pathology KW - Acetaminophen -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73423466?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+detection+and+prevention&rft.atitle=The+effects+of+iodinated+glycerol%2C+trichlorfon%2C+and+acetaminophen+on+tumor+progression+in+a+Fischer+rat+leukemia+transplant+model.&rft.au=Dieter%2C+M+P%3BMaronpot%2C+R+R%3BJameson%2C+C+W%3BWard%2C+S+M&rft.aulast=Dieter&rft.aufirst=M&rft.date=1992-01-01&rft.volume=16&rft.issue=3&rft.spage=173&rft.isbn=&rft.btitle=&rft.title=Cancer+detection+and+prevention&rft.issn=0361090X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-14 N1 - Date created - 1993-01-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Rational use of antiepileptic drug levels. AN - 73412367; 1465479 AB - Antiepileptic drug (AED) levels are obtained frequently in clinical practice, but their complex relation to seizures or drug toxicity often makes interpretation of the results difficult. Research studies have not always taken into account clinical, as well as pharmacokinetic and pharmacodynamic, factors which may influence the drug level-effect relationship. AED levels should be drawn at an appropriate time in relation to drug ingestion and clinical symptoms. Systematic investigations in selected patients, during which several levels are obtained, may be more rewarding than routine measurements in a large clinic population. JF - Pharmacology & therapeutics AU - Theodore, W H AD - Clinical Epilepsy Section, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 297 EP - 305 VL - 54 IS - 3 SN - 0163-7258, 0163-7258 KW - Carbamazepine KW - 33CM23913M KW - Valproic Acid KW - 614OI1Z5WI KW - Phenytoin KW - 6158TKW0C5 KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Half-Life KW - Humans KW - Phenobarbital -- blood KW - Seizures -- blood KW - Phenytoin -- pharmacokinetics KW - Carbamazepine -- pharmacokinetics KW - Phenytoin -- therapeutic use KW - Carbamazepine -- blood KW - Phenobarbital -- pharmacokinetics KW - Valproic Acid -- blood KW - Phenytoin -- blood KW - Carbamazepine -- therapeutic use KW - Seizures -- prevention & control KW - Valproic Acid -- therapeutic use KW - Phenobarbital -- therapeutic use KW - Valproic Acid -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73412367?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology+%26+therapeutics&rft.atitle=Rational+use+of+antiepileptic+drug+levels.&rft.au=Theodore%2C+W+H&rft.aulast=Theodore&rft.aufirst=W&rft.date=1992-01-01&rft.volume=54&rft.issue=3&rft.spage=297&rft.isbn=&rft.btitle=&rft.title=Pharmacology+%26+therapeutics&rft.issn=01637258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-15 N1 - Date created - 1993-01-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulatory influences of estrogen and progesterone on cervical dysplasia in mice model system. AN - 73406105; 1473535 AB - The effectiveness of estrogen and progesterone on the different types of cervical dysplasia are poorly documented compared to their effects on the total process of cervical carcinogenesis. In the present study, an attempt has been made to evaluate the influences of estrogen and progesterone on the different types of cervical dysplasia which are believed to be the antecedents of cervical carcinoma induced by chemical carcinogen (20-Methy cholanthrene) in the mice model system. It was observed that moderate dysplasia is less aberrant than that of marked dysplasia which could not be modified by either of the hormones. JF - European journal of gynaecological oncology AU - Sengupta, A AU - Dutta, S AU - Mallick, R AD - Chittaranjan National Cancer Institute, Department of Experimental Carcinology, Calcutta, India. Y1 - 1992 PY - 1992 DA - 1992 SP - 533 EP - 538 VL - 13 IS - 6 SN - 0392-2936, 0392-2936 KW - Benz(a)Anthracenes KW - 0 KW - Carcinogens KW - Estrogens KW - cholanthrene KW - 429L45KABE KW - Progesterone KW - 4G7DS2Q64Y KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Ovariectomy KW - Mice KW - Drug Synergism KW - Female KW - Uterine Cervical Dysplasia -- pathology KW - Estrogens -- pharmacology KW - Progesterone -- pharmacology KW - Uterine Cervical Dysplasia -- prevention & control KW - Uterine Cervical Dysplasia -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73406105?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+gynaecological+oncology&rft.atitle=Modulatory+influences+of+estrogen+and+progesterone+on+cervical+dysplasia+in+mice+model+system.&rft.au=Sengupta%2C+A%3BDutta%2C+S%3BMallick%2C+R&rft.aulast=Sengupta&rft.aufirst=A&rft.date=1992-01-01&rft.volume=13&rft.issue=6&rft.spage=533&rft.isbn=&rft.btitle=&rft.title=European+journal+of+gynaecological+oncology&rft.issn=03922936&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-04 N1 - Date created - 1993-02-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Renal lesions induced by ochratoxin A exposure in the F344 rat. AN - 73404567; 1475584 AB - Groups of 80 male and female F344 rats were exposed by gavage to ochratoxin A, a naturally occurring mycotoxin, at levels of 21, 70, and 210 micrograms/kg body weight for up to 2 years. Ochratoxin A induced non-neoplastic renal tubular epithelial changes consisting of cytoplasmic alteration, karyomegaly, degeneration, and cysts. Exposure-related renal tubular proliferative lesions included focal hyperplasia, tubular cell adenoma, and tubular cell carcinoma. Renal tubular cell adenoma occurred as early as 9 months in 1 high-dose male rat, and both adenomas and carcinomas were seen in males by 15 months. At the terminal sacrifice, renal tubular cell tumors were found in both male and female rats, but the response was more pronounced in the males. The incidence of renal tumors in the high-dose rats was the highest of any National Toxicology Program (NTP) study completed to date. In the high-dose males approximately one-third of the renal carcinomas developed metastases. This study demonstrates that ochratoxin A is a potent renal carcinogen in the F344 rat and suggests that contamination of feedstuff by this mycotoxin may pose a potential hazard to domestic animals and man. JF - Toxicologic pathology AU - Boorman, G A AU - McDonald, M R AU - Imoto, S AU - Persing, R AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 236 EP - 245 VL - 20 IS - 2 SN - 0192-6233, 0192-6233 KW - Ochratoxins KW - 0 KW - ochratoxin A KW - 1779SX6LUY KW - Index Medicus KW - Animals KW - Hyperplasia -- pathology KW - Kidney Neoplasms -- pathology KW - Kidney -- pathology KW - Kidney Tubules -- pathology KW - Kidney Neoplasms -- chemically induced KW - Rats KW - Rats, Inbred F344 KW - Hyperplasia -- chemically induced KW - Carcinoma -- pathology KW - Adenoma -- chemically induced KW - Adenoma -- pathology KW - Male KW - Female KW - Carcinoma -- chemically induced KW - Kidney Diseases -- pathology KW - Ochratoxins -- toxicity KW - Kidney Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73404567?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Renal+lesions+induced+by+ochratoxin+A+exposure+in+the+F344+rat.&rft.au=Boorman%2C+G+A%3BMcDonald%2C+M+R%3BImoto%2C+S%3BPersing%2C+R&rft.aulast=Boorman&rft.aufirst=G&rft.date=1992-01-01&rft.volume=20&rft.issue=2&rft.spage=236&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=01926233&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-02 N1 - Date created - 1993-02-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intermediate biomarkers of precancer and their application in chemoprevention. AN - 73393920; 1469895 AB - The Chemoprevention Branch of the National Cancer Institute has established a program for the development of safe and effective cancer chemopreventive agents. This program includes identification of new agents, testing for efficacy in vitro and in animals, studies in animals to model clinical use, and preclinical toxicity and metabolism evaluation. Ultimately, the most promising agents progress to clinical trials. The long period required for cancer onset presents a significant challenge to the design of clinical trials for chemoprevention. Phase III trials in which cancer reduction is the endpoint require large subject groups (tens of thousands) and follow-up duration of more than five years. Because of these requirements, the cost of such trials are high. The Chemoprevention Branch is addressing this challenge by expansion of the preclinical and Phase II clinical efficacy efforts to include intermediate biomarkers of carcinogenesis as study endpoints. The Chemoprevention Branch's studies focus on the development of biomarkers with high reliability and predictive value for cancer. Both single markers and batteries of complementary and parallel markers are evaluated. Among the criteria for biomarkers for chemoprevention studies are the following: (1) differential expression in normal and high risk tissue, (2) appearance early in carcinogenesis (the earlier a reliable biomarker appears, the greater is the chance for successful intervention with a chemopreventive agent), (3) high sensitivity, specificity, and accuracy relative to cancer, (4) ease of measurement (use of non-invasive techniques and small tissue samples is preferable), (5) demonstration of modulation by chemopreventive agents, and (6) correlation of modulation with decreased cancer incidence. JF - Journal of cellular biochemistry. Supplement AU - Kelloff, G J AU - Malone, W F AU - Boone, C W AU - Steele, V E AU - Doody, L A AD - Chemoprevention Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 15 EP - 21 VL - 16G SN - 0733-1959, 0733-1959 KW - Anticarcinogenic Agents KW - 0 KW - Biomarkers, Tumor KW - Index Medicus KW - Humans KW - Clinical Trials as Topic KW - Cell Differentiation KW - Research Design KW - Cell Division KW - Anticarcinogenic Agents -- therapeutic use KW - Biomarkers, Tumor -- analysis KW - Precancerous Conditions -- diagnosis KW - Precancerous Conditions -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73393920?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cellular+biochemistry.+Supplement&rft.atitle=Intermediate+biomarkers+of+precancer+and+their+application+in+chemoprevention.&rft.au=Kelloff%2C+G+J%3BMalone%2C+W+F%3BBoone%2C+C+W%3BSteele%2C+V+E%3BDoody%2C+L+A&rft.aulast=Kelloff&rft.aufirst=G&rft.date=1992-01-01&rft.volume=16G&rft.issue=&rft.spage=15&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+biochemistry.+Supplement&rft.issn=07331959&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-25 N1 - Date created - 1993-01-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Approach to lupus nephritis based upon randomized trials. AN - 73393103; 1458925 JF - Contributions to nephrology AU - Steinberg, A D AU - Muir, J AU - Scott, D E AU - Gourley, M F AD - Arthritis and Rheumatism Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Md. Y1 - 1992 PY - 1992 DA - 1992 SP - 46 EP - 54 VL - 99 SN - 0302-5144, 0302-5144 KW - Cyclophosphamide KW - 8N3DW7272P KW - Azathioprine KW - MRK240IY2L KW - Prednisone KW - VB0R961HZT KW - Methylprednisolone KW - X4W7ZR7023 KW - Index Medicus KW - Drug Therapy, Combination KW - Methylprednisolone -- administration & dosage KW - Humans KW - Azathioprine -- administration & dosage KW - Prednisone -- administration & dosage KW - Male KW - Female KW - Cyclophosphamide -- administration & dosage KW - Lupus Nephritis -- drug therapy KW - Cyclophosphamide -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73393103?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Contributions+to+nephrology&rft.atitle=Approach+to+lupus+nephritis+based+upon+randomized+trials.&rft.au=Steinberg%2C+A+D%3BMuir%2C+J%3BScott%2C+D+E%3BGourley%2C+M+F&rft.aulast=Steinberg&rft.aufirst=A&rft.date=1992-01-01&rft.volume=99&rft.issue=&rft.spage=46&rft.isbn=&rft.btitle=&rft.title=Contributions+to+nephrology&rft.issn=03025144&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-08 N1 - Date created - 1993-01-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Acrylamide-induced alterations in axonal transport. Biochemical and autoradiographic studies. AN - 73367194; 1282332 AB - Alterations in the axonal transport of proteins, glycoproteins, and gangliosides in sensory neurons of the sciatic nerve were examined in adult male rats exposed to acrylamide (40 mg ip/kg body wt/d for nine consecutive days). Twenty-four hours after the last dose, the L5 dorsal root ganglion (DRG) was injected with either [35S]methionine to label proteins or [3H]glucosamine to label glycoproteins and gangliosides. The downflow patterns of radioactivity for [35S]methionine-labeled proteins and [3H]glucosamine-labeled gangliosides were unaltered by acrylamide treatment. In contrast, the outflow pattern of labeled glycoproteins displayed a severely attenuated crest with no alteration in velocity, suggesting a preferential transfer with the unlabeled stationary components in the axolemma. Retrograde accumulation of transported glycoproteins and gangliosides was unaltered for at least 6 h; however, by 24 h, there was a 75% decrease in the amount of accumulated material. The accumulation of [35S]methionine-labeled proteins was not altered. Autoradiographic analysis revealed an acrylamide-induced paucity of transported radiolabeled glycoproteins selectively in myelinated axons with no effect on "nonmyelinated" axons. The pattern of transported proteins was similar in both control and acrylamide-exposed animals. These results suggest a preferential inhibition of glycosylation or axonal transport of glycoproteins in neurons bearing myelinated axons. More importantly, it suggests that interpretations of axonal transport data must be made with the consideration of alterations in selective nerve fibers and not with the tacit assumption that all fibers in the nerve population are equally affected. JF - Molecular neurobiology AU - Harry, G J AD - Systems Toxicity Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1992 SP - 203 EP - 216 VL - 6 IS - 2-3 SN - 0893-7648, 0893-7648 KW - Acrylamides KW - 0 KW - Gangliosides KW - Glycoproteins KW - Neurotoxins KW - Sulfur Radioisotopes KW - Tritium KW - 10028-17-8 KW - Acrylamide KW - 20R035KLCI KW - Methionine KW - AE28F7PNPL KW - Glucosamine KW - N08U5BOQ1K KW - Index Medicus KW - Animals KW - Glycoproteins -- biosynthesis KW - Methionine -- metabolism KW - Rats KW - Glycoproteins -- metabolism KW - Glucosamine -- metabolism KW - Models, Neurological KW - Autoradiography -- methods KW - Gangliosides -- biosynthesis KW - Male KW - Gangliosides -- metabolism KW - Axons -- drug effects KW - Ganglia, Spinal -- physiology KW - Neurons -- drug effects KW - Axonal Transport -- drug effects KW - Acrylamides -- toxicity KW - Neurons -- physiology KW - Sciatic Nerve -- physiology KW - Neurons, Afferent -- drug effects KW - Neurotoxins -- toxicity KW - Neurons, Afferent -- physiology KW - Axons -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73367194?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+neurobiology&rft.atitle=Acrylamide-induced+alterations+in+axonal+transport.+Biochemical+and+autoradiographic+studies.&rft.au=Harry%2C+G+J&rft.aulast=Harry&rft.aufirst=G&rft.date=1992-01-01&rft.volume=6&rft.issue=2-3&rft.spage=203&rft.isbn=&rft.btitle=&rft.title=Molecular+neurobiology&rft.issn=08937648&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-10 N1 - Date created - 1993-02-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intrathecal 5-fluorouracil in the rhesus monkey. AN - 73363963; 1451233 AB - Because meningeal spread of both leukemia and solid tumors remains a difficult therapeutic problem, there is a compelling need to develop new agents for intrathecal administration. 5-Fluorouracil (5FU), an active anticancer agent, penetrates into the central nervous system to some degree following intravenous dosing. Significant systemic toxicity, however, is associated with this route of administration. Therefore, the pharmacokinetic behavior of 5FU following its intrathecal administration was studied in a rhesus monkey model. After a 10-mg intraventricular dose, the disappearance of the drug from ventricular cerebrospinal fluid was monoexponential, the half-life being 51 min; the area under the concentration-time curve (AUC) being greater than 18 mM h-1; and the peak ventricular 5FU concentrations ranging between 10 and 15 mM. After a 1-mg intralumbar dose, the AUC was 1235 microM h-1. No toxicity was observed following intraventricular administration of 5FU. After intralumbar administration of either a 10-mg or a 1-mg dose, however, local toxicity was observed in the lumbar spinal cord. These findings suggest that intrathecal administration of 5FU is not presently a feasible means of achieving cytotoxic cerebrospinal fluid concentrations. JF - Cancer chemotherapy and pharmacology AU - Berg, S L AU - Balis, F M AU - McCully, C L AU - Parker, G A AU - Murphy, R F AU - Poplack, D G AD - Pediatric Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 127 EP - 130 VL - 31 IS - 2 SN - 0344-5704, 0344-5704 KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - Animals KW - Spinal Cord -- metabolism KW - Paralysis -- chemically induced KW - Necrosis -- chemically induced KW - Injections, Spinal KW - Cerebral Ventricles -- metabolism KW - Spinal Cord -- pathology KW - Macaca mulatta KW - Male KW - Fluorouracil -- administration & dosage KW - Fluorouracil -- toxicity KW - Fluorouracil -- cerebrospinal fluid KW - Fluorouracil -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73363963?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+chemotherapy+and+pharmacology&rft.atitle=Intrathecal+5-fluorouracil+in+the+rhesus+monkey.&rft.au=Berg%2C+S+L%3BBalis%2C+F+M%3BMcCully%2C+C+L%3BParker%2C+G+A%3BMurphy%2C+R+F%3BPoplack%2C+D+G&rft.aulast=Berg&rft.aufirst=S&rft.date=1992-01-01&rft.volume=31&rft.issue=2&rft.spage=127&rft.isbn=&rft.btitle=&rft.title=Cancer+chemotherapy+and+pharmacology&rft.issn=03445704&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-31 N1 - Date created - 1992-12-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Efficacy of urinalysis in monitoring heroin and cocaine abuse patterns: implications in clinical trials for treatment of drug dependence. AN - 73353038; 1436015 AB - Urinalysis can be used as an objective criterion for monitoring the outcome of a treatment program or a clinical trial. Important factors to consider when implementing a drug testing program include standardization of assay technology and cutoffs between participating centers and selection of identical testing schedules. Also, it is vitally important to minimize the amount of safe time (time that drug use can go undetected) occurring in a testing schedule. The detection times for cocaine and heroin have been shown to vary with selection of cutoff and with the drug dose. Obviously, the selection of cutoffs is under program control, whereas the amount of illicit drug use is under subject control. Fortunately, changes in the illicit drug dose by the subject demonstrate a log-linear relationship to detection time. Hence, a higher drug dose by the subject only extends the detection time slightly (and improves the probability of detection) without greatly increasing the risks of drug carryover from one urine test to another. The most efficient testing schedule for judging the outcome of clinical trials for cocaine and heroin appears to be a 3-days-a-week schedule (Monday, Wednesday, Friday or Tuesday, Thursday, Saturday). When different schedules were challenged by simulating random times at which cocaine use might occur during the week, the 3-days-per-week schedule was the most efficient without the risk of carryover. The 3-days-per-week schedule also performed better than 1-day-per-week when multiple random drug use was simulated. Overall, the 3-days-per-week testing schedule with specified assay technology and cutoffs was the best compromise for maximizing detection of drug use, minimizing carryover, and providing a standardized methodology for outcome comparison between programs. JF - NIDA research monograph AU - Cone, E J AU - Dickerson, S L AD - Laboratory of Chemistry and Drug Metabolism, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1992 PY - 1992 DA - 1992 SP - 46 EP - 58; discussion 59-63 VL - 128 SN - 1046-9516, 1046-9516 KW - Heroin KW - 70D95007SX KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Humans KW - Data Interpretation, Statistical KW - Substance Abuse Detection -- methods KW - Heroin Dependence -- urine KW - Cocaine -- urine KW - Clinical Trials as Topic KW - Heroin Dependence -- rehabilitation KW - Substance-Related Disorders -- urine KW - Heroin -- urine KW - Substance-Related Disorders -- rehabilitation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73353038?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Efficacy+of+urinalysis+in+monitoring+heroin+and+cocaine+abuse+patterns%3A+implications+in+clinical+trials+for+treatment+of+drug+dependence.&rft.au=Cone%2C+E+J%3BDickerson%2C+S+L&rft.aulast=Cone&rft.aufirst=E&rft.date=1992-01-01&rft.volume=128&rft.issue=&rft.spage=46&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-17 N1 - Date created - 1992-12-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Case management community advocacy for substance abuse clients. AN - 73352995; 1436005 JF - NIDA research monograph AU - Ashery, R S AD - Division of Applied Research, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 383 EP - 394 VL - 127 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - Models, Organizational KW - Humans KW - Health Services Research KW - Cost Control KW - Outcome Assessment (Health Care) KW - Organizational Objectives KW - Substance-Related Disorders -- therapy KW - Community Health Services -- standards KW - Patient Advocacy KW - Patient Care Planning -- standards KW - Community Health Services -- economics KW - Patient Care Planning -- organization & administration KW - Patient Care Planning -- economics KW - Community Health Services -- organization & administration UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73352995?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Case+management+community+advocacy+for+substance+abuse+clients.&rft.au=Ashery%2C+R+S&rft.aulast=Ashery&rft.aufirst=R&rft.date=1992-01-01&rft.volume=127&rft.issue=&rft.spage=383&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-21 N1 - Date created - 1992-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Analysis of clinical trials for treatment of opiate dependence: what are the possibilities? AN - 73342305; 1436010 JF - NIDA research monograph AU - Jain, R B AD - Biometrics Branch, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 116 EP - 34; discussion 135-6 VL - 128 SN - 1046-9516, 1046-9516 KW - Narcotics KW - 0 KW - Buprenorphine KW - 40D3SCR4GZ KW - Methadone KW - UC6VBE7V1Z KW - Index Medicus KW - Buprenorphine -- urine KW - Probability KW - Methadone -- therapeutic use KW - Buprenorphine -- therapeutic use KW - Patient Compliance KW - Humans KW - Patient Dropouts KW - Methadone -- urine KW - Narcotics -- urine KW - Clinical Trials as Topic KW - Opioid-Related Disorders -- rehabilitation KW - Data Interpretation, Statistical KW - Opioid-Related Disorders -- urine UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73342305?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Analysis+of+clinical+trials+for+treatment+of+opiate+dependence%3A+what+are+the+possibilities%3F&rft.au=Jain%2C+R+B&rft.aulast=Jain&rft.aufirst=R&rft.date=1992-01-01&rft.volume=128&rft.issue=&rft.spage=116&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-17 N1 - Date created - 1992-12-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Case management models for homeless persons with alcohol and other drug problems: an overview of the NIAAA research demonstration program. AN - 73342246; 1435996 JF - NIDA research monograph AU - Perl, H I AU - Jacobs, M L AD - Homeless Demonstration and Evaluation Branch, Division of Clinical Prevention Research, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 208 EP - 222 VL - 127 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - United States KW - Urban Health KW - Humans KW - National Institutes of Health (U.S.) KW - Health Services Research KW - Health Services Accessibility -- standards KW - Program Development KW - Program Evaluation KW - Outcome Assessment (Health Care) KW - Models, Organizational KW - Substance-Related Disorders -- therapy KW - Patient Care Planning -- standards KW - Homeless Persons KW - Patient Care Planning -- organization & administration UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73342246?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Case+management+models+for+homeless+persons+with+alcohol+and+other+drug+problems%3A+an+overview+of+the+NIAAA+research+demonstration+program.&rft.au=Perl%2C+H+I%3BJacobs%2C+M+L&rft.aulast=Perl&rft.aufirst=H&rft.date=1992-01-01&rft.volume=127&rft.issue=&rft.spage=208&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-21 N1 - Date created - 1992-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The continuing interrelationship of CPDD and NIDDK. AN - 73341796; 1435982 JF - NIDA research monograph AU - Jacobson, A E AU - Rice, K C AD - Laboratory of Medicinal Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 49 EP - 53 VL - 119 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - History of medicine KW - United States KW - Animals KW - History, 20th Century KW - Digestive System KW - Humans KW - Kidney KW - Diabetes Mellitus KW - Substance-Related Disorders -- physiopathology KW - National Institutes of Health (U.S.) -- organization & administration KW - Substance-Related Disorders -- history KW - National Institutes of Health (U.S.) -- history UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73341796?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=The+continuing+interrelationship+of+CPDD+and+NIDDK.&rft.au=Jacobson%2C+A+E%3BRice%2C+K+C&rft.aulast=Jacobson&rft.aufirst=A&rft.date=1992-01-01&rft.volume=119&rft.issue=&rft.spage=49&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-07 N1 - Date created - 1992-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Design of clinical trials for treatment of opiate dependence: what is missing? AN - 73339074; 1436014 JF - NIDA research monograph AU - Jain, R B AD - Biometrics Branch, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 29 EP - 36; discussion 37-45 VL - 128 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - Probability KW - Patient Compliance KW - Humans KW - Time Factors KW - Substance Abuse Detection -- methods KW - Clinical Trials as Topic KW - Opioid-Related Disorders -- rehabilitation KW - Data Interpretation, Statistical KW - Opioid-Related Disorders -- urine KW - Research Design UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73339074?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Design+of+clinical+trials+for+treatment+of+opiate+dependence%3A+what+is+missing%3F&rft.au=Jain%2C+R+B&rft.aulast=Jain&rft.aufirst=R&rft.date=1992-01-01&rft.volume=128&rft.issue=&rft.spage=29&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-17 N1 - Date created - 1992-12-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cellular pattern of multidrug-resistance gene expression during chemical hepatocarcinogenesis in the rat. AN - 73324905; 1359897 AB - Increased expression of multidrug-resistance (mdr) gene transcripts and of the encoded protein, P-glycoprotein, is found in many types of tumors. The biological significance of mdr overexpression during the stepwise process of neoplastic development, however, is not well understood. To assess the possible significance of mdr overexpression in carcinogenesis, we examined the cellular distributions of both mdr gene transcripts and P-glycoprotein during hepatocarcinogenesis induced in rats by the Solt-Farber protocol and then compared them to the distributions of the placental form of glutathione S-transferase (GST-P), a known marker of preneoplastic and neoplastic lesions in the liver. In situ hybridization and immunohistochemical techniques were employed. Neither mdr transcripts nor P-glycoprotein was expressed in oval cells that appeared early in the carcinogenic process. GST-P was strongly expressed in the early focal lesions, whereas the levels of mdr transcripts and P-glycoprotein expressed were low and heterogeneous. Expression of mdr transcripts and P-glycoprotein was increased and became more uniform in hyperplastic nodules and carcinomas, although considerable heterogeneity of expression was still found, particularly at the nodular stage. These data suggest that increased expression of mdr is associated with later stages of neoplastic development in the liver. Furthermore, that no chemical treatment of the animals was employed when the expression of mdr was increasing in the preneoplastic and neoplastic lesions suggests that the enhanced mdr expression is intrinsic to the carcinogenic process. JF - Molecular carcinogenesis AU - Nakatsukasa, H AU - Evarts, R P AU - Burt, R K AU - Nagy, P AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-0037. Y1 - 1992 PY - 1992 DA - 1992 SP - 190 EP - 198 VL - 6 IS - 3 SN - 0899-1987, 0899-1987 KW - mdr KW - Membrane Glycoproteins KW - 0 KW - P-Glycoprotein KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Index Medicus KW - Rats KW - Gene Expression Regulation, Neoplastic KW - Animals KW - Rats, Inbred F344 KW - In Situ Hybridization KW - Membrane Glycoproteins -- biosynthesis KW - Glutathione Transferase -- biosynthesis KW - Liver -- metabolism KW - Disease Models, Animal KW - Immunohistochemistry KW - Liver Neoplasms -- metabolism KW - Drug Resistance -- genetics KW - Cell Transformation, Neoplastic -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73324905?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Cellular+pattern+of+multidrug-resistance+gene+expression+during+chemical+hepatocarcinogenesis+in+the+rat.&rft.au=Nakatsukasa%2C+H%3BEvarts%2C+R+P%3BBurt%2C+R+K%3BNagy%2C+P%3BThorgeirsson%2C+S+S&rft.aulast=Nakatsukasa&rft.aufirst=H&rft.date=1992-01-01&rft.volume=6&rft.issue=3&rft.spage=190&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-30 N1 - Date created - 1992-12-30 N1 - Date revised - 2017-01-13 N1 - Gene symbol - mdr N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Radiation from Chernobyl and risk of childhood leukaemia. AN - 73323957; 1445724 JF - European journal of cancer (Oxford, England : 1990) AU - Linet, M S AU - Boice, J D AD - Analytic Studies Section, National Cancer Institute, Bethesda, Maryland. Y1 - 1992 PY - 1992 DA - 1992 SP - 1 EP - 3 VL - 29A IS - 1 SN - 0959-8049, 0959-8049 KW - Radioactive Fallout KW - 0 KW - Index Medicus KW - Ukraine -- epidemiology KW - Occupational Exposure KW - Radiation Dosage KW - Humans KW - Environmental Exposure KW - Incidence KW - Child KW - Accidents KW - Leukemia, Radiation-Induced -- epidemiology KW - Nuclear Reactors KW - Radioactive Fallout -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73323957?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+cancer+%28Oxford%2C+England+%3A+1990%29&rft.atitle=Radiation+from+Chernobyl+and+risk+of+childhood+leukaemia.&rft.au=Linet%2C+M+S%3BBoice%2C+J+D&rft.aulast=Linet&rft.aufirst=M&rft.date=1992-01-01&rft.volume=29A&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=European+journal+of+cancer+%28Oxford%2C+England+%3A+1990%29&rft.issn=09598049&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-29 N1 - Date created - 1992-12-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chemical toxicity and chemical carcinogenesis. Is there a causal connection? A comparative morphological evaluation of 1500 experiments. AN - 73322313; 1428093 AB - Chemicals cause toxic and carcinogenic effects as well as beneficial and other adverse effects in animals and in humans. The purpose of this paper is to assess whether there is a direct, uniform causal relationship between toxicity and carcinogenicity. Within this context, specific issues receive attention: the influence of exposure concentrations on carcinogenesis; kidney cancer and alpha 2 mu-globulin; urinary calculi and tumours; and cell turnover or proliferation and cancer. The data used to evaluate histopathological site-specific correspondence between these two end-points comes from 130 studies of chemical carcinogenesis designed and conducted by the US National Toxicology Program (NTP). Nearly 1500 sex-species-exposure group experiments were evaluated for morphological evidence of toxicity and/or carcinogenicity, for dose-response relationships, and for site-specific correlations of toxicity and carcinogenicity. The major conclusions are that chemicals evaluated for long-term toxicity and carcinogenicity in experimental animals can be divided into three categories: (1) those that cause organ toxicity without cancer, (2) those that cause site-specific cancer with no associated toxicity and (3) those that cause toxicity and cancer in the same organ. Examples are given to illustrate each category. On the basis of this comparative analysis, in the great majority of cases the available data do not support a correlation between chemically induced toxicity and carcinogenicity. Moreover, until considerably more scientific knowledge about molecular mechanisms of carcinogenesis becomes available and accepted, attempts to use findings on toxicity to modify the risk assessment process will be fraught with uncertainty and might even have a negative impact on public health. JF - IARC scientific publications AU - Huff, J E AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC. Y1 - 1992 PY - 1992 DA - 1992 SP - 437 EP - 475 IS - 116 SN - 0300-5038, 0300-5038 KW - Carcinogens KW - 0 KW - Index Medicus KW - Rats KW - Animals KW - Urinary Calculi -- complications KW - Urinary Bladder Neoplasms -- etiology KW - Dose-Response Relationship, Drug KW - Humans KW - Kidney -- drug effects KW - Kidney Neoplasms -- etiology KW - Time Factors KW - Urinary Bladder -- drug effects KW - Carcinogens -- pharmacology KW - Neoplasms, Experimental -- etiology KW - Neoplasms, Experimental -- chemically induced KW - Toxicology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73322313?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IARC+scientific+publications&rft.atitle=Chemical+toxicity+and+chemical+carcinogenesis.+Is+there+a+causal+connection%3F+A+comparative+morphological+evaluation+of+1500+experiments.&rft.au=Huff%2C+J+E&rft.aulast=Huff&rft.aufirst=J&rft.date=1992-01-01&rft.volume=&rft.issue=116&rft.spage=437&rft.isbn=&rft.btitle=&rft.title=IARC+scientific+publications&rft.issn=03005038&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-22 N1 - Date created - 1992-12-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 12-O-tetradecanoylphorbol-13-acetate--induced levels of AP-1 proteins: a 46-kDa protein immunoprecipitated by anti-fra-1 and induced in promotion-resistant but not promotion-sensitive JB6 cells. AN - 73322132; 1445622 AB - Neoplastic transformation and transcriptional activation by activator protein-1 (AP-1) complex are stimulated by tumor-promoting agents in promotion-sensitive (P+) but not promotion-resistant (P-) mouse epidermal JB6 cells in culture. This implicates AP-1 as a specific regulator of signal transduction pathways in the promotion phase of neoplastic transformation. We therefore hypothesized that the defective P- responsiveness may be due to limiting levels of AP-1 protein components in those cells. In this investigation, steady-state levels of AP-1 protein components were measured by immunoprecipitating proteins from 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated P+ and P- cells to discern what may limit the AP-1 response. Whereas the AP-1 proteins junB, junD, and fosB did not show differential basal or TPA-inducible levels in P+ and P- cells, a 46-kDa species precipitated by anti-fra-1 antibody was TPA-inducible in P- cells but not in P+ cells, and c-jun protein was present at higher levels in TPA-treated and untreated P+ cells than in P- cells. These data raise the possibility that the 46-kDa fra-1-related protein may be a negative modulator of AP-1 activity and suggest that elevated levels of this 46-kDa species and limiting levels of c-jun may significantly impair AP-1 function or transformation response in P- cells or both. JF - Molecular carcinogenesis AU - Bernstein, L R AU - Bravo, R AU - Colburn, N H AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702. Y1 - 1992 PY - 1992 DA - 1992 SP - 221 EP - 229 VL - 6 IS - 3 SN - 0899-1987, 0899-1987 KW - Proto-Oncogene Proteins c-fos KW - 0 KW - Proto-Oncogene Proteins c-jun KW - fos-related antigen 1 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Electrophoresis, Polyacrylamide Gel KW - Signal Transduction -- drug effects KW - Molecular Sequence Data KW - Transcriptional Activation -- drug effects KW - Mice KW - Amino Acid Sequence KW - Time Factors KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Cell Line KW - Proto-Oncogene Proteins c-fos -- biosynthesis KW - Proto-Oncogene Proteins c-jun -- physiology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Transformation, Neoplastic -- drug effects KW - Proto-Oncogene Proteins c-jun -- metabolism KW - Proto-Oncogene Proteins c-jun -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73322132?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=12-O-tetradecanoylphorbol-13-acetate--induced+levels+of+AP-1+proteins%3A+a+46-kDa+protein+immunoprecipitated+by+anti-fra-1+and+induced+in+promotion-resistant+but+not+promotion-sensitive+JB6+cells.&rft.au=Bernstein%2C+L+R%3BBravo%2C+R%3BColburn%2C+N+H&rft.aulast=Bernstein&rft.aufirst=L&rft.date=1992-01-01&rft.volume=6&rft.issue=3&rft.spage=221&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-30 N1 - Date created - 1992-12-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Managed care and case management of substance abuse treatment. AN - 73314222; 1436002 AB - Managed care has become an important subject for health service research and is used increasingly by health care payers to control health care use and costs. Health services research on managed care has relevance to the evaluation of case management of persons with substance abuse problems. Two issues in managed care that are particularly relevant to case management are the lack of explicit, widely accepted criteria for managed care and the lack of demonstrated cost savings attributable to managed care. Thorough, systematic evaluative research needs to be done before these issues are well understood. JF - NIDA research monograph AU - Woodward, A AD - Financing and Services Research Branch, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 34 EP - 53 VL - 127 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - Humans KW - Health Services Research KW - Cost Savings KW - Substance-Related Disorders -- therapy KW - Managed Care Programs -- economics KW - Managed Care Programs -- organization & administration KW - Patient Care Planning -- organization & administration KW - Managed Care Programs -- standards UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73314222?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Managed+care+and+case+management+of+substance+abuse+treatment.&rft.au=Woodward%2C+A&rft.aulast=Woodward&rft.aufirst=A&rft.date=1992-01-01&rft.volume=127&rft.issue=&rft.spage=34&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-21 N1 - Date created - 1992-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Case management systems represented in the NIDA-supported "Perinatal-20" treatment research demonstration projects. AN - 73314173; 1435998 JF - NIDA research monograph AU - Rahdert, E R AD - Division of Clinical Research, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 251 EP - 260 VL - 127 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - Urban Health KW - Interinstitutional Relations KW - Humans KW - Adult KW - Referral and Consultation KW - Program Development KW - Patient Advocacy KW - Program Evaluation KW - Organizational Objectives KW - Adolescent KW - Female KW - Pregnancy KW - Substance-Related Disorders -- therapy KW - Perinatology -- standards KW - Pregnancy Complications -- therapy KW - Perinatology -- organization & administration KW - Perinatology -- economics KW - Patient Care Planning -- standards KW - Health Services Research -- organization & administration KW - Patient Care Planning -- organization & administration KW - Patient Care Planning -- economics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73314173?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Case+management+systems+represented+in+the+NIDA-supported+%22Perinatal-20%22+treatment+research+demonstration+projects.&rft.au=Rahdert%2C+E+R&rft.aulast=Rahdert&rft.aufirst=E&rft.date=1992-01-01&rft.volume=127&rft.issue=&rft.spage=251&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-21 N1 - Date created - 1992-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Issues in the analysis of clinical trials for opiate dependence. AN - 73313466; 1436019 JF - NIDA research monograph AU - Follmann, D AU - Wu, M AU - Geller, N AD - Biostatistics Research Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 97 EP - 113; discussion 114-5 VL - 128 SN - 1046-9516, 1046-9516 KW - Buprenorphine KW - 40D3SCR4GZ KW - Methadone KW - UC6VBE7V1Z KW - Index Medicus KW - Methadone -- therapeutic use KW - Buprenorphine -- therapeutic use KW - Patient Compliance KW - Humans KW - Patient Dropouts KW - Models, Statistical KW - Bias (Epidemiology) KW - Clinical Trials as Topic KW - Opioid-Related Disorders -- rehabilitation KW - Data Interpretation, Statistical UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73313466?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Issues+in+the+analysis+of+clinical+trials+for+opiate+dependence.&rft.au=Follmann%2C+D%3BWu%2C+M%3BGeller%2C+N&rft.aulast=Follmann&rft.aufirst=D&rft.date=1992-01-01&rft.volume=128&rft.issue=&rft.spage=97&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-17 N1 - Date created - 1992-12-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Aftercare for formerly homeless, recovering women: issues for case management. AN - 73310396; 1331802 JF - NIDA research monograph AU - McMillan, D AU - Cheney, R AD - National Institute on Drug Abuse Aftercare Project, Philadelphia, PA 19102. Y1 - 1992 PY - 1992 DA - 1992 SP - 274 EP - 288 VL - 127 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - Interinstitutional Relations KW - Humans KW - Philadelphia KW - Health Services Research KW - Health Services Accessibility -- standards KW - Program Evaluation KW - Research Design KW - Female KW - Health Care Costs KW - Models, Organizational KW - Aftercare -- organization & administration KW - Aftercare -- standards KW - Patient Care Planning -- standards KW - Substance-Related Disorders -- rehabilitation KW - Aftercare -- economics KW - Homeless Persons KW - Patient Care Planning -- organization & administration KW - Patient Care Planning -- economics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73310396?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Aftercare+for+formerly+homeless%2C+recovering+women%3A+issues+for+case+management.&rft.au=McMillan%2C+D%3BCheney%2C+R&rft.aulast=McMillan&rft.aufirst=D&rft.date=1992-01-01&rft.volume=127&rft.issue=&rft.spage=274&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-21 N1 - Date created - 1992-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genetic stability and oxidative stress: common mechanisms in aging and cancer. AN - 73309144; 1450594 AB - Much evidence indicates that age-related diseases as well as the aging process itself may be a result of genetic instability, resulting in cells changing their proper state of differentiation. Such genetic changes could be of an epigenetic or genetic nature (or both) and suggest that mechanisms acting to stabilize the differentiated state of cells could be major determinants of animal species' general health and longevity. There is also much data indicating that a causative factor in cancer is genetic instability, suggesting the importance of genetic stabilized factors governing the frequency of this disease. Possibly related to these two observations is the good positive correlation between rate of cancer and the rate of aging of different mammalian species. In addition, cells from longer-lived species appear to have a higher intrinsic ability to maintain their proper differentiated state and animals whose life span has been extended by food restriction also have a postponed onset of cancer. These data suggest the possibility that genetic instability may represent a common causative mechanism for both aging and cancer. This suggestion is supported by evidence indicating that oxidative stress can increase cancer frequency and that longer-lived species appear to have a lower oxidative stress state. However, there appears to be a serious lack of evidence indicating that physical and chemical mutagenic agents accelerate aging as they do cancer. For these and other considerations, it is proposed that aging is not a result of genetic instability as are many different age-related diseases. Thus, physiological aging and some age-related diseases could have separate and distinct mechanisms of causation and control. JF - EXS AU - Cutler, R G AD - Gerontology Research Center, National Institute on Aging, Baltimore, MD 21224. Y1 - 1992 PY - 1992 DA - 1992 SP - 31 EP - 46 VL - 62 SN - 1023-294X, 1023-294X KW - Antioxidants KW - 0 KW - Free Radicals KW - Index Medicus KW - Animals KW - Antioxidants -- metabolism KW - Longevity -- genetics KW - Humans KW - Hominidae -- genetics KW - Aging -- physiology KW - Neoplasms -- physiopathology KW - Neoplasms -- etiology KW - Aging -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73309144?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=EXS&rft.atitle=Genetic+stability+and+oxidative+stress%3A+common+mechanisms+in+aging+and+cancer.&rft.au=Cutler%2C+R+G&rft.aulast=Cutler&rft.aufirst=R&rft.date=1992-01-01&rft.volume=62&rft.issue=&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=EXS&rft.issn=1023294X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-06 N1 - Date created - 1993-01-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Flow cytometric quantitation of circulating hematopoietic progenitor cells in breast cancer patients on chemotherapy. AN - 73308895; 1279720 JF - Progress in clinical and biological research AU - Read, E J AU - O'Shaughnessy, J A AU - Yu, M Y AU - Cottler-Fox, M AU - Denicoff, A M AU - Cowan, K H AU - Gress, R E AD - Department of Transfusion Medicine, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1992 PY - 1992 DA - 1992 SP - 523 EP - 530 VL - 377 SN - 0361-7742, 0361-7742 KW - Antigens, CD KW - 0 KW - Antigens, CD34 KW - Antineoplastic Agents KW - Index Medicus KW - Blood Transfusion, Autologous KW - Leukopenia -- chemically induced KW - Humans KW - Hematopoietic Stem Cell Transplantation KW - Colony-Forming Units Assay KW - Antineoplastic Agents -- therapeutic use KW - Female KW - Blood Cell Count KW - Leukopenia -- blood KW - Breast Neoplasms -- drug therapy KW - Hematopoietic Stem Cells -- pathology KW - Hematopoietic Stem Cells -- immunology KW - Blood Cells -- pathology KW - Breast Neoplasms -- therapy KW - Blood Cells -- immunology KW - Breast Neoplasms -- blood KW - Blood Cells -- transplantation KW - Flow Cytometry -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73308895?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Progress+in+clinical+and+biological+research&rft.atitle=Flow+cytometric+quantitation+of+circulating+hematopoietic+progenitor+cells+in+breast+cancer+patients+on+chemotherapy.&rft.au=Read%2C+E+J%3BO%27Shaughnessy%2C+J+A%3BYu%2C+M+Y%3BCottler-Fox%2C+M%3BDenicoff%2C+A+M%3BCowan%2C+K+H%3BGress%2C+R+E&rft.aulast=Read&rft.aufirst=E&rft.date=1992-01-01&rft.volume=377&rft.issue=&rft.spage=523&rft.isbn=&rft.btitle=&rft.title=Progress+in+clinical+and+biological+research&rft.issn=03617742&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-07 N1 - Date created - 1992-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Drug dependence (addiction) and its treatment. AN - 73304923; 1436016 JF - NIDA research monograph AU - Vocci, F J AU - Jaffe, J H AU - Jain, R B AD - Medications Development Division, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 6 EP - 13 VL - 128 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - Humans KW - Opioid-Related Disorders -- rehabilitation KW - Substance-Related Disorders -- physiopathology KW - Substance-Related Disorders -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73304923?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Drug+dependence+%28addiction%29+and+its+treatment.&rft.au=Vocci%2C+F+J%3BJaffe%2C+J+H%3BJain%2C+R+B&rft.aulast=Vocci&rft.aufirst=F&rft.date=1992-01-01&rft.volume=128&rft.issue=&rft.spage=6&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-17 N1 - Date created - 1992-12-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Biological evaluation of compounds for their physical dependence potential and abuse liability, XIV. Animal Testing Committee of the Committee on Problems of Drug Dependence, Inc. (1991). AN - 73303404; 1435983 JF - NIDA research monograph AU - Jacobson, A E AD - Drug Evaluation Committee, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 490 EP - 512 VL - 119 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - Animals KW - Humans KW - Research Design KW - Substance-Related Disorders -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73303404?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Biological+evaluation+of+compounds+for+their+physical+dependence+potential+and+abuse+liability%2C+XIV.+Animal+Testing+Committee+of+the+Committee+on+Problems+of+Drug+Dependence%2C+Inc.+%281991%29.&rft.au=Jacobson%2C+A+E&rft.aulast=Jacobson&rft.aufirst=A&rft.date=1992-01-01&rft.volume=119&rft.issue=&rft.spage=490&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-07 N1 - Date created - 1992-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of corn oil, time-related changes, and inter-laboratory variability on tumor occurrence in control Fischer 344 (F344/N) rats. AN - 73298871; 1411131 AB - Survival, body weight, and site-specific tumor rates in untreated, corn oil gavage, and water gavage control Fischer 344 (F344/N) rats from 88 National Toxicology Program (NTP) long term carcinogenicity studies were evaluated to determine which factors were primarily responsible for inter-study variability. For male rats, previously-reported decreases in leukemia and increases in body weight, survival, and pancreatic acinar cell tumors attributable to corn oil gavage were confirmed. Corn oil did not appear to affect tumor rates in female rats. The gavage technique per se did not appear to influence tumor rates in rats of either sex. Previously reported time-related increases in certain site-specific neoplasia in control rats appeared to have stabilized in recent years, but control tumor rates are still much greater than those seen a decade ago. More recent studies continue to show increasing rates of leukemia and mammary gland tumors and decreasing survival. Female rats also continue to show time-related increases in maximum mean body weight. Inter-laboratory variability in body weight and in the rates of a number of site-specific neoplasms were also significant. High mean body weights in control groups were found to be associated with increased rates of mammary and pituitary tumors. Our evaluation supports the view that if historical control data are to be utilized in the interpretation of experimental results, primary emphasis should be given to lab and route of administration-specific tumor rates for studies that are contemporary to the study under evaluation. It also suggests that certain experimental design changes (e.g., dietary modifications) may be needed to reduce tumor rates and to increase survival. JF - Toxicologic pathology AU - Haseman, J K AU - Rao, G N AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 52 EP - 60 VL - 20 IS - 1 SN - 0192-6233, 0192-6233 KW - Corn Oil KW - 8001-30-7 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Body Weight -- drug effects KW - Carcinogenicity Tests KW - Time Factors KW - Male KW - Female KW - Neoplasms, Experimental -- chemically induced KW - Corn Oil -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73298871?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Effects+of+corn+oil%2C+time-related+changes%2C+and+inter-laboratory+variability+on+tumor+occurrence+in+control+Fischer+344+%28F344%2FN%29+rats.&rft.au=Haseman%2C+J+K%3BRao%2C+G+N&rft.aulast=Haseman&rft.aufirst=J&rft.date=1992-01-01&rft.volume=20&rft.issue=1&rft.spage=52&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=01926233&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-04 N1 - Date created - 1992-11-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanisms of action of known human carcinogens. AN - 73294281; 1428078 AB - Mutational mechanisms can be proposed for most, if not all, known human carcinogens. Many of these are electrophilic or metabolically activated to reactive molecules which can alter DNA, causing genetic damage and different types of mutations. Even some human carcinogens previously proposed to be nongenotoxic (e.g., hormones and asbestos) exhibit mutational activity in assays for chromosomal mutations. Since such chemicals are usually inactive in the Salmonella assay and other assays for gene mutation, more emphasis has been placed on their nonmutational mechanisms. Clear evidence exists that these carcinogens can alter gene expression and stimulate cell proliferation by epigenetic mechanisms. Such properties are undoubtedly important in their carcinogenic activity. Although they are less well studied, DNA reactive, genotoxic carcinogens also alter gene expression and increase cell turnover by epigenetic mechanisms. These findings are consistent with the current understanding of the molecular basis of multistep carcinogenesis. Most common human cancers evolve as the result of multiple mutational events. The molecular basis of these mutations is varied, and they include point mutations, deletion mutations, chromosomal rearrangements, gene amplification and chromosomal losses and gains. Therefore, different mutational activities of carcinogens can influence the carcinogenic process at different steps. Influences on gene expression and cell proliferation are also important in allowing clonal expansion of preneoplastic cells and in disrupting the suppressive effects of surrounding normal cells on preneoplastic cells (Dotto et al., 1988). The mechanisms of action of human carcinogens, and very probably many rodent carcinogens, include both genetic and epigenetic processes. Carcinogenesis is a multistep, multigenic, multicausal process (Barrett, 1987b), so both epigenetic and genetic factors are probably important.(ABSTRACT TRUNCATED AT 250 WORDS) JF - IARC scientific publications AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC. Y1 - 1992 PY - 1992 DA - 1992 SP - 115 EP - 134 IS - 116 SN - 0300-5038, 0300-5038 KW - Carcinogens KW - 0 KW - Index Medicus KW - Humans KW - Carcinogens -- pharmacology KW - Neoplasms -- pathology KW - Neoplasms -- chemically induced KW - Neoplasms -- genetics KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73294281?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IARC+scientific+publications&rft.atitle=Mechanisms+of+action+of+known+human+carcinogens.&rft.au=Barrett%2C+J+C&rft.aulast=Barrett&rft.aufirst=J&rft.date=1992-01-01&rft.volume=&rft.issue=116&rft.spage=115&rft.isbn=&rft.btitle=&rft.title=IARC+scientific+publications&rft.issn=03005038&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-22 N1 - Date created - 1992-12-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tumour suppressor genes, multistage carcinogenesis and molecular epidemiology. AN - 73293492; 1428103 JF - IARC scientific publications AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 1992 PY - 1992 DA - 1992 SP - 67 EP - 85 IS - 116 SN - 0300-5038, 0300-5038 KW - Carcinogens KW - 0 KW - Index Medicus KW - Risk Factors KW - Humans KW - Carcinogens -- pharmacology KW - Genes, Tumor Suppressor -- drug effects KW - Genes, Tumor Suppressor -- genetics KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73293492?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IARC+scientific+publications&rft.atitle=Tumour+suppressor+genes%2C+multistage+carcinogenesis+and+molecular+epidemiology.&rft.au=Harris%2C+C+C&rft.aulast=Harris&rft.aufirst=C&rft.date=1992-01-01&rft.volume=&rft.issue=116&rft.spage=67&rft.isbn=&rft.btitle=&rft.title=IARC+scientific+publications&rft.issn=03005038&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-22 N1 - Date created - 1992-12-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Receptor-mediated carcinogenesis. AN - 73289265; 1428104 JF - IARC scientific publications AU - Lucier, G W AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC. Y1 - 1992 PY - 1992 DA - 1992 SP - 87 EP - 112 IS - 116 SN - 0300-5038, 0300-5038 KW - Carcinogens KW - 0 KW - Estrogens KW - Phorbol Esters KW - Polychlorinated Dibenzodioxins KW - Receptors, Drug KW - Index Medicus KW - Phorbol Esters -- pharmacology KW - Estrogens -- pharmacology KW - Receptors, Drug -- drug effects KW - Humans KW - Polychlorinated Dibenzodioxins -- pharmacology KW - Carcinogens -- pharmacology KW - Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73289265?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IARC+scientific+publications&rft.atitle=Receptor-mediated+carcinogenesis.&rft.au=Lucier%2C+G+W&rft.aulast=Lucier&rft.aufirst=G&rft.date=1992-01-01&rft.volume=&rft.issue=116&rft.spage=87&rft.isbn=&rft.btitle=&rft.title=IARC+scientific+publications&rft.issn=03005038&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-22 N1 - Date created - 1992-12-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Implementation issues and techniques in randomized trials of outpatient psychosocial treatments for drug abusers: recruitment of subjects. AN - 73287762; 1329493 AB - We reviewed nine randomized clinical trials of outpatient psychosocial treatments for drug abuse to ascertain implementation problems and solutions that the researchers developed. The most common problem was subject recruitment. Inadequate recruitment can disrupt a project's timetable, preoccupy its staff, reduce the trial's ability to detect treatment differences, and perhaps result in the trial's abandonment. The causes of recruitment problems include the need for large samples and multiple eligibility criteria, subject reluctance to be a "guinea pig," low client treatment motivation, client dislike of research procedures, clinicians' distrust of research, and difficulties collaborating with treatment agencies. Solutions include realistic assessment of the target population's size, use of mass media, statistical adjustments to minimize unnecessary sample exclusions, variable treatment assignment ratios, and prevention of common collaboration difficulties. JF - The American journal of drug and alcohol abuse AU - Ashery, R S AU - McAuliffe, W E AD - National Institute on Drug Abuse, Rockville, Maryland 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 305 EP - 329 VL - 18 IS - 3 SN - 0095-2990, 0095-2990 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Humans KW - Referral and Consultation KW - Research Design KW - Health Promotion KW - Substance Abuse Treatment Centers KW - Behavior Therapy KW - Patient Compliance KW - Adult KW - Treatment Outcome KW - Middle Aged KW - Adolescent KW - Female KW - Male KW - Substance-Related Disorders -- therapy KW - Randomized Controlled Trials as Topic KW - Substance-Related Disorders -- prevention & control KW - Ambulatory Care UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73287762?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+drug+and+alcohol+abuse&rft.atitle=Implementation+issues+and+techniques+in+randomized+trials+of+outpatient+psychosocial+treatments+for+drug+abusers%3A+recruitment+of+subjects.&rft.au=Ashery%2C+R+S%3BMcAuliffe%2C+W+E&rft.aulast=Ashery&rft.aufirst=R&rft.date=1992-01-01&rft.volume=18&rft.issue=3&rft.spage=305&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+drug+and+alcohol+abuse&rft.issn=00952990&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-05 N1 - Date created - 1992-11-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transgenic mice in carcinogenicity testing. AN - 73284143; 1428092 AB - The biological effects of the expression of single genes can be evaluated in transgenic animals. Transgenic techniques have been used to investigate a wide variety of biomedical topics, including the consequences of oncogene expression, but their use in carcinogenicity testing is just beginning. Probable future developments involving transgenic animals are new short-term assays for carcinogenicity in vivo and methods for detecting and characterizing the critical genotoxic events in carcinogenesis. JF - IARC scientific publications AU - Griesemer, R AU - Tennant, R AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC. Y1 - 1992 PY - 1992 DA - 1992 SP - 429 EP - 436 IS - 116 SN - 0300-5038, 0300-5038 KW - Carcinogens KW - 0 KW - Index Medicus KW - Animals KW - Carcinogenicity Tests KW - Mice KW - Carcinogens -- pharmacology KW - Neoplasms, Experimental -- chemically induced KW - Mice, Transgenic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73284143?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IARC+scientific+publications&rft.atitle=Transgenic+mice+in+carcinogenicity+testing.&rft.au=Griesemer%2C+R%3BTennant%2C+R&rft.aulast=Griesemer&rft.aufirst=R&rft.date=1992-01-01&rft.volume=&rft.issue=116&rft.spage=429&rft.isbn=&rft.btitle=&rft.title=IARC+scientific+publications&rft.issn=03005038&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-22 N1 - Date created - 1992-12-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A historical perspective on the classification developed and used for chemical carcinogens by the National Toxicology Program during 1983-1992. AN - 73279269; 1411383 AB - To evaluate, interpret, and better communicate the data and findings from long-term chemical carcinogenesis studies on laboratory animals, the National Toxicology Program began using five categories or levels of evidence of carcinogenicity in 1983 (clear, some, equivocal, and no evidence and inadequate experiment). Through July 1991 these defined terms had been used to describe 144 chemical carcinogenesis studies comprising 530 sex-species experiments. Together with a selected descriptor of the chemically associated level of evidence for each experimental unit (male rats, female rats, male mice, female mice), mention is made of the length of the experiment, route of exposure, and the particular tumor type or types for each organ or system affected. The scientific judgements are comprised of this relevant information to inform the readers and users of these evaluations. In this paper the background rationale for the development and proper use of these categories of evidence of carcinogenicity are detailed, together with some personal reflections. JF - Scandinavian journal of work, environment & health AU - Huff, J AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 74 EP - 82 VL - 18 Suppl 1 SN - 0355-3140, 0355-3140 KW - Carcinogens KW - 0 KW - Index Medicus KW - Animals KW - Carcinogenicity Tests KW - Toxicology KW - Carcinogens -- classification KW - Neoplasms -- chemically induced KW - Program Development KW - Carcinogens -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73279269?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scandinavian+journal+of+work%2C+environment+%26+health&rft.atitle=A+historical+perspective+on+the+classification+developed+and+used+for+chemical+carcinogens+by+the+National+Toxicology+Program+during+1983-1992.&rft.au=Huff%2C+J&rft.aulast=Huff&rft.aufirst=J&rft.date=1992-01-01&rft.volume=18+Suppl+1&rft.issue=&rft.spage=74&rft.isbn=&rft.btitle=&rft.title=Scandinavian+journal+of+work%2C+environment+%26+health&rft.issn=03553140&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-29 N1 - Date created - 1992-10-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vivo trapping of hydroxyl free radicals in the striatum utilizing intracranial microdialysis perfusion of salicylate: effects of MPTP, MPDP+, and MPP+. AN - 73271599; 1329855 AB - Increased formation of hydroxyl free radicals (.OH) reflected by .OH adduct of salicylate in brain dialysate was demonstrated during the sustained (more than 2 hours) dopamine overflow elicited by 75 nmol of 1-methyl-4-phenyldihydropyridine (MPDP+) and 1-methyl-4-phenylpyridinium (MPP+) in the rat striatum. Owing to its weak dopamine releasing action, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) did not significantly increase the .OH formation. This data suggests that sustained elevation of dopamine in the extracellular fluid elicited by MPTP analogues can be auto-oxidized, which in turn leads (possibly by indirect mechanisms) to the formation of cytotoxic .OH free radicals near the nigrostriatal terminals. JF - Journal of neural transmission. General section AU - Obata, T AU - Chiueh, C C AD - National Institute of Neurological Disorders and Stroke, Bethesda, Md. Y1 - 1992 PY - 1992 DA - 1992 SP - 139 EP - 145 VL - 89 IS - 1-2 KW - Free Radicals KW - 0 KW - Hydroxides KW - Pyridinium Compounds KW - Salicylates KW - Hydroxyl Radical KW - 3352-57-6 KW - 1-(4-methoxyphenyl)pyridinium KW - 42850-10-2 KW - 1-methyl-4-phenyl-2,3-dihydropyridinium KW - 94613-45-3 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Salicylic Acid KW - O414PZ4LPZ KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Animals KW - Dialysis KW - Perfusion KW - Dopamine -- physiology KW - Substantia Nigra -- drug effects KW - Substantia Nigra -- metabolism KW - Nerve Endings -- metabolism KW - Rats KW - Rats, Sprague-Dawley KW - Male KW - Nerve Endings -- drug effects KW - Corpus Striatum -- metabolism KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- pharmacology KW - Pyridinium Compounds -- pharmacology KW - Hydroxides -- metabolism KW - Salicylates -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73271599?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neural+transmission.+General+section&rft.atitle=In+vivo+trapping+of+hydroxyl+free+radicals+in+the+striatum+utilizing+intracranial+microdialysis+perfusion+of+salicylate%3A+effects+of+MPTP%2C+MPDP%2B%2C+and+MPP%2B.&rft.au=Obata%2C+T%3BChiueh%2C+C+C&rft.aulast=Obata&rft.aufirst=T&rft.date=1992-01-01&rft.volume=89&rft.issue=1-2&rft.spage=139&rft.isbn=&rft.btitle=&rft.title=Journal+of+neural+transmission.+General+section&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-04 N1 - Date created - 1992-12-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Age at first injection and HIV risk among intravenous drug users. AN - 73261922; 1415084 AB - The relationship of age at first injection and HIV risk was explored in a nonblinded HIV seroprevalence study of intravenous drug users (IVDUs) admitted to methadone treatment in seven United States cities between February 1987 and June 1989. Comparisons were made of IVDUs who began injecting as adolescents, young adults, and adults in terms of drug use and sexual HIV risk behaviors and HIV serostatus. Early injectors consistently reported higher levels of drug-using risk behaviors (e.g., frequency of injection, frequency of needle sharing, and use of shooting galleries), and were more likely to be HIV seropositive. Among females, early injectors were also more likely to report sexual risk behaviors (e.g., multiple sex partners, prostitution). The relationship of age at first injection with selected risk behaviors and HIV serostatus was independent of subjects' age at interview, gender, and race/ethnicity. This study suggests that adolescent injectors are an important target group for HIV prevention efforts. JF - The American journal of drug and alcohol abuse AU - Battjes, R J AU - Leukefeld, C G AU - Pickens, R W AD - Division of Clinical Research, National Institute on Drug Abuse, Rockville, Maryland. Y1 - 1992 PY - 1992 DA - 1992 SP - 263 EP - 273 VL - 18 IS - 3 SN - 0095-2990, 0095-2990 KW - Index Medicus KW - AIDS/HIV KW - Age Factors KW - Risk-Taking KW - Attitude to Health KW - Humans KW - Child KW - Ethnic Groups KW - Risk Factors KW - Adult KW - Cohort Studies KW - Middle Aged KW - Adolescent KW - United States -- epidemiology KW - Female KW - Male KW - Sexual Behavior -- statistics & numerical data KW - HIV Seroprevalence KW - Substance Abuse, Intravenous -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73261922?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+drug+and+alcohol+abuse&rft.atitle=Age+at+first+injection+and+HIV+risk+among+intravenous+drug+users.&rft.au=Battjes%2C+R+J%3BLeukefeld%2C+C+G%3BPickens%2C+R+W&rft.aulast=Battjes&rft.aufirst=R&rft.date=1992-01-01&rft.volume=18&rft.issue=3&rft.spage=263&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+drug+and+alcohol+abuse&rft.issn=00952990&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-05 N1 - Date created - 1992-11-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Perspective and overview of the concepts and value of hazard identification as the initial phase of risk assessment for cancer and human health. AN - 73258005; 1411384 AB - The identification of potential human health hazards stems from the obvious need to prevent, avoid, reduce, and eliminate exposure to hazardous agents, mixtures of agents, or exposure circumstances. The first step in the risk assessment process centers on determining if a hazard exists. The following strategies are used for this purpose: (i) epidemiologic investigations, (ii) long-term chemical toxicology and carcinogenesis studies on laboratory animals, (ii) shorter-term in vivo and in vitro assays, and (iv) physicochemical structure-activity relationships. Indicator 1 is the most relevant and reliable if adequate data are available; indicator 2 is the most valid and useful alternative for human experience; indicator 3 allows certain toxicologic end points to be identified, but generally needs confirmatory and supportive information; and indicator 4 has made gains in the area of predictivity. The advantages and limitations of each are given. The magnitude of the overall cancer hazard identification effort and a likelihood number of eventual chemical carcinogens have also been estimated. JF - Scandinavian journal of work, environment & health AU - Huff, J AU - Hoel, D AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 83 EP - 89 VL - 18 Suppl 1 SN - 0355-3140, 0355-3140 KW - Hazardous Substances KW - 0 KW - Index Medicus KW - Animals KW - Risk Factors KW - Humans KW - Forecasting KW - Time Factors KW - Public Health KW - Hazardous Substances -- adverse effects KW - Neoplasms -- chemically induced KW - Hazardous Substances -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73258005?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scandinavian+journal+of+work%2C+environment+%26+health&rft.atitle=Perspective+and+overview+of+the+concepts+and+value+of+hazard+identification+as+the+initial+phase+of+risk+assessment+for+cancer+and+human+health.&rft.au=Huff%2C+J%3BHoel%2C+D&rft.aulast=Huff&rft.aufirst=J&rft.date=1992-01-01&rft.volume=18+Suppl+1&rft.issue=&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=Scandinavian+journal+of+work%2C+environment+%26+health&rft.issn=03553140&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-29 N1 - Date created - 1992-10-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Design strategies, results and evaluations of long-term chemical carcinogenesis studies. AN - 73251369; 1411375 AB - Long-term toxicology and chemical carcinogenesis experiments typically involve both sexes of two species of rodents divided randomly into sets of 50-60 animals per control and exposure groups. Ordinarily three exposure concentrations are gradated down from a top level likely to show some chemically associated toxicity, but which should not compromise the normal well-being or growth and survival patterns of the animals unduly. Duration of exposure is generally two years. Single, intermittent, or varied exposures are used to mimic specific occupational or environmental situations. Exposures are started prior to conception, during gestation and lactation, or at specified times thereafter. Extensive gross observations and microscopic pathology are performed on each animal, and incidences of neoplastic and nonneoplastic lesions are evaluated in age-adjusted statistical comparisons. The collated findings are then interpreted, evaluated, and presented for scientific peer review in public meetings, the aim being to identify qualitatively those environmental and occupational exposures that may likely induce cancer in humans. JF - Scandinavian journal of work, environment & health AU - Huff, J AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 31 EP - 37 VL - 18 Suppl 1 SN - 0355-3140, 0355-3140 KW - Carcinogens KW - 0 KW - Index Medicus KW - Rats KW - Animals KW - Mice KW - Time Factors KW - Research Design KW - Male KW - Neoplasms, Experimental -- genetics KW - Carcinogens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73251369?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scandinavian+journal+of+work%2C+environment+%26+health&rft.atitle=Design+strategies%2C+results+and+evaluations+of+long-term+chemical+carcinogenesis+studies.&rft.au=Huff%2C+J&rft.aulast=Huff&rft.aufirst=J&rft.date=1992-01-01&rft.volume=18+Suppl+1&rft.issue=&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=Scandinavian+journal+of+work%2C+environment+%26+health&rft.issn=03553140&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-29 N1 - Date created - 1992-10-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The national impact of alcohol and drug problems and HIV infection and AIDS among the poor and underserved. AN - 73226252; 1391385 JF - Journal of health care for the poor and underserved AU - Millstein, R A AD - National Institute on Drug Abuse, Alcohol, Drug Abuse, and Mental Health Administration, U.S. Department of Health and Human Services, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 21 EP - 9; discussion 30-2 VL - 3 IS - 1 SN - 1049-2089, 1049-2089 KW - Street Drugs KW - 0 KW - Index Medicus KW - AIDS/HIV KW - Demography KW - Risk-Taking KW - Humans KW - Adult KW - Delivery of Health Care KW - Middle Aged KW - United States -- epidemiology KW - Male KW - Female KW - Pregnancy KW - HIV Infections -- transmission KW - Poverty KW - HIV Infections -- prevention & control KW - Substance-Related Disorders -- prevention & control KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73226252?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+health+care+for+the+poor+and+underserved&rft.atitle=The+national+impact+of+alcohol+and+drug+problems+and+HIV+infection+and+AIDS+among+the+poor+and+underserved.&rft.au=Millstein%2C+R+A&rft.aulast=Millstein&rft.aufirst=R&rft.date=1992-01-01&rft.volume=3&rft.issue=1&rft.spage=21&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+care+for+the+poor+and+underserved&rft.issn=10492089&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-12 N1 - Date created - 1992-11-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Early events in the neoplastic transformation of respiratory epithelium. AN - 73217528; 1389694 AB - The complex process of epithelial carcinogenesis is composed of discrete biologic events including the early activation events of "initiation" and "promotion." For lung cancer, these events are only now being elucidated. Despite the identification of possible target genes and their mutations, the "initiation" events for lung cancer remain poorly understood. The identification of these "initiation" events is a crucial step toward the development of practical molecular markers for early detection of this disease. The reversible process of tumor promotion remains somewhat enigmatic but is a promising target for chemoprevention. A wide range of substances, including asbestos and various substances in cigarette smoke, behave as tumor promoters for lung cancer. They appear to promote tumor formation by inducing cellular proliferation mediated in part by growth factors. The intracellular signals these factors provide are ultimately translated into cellular growth via steps involving nuclear transcription factors. Early response genes such as the jun and fos gene family members encode such nuclear transcription factors which are expressed in lung cancer cells and primary bronchial epithelial cells. The expression of these transcription factors is highly responsive to stimulation by growth factors including serum, transforming growth factor, and gastrin-releasing peptide. A more thorough understanding of this process will allow the development of molecular and/or pharmacologic antagonists that can interfere with the biologic process of tumor promotion and therefore function as chemoprevention agents. JF - Journal of the National Cancer Institute. Monographs AU - Birrer, M J AU - Alani, R AU - Cuttitta, F AU - Preis, L H AU - Sabich, A L AU - Sanders, D A AU - Siegfried, J M AU - Szabo, E AU - Brown, P H AD - National Cancer Institute-Navy Medical Oncology Branch, National Naval Medical Center, Bethesda, Md 20895. Y1 - 1992 PY - 1992 DA - 1992 SP - 31 EP - 37 IS - 13 SN - 1052-6773, 1052-6773 KW - Biomarkers, Tumor KW - 0 KW - Carcinogens KW - Proto-Oncogene Proteins c-fos KW - Proto-Oncogene Proteins c-jun KW - Transcription Factors KW - Index Medicus KW - Proto-Oncogene Proteins c-fos -- metabolism KW - Transcription Factors -- metabolism KW - Humans KW - Carcinogens -- toxicity KW - Proto-Oncogene Proteins c-jun -- metabolism KW - Proto-Oncogenes KW - Time Factors KW - Lung Neoplasms -- etiology KW - Cell Transformation, Neoplastic KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73217528?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute.+Monographs&rft.atitle=Early+events+in+the+neoplastic+transformation+of+respiratory+epithelium.&rft.au=Birrer%2C+M+J%3BAlani%2C+R%3BCuttitta%2C+F%3BPreis%2C+L+H%3BSabich%2C+A+L%3BSanders%2C+D+A%3BSiegfried%2C+J+M%3BSzabo%2C+E%3BBrown%2C+P+H&rft.aulast=Birrer&rft.aufirst=M&rft.date=1992-01-01&rft.volume=&rft.issue=13&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute.+Monographs&rft.issn=10526773&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-06 N1 - Date created - 1992-11-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pharmacotherapies for treatment of opioid dependence. AN - 73210721; 1356495 JF - Journal of health care for the poor and underserved AU - Vocci, F J AU - Sorer, H AD - Medications Development Division, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 109 EP - 24; discussion 125-7 VL - 3 IS - 1 SN - 1049-2089, 1049-2089 KW - Analgesics, Opioid KW - 0 KW - Narcotic Antagonists KW - Index Medicus KW - Narcotic Antagonists -- pharmacokinetics KW - Drug Evaluation KW - Animals KW - Narcotic Antagonists -- therapeutic use KW - Humans KW - Analgesics, Opioid -- therapeutic use KW - Analgesics, Opioid -- pharmacokinetics KW - Mice KW - Haplorhini KW - Opioid-Related Disorders -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73210721?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+health+care+for+the+poor+and+underserved&rft.atitle=Pharmacotherapies+for+treatment+of+opioid+dependence.&rft.au=Vocci%2C+F+J%3BSorer%2C+H&rft.aulast=Vocci&rft.aufirst=F&rft.date=1992-01-01&rft.volume=3&rft.issue=1&rft.spage=109&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+care+for+the+poor+and+underserved&rft.issn=10492089&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-12 N1 - Date created - 1992-11-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Rational targets for the early detection of lung cancer. AN - 73204939; 1389692 AB - The fact that routinely effective treatments for disseminated lung cancer are not available has prompted the search for effective early detection systems. It is important to identify lung cancer while it is still confined to the bronchial epithelium and is potentially curable with local modalities. We have previously reported on an immunologically based assay to identify antigens expressed on shed bronchial epithelial cells. This assay resulted in a statistically significant correlation of immunostaining with the eventual development of lung cancer 2-4 years prior to routine clinical detection. Attempts to further improve this approach require an understanding of the basis for its success. Based on the work of Hakomori and coworkers, this difucosylated Lewis X structure would be a likely marker of carcinogenic transformation of the bronchial epithelium. In fact, an antibody to this structure was useful for sputum immunocytochemistry analysis for early lung cancer detection. Other carbohydrate structures would also be reasonable markers to evaluate for early detection application, based on the known pattern of expression of these structures in fetal, dysplastic, and neoplastic lung tissue. Another antibody used for sputum immunostaining recognizes a 31-kd protein structure; the antibody is not a known member of a likely class of early detection targets. The reported cases of lung cancer missed by the immunostaining approach included principally adenocarcinoma of the lung, suggesting that the addition of a marker(s) of that type of morphologic differentiation should be considered. Markers to dissect the various forms of lung adenocarcinoma are being characterized and are available for evaluation in early detection applications.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Journal of the National Cancer Institute. Monographs AU - Mulshine, J L AU - Linnoila, R I AU - Jensen, S M AU - Magnani, J L AU - Tockman, M S AU - Gupta, P K AU - Scott, F S AU - Avis, I AU - Quinn, K AU - Birrer, M J AD - Biomarkers and Prevention Research Branch, National Cancer Institute, Bethesda, Md. Y1 - 1992 PY - 1992 DA - 1992 SP - 183 EP - 190 IS - 13 SN - 1052-6773, 1052-6773 KW - Antigens, Neoplasm KW - 0 KW - Biomarkers, Tumor KW - Growth Substances KW - Index Medicus KW - Oncogenes KW - Cytodiagnosis KW - Humans KW - Neoplasm Metastasis KW - Antigens, Neoplasm -- analysis KW - Growth Substances -- analysis KW - Cell Transformation, Neoplastic KW - Carbohydrate Metabolism KW - Lung Neoplasms -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73204939?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute.+Monographs&rft.atitle=Rational+targets+for+the+early+detection+of+lung+cancer.&rft.au=Mulshine%2C+J+L%3BLinnoila%2C+R+I%3BJensen%2C+S+M%3BMagnani%2C+J+L%3BTockman%2C+M+S%3BGupta%2C+P+K%3BScott%2C+F+S%3BAvis%2C+I%3BQuinn%2C+K%3BBirrer%2C+M+J&rft.aulast=Mulshine&rft.aufirst=J&rft.date=1992-01-01&rft.volume=&rft.issue=13&rft.spage=183&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute.+Monographs&rft.issn=10526773&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-06 N1 - Date created - 1992-11-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alteration of brain catecholamines during growth of benzo(a)pyrene induced murine fibrosarcoma. AN - 73203865; 1528321 AB - Brain catecholamines (CA) were studied in discrete brain areas of benzo(a)pyrene (b(a)p) induced fibrosarcoma bearing mice. Dopamine (DA) and norepinephrine (NE) levels decreased significantly in different brain areas especially in corpus striatum and hypothalamus with the tumor progression, indicating an inverse relationship between brain DA and NE levels and tumor growth. Since impaired hormonal and immunological functions are manifestation of systemic alteration during tumor growth, it appears that during malignant growth an alteration of these brain CA may play an important role in the regulation of systemic alterations. JF - Neoplasma AU - Dasgupta, P S AU - Lahiri, T AD - Department of Endocrinology, Chittaranjan National Cancer Institute (Research Centre), Calcutta, India. Y1 - 1992 PY - 1992 DA - 1992 SP - 163 EP - 165 VL - 39 IS - 3 SN - 0028-2685, 0028-2685 KW - Catecholamines KW - 0 KW - Benzo(a)pyrene KW - 3417WMA06D KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Epinephrine KW - YKH834O4BH KW - Index Medicus KW - Mice, Inbred A KW - Animals KW - Norepinephrine -- metabolism KW - Hypothalamus -- metabolism KW - Corpus Striatum -- metabolism KW - Cell Division -- physiology KW - Dopamine -- metabolism KW - Mice KW - Epinephrine -- metabolism KW - Male KW - Fibrosarcoma -- metabolism KW - Catecholamines -- metabolism KW - Neoplasms, Experimental -- chemically induced KW - Fibrosarcoma -- chemically induced KW - Cell Transformation, Neoplastic -- metabolism KW - Cell Transformation, Neoplastic -- chemically induced KW - Neoplasms, Experimental -- metabolism KW - Brain -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73203865?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neoplasma&rft.atitle=Alteration+of+brain+catecholamines+during+growth+of+benzo%28a%29pyrene+induced+murine+fibrosarcoma.&rft.au=Dasgupta%2C+P+S%3BLahiri%2C+T&rft.aulast=Dasgupta&rft.aufirst=P&rft.date=1992-01-01&rft.volume=39&rft.issue=3&rft.spage=163&rft.isbn=&rft.btitle=&rft.title=Neoplasma&rft.issn=00282685&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-20 N1 - Date created - 1992-10-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular carcinogenesis in humans and rodents. AN - 73201654; 1528915 JF - Progress in clinical and biological research AU - Barrett, J C AU - Wiseman, R W AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 1 EP - 30 VL - 376 SN - 0361-7742, 0361-7742 KW - Index Medicus KW - Animals KW - Risk Factors KW - Humans KW - Confounding Factors (Epidemiology) KW - Aging -- genetics KW - Neoplasms, Experimental -- etiology KW - Neoplasms, Experimental -- genetics KW - Rodentia -- genetics KW - Neoplasms -- genetics KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73201654?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Progress+in+clinical+and+biological+research&rft.atitle=Molecular+carcinogenesis+in+humans+and+rodents.&rft.au=Barrett%2C+J+C%3BWiseman%2C+R+W&rft.aulast=Barrett&rft.aufirst=J&rft.date=1992-01-01&rft.volume=376&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Progress+in+clinical+and+biological+research&rft.issn=03617742&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Suramin in advanced platinum-resistant ovarian cancer. AN - 73198929; 1524910 AB - 10 patients with ovarian cancer, whose disease had progressed while receiving platinum-based therapy, were entered onto a phase II clinical trial of the antiproliferative agent suramin. Suramin was administered in a fashion that is associated with durable objective disease response in patients with hormonally resistant metastatic prostate cancer. No individual had an objective response to therapy in this study, but 3 of 9 evaluable patients (33%) experienced disease stabilisation and subjective clinical improvement for periods ranging from 2 to 5 months. Disease stabilisation was associated with prolonged periods of comparatively high plasma levels of drug, which appeared to be determined primarily by reduced drug clearance. We conclude that suramin has potential activity in platinum-resistant ovarian cancer, and we have initiated a second clinical trial using pharmacological information derived from this study. JF - European journal of cancer (Oxford, England : 1990) AU - Reed, E AU - Cooper, M R AU - LaRocca, R V AU - Bostick-Bruton, F AU - Myers, C E AD - Medicine Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 864 EP - 866 VL - 28A IS - 4-5 SN - 0959-8049, 0959-8049 KW - Suramin KW - 6032D45BEM KW - Carboplatin KW - BG3F62OND5 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Drug Evaluation KW - Humans KW - Adult KW - Drug Resistance KW - Aged KW - Middle Aged KW - Female KW - Suramin -- adverse effects KW - Carboplatin -- pharmacology KW - Cisplatin -- pharmacology KW - Ovarian Neoplasms -- drug therapy KW - Suramin -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73198929?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+cancer+%28Oxford%2C+England+%3A+1990%29&rft.atitle=Suramin+in+advanced+platinum-resistant+ovarian+cancer.&rft.au=Reed%2C+E%3BCooper%2C+M+R%3BLaRocca%2C+R+V%3BBostick-Bruton%2C+F%3BMyers%2C+C+E&rft.aulast=Reed&rft.aufirst=E&rft.date=1992-01-01&rft.volume=28A&rft.issue=4-5&rft.spage=864&rft.isbn=&rft.btitle=&rft.title=European+journal+of+cancer+%28Oxford%2C+England+%3A+1990%29&rft.issn=09598049&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-19 N1 - Date created - 1992-10-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alterations in the biology and biochemistry of keratinocytes induced by the ras oncogene. AN - 73198707; 1528916 JF - Progress in clinical and biological research AU - Yuspa, S H AU - Punnonen, K AU - Lee, E AU - Hennings, H AU - Strickland, J E AU - Cheng, C AU - Glick, A AU - Dlugosz, A AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 103 EP - 115 VL - 376 SN - 0361-7742, 0361-7742 KW - Index Medicus KW - Phenotype KW - Signal Transduction -- physiology KW - Animals KW - Cell Differentiation -- genetics KW - Neoplasms, Experimental -- physiopathology KW - Cell Division -- genetics KW - Keratinocytes -- physiology KW - Keratinocytes -- drug effects KW - Genes, ras -- physiology KW - Keratinocytes -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73198707?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Progress+in+clinical+and+biological+research&rft.atitle=Alterations+in+the+biology+and+biochemistry+of+keratinocytes+induced+by+the+ras+oncogene.&rft.au=Yuspa%2C+S+H%3BPunnonen%2C+K%3BLee%2C+E%3BHennings%2C+H%3BStrickland%2C+J+E%3BCheng%2C+C%3BGlick%2C+A%3BDlugosz%2C+A&rft.aulast=Yuspa&rft.aufirst=S&rft.date=1992-01-01&rft.volume=376&rft.issue=&rft.spage=103&rft.isbn=&rft.btitle=&rft.title=Progress+in+clinical+and+biological+research&rft.issn=03617742&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sequential administration of camptothecin and etoposide circumvents the antagonistic cytotoxicity of simultaneous drug administration in slowly growing human colon carcinoma HT-29 cells. AN - 73198667; 1326304 AB - We compared the cytotoxicity of simultaneous and sequential combination chemotherapy with camptothecin and etoposide, in slowly growing human colon carcinoma, HT-29 cells. Simultaneous treatments of HT-29 cells with etoposide and camptothecin produced no marked enhancement of cytotoxicity over single agent administration. This finding demonstrates antagonism of one drug's cytotoxicity over the other. When these studies were repeated in sequential treatment protocols, we observed that antagonism could be circumvented if the period between individual drug administration was separated by 6-8 h. The cytotoxicity that was observed with this approach was never more than additive and the order of camptothecin or etoposide administration did not significantly affect the extent of combined cytotoxicity observed. The protective effect of simultaneous camptothecin and etoposide exposure was not due to reduced formation or alterations in the rate of cleavable complex reversal, and protection persisted for a considerably longer period of time than DNA strand breaks. Protection correlated with the kinetics of DNA and RNA synthesis inhibition produced by either drug. Remarkably, full cytotoxic protection could be afforded by one drug over the other, in the presence of only partial inhibition of DNA or RNA synthesis (50-60%). Our findings suggest that sequential rather than simultaneous administration of topoisomerase I and II inhibitors in future cancer chemotherapy schedules will enhance cytotoxicity over single-agent administration. JF - European journal of cancer (Oxford, England : 1990) AU - Bertrand, R AU - O'Connor, P M AU - Kerrigan, D AU - Pommier, Y AD - Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 743 EP - 748 VL - 28A IS - 4-5 SN - 0959-8049, 0959-8049 KW - DNA, Neoplasm KW - 0 KW - DNA, Single-Stranded KW - RNA, Neoplasm KW - Topoisomerase I Inhibitors KW - Topoisomerase II Inhibitors KW - Etoposide KW - 6PLQ3CP4P3 KW - Camptothecin KW - XT3Z54Z28A KW - Index Medicus KW - RNA, Neoplasm -- biosynthesis KW - Drug Interactions KW - Drug Administration Schedule KW - DNA, Single-Stranded -- drug effects KW - Tumor Cells, Cultured -- drug effects KW - DNA Damage KW - Kinetics KW - Humans KW - Cell Division -- drug effects KW - DNA, Neoplasm -- biosynthesis KW - Etoposide -- antagonists & inhibitors KW - Camptothecin -- antagonists & inhibitors KW - Etoposide -- administration & dosage KW - Colonic Neoplasms -- drug therapy KW - Colonic Neoplasms -- metabolism KW - Antineoplastic Combined Chemotherapy Protocols -- pharmacology KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage KW - Colonic Neoplasms -- pathology KW - Camptothecin -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73198667?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+cancer+%28Oxford%2C+England+%3A+1990%29&rft.atitle=Sequential+administration+of+camptothecin+and+etoposide+circumvents+the+antagonistic+cytotoxicity+of+simultaneous+drug+administration+in+slowly+growing+human+colon+carcinoma+HT-29+cells.&rft.au=Bertrand%2C+R%3BO%27Connor%2C+P+M%3BKerrigan%2C+D%3BPommier%2C+Y&rft.aulast=Bertrand&rft.aufirst=R&rft.date=1992-01-01&rft.volume=28A&rft.issue=4-5&rft.spage=743&rft.isbn=&rft.btitle=&rft.title=European+journal+of+cancer+%28Oxford%2C+England+%3A+1990%29&rft.issn=09598049&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-19 N1 - Date created - 1992-10-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Oncogenes in mouse liver tumors. AN - 73198450; 1528919 JF - Progress in clinical and biological research AU - Anderson, M AU - Stanley, L AU - Devereux, T AU - Reynolds, S AU - Maronpot, R AD - Laboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 187 EP - 201 VL - 376 SN - 0361-7742, 0361-7742 KW - Carcinogens KW - 0 KW - Index Medicus KW - Animals KW - Proto-Oncogenes -- genetics KW - Gene Expression Regulation, Neoplastic -- physiology KW - Carcinogens -- toxicity KW - Mice KW - Liver Neoplasms, Experimental -- genetics KW - Oncogenes -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73198450?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Progress+in+clinical+and+biological+research&rft.atitle=Oncogenes+in+mouse+liver+tumors.&rft.au=Anderson%2C+M%3BStanley%2C+L%3BDevereux%2C+T%3BReynolds%2C+S%3BMaronpot%2C+R&rft.aulast=Anderson&rft.aufirst=M&rft.date=1992-01-01&rft.volume=376&rft.issue=&rft.spage=187&rft.isbn=&rft.btitle=&rft.title=Progress+in+clinical+and+biological+research&rft.issn=03617742&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Stimulus functions of caffeine in humans: relation to dependence potential. AN - 73188138; 1528521 AB - The interoceptive stimulus functions common to drugs of dependence include positive subjective effects, discriminative functions, and reinforcing functions. Data from studies measuring these stimulus functions constitute the objective assessment of a drug's dependence potential. This paper reviews the subjective effects, discriminative stimulus, and reinforcing stimulus functions of caffeine in humans to assess the dependence potential of caffeine. The stimulus effects of caffeine are compared with those of d-amphetamine, a prototypic CNS stimulant that has been studied under similar conditions, to evaluate the relative dependence potential of caffeine. Finally, caffeine's effects are evaluated in terms of generally accepted criteria for defining drug dependence. It is concluded that caffeine partially meets the primary criteria of drug dependence: 1) the majority of caffeine use is highly controlled, but not compulsive; 2) caffeine is psychoactive; and 3) caffeine functions as a reinforcer under certain conditions in humans, but not in animals. Caffeine thus has limited dependence potential. Additionally, although caffeine shares stimulus functions with d-amphetamine, it does so under limited conditions and should be considered to have a relatively lower dependence potential. JF - Neuroscience and biobehavioral reviews AU - Heishman, S J AU - Henningfield, J E AD - Clinical Pharmacology Branch, National Institute on Drug Abuse, Baltimore, Maryland 21224. Y1 - 1992 PY - 1992 DA - 1992 SP - 273 EP - 287 VL - 16 IS - 3 SN - 0149-7634, 0149-7634 KW - Caffeine KW - 3G6A5W338E KW - Index Medicus KW - Humans KW - Caffeine -- pharmacology KW - Substance-Related Disorders -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73188138?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+and+biobehavioral+reviews&rft.atitle=Stimulus+functions+of+caffeine+in+humans%3A+relation+to+dependence+potential.&rft.au=Heishman%2C+S+J%3BHenningfield%2C+J+E&rft.aulast=Heishman&rft.aufirst=S&rft.date=1992-01-01&rft.volume=16&rft.issue=3&rft.spage=273&rft.isbn=&rft.btitle=&rft.title=Neuroscience+and+biobehavioral+reviews&rft.issn=01497634&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intensive combination chemotherapy (TTL-I protocol) of large cell and immunoblastic lymphomas--long-term observation. AN - 73182780; 1382234 AB - Fifty patients with advanced (Stage III and IV) large cell and immunoblastic lymphoma were treated with eight 4-week courses of chemotherapy. The first two identical A courses were composed of high dose cyclophosphamide, vincristine, 5-day administration of bleomycin, 2-week prednisone, and methotrexate with calcium leucovorin. The next two "B" courses were composed of vincristine, 3-day administration of doxorubicin together with bleomycin, and prednisone. The next two "C" courses were composed of cyclophosphamide, vincristine, bleomycin, prednisone, methotrexate, and calcium leucovorin. The last two "D" courses were the same as "B" courses. CNS prophylaxis was done with intrathecal methotrexate. Fourty-two patients (84%) achieved complete remission, 7 patients entered partial remission, and 1 patient failed to respond. The median survival of all groups was 80 + months (range 2-181 + months). Nine patients relapsed (21%), and seven patients died in complete remission, three of them died of toxicity. The most frequent toxicity was myelosuppression, mostly leukopenia, frequently followed by infection, sometimes severe. Neurotoxicity and stomatitis were frequent, but usually not severe. Two patients developed secondary malignancies. Most of the patients (54%) are alive without evidence of disease at present. JF - Neoplasma AU - Koza, I AU - Mardiak, J AU - Bohunický, L AU - Svancárová, L AU - Fuchsberger, P AU - Gyárfás, J AU - Horák, I AU - Spánik, S AU - Sufliarsky, J AU - Thalmeinerová, Z AD - National Cancer Institute, Bratislava, Czechoslovakia. Y1 - 1992 PY - 1992 DA - 1992 SP - 43 EP - 47 VL - 39 IS - 1 SN - 0028-2685, 0028-2685 KW - Bleomycin KW - 11056-06-7 KW - Vincristine KW - 5J49Q6B70F KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Leucovorin KW - Q573I9DVLP KW - Prednisone KW - VB0R961HZT KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Doxorubicin -- adverse effects KW - Vincristine -- adverse effects KW - Bleomycin -- administration & dosage KW - Humans KW - Leucovorin -- administration & dosage KW - Vincristine -- administration & dosage KW - Aged KW - Leucovorin -- adverse effects KW - Doxorubicin -- administration & dosage KW - Bleomycin -- adverse effects KW - Cyclophosphamide -- adverse effects KW - Prednisone -- adverse effects KW - Methotrexate -- adverse effects KW - Adult KW - Middle Aged KW - Methotrexate -- administration & dosage KW - Prednisone -- administration & dosage KW - Male KW - Female KW - Lymphoma, Large B-Cell, Diffuse -- drug therapy KW - Lymphoma, Large-Cell, Immunoblastic -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73182780?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neoplasma&rft.atitle=Intensive+combination+chemotherapy+%28TTL-I+protocol%29+of+large+cell+and+immunoblastic+lymphomas--long-term+observation.&rft.au=Koza%2C+I%3BMardiak%2C+J%3BBohunick%C3%BD%2C+L%3BSvanc%C3%A1rov%C3%A1%2C+L%3BFuchsberger%2C+P%3BGy%C3%A1rf%C3%A1s%2C+J%3BHor%C3%A1k%2C+I%3BSp%C3%A1nik%2C+S%3BSufliarsky%2C+J%3BThalmeinerov%C3%A1%2C+Z&rft.aulast=Koza&rft.aufirst=I&rft.date=1992-01-01&rft.volume=39&rft.issue=1&rft.spage=43&rft.isbn=&rft.btitle=&rft.title=Neoplasma&rft.issn=00282685&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of prior exposure to cocaine: interaction of reinforcing and suppressant effects. AN - 73178110; 1522757 AB - Squirrel monkeys were trained to respond under second-order schedules of food presentation and then sequentially exposed to either a self-administration (SA) and then a conditioned taste aversion (CTA) procedure, or a CTA procedure and then a SA procedure. Initial exposure to stimuli associated with post-session delivery of cocaine (0.3 mg/kg) either maintained (SA) or suppressed (CTA) responding, respectively. In contrast, following exposure to CTA, SA procedures failed to maintain levels of responding comparable to those seen with initial exposure to SA. Following exposure to SA, the CTA procedure failed to suppress responding. Thus, prior exposure to either the reinforcing or suppressant effects of cocaine modified its subsequent behavioral effects, suggesting a unique role for behavioral history in the abuse potential of cocaine. JF - Life sciences AU - Glowa, J R AU - Williams, A N AD - Biopsychology Unit, CNE, NIMH Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 987 EP - 994 VL - 51 IS - 13 SN - 0024-3205, 0024-3205 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Saimiri KW - Animals KW - Drug Administration Schedule KW - Self Administration KW - Reinforcement Schedule KW - Aversive Therapy KW - Taste KW - Male KW - Behavior, Animal KW - Conditioning (Psychology) KW - Reinforcement (Psychology) KW - Substance-Related Disorders -- psychology KW - Cocaine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73178110?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Life+sciences&rft.atitle=Effects+of+prior+exposure+to+cocaine%3A+interaction+of+reinforcing+and+suppressant+effects.&rft.au=Glowa%2C+J+R%3BWilliams%2C+A+N&rft.aulast=Glowa&rft.aufirst=J&rft.date=1992-01-01&rft.volume=51&rft.issue=13&rft.spage=987&rft.isbn=&rft.btitle=&rft.title=Life+sciences&rft.issn=00243205&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-09 N1 - Date created - 1992-10-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Protooncogene activation in spontaneously occurring and chemically induced rodent and human lung tumors. AN - 73177830; 1528924 JF - Progress in clinical and biological research AU - Reynolds, S H AU - Wiest, J S AU - Devereux, T R AU - Anderson, M W AU - You, M AD - Laboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 303 EP - 320 VL - 376 SN - 0361-7742, 0361-7742 KW - Index Medicus KW - Animals KW - Humans KW - Proto-Oncogenes -- genetics KW - Gene Expression Regulation, Neoplastic -- physiology KW - Lung Neoplasms -- genetics KW - Rodentia -- genetics KW - Lung Neoplasms -- chemically induced KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Proto-Oncogenes -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73177830?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Progress+in+clinical+and+biological+research&rft.atitle=Protooncogene+activation+in+spontaneously+occurring+and+chemically+induced+rodent+and+human+lung+tumors.&rft.au=Reynolds%2C+S+H%3BWiest%2C+J+S%3BDevereux%2C+T+R%3BAnderson%2C+M+W%3BYou%2C+M&rft.aulast=Reynolds&rft.aufirst=S&rft.date=1992-01-01&rft.volume=376&rft.issue=&rft.spage=303&rft.isbn=&rft.btitle=&rft.title=Progress+in+clinical+and+biological+research&rft.issn=03617742&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Does early exposure to maternal smoking affect future fertility in adult males? AN - 73170091; 1521002 AB - Animal data suggest that prenatal exposure to certain tobacco smoke components such as nicotine may affect the development of the male gonadal axis, which may in turn affect future adult fertility. There are no previous epidemiologic studies on the potential effects of early (prenatal and childhood) exposure to maternal smoking on the reproductive system in adult male offspring. To investigate this question, we used data from a follow-up study of reproductive function and fertility among young adult sons of mothers who had participated in a randomized clinical trial of diethylstilbestrol use during pregnancy. We observed no significant effects of early exposure to maternal smoking on conventional semen characteristics, hormone levels (follicle stimulating hormone [FSH], luteinizing hormone [LH] and testosterone), urogenital abnormalities and diseases, or perceived infertility problems. Current active smoking by the men was, however, associated with a significant decrease in the percentage of sperm with normal morphology. JF - Reproductive toxicology (Elmsford, N.Y.) AU - Ratcliffe, J M AU - Gladen, B C AU - Wilcox, A J AU - Herbst, A L AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 297 EP - 307 VL - 6 IS - 4 SN - 0890-6238, 0890-6238 KW - Gonadal Steroid Hormones KW - 0 KW - Testosterone KW - 3XMK78S47O KW - Luteinizing Hormone KW - 9002-67-9 KW - Follicle Stimulating Hormone KW - 9002-68-0 KW - Index Medicus KW - Male Urogenital Diseases KW - Female Urogenital Diseases -- chemically induced KW - Urogenital Abnormalities KW - Humans KW - Testosterone -- blood KW - Semen -- chemistry KW - Adult KW - Luteinizing Hormone -- blood KW - Gonadal Steroid Hormones -- blood KW - Male KW - Follicle Stimulating Hormone -- blood KW - Female KW - Pregnancy KW - Smoking -- adverse effects KW - Fertility -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73170091?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.atitle=Does+early+exposure+to+maternal+smoking+affect+future+fertility+in+adult+males%3F&rft.au=Ratcliffe%2C+J+M%3BGladen%2C+B+C%3BWilcox%2C+A+J%3BHerbst%2C+A+L&rft.aulast=Ratcliffe&rft.aufirst=J&rft.date=1992-01-01&rft.volume=6&rft.issue=4&rft.spage=297&rft.isbn=&rft.btitle=&rft.title=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.issn=08906238&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-14 N1 - Date created - 1992-10-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of radical adduct reduction and reoxidation of the corresponding hydroxylamines in in vivo spin trapping of carbon tetrachloride-derived radicals. AN - 73163974; 1325396 AB - In vivo spin trapping of radical metabolites has become a promising tool in understanding and predicting toxicities caused by different xenobiotics. However, in biological systems radical adducts can be reduced to electron paramagnetic resonance (EPR)-silent hydroxylamines. To overcome this difficulty, different procedures for reoxidation of the reduced radical adducts were systematically investigated and some metabolic inhibitors of nitroxide reduction were tested. As a test system, carbon tetrachloride (CCl4), a known hepatotoxic substance, was used. CCl4 is metabolized by liver to .CCl3 and, in the presence of the spin trap phenyl N-t-butylnitrone (PBN), forms the PBN/.CCl3 and PBN/.CO2- radical adducts. These radical adducts were measured in the bile using electron paramagnetic resonance after administration of CCl4 and PBN to the rat. We have shown that these radical adducts were reduced to the corresponding hydroxylamines in vivo, since immediately after the collection of bile only traces of the radical adducts could be detected, but after oxidation by different procedures such as bubbling with oxygen, addition of mild oxidant potassium ferricyanide or autoxidation the EPR spectra intensity increases, indicating that the hydroxylamines had been re-oxidized back to nitroxides. The collection of bile into plastic Eppendorf tubes containing the sulfhydryl reagent N-ethylmaleimide (NEM) or the enzyme ascorbate oxidase did not increase the intensity of the spectra significantly, demonstrating that neither reduction by reduced glutathione (GSH) nor ascorbic acid occurred ex vivo. However in the presence of NEM faster re-oxidation was observed. A new radical adduct that was not observed previously in any in vivo experiment and which exhibited 13C hyperfine coupling was detected when the rats were injected with 13CCl4. We have proven that this is the same adduct detected previously in vitro in microsomal incubations of CCl4, PBN, GSH, and reduced nicotinamide adenine dinucleotide phosphate (NADPH). As a general rule, we have shown that a variety of oxidation procedures should be tried to detect the different radical adducts which are otherwise not observable due to the in vivo reduction of radical adducts. JF - Free radical biology & medicine AU - Sentjurc, M AU - Mason, R P AD - National Institute of Environmental Health Sciences, National Institutes of Health, Laboratory of Molecular Biophysics, Research Triangle Park, NC 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 151 EP - 160 VL - 13 IS - 2 SN - 0891-5849, 0891-5849 KW - Antimetabolites KW - 0 KW - Cyclic N-Oxides KW - Ferricyanides KW - Free Radicals KW - Hydroxylamines KW - Nitrogen Oxides KW - Spin Labels KW - phenyl-N-tert-butylnitrone KW - 3I91332OPG KW - Carbon Tetrachloride KW - CL2T97X0V0 KW - Glutathione KW - GAN16C9B8O KW - Oxygen KW - S88TT14065 KW - potassium ferricyanide KW - U4MAF9C813 KW - Index Medicus KW - Animals KW - Oxygen -- metabolism KW - Glutathione -- metabolism KW - Bile -- metabolism KW - Free Radicals -- metabolism KW - Hydroxylamines -- metabolism KW - Rats KW - Antimetabolites -- pharmacology KW - Ferricyanides -- pharmacology KW - Oxidation-Reduction KW - Electron Spin Resonance Spectroscopy KW - Male KW - Carbon Tetrachloride -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73163974?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Free+radical+biology+%26+medicine&rft.atitle=Inhibition+of+radical+adduct+reduction+and+reoxidation+of+the+corresponding+hydroxylamines+in+in+vivo+spin+trapping+of+carbon+tetrachloride-derived+radicals.&rft.au=Sentjurc%2C+M%3BMason%2C+R+P&rft.aulast=Sentjurc&rft.aufirst=M&rft.date=1992-01-01&rft.volume=13&rft.issue=2&rft.spage=151&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=08915849&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-02 N1 - Date created - 1992-10-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sulfonic acid dyes: inhibition of the human immunodeficiency virus and mechanism of action. AN - 73156700; 1517963 AB - Over 50 different commercially available sulfonic acid-containing dyes were analyzed for their ability to prevent HIV-1-induced cell killing and in inhibiting HIV-1 replication. Compounds of remarkably similar structure, but with differing patterns of sulfonic acid group substitutions, had a wide range of potency in inhibiting HIV-1. Chicago sky blue (CSB) was highly effective in the inhibition of HIV-1 with less toxicity to CEM-SS cells than most of the other sulfonated dyes tested. Synthesis of CSB was undertaken to produce a product greater than 98% pure and this compound was used to elucidate the possible mechanisms by which this class of structurally related compounds inhibits HIV-1. Addition of CSB to cells infected at high multiplicity at any time up to 24 h after infection, unlike dideoxycytidine (ddC) or oxathiin carboxanilide (OC), inhibited HIV-1-induced cell killing. Other postinfection time course studies revealed that CSB had to be present for 24 h or longer immediately after infection to be protective. Virus binding to cells occurred in the presence of CSB, but the requirement for virion envelope-cell membrane fusion was delayed. CSB was a potent inhibitor of the reverse transcriptase (RT) of both HIV-1 and HIV-2, although it was less active against HIV-2 in a cell killing-based assay. CSB also inhibited Rauscher and LP-BM5 murine leukemia viruses. CSB appears to disrupt the interaction between viral proteins and cell membranes, both in the fusion step early in the infection cycle and in the development of syncytia in the late stages of virus infection. JF - Journal of acquired immune deficiency syndromes AU - Clanton, D J AU - Moran, R A AU - McMahon, J B AU - Weislow, O S AU - Buckheit, R W AU - Hollingshead, M G AU - Ciminale, V AU - Felber, B K AU - Pavlakis, G N AU - Bader, J P AD - Antiviral Evaluation Branch, National Cancer Institute, Bethesda, Maryland. Y1 - 1992 PY - 1992 DA - 1992 SP - 771 EP - 781 VL - 5 IS - 8 SN - 0894-9255, 0894-9255 KW - Antiviral Agents KW - 0 KW - Azo Compounds KW - Coloring Agents KW - Sulfonic Acids KW - Index Medicus KW - AIDS/HIV KW - Molecular Structure KW - Giant Cells -- microbiology KW - Virus Replication -- drug effects KW - Humans KW - Azo Compounds -- pharmacology KW - Cell Line KW - Coloring Agents -- pharmacology KW - Antiviral Agents -- pharmacology KW - Antiviral Agents -- chemistry KW - Coloring Agents -- chemistry KW - HIV-1 -- physiology KW - HIV-1 -- drug effects KW - Sulfonic Acids -- chemistry KW - Sulfonic Acids -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73156700?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+acquired+immune+deficiency+syndromes&rft.atitle=Sulfonic+acid+dyes%3A+inhibition+of+the+human+immunodeficiency+virus+and+mechanism+of+action.&rft.au=Clanton%2C+D+J%3BMoran%2C+R+A%3BMcMahon%2C+J+B%3BWeislow%2C+O+S%3BBuckheit%2C+R+W%3BHollingshead%2C+M+G%3BCiminale%2C+V%3BFelber%2C+B+K%3BPavlakis%2C+G+N%3BBader%2C+J+P&rft.aulast=Clanton&rft.aufirst=D&rft.date=1992-01-01&rft.volume=5&rft.issue=8&rft.spage=771&rft.isbn=&rft.btitle=&rft.title=Journal+of+acquired+immune+deficiency+syndromes&rft.issn=08949255&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-08 N1 - Date created - 1992-10-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Neurotoxicology of PCBs and related compounds. AN - 73145284; 1508429 AB - Polychlorinated biphenyls (PCBs) are a family of 209 chemicals with two linked phenyl rings and variable chlorination. They are clear oils at room temperature. They were produced from the 1930s until banned in the 1970s because of toxicity and evidence of widespread environmental contamination. They were used mostly as insulators in electrical equipment; their widespread occurrence in the environment is more a consequence of uncontrolled disposal than of deliberate dissemination. In Asia, there have been two outbreaks of poisoning due to cooking oil contaminated by thermally degraded PCBs. Studies in workers exposed chronically to "clean" PCBs, workers exposed acutely to thermally degraded PCBs in clean-up of fires, and adult patients in Asia who ingested contaminated rice oil consistently show slowed nerve conduction and sometimes show headache, lassitude, and other CNS symptoms. In children exposed to background levels in the US, those with the highest transplacental exposure show hypotonia and hyporeflexia at birth and slowed motor development through age two, a defect in visual memory processing at 7 mon, and defects in short term memory at 4 years. Despite the presence of PCBs in breast milk, no association between breast milk exposure and any measured outcome has been seen other than lower activity levels at 4 years among long term breast fed children at the highest PCB levels. In Asia, children who were in utero at or after the 1968 exposure in Japan or the 1979 exposure in Taiwan showed clinically evident developmental delay. In Taiwan, the children were shown to have a variety of ectodermal defects, but the association between these defects and developmental delay was weak.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Neurotoxicology AU - Rogan, W J AU - Gladen, B C AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 27 EP - 35 VL - 13 IS - 1 SN - 0161-813X, 0161-813X KW - Polychlorinated Biphenyls KW - DFC2HB4I0K KW - Index Medicus KW - Humans KW - Occupational Diseases -- chemically induced KW - Polychlorinated Biphenyls -- toxicity KW - Nervous System -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73145284?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurotoxicology&rft.atitle=Neurotoxicology+of+PCBs+and+related+compounds.&rft.au=Rogan%2C+W+J%3BGladen%2C+B+C&rft.aulast=Rogan&rft.aufirst=W&rft.date=1992-01-01&rft.volume=13&rft.issue=1&rft.spage=27&rft.isbn=&rft.btitle=&rft.title=Neurotoxicology&rft.issn=0161813X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-22 N1 - Date created - 1992-09-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The basic neurobiology of addiction. AN - 73135141; 1501690 AB - This overview on cocaine's addiction liability is presented in this monograph on the blood-brain barrier (BBB) because the National Institute on Drug Abuse has been given the task of finding pharmacotherapies to treat addiction. Knowledge about the BBB might help researchers design better drugs or approaches to keep the "good" drugs inside and/or the "bad" drugs outside. It is to be hoped that the BBB community can be convinced that drug abuse is an exciting area and that work on biological barriers has something to offer. JF - NIDA research monograph AU - Brown, R M AD - Neuroscience Branch, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 4 EP - 12 VL - 120 SN - 1046-9516, 1046-9516 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Reward KW - Humans KW - Brain -- drug effects KW - Blood-Brain Barrier KW - Substance-Related Disorders -- etiology KW - Cocaine -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73135141?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=The+basic+neurobiology+of+addiction.&rft.au=Brown%2C+R+M&rft.aulast=Brown&rft.aufirst=R&rft.date=1992-01-01&rft.volume=120&rft.issue=&rft.spage=4&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-17 N1 - Date created - 1992-09-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Relationship of diagnostic, demographic, and personality variables to self-reported stimuli for chemical use. AN - 73126018; 1502969 AB - While extensive research has been conducted to determine internal and external stimuli for drinking by alcoholics, the topic of how demographic, diagnostic, and personality variables may relate to these precipitants is largely unexplored. This study suggests that stimuli to use alcohol or drugs differ partly as a function of diagnosis (alcohol dependence vs. concurrent alcohol and drug dependence). Age, education, and gender do not appear related to the stimuli in either diagnostic group. Personality characteristics of cognitive reflectiveness, impulse control, sociability, and intrapunitiveness, however, seem to be associated with certain classes of high risk stimuli. JF - Addictive behaviors AU - Allen, J P AU - Faden, V AU - Rawlings, R AD - Treatment Research Branch, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 359 EP - 366 VL - 17 IS - 4 SN - 0306-4603, 0306-4603 KW - Index Medicus KW - Age Factors KW - Educational Status KW - Sex Factors KW - Behavior, Addictive -- etiology KW - Humans KW - Behavior, Addictive -- psychology KW - Personality Inventory KW - Behavior, Addictive -- diagnosis KW - Psychiatric Status Rating Scales KW - Risk Factors KW - Adult KW - Female KW - Male KW - Substance-Related Disorders -- diagnosis KW - Alcoholism -- etiology KW - Alcoholism -- diagnosis KW - Substance-Related Disorders -- etiology KW - Personality KW - Substance-Related Disorders -- psychology KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73126018?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Addictive+behaviors&rft.atitle=Relationship+of+diagnostic%2C+demographic%2C+and+personality+variables+to+self-reported+stimuli+for+chemical+use.&rft.au=Allen%2C+J+P%3BFaden%2C+V%3BRawlings%2C+R&rft.aulast=Allen&rft.aufirst=J&rft.date=1992-01-01&rft.volume=17&rft.issue=4&rft.spage=359&rft.isbn=&rft.btitle=&rft.title=Addictive+behaviors&rft.issn=03064603&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-16 N1 - Date created - 1992-09-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Recombinant toxins as novel therapeutic agents. AN - 73124162; 1497314 JF - Annual review of biochemistry AU - Pastan, I AU - Chaudhary, V AU - FitzGerald, D J AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20829. Y1 - 1992 PY - 1992 DA - 1992 SP - 331 EP - 354 VL - 61 SN - 0066-4154, 0066-4154 KW - Diphtheria Toxin KW - 0 KW - Exotoxins KW - Immunotoxins KW - Recombinant Proteins KW - Toxins, Biological KW - Ricin KW - 9009-86-3 KW - Index Medicus KW - Animals KW - Ricin -- therapeutic use KW - Immunotoxins -- therapeutic use KW - Diphtheria Toxin -- therapeutic use KW - Pseudomonas KW - Neoplasms, Experimental -- drug therapy KW - Exotoxins -- therapeutic use KW - Recombinant Proteins -- therapeutic use KW - Toxins, Biological -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73124162?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annual+review+of+biochemistry&rft.atitle=Recombinant+toxins+as+novel+therapeutic+agents.&rft.au=Pastan%2C+I%3BChaudhary%2C+V%3BFitzGerald%2C+D+J&rft.aulast=Pastan&rft.aufirst=I&rft.date=1992-01-01&rft.volume=61&rft.issue=&rft.spage=331&rft.isbn=&rft.btitle=&rft.title=Annual+review+of+biochemistry&rft.issn=00664154&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-08 N1 - Date created - 1992-09-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Relationship between the expression of differentiation-specific keratins 1 and 10 and cell proliferation in epidermal tumors. AN - 73123195; 1380247 AB - In normal epidermis, the expression of keratins 1 and 10 is associated with the loss of proliferative capacity and the onset of terminal differentiation. Keratins 1 (K1) and 10 (K10) are commonly expressed in the differentiating layer of benign tumors, but are lost during progression from the benign to the malignant state in skin carcinogenesis. Active gene constructs of mouse K1 and K10 were introduced into papilloma and carcinoma cell lines derived from keratinocytes to analyze the consequences of the expression of these keratins on the organization of the endogenous cytoskeletal network and on the mitotic activity of the recipient cells. Exogenous K1 integrated into the preexisting keratin K5/K14 network of both SLC-1 carcinoma and 308 papilloma cells. The formation of a recombinant cytoskeleton was more restricted for K10 than for K1 and appeared to be related to a requirement for cessation of cell division before K10 could integrate. The integration of exogenous K1 filaments into the endogenous keratin network was compatible with sustained proliferation of SLC-1 carcinoma cells in vitro. However, the exogenous gene was not expressed in tumor grafts in vivo. In contrast, stable K1 or K10 transfectants could not be selected in 308 cells, suggesting that benign tumor cells expressing suprabasal keratins cannot sustain proliferation. JF - Molecular carcinogenesis AU - Kartasova, T AU - Roop, D R AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 18 EP - 25 VL - 6 IS - 1 SN - 0899-1987, 0899-1987 KW - RNA, Neoplasm KW - 0 KW - Keratins KW - 68238-35-7 KW - Index Medicus KW - Animals KW - Blotting, Northern KW - Papilloma -- pathology KW - Carcinoma, Squamous Cell -- metabolism KW - Mice KW - RNA, Neoplasm -- analysis KW - Papilloma -- genetics KW - Mice, Inbred BALB C KW - Neoplasm Transplantation KW - Blotting, Western KW - Transfection KW - Carcinoma, Squamous Cell -- pathology KW - Carcinoma, Squamous Cell -- genetics KW - Cytoskeleton -- pathology KW - Papilloma -- metabolism KW - Cell Line KW - Cell Division KW - Skin Neoplasms -- genetics KW - Keratins -- metabolism KW - Skin Neoplasms -- pathology KW - Skin Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73123195?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Relationship+between+the+expression+of+differentiation-specific+keratins+1+and+10+and+cell+proliferation+in+epidermal+tumors.&rft.au=Kartasova%2C+T%3BRoop%2C+D+R%3BYuspa%2C+S+H&rft.aulast=Kartasova&rft.aufirst=T&rft.date=1992-01-01&rft.volume=6&rft.issue=1&rft.spage=18&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-24 N1 - Date created - 1992-09-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Monoaminergic actions of ECT. AN - 73122909; 1498997 JF - Clinical neuropharmacology AU - Rudorfer, M V AU - Manji, H K AU - Potter, W Z AD - Section on Clinical Pharmacology, National Institute of Mental Health, Bethesda, MD. Y1 - 1992 PY - 1992 DA - 1992 SP - 677A EP - 678A VL - 15 Suppl 1 Pt A SN - 0362-5664, 0362-5664 KW - Antidepressive Agents KW - 0 KW - Biogenic Monoamines KW - Index Medicus KW - Rats KW - Animals KW - Humans KW - Antidepressive Agents -- therapeutic use KW - Antidepressive Agents -- adverse effects KW - Biogenic Monoamines -- cerebrospinal fluid KW - Biogenic Monoamines -- blood KW - Biogenic Monoamines -- physiology KW - Mood Disorders -- therapy KW - Mood Disorders -- physiopathology KW - Electroconvulsive Therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73122909?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+neuropharmacology&rft.atitle=Monoaminergic+actions+of+ECT.&rft.au=Rudorfer%2C+M+V%3BManji%2C+H+K%3BPotter%2C+W+Z&rft.aulast=Rudorfer&rft.aufirst=M&rft.date=1992-01-01&rft.volume=15+Suppl+1+Pt+A&rft.issue=&rft.spage=677A&rft.isbn=&rft.btitle=&rft.title=Clinical+neuropharmacology&rft.issn=03625664&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-14 N1 - Date created - 1992-09-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transcripts encoding protein kinase C-alpha, -delta, -epsilon, -zeta, and -eta are expressed in basal and differentiating mouse keratinocytes in vitro and exhibit quantitative changes in neoplastic cells. AN - 73109858; 1379814 AB - The protein kinase C (PKC) family of phospholipid-dependent serine-threonine kinases has been implicated in keratinocyte differentiation and neoplastic transformation. To determine if Ca(2+)-mediated keratinocyte differentiation is associated with changes in PKC isozyme gene expression, RNA was isolated from primary mouse keratinocytes grown in medium with 0.05, 0.12, or 1.4 mM Ca2+. Based on northern blot analysis, primary keratinocytes expressed mRNA encoding PKC-alpha, -delta, -epsilon, -zeta, and -eta, but not PKC-beta or -gamma. Relatively little change was detected in the level of these transcripts in cells induced to differentiate by exposure to elevated extracellular Ca2+. Interestingly, the PKC-zeta transcripts detected in RNA isolated from keratinocytes were approximately 200 nucleotides longer than those from mouse brain, suggesting the existence of an alternative form of this isozyme. An early change in benign neoplastic transformation of keratinocytes is the inability to differentiate in response to Ca2+ or the PKC activator 12-O-tetradecanoylphorbol-13-acetate, which is consistent with altered PKC function in these cells. The PKC isozyme mRNA profile was examined in two benign neoplastic keratinocyte cell lines, 308 and SP-1, which contain an activating mutation of the c-Ha-ras gene. Like normal keratinocytes. 308 and SP-1 cells expressed mRNA encoding PKC-alpha, -delta, -epsilon, -zeta, and -eta. However, the abundance of PKC-zeta transcripts in both cell lines was reduced by 74-89% when compared with normal keratinocytes at similar Ca2+ levels. In addition, SP-1 but not 308 cells exhibited a sevenfold increase in PKC-eta mRNA when cultured in medium with 1.4 mM Ca2+. To address whether these changes were related to the presence of an activated ras gene, RNA was isolated from primary keratinocytes transduced to a benign neoplastic phenotype with the v-Ha-ras oncogene. As with normal, 308, and SP-1 cells, v-Ha-ras keratinocytes expressed mRNA encoding PKC-alpha, -delta, -epsilon, -zeta and -eta. The level of PKC-zeta transcripts was similar in normal and v-Ha-ras keratinocytes, indicating that reduction of this mRNA in both 308 and SP-1 cells was not a direct result of ras activation. As in SP-1 cells, PKC-eta in v-Ha-ras keratinocytes was responsive to extracellular Ca2+, with a four-fold increase in transcript abundance in 0.12 mM Ca2+ medium relative to 0.05 mM Ca2+ medium.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Molecular carcinogenesis AU - Dlugosz, A A AU - Mischak, H AU - Mushinski, J F AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 286 EP - 292 VL - 5 IS - 4 SN - 0899-1987, 0899-1987 KW - v-Ha-ras KW - Isoenzymes KW - 0 KW - RNA, Messenger KW - Poly A KW - 24937-83-5 KW - RNA KW - 63231-63-0 KW - Protein Kinases KW - EC 2.7.- KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Poly A -- isolation & purification KW - Animals KW - Blotting, Northern KW - Humans KW - Cell Differentiation KW - Calcium -- pharmacology KW - Mice KW - RNA, Messenger -- genetics KW - Gene Expression Regulation, Neoplastic KW - Animals, Newborn KW - Gene Expression Regulation, Enzymologic KW - Tumor Cells, Cultured KW - RNA, Messenger -- metabolism KW - Cells, Cultured KW - RNA -- isolation & purification KW - Poly A -- genetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - RNA, Messenger -- isolation & purification KW - RNA -- genetics KW - Genes, ras KW - Keratinocytes -- enzymology KW - Protein Kinases -- genetics KW - Keratinocytes -- cytology KW - Transcription, Genetic KW - Isoenzymes -- genetics KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73109858?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Transcripts+encoding+protein+kinase+C-alpha%2C+-delta%2C+-epsilon%2C+-zeta%2C+and+-eta+are+expressed+in+basal+and+differentiating+mouse+keratinocytes+in+vitro+and+exhibit+quantitative+changes+in+neoplastic+cells.&rft.au=Dlugosz%2C+A+A%3BMischak%2C+H%3BMushinski%2C+J+F%3BYuspa%2C+S+H&rft.aulast=Dlugosz&rft.aufirst=A&rft.date=1992-01-01&rft.volume=5&rft.issue=4&rft.spage=286&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-11 N1 - Date created - 1992-09-11 N1 - Date revised - 2017-01-13 N1 - Gene symbol - v-Ha-ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - p53 gene mutations in human endometrial carcinoma. AN - 73109822; 1497800 AB - Although carcinoma of the uterine endometrium is the most frequently diagnosed malignancy of the female reproductive tract, the molecular genetic features of this tumor have yet to be described in significant detail. Since mutations of the p53 tumor suppressor gene are the single most common genetic alteration found in human malignancies, we examined the hypothesis that p53 mutations occur in human endometrial carcinoma. Sequencing analysis of exons 5-8 revealed point mutations in 3 of 21 (14%) tumors; one mutation was an unusual single-base insertion at codons 176-177, resulting in a premature stop codon, whereas the other two were CGG----TGG transitions at codon 248. Two of these tumors showed reduction to homozygosity at the p53 allele, but one tumor apparently retained heterozygosity. These data indicate that p53 mutations occur in human endometrial carcinoma, although relatively infrequently, and that loss of the normal p53 allele does not necessarily occur with point mutation of the p53 gene in this tumor type. JF - Molecular carcinogenesis AU - Risinger, J I AU - Dent, G A AU - Ignar-Trowbridge, D AU - McLachlan, J A AU - Tsao, M S AU - Senterman, M AU - Boyd, J AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 250 EP - 253 VL - 5 IS - 4 SN - 0899-1987, 0899-1987 KW - p53 KW - Codon KW - 0 KW - DNA, Neoplasm KW - Index Medicus KW - Polymerase Chain Reaction KW - Reference Values KW - Chromosome Deletion KW - Base Sequence KW - Alleles KW - Codon -- genetics KW - Exons KW - Humans KW - Molecular Sequence Data KW - DNA, Neoplasm -- genetics KW - DNA, Neoplasm -- isolation & purification KW - Female KW - Genes, p53 KW - Endometrial Neoplasms -- pathology KW - Endometrial Neoplasms -- genetics KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73109822?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=p53+gene+mutations+in+human+endometrial+carcinoma.&rft.au=Risinger%2C+J+I%3BDent%2C+G+A%3BIgnar-Trowbridge%2C+D%3BMcLachlan%2C+J+A%3BTsao%2C+M+S%3BSenterman%2C+M%3BBoyd%2C+J&rft.aulast=Risinger&rft.aufirst=J&rft.date=1992-01-01&rft.volume=5&rft.issue=4&rft.spage=250&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-11 N1 - Date created - 1992-09-11 N1 - Date revised - 2017-01-13 N1 - Gene symbol - p53 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The use of pharmacogenetic techniques in drug abuse research. AN - 73108916; 1641407 AB - Pharmacogenetics, the study of genetic factors underlying individual differences in response to drugs, has proven useful for demonstrating that there are large genetic differences in response to a number of abused drugs. Pharmacogenetics also provides a number of useful tools for studying mechanisms underlying the effects of drugs. This review discusses pharmacogenetic techniques with potential utility for drug abuse research and provides examples of their use in studies of the effects of acute and chronic nicotine, cocaine and opiate administration. The importance of using genetically standardized animal models in behavioral and pharmacological research is also discussed. JF - Pharmacology & therapeutics AU - Marley, R J AU - Elmer, G I AU - Goldberg, S R AD - National Institute on Drug Abuse, Addiction Research Center, Baltimore, MD 21224. Y1 - 1992 PY - 1992 DA - 1992 SP - 217 EP - 237 VL - 53 IS - 2 SN - 0163-7258, 0163-7258 KW - Narcotics KW - 0 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Behavior, Animal -- drug effects KW - Animals KW - Kindling, Neurologic -- drug effects KW - Humans KW - Research KW - Species Specificity KW - Pharmacogenetics -- methods KW - Substance-Related Disorders -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73108916?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology+%26+therapeutics&rft.atitle=The+use+of+pharmacogenetic+techniques+in+drug+abuse+research.&rft.au=Marley%2C+R+J%3BElmer%2C+G+I%3BGoldberg%2C+S+R&rft.aulast=Marley&rft.aufirst=R&rft.date=1992-01-01&rft.volume=53&rft.issue=2&rft.spage=217&rft.isbn=&rft.btitle=&rft.title=Pharmacology+%26+therapeutics&rft.issn=01637258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-03 N1 - Date created - 1992-09-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Possible role of free radical formation in drug-induced agranulocytosis. AN - 73106561; 1503677 AB - The use of clozapine, a unique antipsychotic drug, has been restricted due to a 1 to 2% incidence of drug-induced agranulocytosis. Many other drugs, including paracetamol (acetaminophen), can cause agranulocytosis, although with a much lower incidence. Metabolic activation of these drugs by neutrophils or stem cells could be the molecular mechanism underlying this adverse effect. Drug oxidation by myeloperoxidase leads to free radical metabolite formation; these reactive free radicals can oxidise glutathione to a thiyl free radical, which in the presence of oxygen forms oxygen-derived free radicals. In contrast to glutathione, when these free radical metabolites oxidise ascorbate an unreactive free radical is formed, which does not even react with oxygen. In both reactions, the free radical metabolite is reduced to the original drug, although ascorbate is the more effective reducing agent. Thus ascorbate, when coadministered with agranulocytosis-causing drugs, may inhibit free radical chain reactions and other free radical-mediated reactions, such as protein adduct formation, and thereby prevent drug-induced agranulocytosis. JF - Drug safety AU - Mason, R P AU - Fischer, V AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina. Y1 - 1992 PY - 1992 DA - 1992 SP - 45 EP - 50 VL - 7 Suppl 1 SN - 0114-5916, 0114-5916 KW - Free Radicals KW - 0 KW - Pharmaceutical Preparations KW - Peroxidases KW - EC 1.11.1.- KW - Clozapine KW - J60AR2IKIC KW - Index Medicus KW - Oxidation-Reduction KW - Pharmaceutical Preparations -- metabolism KW - Peroxidases -- physiology KW - Humans KW - Clozapine -- metabolism KW - Clozapine -- adverse effects KW - Drug-Related Side Effects and Adverse Reactions KW - Agranulocytosis -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73106561?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+safety&rft.atitle=Possible+role+of+free+radical+formation+in+drug-induced+agranulocytosis.&rft.au=Mason%2C+R+P%3BFischer%2C+V&rft.aulast=Mason&rft.aufirst=R&rft.date=1992-01-01&rft.volume=7+Suppl+1&rft.issue=&rft.spage=45&rft.isbn=&rft.btitle=&rft.title=Drug+safety&rft.issn=01145916&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-23 N1 - Date created - 1992-09-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Progressive slowing of reaction time and increasing cerebrospinal fluid concentrations of quinolinic acid in HIV-infected individuals. AN - 73099570; 1386770 AB - Neuropsychological functioning and cerebrospinal fluid concentrations of an endogenous neurotoxin, quinolinic acid (QUIN) were evaluated in 52 HIV-positive individuals (71% without constitutional symptoms) and 33 HIV-seronegative controls (including 15 psychiatric patients with adjustment disorders). Although the HIV-positive subjects did not differ from controls on standard neuropsychological tests, simple and choice reactions times (RT) were slow at initial evaluation (P less than 0.01) and became progressively slower at 6-month re-evaluation (P less than 0.05). Cerebrospinal fluid (CSF) QUIN was elevated at initial evaluation and increased during the 6-month interval (P less than 0.05). Moreover, during this 6-month interval, progressive slowing of RT was highly correlated with increasing levels of CSF QUIN (r = 0.85, df = 15, P less than 0.0001) but not with changes in mood, constitutional symptoms, or CD4 cell count. These findings suggest that RT may provide a sensitive behavioral measure of relatively early central nervous system involvement in HIV-infected individuals and that QUIN may play an important role in the pathogenesis of HIV-related neurological dysfunction. JF - The Journal of neuropsychiatry and clinical neurosciences AU - Martin, A AU - Heyes, M P AU - Salazar, A M AU - Kampen, D L AU - Williams, J AU - Law, W A AU - Coats, M E AU - Markey, S P AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 270 EP - 279 VL - 4 IS - 3 SN - 0895-0172, 0895-0172 KW - Neurotoxins KW - 0 KW - Quinolinic Acids KW - Quinolinic Acid KW - F6F0HK1URN KW - Index Medicus KW - AIDS/HIV KW - HIV Seropositivity -- psychology KW - Anxiety Disorders -- psychology KW - Depressive Disorder -- psychology KW - Anxiety Disorders -- diagnosis KW - Humans KW - Neurologic Examination KW - Depressive Disorder -- cerebrospinal fluid KW - Leukocyte Count KW - HIV Seropositivity -- diagnosis KW - Adult KW - Anxiety Disorders -- cerebrospinal fluid KW - Depressive Disorder -- diagnosis KW - HIV Seropositivity -- cerebrospinal fluid KW - Neuropsychological Tests KW - Male KW - Female KW - AIDS Dementia Complex -- diagnosis KW - AIDS Dementia Complex -- cerebrospinal fluid KW - Neurotoxins -- cerebrospinal fluid KW - Quinolinic Acids -- cerebrospinal fluid KW - Reaction Time -- physiology KW - AIDS Dementia Complex -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73099570?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+neuropsychiatry+and+clinical+neurosciences&rft.atitle=Progressive+slowing+of+reaction+time+and+increasing+cerebrospinal+fluid+concentrations+of+quinolinic+acid+in+HIV-infected+individuals.&rft.au=Martin%2C+A%3BHeyes%2C+M+P%3BSalazar%2C+A+M%3BKampen%2C+D+L%3BWilliams%2C+J%3BLaw%2C+W+A%3BCoats%2C+M+E%3BMarkey%2C+S+P&rft.aulast=Martin&rft.aufirst=A&rft.date=1992-01-01&rft.volume=4&rft.issue=3&rft.spage=270&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+neuropsychiatry+and+clinical+neurosciences&rft.issn=08950172&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-16 N1 - Date created - 1992-09-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The psychobiology of dysphoric mania. AN - 73097842; 1498976 JF - Clinical neuropharmacology AU - Post, R M AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, MD. Y1 - 1992 PY - 1992 DA - 1992 SP - 624A EP - 625A VL - 15 Suppl 1 Pt A SN - 0362-5664, 0362-5664 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Humans KW - Bipolar Disorder -- psychology KW - Bipolar Disorder -- metabolism KW - Bipolar Disorder -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73097842?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+neuropharmacology&rft.atitle=The+psychobiology+of+dysphoric+mania.&rft.au=Post%2C+R+M&rft.aulast=Post&rft.aufirst=R&rft.date=1992-01-01&rft.volume=15+Suppl+1+Pt+A&rft.issue=&rft.spage=624A&rft.isbn=&rft.btitle=&rft.title=Clinical+neuropharmacology&rft.issn=03625664&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-14 N1 - Date created - 1992-09-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of the Syrian hamster c-Ha-ras gene and intron-D-exon transcript. AN - 73094937; 1497801 AB - The coding sequences as well as 5'- and 3'-flanking sequences of the Syrian hamster c-Ha-ras gene were deduced from cDNA clones derived from embryo fibroblast cell lines. Sequences of introns B, C, and D were obtained from genomic DNA after amplification by the polymerase chain reaction. Sequence comparisons with rat, mouse, and human c-Ha-ras genes revealed a high degree of homology. One of 12 cDNA clones contained intron-D-exon (IDX) sequences due to alternative splicing that would encode a p19 Ha-ras gene product. Conservation between species suggests a functional role for the IDX, possibly as a negative control of p21 Ha-ras expression. JF - Molecular carcinogenesis AU - Ebert, R AU - Wiseman, R W AU - Barrett, J C AU - Reiss, E AU - Rollich, G AU - Schiffmann, D AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 254 EP - 258 VL - 5 IS - 4 SN - 0899-1987, 0899-1987 KW - c-Ha-ras KW - DNA KW - 9007-49-2 KW - HRAS protein, human KW - EC 3.6.5.2 KW - Proto-Oncogene Proteins p21(ras) KW - Index Medicus KW - Animals KW - Sequence Homology, Nucleic Acid KW - Humans KW - Amino Acid Sequence KW - Cloning, Molecular KW - DNA -- isolation & purification KW - Base Sequence KW - DNA -- genetics KW - Molecular Sequence Data KW - Mesocricetus KW - Cell Line, Transformed KW - Cell Line KW - Proto-Oncogene Proteins p21(ras) -- genetics KW - Cricetinae KW - Genes, ras KW - Exons KW - Introns KW - Transcription, Genetic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73094937?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Characterization+of+the+Syrian+hamster+c-Ha-ras+gene+and+intron-D-exon+transcript.&rft.au=Ebert%2C+R%3BWiseman%2C+R+W%3BBarrett%2C+J+C%3BReiss%2C+E%3BRollich%2C+G%3BSchiffmann%2C+D&rft.aulast=Ebert&rft.aufirst=R&rft.date=1992-01-01&rft.volume=5&rft.issue=4&rft.spage=254&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-11 N1 - Date created - 1992-09-11 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-Ha-ras N1 - Genetic sequence - M84166; GENBANK; J00277 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Substance abuse treatment services: an introduction. AN - 73089427; 10171033 JF - Journal of mental health administration AU - Lowman, C AD - National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 1 EP - 4 VL - 19 IS - 1 SN - 0092-8623, 0092-8623 KW - Health administration KW - United States KW - Humans KW - Cost-Benefit Analysis KW - Financing, Organized -- methods KW - Substance Abuse Treatment Centers -- organization & administration KW - Substance Abuse Treatment Centers -- trends KW - Management Information Systems -- trends KW - Substance-Related Disorders -- economics KW - Substance Abuse Treatment Centers -- economics KW - Substance-Related Disorders -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73089427?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+mental+health+administration&rft.atitle=Substance+abuse+treatment+services%3A+an+introduction.&rft.au=Lowman%2C+C&rft.aulast=Lowman&rft.aufirst=C&rft.date=1992-01-01&rft.volume=19&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Journal+of+mental+health+administration&rft.issn=00928623&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-21 N1 - Date created - 1992-08-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Xenobiotic metabolism by prostaglandin H synthase. AN - 73088277; 1641409 AB - During the metabolism of arachidonic acid by prostaglandin H synthase many chemicals including carcinogens are metabolized. These chemicals are metabolized by either the peroxidase activity of prostaglandin H synthase, the peroxyl radicals generated during arachidonic acid oxygenation, or a combination of these two mechanisms. In many cases, the chemical metabolism results in the formation of reactive metabolites that have mutagenic activity and potential carcinogenic activity. In other cases, the chemicals are detoxified. Chemical metabolism that occurs during arachidonic acid oxygenation may be an important determinate of chemical toxicity in extra-hepatic tissues. JF - Pharmacology & therapeutics AU - Eling, T E AU - Curtis, J F AD - Eicosanoid Biochemistry Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 261 EP - 273 VL - 53 IS - 2 SN - 0163-7258, 0163-7258 KW - Mutagens KW - 0 KW - Arachidonic Acid KW - 27YG812J1I KW - Prostaglandin-Endoperoxide Synthases KW - EC 1.14.99.1 KW - Index Medicus KW - Oxidation-Reduction KW - Animals KW - Inactivation, Metabolic KW - Mutagens -- metabolism KW - Humans KW - Prostaglandin-Endoperoxide Synthases -- physiology KW - Prostaglandin-Endoperoxide Synthases -- metabolism KW - Arachidonic Acid -- pharmacokinetics KW - Arachidonic Acid -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73088277?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology+%26+therapeutics&rft.atitle=Xenobiotic+metabolism+by+prostaglandin+H+synthase.&rft.au=Eling%2C+T+E%3BCurtis%2C+J+F&rft.aulast=Eling&rft.aufirst=T&rft.date=1992-01-01&rft.volume=53&rft.issue=2&rft.spage=261&rft.isbn=&rft.btitle=&rft.title=Pharmacology+%26+therapeutics&rft.issn=01637258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-03 N1 - Date created - 1992-09-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Generation of chimeric toxins. AN - 73085340; 1633306 JF - Targeted diagnosis and therapy AU - FitzGerald, D AU - Chaudhary, V K AU - Kreitman, R J AU - Siegall, C B AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1992 PY - 1992 DA - 1992 SP - 447 EP - 462 VL - 7 SN - 1046-1906, 1046-1906 KW - Antiviral Agents KW - 0 KW - Immunotoxins KW - Interleukin-6 KW - Receptors, Interleukin-2 KW - Recombinant Fusion Proteins KW - Transforming Growth Factor alpha KW - Index Medicus KW - Animals KW - Transforming Growth Factor alpha -- therapeutic use KW - Interleukin-6 -- therapeutic use KW - Humans KW - Antiviral Agents -- pharmacology KW - Recombinant Fusion Proteins -- genetics KW - Recombinant Fusion Proteins -- toxicity KW - Recombinant Fusion Proteins -- therapeutic use KW - Cell Line KW - Receptors, Interleukin-2 -- drug effects KW - Cloning, Molecular KW - Immunotoxins -- toxicity KW - Immunotoxins -- therapeutic use KW - Immunotoxins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73085340?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Targeted+diagnosis+and+therapy&rft.atitle=Generation+of+chimeric+toxins.&rft.au=FitzGerald%2C+D%3BChaudhary%2C+V+K%3BKreitman%2C+R+J%3BSiegall%2C+C+B%3BPastan%2C+I&rft.aulast=FitzGerald&rft.aufirst=D&rft.date=1992-01-01&rft.volume=7&rft.issue=&rft.spage=447&rft.isbn=&rft.btitle=&rft.title=Targeted+diagnosis+and+therapy&rft.issn=10461906&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-21 N1 - Date created - 1992-08-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interactions of HPV E6 and E7 oncoproteins with tumour suppressor gene products. AN - 73084642; 1322242 AB - The HPVs associated with anogenital cancers encode two oncoproteins, E6 and E7. Both E6 and E7 can form specific complexes with tumour suppressor gene products. The E7 protein binds to the retinoblastoma tumour suppressor gene product pRB, with a preference for the underphosphorylated, "active" form of pRB. The E7 proteins derived from the "high risk" HPVs bind to pRB with a higher affinity than the E7 proteins from the "low risk" HPVs. The "high risk" HPV E6 proteins can associate with the p53 tumour suppressor protein. This interaction promotes the degradation of p53 in vitro, which presumably accounts for the very low levels of p53 in cervical carcinoma cell lines. The functional inactivation of pRB and p53 by the HPV oncoproteins E7 and E6, respectively, are likely to be important steps in cervical carcinogenesis, since mutations in the RB and p53 genes were detected in HPV negative but not HPV positive cervical carcinoma cell lines. Cytogenetic studies strongly suggest, however, that additional chromosomal changes may be necessary for carcinogenic progression of HPV induced anogenital lesions. JF - Cancer surveys AU - Münger, K AU - Scheffner, M AU - Huibregtse, J M AU - Howley, P M AD - Laboratory of Tumour Virus Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 197 EP - 217 VL - 12 SN - 0261-2429, 0261-2429 KW - DNA, Viral KW - 0 KW - DNA-Binding Proteins KW - E6 protein, Human papillomavirus type 18 KW - E7 protein, Human papillomavirus type 18 KW - Oncogene Proteins, Viral KW - Retinoblastoma Protein KW - Tumor Suppressor Protein p53 KW - Index Medicus KW - Humans KW - Uterine Cervical Neoplasms -- genetics KW - DNA, Viral -- genetics KW - Transcriptional Activation KW - Female KW - Oncogene Proteins, Viral -- chemistry KW - Tumor Virus Infections -- genetics KW - Retinoblastoma Protein -- metabolism KW - Papillomaviridae -- genetics KW - Oncogene Proteins, Viral -- physiology KW - Tumor Suppressor Protein p53 -- metabolism KW - Oncogene Proteins, Viral -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73084642?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+surveys&rft.atitle=Interactions+of+HPV+E6+and+E7+oncoproteins+with+tumour+suppressor+gene+products.&rft.au=M%C3%BCnger%2C+K%3BScheffner%2C+M%3BHuibregtse%2C+J+M%3BHowley%2C+P+M&rft.aulast=M%C3%BCnger&rft.aufirst=K&rft.date=1992-01-01&rft.volume=12&rft.issue=&rft.spage=197&rft.isbn=&rft.btitle=&rft.title=Cancer+surveys&rft.issn=02612429&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-01 N1 - Date created - 1992-09-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The structure of diphtheria toxin as a guide to rational design. AN - 73076099; 1633298 JF - Targeted diagnosis and therapy AU - Nicholls, P J AU - Youle, R J AD - National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland. Y1 - 1992 PY - 1992 DA - 1992 SP - 339 EP - 363 VL - 7 SN - 1046-1906, 1046-1906 KW - tox KW - Diphtheria Toxin KW - 0 KW - Index Medicus KW - Genes, Bacterial KW - Corynebacterium diphtheriae -- genetics KW - Drug Design KW - Structure-Activity Relationship KW - Diphtheria Toxin -- chemistry KW - Diphtheria Toxin -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73076099?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Targeted+diagnosis+and+therapy&rft.atitle=The+structure+of+diphtheria+toxin+as+a+guide+to+rational+design.&rft.au=Nicholls%2C+P+J%3BYoule%2C+R+J&rft.aulast=Nicholls&rft.aufirst=P&rft.date=1992-01-01&rft.volume=7&rft.issue=&rft.spage=339&rft.isbn=&rft.btitle=&rft.title=Targeted+diagnosis+and+therapy&rft.issn=10461906&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-21 N1 - Date created - 1992-08-21 N1 - Date revised - 2017-01-13 N1 - Gene symbol - tox N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Regional cerebral glucose utilization in chronic organic mental disorders associated with alcoholism. AN - 73071834; 1627977 AB - Localized cerebral utilization rates for glucose (CMRglu) were determined in 10 detoxified patients with alcoholic organic mental disorders and in 7 age-equivalent normal volunteers using [18F]2-fluoro-2-deoxyglucose positron emission tomography. Although gray and white matter CMRglu were not significantly different, normalized CMRglu was increased in the left cerebellar and parietal cortical regions and decreased in the right posterior white matter and anterior temporal regions of alcoholic patients, and the pattern of regional CMRglu differed between the two groups. The results suggest functional disruption of right-sided and frontal brain regions and hyperactivity of cerebellar-cortical connections in alcoholic chronic organic mental disorders. JF - The Journal of neuropsychiatry and clinical neurosciences AU - Martin, P R AU - Rio, D AU - Adinoff, B AU - Johnson, J L AU - Bisserbe, J C AU - Rawlings, R R AU - Rohrbaugh, J W AU - Stapleton, J M AU - Eckardt, M J AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland. Y1 - 1992 PY - 1992 DA - 1992 SP - 159 EP - 167 VL - 4 IS - 2 SN - 0895-0172, 0895-0172 KW - Blood Glucose KW - 0 KW - Fluorodeoxyglucose F18 KW - 0Z5B2CJX4D KW - Deoxyglucose KW - 9G2MP84A8W KW - Index Medicus KW - Dominance, Cerebral -- physiology KW - Humans KW - Aged KW - Alcohol Amnestic Disorder -- diagnostic imaging KW - Wernicke Encephalopathy -- diagnostic imaging KW - Cerebral Cortex -- diagnostic imaging KW - Brain Mapping KW - Dementia -- diagnostic imaging KW - Deoxyglucose -- analogs & derivatives KW - Middle Aged KW - Male KW - Deoxyglucose -- metabolism KW - Blood Glucose -- metabolism KW - Alcoholism -- diagnostic imaging KW - Tomography, Emission-Computed KW - Substance-Related Disorders -- diagnostic imaging KW - Brain -- diagnostic imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73071834?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+neuropsychiatry+and+clinical+neurosciences&rft.atitle=Regional+cerebral+glucose+utilization+in+chronic+organic+mental+disorders+associated+with+alcoholism.&rft.au=Martin%2C+P+R%3BRio%2C+D%3BAdinoff%2C+B%3BJohnson%2C+J+L%3BBisserbe%2C+J+C%3BRawlings%2C+R+R%3BRohrbaugh%2C+J+W%3BStapleton%2C+J+M%3BEckardt%2C+M+J&rft.aulast=Martin&rft.aufirst=P&rft.date=1992-01-01&rft.volume=4&rft.issue=2&rft.spage=159&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+neuropsychiatry+and+clinical+neurosciences&rft.issn=08950172&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-18 N1 - Date created - 1992-08-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Renal cell cancer among architects and allied professionals in Sweden. AN - 73057665; 1621695 AB - The Swedish Cancer-Environment Registry was used to evaluate a recent report of a large excess risk of renal cell cancer among architects in Los Angeles. We identified 131 renal cell cancers among male Swedish architects and allied professionals during a 19-year follow-up period (1961-1979). Compared with the Swedish population, there was no significant excess of renal cell cancer among architects and allied professionals (standardized incidence ratio (SIR) = 1.15; 131 cases). Although it was not possible to estimate the risk for architects alone, the SIR was only 1.06 (16 cases) in a subset of professionals employed in architectural and engineering firms. However, a significant increase in risk (SIR = 1.38) was observed in a related group of workers employed as engineers and construction supervisors in the home construction industry. JF - American journal of industrial medicine AU - McLaughlin, J K AU - Malker, H S AU - Blot, W J AU - Weiner, J A AU - Stone, B J AU - Ericsson, J L AU - Fraumeni, J F AD - National Cancer Institute, Division of Cancer Etiology, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 873 EP - 876 VL - 21 IS - 6 SN - 0271-3586, 0271-3586 KW - Index Medicus KW - Risk Factors KW - Humans KW - Sweden -- epidemiology KW - Incidence KW - Male KW - Housing KW - Occupational Diseases -- epidemiology KW - Kidney Neoplasms -- epidemiology KW - Architecture as Topic KW - Carcinoma, Renal Cell -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73057665?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+industrial+medicine&rft.atitle=Renal+cell+cancer+among+architects+and+allied+professionals+in+Sweden.&rft.au=McLaughlin%2C+J+K%3BMalker%2C+H+S%3BBlot%2C+W+J%3BWeiner%2C+J+A%3BStone%2C+B+J%3BEricsson%2C+J+L%3BFraumeni%2C+J+F&rft.aulast=McLaughlin&rft.aufirst=J&rft.date=1992-01-01&rft.volume=21&rft.issue=6&rft.spage=873&rft.isbn=&rft.btitle=&rft.title=American+journal+of+industrial+medicine&rft.issn=02713586&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-03 N1 - Date created - 1992-08-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of the effector functions of cytolytic T-lymphocytes with synthetic peptide inhibitors of protein kinases. AN - 73055139; 1619567 AB - The hypothesis was tested that it is possible to influence cellular responses of intact cells using synthetic peptide substrates, pseudosubstrates, and inhibitors of protein kinases. Using cytotoxic T-cells (CTL), we demonstrate here that some basic amino acid-containing synthetic peptide substrates of protein kinases [e.g., of cGMP-dependent protein kinase (peptide PKG-S), synthetic peptide inhibitor of cGMP-dependent protein kinase (peptide PKG-I), and peptide corresponding to the tyrosine phosphorylation site in pp60src (peptide RR-src)] were strongly inhibitory in T-cell receptor (TCR) and T-cell growth factor, interleukin 2 (IL-2)-triggered proliferation of CTL. These peptides also inhibited other cellular responses of CTL. Peptides which contain basic amino acids, but do not have substrate specificity determinants for protein kinase, were not inhibitory. The inhibition with peptides is not due to their toxicity, since no cell death was observed by the trypan blue exclusion test and by lactate dehydrogenase release. Use of the granule exocytosis assay provided opportunities to clarify the mechanism of the peptide action. Tested peptides inhibited not only cell-surface ligand-induced CTL activation, but also affected cell-surface receptor-independent CTL activation (granule exocytosis and gamma-interferon secretion) induced by the synergistic action of the protein kinase C activator (PMA) and ionophore A23187. It was found that minor changes in amino acid composition or amino acid position in the synthetic peptides dramatically change their ability to affect lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Journal of pharmaceutical sciences AU - Taffs, R E AU - Sitkovsky, M V AD - Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 37 EP - 44 VL - 81 IS - 1 SN - 0022-3549, 0022-3549 KW - Interleukin-2 KW - 0 KW - Oligopeptides KW - Peptides KW - Protein Kinase Inhibitors KW - protein kinase inhibitor peptide KW - 128022-93-5 KW - Interferon-gamma KW - 82115-62-6 KW - Index Medicus KW - Lymphocyte Activation -- drug effects KW - Interleukin-2 -- pharmacology KW - Animals KW - Interferon-gamma -- secretion KW - Molecular Sequence Data KW - Cell Division -- drug effects KW - Enzyme-Linked Immunosorbent Assay KW - Mice KW - Amino Acid Sequence KW - Cell Degranulation -- drug effects KW - T-Lymphocytes, Cytotoxic -- physiology KW - Oligopeptides -- chemistry KW - Oligopeptides -- metabolism KW - T-Lymphocytes, Cytotoxic -- immunology KW - Oligopeptides -- pharmacology KW - Peptides -- pharmacology KW - T-Lymphocytes, Cytotoxic -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73055139?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+pharmaceutical+sciences&rft.atitle=Modulation+of+the+effector+functions+of+cytolytic+T-lymphocytes+with+synthetic+peptide+inhibitors+of+protein+kinases.&rft.au=Taffs%2C+R+E%3BSitkovsky%2C+M+V&rft.aulast=Taffs&rft.aufirst=R&rft.date=1992-01-01&rft.volume=81&rft.issue=1&rft.spage=37&rft.isbn=&rft.btitle=&rft.title=Journal+of+pharmaceutical+sciences&rft.issn=00223549&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-06 N1 - Date created - 1992-08-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanisms of human carcinogens. AN - 73050924; 1620716 AB - Mutational mechanisms can be proposed as contributing to the activity of most human carcinogens. Many of these chemicals are electrophilic or are metabolically activated to reactive molecules that can alter DNA. Even human carcinogens that do not exhibit direct chemical interaction with DNA, e.g., hormones and asbestos, have been shown to induce genetic effects when in vitro assays for chromosomal mutations are employed. Since these chemicals are usually inactive in the Salmonella assay and other gene mutational assays, more emphasis has been placed on their nonmutational mechanisms. Evidence exists that these carcinogens alter gene expression and stimulate cell proliferation by epigenetic mechanisms; such properties almost certainly contribute to the carcinogenic activity of these chemicals. Although less well studied, DNA reactive, genotoxic carcinogens also alter gene expression and cell proliferation by epigenetic mechanisms. These findings are consistent with the current understanding of the molecular basis of multistep carcinogenesis. The neoplastic evolution of most common human cancers occurs as the result of multiple mutational events. The molecular basis for these mutations is varied and includes point mutations, deletion mutations, chromosome rearrangements, gene amplification, and chromosome losses and gains. Therefore, different mutational activities of carcinogens may influence the carcinogenic process at different steps. In addition, chemical influences on gene expression and cell proliferation are important in allowing clonal expansion of preneoplastic cells and in disrupting the suppressive effects of surrounding normal cells on preneoplastic cells (Dotto et al., 1988). Therefore, the mechanisms of action of human carcinogens, and very likely many rodent carcinogens, will include both genetic and epigenetic processes. JF - Progress in clinical and biological research AU - Barrett, J C AU - Shelby, M D AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 415 EP - 434 VL - 374 SN - 0361-7742, 0361-7742 KW - Carcinogens KW - 0 KW - Index Medicus KW - Animals KW - Mutagenicity Tests KW - Genes, Tumor Suppressor KW - Humans KW - Carcinogenicity Tests KW - Proto-Oncogenes KW - Carcinogens -- pharmacology KW - Neoplasms, Experimental -- chemically induced KW - Neoplasms -- chemically induced KW - Carcinogens -- toxicity KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73050924?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Progress+in+clinical+and+biological+research&rft.atitle=Mechanisms+of+human+carcinogens.&rft.au=Barrett%2C+J+C%3BShelby%2C+M+D&rft.aulast=Barrett&rft.aufirst=J&rft.date=1992-01-01&rft.volume=374&rft.issue=&rft.spage=415&rft.isbn=&rft.btitle=&rft.title=Progress+in+clinical+and+biological+research&rft.issn=03617742&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-04 N1 - Date created - 1992-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The challenge of drug abuse treatment in prisons and jails. AN - 73049617; 1620215 JF - NIDA research monograph AU - Tims, F M AU - Leukefeld, C G AD - Division of Clinical Research, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 1 EP - 7 VL - 118 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - Humans KW - Prisons KW - Substance-Related Disorders -- rehabilitation KW - Substance-Related Disorders -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73049617?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=The+challenge+of+drug+abuse+treatment+in+prisons+and+jails.&rft.au=Tims%2C+F+M%3BLeukefeld%2C+C+G&rft.aulast=Tims&rft.aufirst=F&rft.date=1992-01-01&rft.volume=118&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-06 N1 - Date created - 1992-08-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Enhancement of cholera toxin-catalyzed ADP-ribosylation by guanine nucleotide-binding proteins. AN - 73046506; 1321019 JF - Current topics in microbiology and immunology AU - Serventi, I M AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 43 EP - 67 VL - 175 SN - 0070-217X, 0070-217X KW - ARF KW - ARF1 KW - ARF2 KW - ARF5 KW - ARF6 KW - ARFs1 KW - ARFs2 KW - ARFs3 KW - ARFs4 KW - CPS1 KW - hARF1 KW - hARF6 KW - mARF KW - sARF KW - yARF KW - yARF1 KW - Bacterial Toxins KW - 0 KW - Enterotoxins KW - Escherichia coli Proteins KW - heat-labile enterotoxin, E coli KW - NAD KW - 0U46U6E8UK KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Cholera Toxin KW - 9012-63-9 KW - Cyclic AMP KW - E0399OZS9N KW - Poly(ADP-ribose) Polymerases KW - EC 2.4.2.30 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - ADP-Ribosylation Factors KW - EC 3.6.5.2 KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Index Medicus KW - Animals KW - Enterotoxins -- metabolism KW - Sequence Homology, Nucleic Acid KW - Humans KW - Adenylyl Cyclases -- metabolism KW - Intestinal Mucosa -- metabolism KW - Amino Acid Sequence KW - Mammals -- genetics KW - Stimulation, Chemical KW - Saccharomyces cerevisiae -- genetics KW - NAD -- metabolism KW - Bacterial Toxins -- metabolism KW - Second Messenger Systems -- drug effects KW - Molecular Sequence Data KW - Carbohydrate Sequence KW - Cyclic AMP -- metabolism KW - Consensus Sequence KW - Species Specificity KW - GTP-Binding Proteins -- metabolism KW - Cholera Toxin -- pharmacology KW - Adenosine Diphosphate Ribose -- metabolism KW - Poly(ADP-ribose) Polymerases -- metabolism KW - GTP-Binding Proteins -- genetics KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73046506?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+topics+in+microbiology+and+immunology&rft.atitle=Enhancement+of+cholera+toxin-catalyzed+ADP-ribosylation+by+guanine+nucleotide-binding+proteins.&rft.au=Serventi%2C+I+M%3BMoss%2C+J%3BVaughan%2C+M&rft.aulast=Serventi&rft.aufirst=I&rft.date=1992-01-01&rft.volume=175&rft.issue=&rft.spage=43&rft.isbn=&rft.btitle=&rft.title=Current+topics+in+microbiology+and+immunology&rft.issn=0070217X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-18 N1 - Date created - 1992-08-18 N1 - Date revised - 2017-01-13 N1 - Gene symbol - ARF; ARF1; ARF2; ARF5; ARF6; ARFs1; ARFs2; ARFs3; ARFs4; CPS1; hARF1; hARF6; mARF; sARF; yARF; yARF1 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lung cancer induction by crystalline silica. AN - 73043938; 1320275 JF - Progress in clinical and biological research AU - Saffiotti, U AD - Laboratory of Experimental Pathology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 51 EP - 69 VL - 374 SN - 0361-7742, 0361-7742 KW - Dust KW - 0 KW - Silicon Dioxide KW - 7631-86-9 KW - Index Medicus KW - Animals KW - Carcinoma -- etiology KW - Humans KW - Mice KW - Mice, Nude KW - Mice, Inbred BALB C KW - Neoplasms, Experimental -- pathology KW - Rats, Inbred Strains KW - Rats KW - Mice, Inbred A KW - Risk Factors KW - Adenoma -- etiology KW - Female KW - Male KW - Lung Neoplasms -- etiology KW - Silicosis -- complications KW - Silicon Dioxide -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73043938?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Progress+in+clinical+and+biological+research&rft.atitle=Lung+cancer+induction+by+crystalline+silica.&rft.au=Saffiotti%2C+U&rft.aulast=Saffiotti&rft.aufirst=U&rft.date=1992-01-01&rft.volume=374&rft.issue=&rft.spage=51&rft.isbn=&rft.btitle=&rft.title=Progress+in+clinical+and+biological+research&rft.issn=03617742&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-04 N1 - Date created - 1992-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Rational design of a chimeric toxin: an intramolecular location for the insertion of transforming growth factor alpha within Pseudomonas exotoxin as a targeting ligand. AN - 73043377; 1616950 AB - To investigate the potential utility of Pseudomonas exotoxin (PE) in forming rationally designed chemotherapeutic agents, we inserted a cDNA encoding transforming growth factor alpha (TGF alpha) at several locations in a gene encoding a mutant full-length PE (PE4E) which does not bind to the PE receptor. After expression in Escherichia coli, we purified the chimeric toxins to near homogeneity and showed that they were specifically cytotoxic to human epidermoid, ovarian, colon, and hepatocellular carcinoma lines. Like the previously reported TGF alpha-PE40, one of the new molecules (TGF alpha-PE4E) contains the ligand at the amino terminus. Two additional chimeras (PE4E-TGF alpha and PE4E-TGF alpha-598-613) each contain TGF alpha inserted near the carboxyl terminus of PE. We show that preservation of the correct PE carboxyl-terminal amino acid sequence, REDLK, allows the toxins containing TGF alpha carboxyl inserts to retain significant cytotoxicity against target cells, since another molecule (PE4E-TGF alpha-ILK) containing a nonfunctional carboxyl-terminal sequence was over 100-fold less active. The chimeric toxins with TGF alpha had the same binding affinity for the EGF receptor whether the ligand occupied the amino or carboxyl position. Molecules with TGF alpha near the carboxyl position were consistently less active against target cells but also less toxic to mice than those with TGF alpha at the amino terminus, indicating both types of molecules might be therapeutically effective. Our results establish that a ligand can be placed near the carboxyl terminus of PE, within the portion of the toxin that translocates to the cytosol. The amino-terminal position in such molecules is then available for the placement of other targeting ligands. JF - Bioconjugate chemistry AU - Kreitman, R J AU - Chaudhary, V K AU - Siegall, C B AU - FitzGerald, D J AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 58 EP - 62 VL - 3 IS - 1 SN - 1043-1802, 1043-1802 KW - Exotoxins KW - 0 KW - Immunotoxins KW - Recombinant Fusion Proteins KW - Transforming Growth Factor alpha KW - transforming growth factor type alpha-Pseudomonas exotoxin A KW - Index Medicus KW - Animals KW - Humans KW - Amino Acid Sequence KW - Mice KW - Mice, Nude KW - Recombinant Fusion Proteins -- toxicity KW - Mice, Inbred BALB C KW - Drug Design KW - Recombinant Fusion Proteins -- chemistry KW - Binding Sites KW - Base Sequence KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - Molecular Sequence Data KW - Lethal Dose 50 KW - Female KW - Immunotoxins -- chemistry KW - Transforming Growth Factor alpha -- toxicity KW - Immunotoxins -- toxicity KW - Exotoxins -- toxicity KW - Exotoxins -- chemistry KW - Transforming Growth Factor alpha -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73043377?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioconjugate+chemistry&rft.atitle=Rational+design+of+a+chimeric+toxin%3A+an+intramolecular+location+for+the+insertion+of+transforming+growth+factor+alpha+within+Pseudomonas+exotoxin+as+a+targeting+ligand.&rft.au=Kreitman%2C+R+J%3BChaudhary%2C+V+K%3BSiegall%2C+C+B%3BFitzGerald%2C+D+J%3BPastan%2C+I&rft.aulast=Kreitman&rft.aufirst=R&rft.date=1992-01-01&rft.volume=3&rft.issue=1&rft.spage=58&rft.isbn=&rft.btitle=&rft.title=Bioconjugate+chemistry&rft.issn=10431802&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-05 N1 - Date created - 1992-08-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Methodological issues: drug abuse treatment research in prisons and jails. AN - 73042632; 1620221 JF - NIDA research monograph AU - Fletcher, B W AU - Tims, F M AD - Treatment Research Branch, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 246 EP - 260 VL - 118 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - Humans KW - Research Design KW - Substance-Related Disorders -- therapy KW - Prisons KW - Substance-Related Disorders -- rehabilitation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73042632?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Methodological+issues%3A+drug+abuse+treatment+research+in+prisons+and+jails.&rft.au=Fletcher%2C+B+W%3BTims%2C+F+M&rft.aulast=Fletcher&rft.aufirst=B&rft.date=1992-01-01&rft.volume=118&rft.issue=&rft.spage=246&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-06 N1 - Date created - 1992-08-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Program models. AN - 73040760; 1620224 JF - NIDA research monograph AU - Brown, B S AD - Division of Applied Research, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 31 EP - 37 VL - 118 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - Humans KW - Prisons KW - Substance-Related Disorders -- rehabilitation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73040760?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Program+models.&rft.au=Brown%2C+B+S&rft.aulast=Brown&rft.aufirst=B&rft.date=1992-01-01&rft.volume=118&rft.issue=&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-06 N1 - Date created - 1992-08-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phenobarbital and related compounds: approaches to interspecies extrapolation. AN - 73037952; 1620706 JF - Progress in clinical and biological research AU - Rice, J M AU - Diwan, B A AU - Ward, J M AU - Nims, R W AU - Lubet, R A AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, Maryland. Y1 - 1992 PY - 1992 DA - 1992 SP - 231 EP - 249 VL - 374 SN - 0361-7742, 0361-7742 KW - Barbiturates KW - 0 KW - Carcinogens KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Animals KW - Liver -- pathology KW - Liver -- drug effects KW - Humans KW - Enzyme Induction KW - Species Specificity KW - Liver Neoplasms, Experimental -- pathology KW - Carcinogens -- toxicity KW - Liver Neoplasms, Experimental -- chemically induced KW - Phenobarbital -- toxicity KW - Barbiturates -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73037952?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Progress+in+clinical+and+biological+research&rft.atitle=Phenobarbital+and+related+compounds%3A+approaches+to+interspecies+extrapolation.&rft.au=Rice%2C+J+M%3BDiwan%2C+B+A%3BWard%2C+J+M%3BNims%2C+R+W%3BLubet%2C+R+A&rft.aulast=Rice&rft.aufirst=J&rft.date=1992-01-01&rft.volume=374&rft.issue=&rft.spage=231&rft.isbn=&rft.btitle=&rft.title=Progress+in+clinical+and+biological+research&rft.issn=03617742&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-04 N1 - Date created - 1992-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment of cocaine dependence in methadone maintenance clients: a pilot study comparing the efficacy of desipramine and amantadine. AN - 73037740; 1319961 AB - We conducted a pilot study (N = 22) comparing the efficacy of desipramine and amantadine for treatment of cocaine dependence in methadone maintenance clients. The study which lasted 12 weeks, was double-blind, randomly assigned, and placebo-controlled. Subjects met DSM-III-R criteria for active cocaine dependence. All three groups' cocaine use, craving, and depressive symptoms declined significantly, but intergroup differences were not significant. Clients receiving desipramine were significantly more likely to remain in treatment and to be cocaine free at study completion. The results emphasize the importance of delivering comprehensive services to the cocaine user in methadone treatment. Further evaluations of these two medications as adjuncts in the treatment of cocaine dependence are needed. JF - The International journal of the addictions AU - Kolar, A F AU - Brown, B S AU - Weddington, W W AU - Haertzen, C C AU - Michaelson, B S AU - Jaffe, J H AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland. Y1 - 1992 PY - 1992 DA - 1992 SP - 849 EP - 868 VL - 27 IS - 7 SN - 0020-773X, 0020-773X KW - Placebos KW - 0 KW - Amantadine KW - BF4C9Z1J53 KW - Cocaine KW - I5Y540LHVR KW - Desipramine KW - TG537D343B KW - Methadone KW - UC6VBE7V1Z KW - Index Medicus KW - United States KW - Baltimore KW - Substance Abuse Treatment Centers KW - Substance Withdrawal Syndrome -- prevention & control KW - Humans KW - Adult KW - Pilot Projects KW - Middle Aged KW - Follow-Up Studies KW - Adolescent KW - Research Design KW - Male KW - Female KW - Amantadine -- administration & dosage KW - Methadone -- therapeutic use KW - Opioid-Related Disorders -- complications KW - Desipramine -- therapeutic use KW - Amantadine -- therapeutic use KW - Desipramine -- administration & dosage KW - Substance-Related Disorders -- drug therapy KW - Opioid-Related Disorders -- rehabilitation KW - Substance-Related Disorders -- complications KW - Substance-Related Disorders -- rehabilitation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73037740?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+International+journal+of+the+addictions&rft.atitle=Treatment+of+cocaine+dependence+in+methadone+maintenance+clients%3A+a+pilot+study+comparing+the+efficacy+of+desipramine+and+amantadine.&rft.au=Kolar%2C+A+F%3BBrown%2C+B+S%3BWeddington%2C+W+W%3BHaertzen%2C+C+C%3BMichaelson%2C+B+S%3BJaffe%2C+J+H&rft.aulast=Kolar&rft.aufirst=A&rft.date=1992-01-01&rft.volume=27&rft.issue=7&rft.spage=849&rft.isbn=&rft.btitle=&rft.title=The+International+journal+of+the+addictions&rft.issn=0020773X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-31 N1 - Date created - 1992-07-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Trends in illicit drug use in the United States: conflicting results from national surveys. AN - 73037689; 1618584 AB - Data from several national studies lead to divergent conclusions regarding trends in illicit drug use in the United States. Two major population studies point to a downturn in drug use dating to the late 1970s. However, a study of drug-related deaths and hospital emergency room visits shows increases in these events in recent years. Studies also show drug use, especially cocaine, continuing to increase among criminals. Additionally, drugs were identified as the most important problem facing the nation in a Gallup poll conducted during the summer of 1989. This paper offers some possible explanations for the divergent trends. Most notably, we suggest that methodological differences in the studies being compared, and lags between trends in the general population and certain subgroups, account for most of the variation in the trend estimates. The paper concludes that illicit drug use is decreasing in the United States. JF - The International journal of the addictions AU - Harrison, L D AD - National Institute on Drug Abuse, Rockville, Maryland 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 817 EP - 847 VL - 27 IS - 7 SN - 0020-773X, 0020-773X KW - Street Drugs KW - 0 KW - Index Medicus KW - Age Factors KW - Culture KW - Epidemiologic Methods KW - Humans KW - Prisoners -- psychology KW - Research Design KW - Smoking KW - Schools KW - Adult KW - Middle Aged KW - Adolescent KW - United States -- epidemiology KW - Female KW - Male KW - Prevalence KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73037689?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+International+journal+of+the+addictions&rft.atitle=Trends+in+illicit+drug+use+in+the+United+States%3A+conflicting+results+from+national+surveys.&rft.au=Harrison%2C+L+D&rft.aulast=Harrison&rft.aufirst=L&rft.date=1992-01-01&rft.volume=27&rft.issue=7&rft.spage=817&rft.isbn=&rft.btitle=&rft.title=The+International+journal+of+the+addictions&rft.issn=0020773X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-31 N1 - Date created - 1992-07-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Properties of chimeric toxins with two recognition domains: interleukin 6 and transforming growth factor alpha at different locations in Pseudomonas exotoxin. AN - 73037002; 1616951 AB - Pseudomonas exotoxin (PE) is a potent cytotoxic agent that is composed of 613 amino acids arranged into three major domains. We have previously identified two positions where ligands can successfully be placed in PE to direct it to cells with specific surface receptors. One site is at the amino terminus and the other is close to but not at the C-terminus. To examine the possibility of constructing oncotoxins with two different recognition elements that will bind to two different receptors, we have placed cDNAs encoding either transforming growth factor alpha (TGF alpha) or interleukin 6 (IL6) at the 5' end of a PE gene and also inserted a cDNA encoding TGF alpha near the 3' end of the PE gene. The plasmids encoding these chimeric toxins were expressed in Escherichia coli and the chimeric proteins purified to near homogeneity. In all the new toxins, the TGF alpha near the C-terminus was inserted after amino acid 607 of PE and followed by amino acids 604-613 so that the correct PE C-terminus (REDLK) was preserved. For each chimera, the toxin portion was either PE4E, in which the cell binding domain (domain Ia) is mutated, PE40, in which domain Ia is deleted, or PE38, in which domain Ia and part of domain Ib are deleted. These derivatives of PE do not bind to the PE receptor and allow 607, 355, or 339 amino acids, respectively, between the two ligands.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Bioconjugate chemistry AU - Kreitman, R J AU - Siegall, C B AU - Chaudhary, V K AU - FitzGerald, D J AU - Pastan, I AD - Laboratory of Molecular Biology, DCBDC, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 63 EP - 68 VL - 3 IS - 1 SN - 1043-1802, 1043-1802 KW - Exotoxins KW - 0 KW - IL-6-PE40 protein, chimeric KW - Immunotoxins KW - Interleukin-6 KW - Recombinant Fusion Proteins KW - Transforming Growth Factor alpha KW - transforming growth factor type alpha-Pseudomonas exotoxin A KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Animals KW - Escherichia coli -- metabolism KW - Receptor, Epidermal Growth Factor -- metabolism KW - Tumor Cells, Cultured KW - Plasmids -- genetics KW - Lethal Dose 50 KW - Escherichia coli -- genetics KW - Mice KW - Mice, Inbred BALB C KW - Binding Sites KW - Exotoxins -- genetics KW - Transforming Growth Factor alpha -- toxicity KW - Interleukin-6 -- chemistry KW - Immunotoxins -- toxicity KW - Interleukin-6 -- metabolism KW - Exotoxins -- chemistry KW - Immunotoxins -- metabolism KW - Transforming Growth Factor alpha -- metabolism KW - Immunotoxins -- chemistry KW - Transforming Growth Factor alpha -- genetics KW - Interleukin-6 -- genetics KW - Exotoxins -- metabolism KW - Exotoxins -- toxicity KW - Immunotoxins -- genetics KW - Transforming Growth Factor alpha -- chemistry KW - Interleukin-6 -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73037002?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioconjugate+chemistry&rft.atitle=Properties+of+chimeric+toxins+with+two+recognition+domains%3A+interleukin+6+and+transforming+growth+factor+alpha+at+different+locations+in+Pseudomonas+exotoxin.&rft.au=Kreitman%2C+R+J%3BSiegall%2C+C+B%3BChaudhary%2C+V+K%3BFitzGerald%2C+D+J%3BPastan%2C+I&rft.aulast=Kreitman&rft.aufirst=R&rft.date=1992-01-01&rft.volume=3&rft.issue=1&rft.spage=63&rft.isbn=&rft.btitle=&rft.title=Bioconjugate+chemistry&rft.issn=10431802&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-05 N1 - Date created - 1992-08-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selective formation of tumor necrosis factor-alpha (TNF) degradation products contributes to TNF mediated cytotoxicity. AN - 73026963; 1319775 AB - We compared tumor necrosis factor (TNF) metabolism by wild-type MCF-7 (WT) cells, by 40-fold doxorubicin resistant (40F) breast cancer cells and by PC3 and LNCaP prostate cancer cell lines. MCF-7 WT and LNCaP cell lines were sensitive to TNF cytotoxicity and both lines produced two major intracellular TNF degradation products of 15 kDa and 5.5 kDa. The MCF-7 40F and the PC3 cell lines were resistant to TNF and produced multiple TNF degradation products with molecular weights lower than 15 kDa. Both the breast and prostate lines showed TNF receptor crosslinking patterns consistent with a molecular weight of 55 kDa. The breast and LNCaP lines expressed TNF receptors with an apparent dissociation constant (Kd) of 0.4 to 0.6 nM, while the TNF resistant line had a Kd of 2 nM. Similar receptor numbers per cell were found for all cell types (4,000 to 8,000/cell), and comparable levels of TNF internalization were noted. TNF-conditioned medium from the TNF-sensitive cell types was cytotoxic toward both the TNF-sensitive and TNF-resistant lines, and the toxicity was significantly blocked by an anti-TNF monoclonal antibody. Hydrophobic interaction column HPLC fractionation of the TNF-degradation products produced by MCF-7 WT and LNCaP cells revealed that the trimeric, monomeric, and 5.5 kDa fractions possessed the greatest in vitro antitumor activity. These findings suggest that a TNF degradation product, produced selectively by TNF-sensitive cells, may contribute to the antitumor action of TNF. JF - Oncology research AU - Fruehauf, J P AU - Sinha, B K AD - Section of Biochemical and Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1992 PY - 1992 DA - 1992 SP - 91 EP - 101 VL - 4 IS - 3 SN - 0965-0407, 0965-0407 KW - her-2 KW - Antibodies, Monoclonal KW - 0 KW - Iodine Radioisotopes KW - RNA, Messenger KW - Receptors, Cell Surface KW - Receptors, Tumor Necrosis Factor KW - Recombinant Proteins KW - Tumor Necrosis Factor-alpha KW - Doxorubicin KW - 80168379AG KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Electrophoresis KW - Humans KW - RNA, Messenger -- analysis KW - Cell Division -- drug effects KW - Drug Resistance KW - Receptor, Epidermal Growth Factor -- physiology KW - RNA, Messenger -- genetics KW - Recombinant Proteins -- toxicity KW - Receptors, Cell Surface -- metabolism KW - Oncogenes -- genetics KW - Tumor Cells, Cultured KW - Receptor, Epidermal Growth Factor -- genetics KW - Doxorubicin -- pharmacology KW - Gene Expression -- genetics KW - Recombinant Proteins -- metabolism KW - Cytotoxicity, Immunologic -- drug effects KW - Recombinant Proteins -- analysis KW - Female KW - Male KW - Prostatic Neoplasms -- metabolism KW - Breast Neoplasms -- genetics KW - Tumor Necrosis Factor-alpha -- toxicity KW - Prostatic Neoplasms -- genetics KW - Breast Neoplasms -- metabolism KW - Tumor Necrosis Factor-alpha -- metabolism KW - Prostatic Neoplasms -- ultrastructure KW - Breast Neoplasms -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73026963?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncology+research&rft.atitle=Selective+formation+of+tumor+necrosis+factor-alpha+%28TNF%29+degradation+products+contributes+to+TNF+mediated+cytotoxicity.&rft.au=Fruehauf%2C+J+P%3BSinha%2C+B+K&rft.aulast=Fruehauf&rft.aufirst=J&rft.date=1992-01-01&rft.volume=4&rft.issue=3&rft.spage=91&rft.isbn=&rft.btitle=&rft.title=Oncology+research&rft.issn=09650407&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-06 N1 - Date created - 1992-08-06 N1 - Date revised - 2017-01-13 N1 - Gene symbol - her-2 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Perspectives on risk assessment impact of recent reports on benzene. AN - 73022211; 1609819 AB - Very sensitive methods that can detect the benzene metabolite muconic acid (MA) in the urine of virtually all members of the general population have recently become available and have been used in a few occupational studies as a marker of benzene exposure. Preliminary findings from these studies suggest that urinary MA may be a reliable marker of occupational exposure to greater than 5 ppm benzene. It was also consistently observed that a certain proportion of the general population have urinary MA levels compatible with those seen in persons occupationally exposed to greater than 1 ppm benzene. It is unlikely that these elevated levels can be explained solely as being artifactual. The frequency with which they occur for a given individual, and the duration with which they are maintained, are not known. Information on these two factors is needed in order to adequately assess whether or not these levels present a significant risk for a segment of the general population. JF - American journal of industrial medicine AU - Johnson, E S AU - Lucier, G AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 749 EP - 757 VL - 21 IS - 5 SN - 0271-3586, 0271-3586 KW - muconic acid KW - 3KD92ZL2KH KW - Benzene KW - J64922108F KW - Sorbic Acid KW - X045WJ989B KW - Index Medicus KW - Risk Factors KW - Humans KW - Urine -- chemistry KW - Male KW - Female KW - Sorbic Acid -- analogs & derivatives KW - Sorbic Acid -- analysis KW - Environmental Exposure -- adverse effects KW - Benzene -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73022211?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+industrial+medicine&rft.atitle=Perspectives+on+risk+assessment+impact+of+recent+reports+on+benzene.&rft.au=Johnson%2C+E+S%3BLucier%2C+G&rft.aulast=Johnson&rft.aufirst=E&rft.date=1992-01-01&rft.volume=21&rft.issue=5&rft.spage=749&rft.isbn=&rft.btitle=&rft.title=American+journal+of+industrial+medicine&rft.issn=02713586&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-20 N1 - Date created - 1992-07-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Postoperative radiotherapy of carcinoma in bilharzial bladder: improved disease free survival through improving local control. AN - 73019975; 1612951 AB - Two hundred thirty-six patients with T3 bladder cancer who survived radical surgery and proved to have P3a, P3b, or P4a tumors were randomized in two phases into three groups: (a) no further treatment (83 patients); (b) postoperative radiotherapy multiple daily fractionation (MDF), using 3 daily fractions of 1.25 Gy each, with 3 hr between fractions, up to a total dose of 37.5 Gy in 12 days (75 patients); and (c) postoperative radiotherapy conventional fractionation (CF), for a total dose of 50 Gy/5 weeks (78 patients). The tolerance of the patients to postoperative radiotherapy was quite acceptable, with equal acute reactions in MDF and CF groups. The 5-year disease-free survival (DFS) rates amounted to 49 and 44% in MDF and CF postoperative radiotherapy groups, respectively, compared to 25% in the cystectomy-alone group. The 5-year local control rates were 87% and 93% for those treated with multiple daily fractionation and conventional fractionation while it was 50% in the surgery-alone group. The therapeutic benefit of postoperative irradiation was consistent for all tumor types, histological grades, and pathological stages for both the disease-free survival and local control. Patients with nodal metastases demonstrated lower recurrence rates in the postoperative radiotherapy groups, but this was not associated with improved disease-free survival. Multivariate analysis using the Cox Model confirmed these results. The independent prognostic factors affecting both disease-free survival and local control were the addition of postoperative radiotherapy, the nodal status, the pathological stage, and the tumor grade. Late complications of radiotherapy in the skin, small intestine, rectum, and the anastomotic site of the urinary division were lower with MDF than with conventional fractionation. JF - International journal of radiation oncology, biology, physics AU - Zaghloul, M S AU - Awwad, H K AU - Akoush, H H AU - Omar, S AU - Soliman, O AU - el Attar, I AD - Dept. of Radiotherapy, National Cancer Institute, Cairo, Egypt. Y1 - 1992 PY - 1992 DA - 1992 SP - 511 EP - 517 VL - 23 IS - 3 SN - 0360-3016, 0360-3016 KW - Index Medicus KW - Random Allocation KW - Cystectomy KW - Combined Modality Therapy KW - Radiotherapy Dosage KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Female KW - Radiotherapy -- adverse effects KW - Schistosomiasis -- therapy KW - Urinary Bladder Neoplasms -- mortality KW - Urinary Bladder Neoplasms -- radiotherapy KW - Urinary Bladder Diseases -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73019975?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.atitle=Postoperative+radiotherapy+of+carcinoma+in+bilharzial+bladder%3A+improved+disease+free+survival+through+improving+local+control.&rft.au=Zaghloul%2C+M+S%3BAwwad%2C+H+K%3BAkoush%2C+H+H%3BOmar%2C+S%3BSoliman%2C+O%3Bel+Attar%2C+I&rft.aulast=Zaghloul&rft.aufirst=M&rft.date=1992-01-01&rft.volume=23&rft.issue=3&rft.spage=511&rft.isbn=&rft.btitle=&rft.title=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.issn=03603016&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-28 N1 - Date created - 1992-07-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nucleotide sequence and genomic organization of a tandem satellite array from the rock vole Microtus chrotorrhinus (Rodentia). AN - 73014576; 1611217 AB - A tandem satellite array (herein named MSAT-160) has been isolated and characterized from the rodent Microtus chrotorrhinus. Sequence data from 15 partial or complete monomers revealed a repeat unit length of 160 bp. This unit length was apparently derived from two shorter sub-motifs, one a tetramer (GAAA), the other a hexamer (CTTTCT), through polymerase slippage and mutation. Collectively, perfect or imperfect variants of these two motifs comprise nearly 60% of the component. Southern blot analyses of genomic DNA digested with 14 different restriction endonucleases indicated that most enzymes yielded either classical type A or type B restriction patterns, while RsaI yielded a pattern that combined features of both the A and B types, and BamHI appeared to lack sites altogether in MSAT-160. An examination of restriction patterns from 16 individuals with three enzymes failed to identify intraspecific variation, while a related study compared 11 species and documented interspecific distinctiveness (Modi, submitted). Fluorescence in situ hybridization indicated that the satellite DNA was located at the centromeres of several autosomes and at sex chromosome heterochromatin. JF - Mammalian genome : official journal of the International Mammalian Genome Society AU - Modi, W S AD - Biological Carcinogenesis Development Program, Program Resources, Inc./DynCorp, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1992 PY - 1992 DA - 1992 SP - 226 EP - 232 VL - 3 IS - 4 SN - 0938-8990, 0938-8990 KW - DNA, Satellite KW - 0 KW - Index Medicus KW - Animals KW - Base Sequence KW - Molecular Sequence Data KW - Repetitive Sequences, Nucleic Acid -- genetics KW - Consensus Sequence KW - Cloning, Molecular KW - DNA, Satellite -- chemistry KW - Arvicolinae -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73014576?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mammalian+genome+%3A+official+journal+of+the+International+Mammalian+Genome+Society&rft.atitle=Nucleotide+sequence+and+genomic+organization+of+a+tandem+satellite+array+from+the+rock+vole+Microtus+chrotorrhinus+%28Rodentia%29.&rft.au=Modi%2C+W+S&rft.aulast=Modi&rft.aufirst=W&rft.date=1992-01-01&rft.volume=3&rft.issue=4&rft.spage=226&rft.isbn=&rft.btitle=&rft.title=Mammalian+genome+%3A+official+journal+of+the+International+Mammalian+Genome+Society&rft.issn=09388990&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-29 N1 - Date created - 1992-07-29 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M86843; GENBANK N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Monoamine oxidase inhibitors: reversible and irreversible. AN - 73012457; 1609042 AB - Coincident with and in part fueling advances in diagnostic nosology and drug development, the recent resurgence of interest in monoamine oxidase inhibitors (MAOIs) is reviewed. Accidentally discovered nearly 40 years ago as the first true antidepressants, the MAOIs soon fell into disfavor due to concerns about toxicity and seemingly lesser efficacy compared with the newer tricyclic compounds. Now that we have better understanding of the nature of the hypertensive and hyperpyrexic interactions of MAOIs with other substances, these medications have assumed a role in the treatment of nonendogenous depressive and anxiety syndromes, especially in operationally defined "atypical depression." The discovery of two MAO isoenzymes has resulted in a new generation of selective inhibitors in the search for enhanced efficacy (i.e., clorgyline) or safety (i.e., l-deprenyl). Most promising is the emerging class of reversible selective MAO-type A inhibitors, such as moclobemide, which combine antidepressant potency with freedom from the risk of dangerous tyramine-type adverse interactions. JF - Psychopharmacology bulletin AU - Rudorfer, M V AD - Clinical Treatment Research Branch, National Institute of Mental Health, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 45 EP - 57 VL - 28 IS - 1 SN - 0048-5764, 0048-5764 KW - Monoamine Oxidase Inhibitors KW - 0 KW - Index Medicus KW - History of medicine KW - History, 20th Century KW - Humans KW - Depressive Disorder -- drug therapy KW - Forecasting KW - Depressive Disorder -- classification KW - Monoamine Oxidase Inhibitors -- classification KW - Monoamine Oxidase Inhibitors -- history KW - Monoamine Oxidase Inhibitors -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73012457?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychopharmacology+bulletin&rft.atitle=Monoamine+oxidase+inhibitors%3A+reversible+and+irreversible.&rft.au=Rudorfer%2C+M+V&rft.aulast=Rudorfer&rft.aufirst=M&rft.date=1992-01-01&rft.volume=28&rft.issue=1&rft.spage=45&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology+bulletin&rft.issn=00485764&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-20 N1 - Date created - 1992-07-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Disclosure of tardive dyskinesia: effect of written policy on risk disclosure. AN - 73009169; 1351688 AB - Over half of the states in the country have written statutory and/or regulatory policies that require psychiatrists treating inpatients within the state mental health system to disclose risks associated with treatment to voluntarily admitted patients. A severe side effect associated with the long-term use of neuroleptic medication is tardive dyskinesia (TD). A nationwide study was conducted to investigate the effect of written risk disclosure policy on psychiatrists' self-reported disclosure of the risks associated with neuroleptics to individuals diagnosed as having schizophrenia of a chronic nature. Participating in the study were 520 psychiatrists from 94 state/county mental hospitals located in 35 states. Fifty-four percent of those psychiatrists reported that they typically disclosed TD to the target patient population. The study results did not support the hypothesis that the presence of statutory and regulatory policy on disclosure of risk results in psychiatrists typically disclosing TD to patients. JF - Psychopharmacology bulletin AU - Kennedy, N J AU - Sanborn, J S AD - Division of Epidemiology and Prevention Research, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 93 EP - 100 VL - 28 IS - 1 SN - 0048-5764, 0048-5764 KW - Antipsychotic Agents KW - 0 KW - Bioethics KW - Index Medicus KW - Mental Health Therapies KW - Empirical Approach KW - Legal Approach KW - Professional Patient Relationship KW - United States KW - Risk Factors KW - Humans KW - Data Collection KW - Physician's Role KW - Hospitals, Psychiatric -- legislation & jurisprudence KW - Dyskinesia, Drug-Induced -- etiology KW - Truth Disclosure KW - Antipsychotic Agents -- adverse effects KW - Patient Advocacy -- legislation & jurisprudence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73009169?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychopharmacology+bulletin&rft.atitle=Disclosure+of+tardive+dyskinesia%3A+effect+of+written+policy+on+risk+disclosure.&rft.au=Kennedy%2C+N+J%3BSanborn%2C+J+S&rft.aulast=Kennedy&rft.aufirst=N&rft.date=1992-01-01&rft.volume=28&rft.issue=1&rft.spage=93&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology+bulletin&rft.issn=00485764&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-20 N1 - Date created - 1992-07-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Psychopharmacologic treatment of cocaine dependence. AN - 73009117; 1609036 JF - Psychopharmacology bulletin AU - Blaine, J D AU - Ling, W AD - National Institute on Drug Abuse, Rockville, MD. Y1 - 1992 PY - 1992 DA - 1992 SP - 11 EP - 14 VL - 28 IS - 1 SN - 0048-5764, 0048-5764 KW - Psychotropic Drugs KW - 0 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Humans KW - United States -- epidemiology KW - Substance-Related Disorders -- drug therapy KW - Psychotropic Drugs -- therapeutic use KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73009117?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychopharmacology+bulletin&rft.atitle=Psychopharmacologic+treatment+of+cocaine+dependence.&rft.au=Blaine%2C+J+D%3BLing%2C+W&rft.aulast=Blaine&rft.aufirst=J&rft.date=1992-01-01&rft.volume=28&rft.issue=1&rft.spage=11&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology+bulletin&rft.issn=00485764&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-20 N1 - Date created - 1992-07-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chronic treatment with 1-aminocyclopropanecarboxylic acid desensitizes behavioral responses to compounds acting at the N-methyl-D-aspartate receptor complex. AN - 73005132; 1534910 AB - Functional antagonists at the N-methyl-D-aspartate (NMDA) receptor complex produce anti-depressant-like actions in preclinical models. Thus, an injection of a glycine partial agonist (1-aminocyclopropanecarboxylic acid; ACPC), a competitive NMDA antagonist (2-amino-7-phosphonoheptanoic acid; AP-7) or a use-dependent cation channel blocker (MK-801) reduced immobility in the forced swim test (FST) with efficacies comparable to imipramine (Trullas and Skolnick 1990). Seven daily injections of ACPC (200-400 mg/kg) abolished the effects of both this compound (200-1200 mg/kg) and AP-7 (200-300 mg/kg) in the FST. The loss in effectiveness of ACPC required 7 days of treatment to become fully manifest, and was reversed by discontinuing treatment. Other agents active in the FST (e.g. MK-801, imipramine, and nifedipine) were unaffected by this regimen. Moreover, ACPC and AP-7 remained active in the FST following repeated injections of MK-801, AP-7, or imipramine. Chronic treatment with ACPC did not affect its actions in the elevated plus-maze, but significantly attenuated the convulsant and lethal effects of NMDA (125 mg/kg). Tissue levels of ACPC indicate the modified behavioral responses produced by chronic treatment are not attributable to pharmacokinetic factors. These findings suggest repeated administration of ACPC may effect an "uncoupling" of NMDA and glycine receptors, resulting in an apparent desensitization of the behavioral actions of substances acting at these sites. JF - Psychopharmacology AU - Skolnick, P AU - Miller, R AU - Young, A AU - Boje, K AU - Trullas, R AD - Laboratory of Neuroscience, NIDDK, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 489 EP - 496 VL - 107 IS - 4 SN - 0033-3158, 0033-3158 KW - Amino Acids KW - 0 KW - Amino Acids, Cyclic KW - Anticonvulsants KW - Antidepressive Agents KW - Receptors, N-Methyl-D-Aspartate KW - 1-aminocyclopropane-1-carboxylic acid KW - 3K9EJ633GL KW - N-Methylaspartate KW - 6384-92-5 KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - 2-Amino-5-phosphonovalerate KW - 76726-92-6 KW - 2-amino-7-phosphonoheptanoic acid KW - P34K80CUSM KW - Index Medicus KW - Seizures -- chemically induced KW - Anticonvulsants -- pharmacology KW - Animals KW - Swimming KW - Antidepressive Agents -- pharmacology KW - Brain Chemistry -- drug effects KW - Learning -- drug effects KW - Mice KW - Seizures -- prevention & control KW - Male KW - Dizocilpine Maleate -- pharmacology KW - Behavior, Animal -- drug effects KW - Receptors, N-Methyl-D-Aspartate -- drug effects KW - 2-Amino-5-phosphonovalerate -- analogs & derivatives KW - Amino Acids -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73005132?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychopharmacology&rft.atitle=Chronic+treatment+with+1-aminocyclopropanecarboxylic+acid+desensitizes+behavioral+responses+to+compounds+acting+at+the+N-methyl-D-aspartate+receptor+complex.&rft.au=Skolnick%2C+P%3BMiller%2C+R%3BYoung%2C+A%3BBoje%2C+K%3BTrullas%2C+R&rft.aulast=Skolnick&rft.aufirst=P&rft.date=1992-01-01&rft.volume=107&rft.issue=4&rft.spage=489&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology&rft.issn=00333158&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-16 N1 - Date created - 1992-07-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A phase II trial of continuous-infusion 6-mercaptopurine for childhood leukemia. AN - 72999147; 1600597 AB - A phase II pediatric trial of a continuous intravenous infusion of 6-mercaptopurine (6MP) in patients with refractory leukemia was performed. The dosing schedule, 50 mg m-2 h-1 for 48 h, was based on the results of a previous phase I trial of this approach. Among the 40 children treated for acute lymphoblastic leukemia (ALL), all of whom had received prior therapy with oral 6MP, 1 complete and 1 partial response were achieved. No response was observed in 17 patients with refractory acute nonlymphocytic leukemia (ANLL). Reversible hepatotoxicity, the primary dose-limiting toxicity, was observed in approximately 50% of cases. Mucositis was encountered infrequently and was usually not severe. 6MP given on the present continuous intravenous infusion schedule overcomes the limited and variable bioavailability of oral 6MP but shows limited activity as induction agent in children with recurrent ALL. JF - Cancer chemotherapy and pharmacology AU - Adamson, P C AU - Zimm, S AU - Ragab, A H AU - Balis, F AU - Steinberg, S M AU - Kamen, B A AU - Vietti, T J AU - Gillespie, A AU - Poplack, D G AD - Pediatric Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 155 EP - 157 VL - 30 IS - 2 SN - 0344-5704, 0344-5704 KW - 6-Mercaptopurine KW - E7WED276I5 KW - Index Medicus KW - Infant KW - Drug Evaluation KW - Drug Administration Schedule KW - Infusions, Intravenous KW - Humans KW - Adult KW - Child KW - Adolescent KW - Child, Preschool KW - 6-Mercaptopurine -- therapeutic use KW - 6-Mercaptopurine -- administration & dosage KW - 6-Mercaptopurine -- adverse effects KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- drug therapy KW - Leukemia, Myeloid, Acute -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72999147?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+chemotherapy+and+pharmacology&rft.atitle=A+phase+II+trial+of+continuous-infusion+6-mercaptopurine+for+childhood+leukemia.&rft.au=Adamson%2C+P+C%3BZimm%2C+S%3BRagab%2C+A+H%3BBalis%2C+F%3BSteinberg%2C+S+M%3BKamen%2C+B+A%3BVietti%2C+T+J%3BGillespie%2C+A%3BPoplack%2C+D+G&rft.aulast=Adamson&rft.aufirst=P&rft.date=1992-01-01&rft.volume=30&rft.issue=2&rft.spage=155&rft.isbn=&rft.btitle=&rft.title=Cancer+chemotherapy+and+pharmacology&rft.issn=03445704&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-10 N1 - Date created - 1992-07-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Subchronic (13-week) toxicity studies of oral phenolphthalein in Fischer 344 rats and B6C3F1 mice. AN - 72991040; 1601209 AB - Phenolphthalein is a cathartic agent that is widely used in over-the-counter laxatives. Thirteen-week toxicity studies of phenolphthalein were performed using F344/N rats and B6C3F1 mice. Rats and mice were fed ad libitum with a NIH 07 diet containing 0; 3000; 6000; 12,000; 25,000; or 50,000 ppm phenolphthalein. On a milligram per kilogram body weight basis, rats and mice fed 50,000 ppm phenolphthalein ingested more drug than would be expected during human laxative abuse. Phenolphthalein produced little evidence of toxicity in rats. There was slightly lower weight gain among the 25,000 and 50,000 ppm groups. Treated rats showed elevated relative kidney weights (males only) and elevated absolute and relative liver weights at 12,000-50,000 ppm phenolphthalein. Rat serum bile acids were depressed early (Days 5 and 6) by phenolphthalein treatment. Several treatment-related toxic effects, however, were identified in mice who received more phenolphthalein per unit body weight than rats. Although there were no effects on body weight gain, elevated liver weights were noted in female mice receiving 6000-50,000 ppm phenolphthalein. The primary treatment-related findings that occurred during the mouse studies involved the reproductive and hematopoietic systems. Reproductive changes including depressed testis and right epididymal weights and sperm density, an elevated production of abnormal sperm, and morphologic alterations in seminiferous tubules occurred at all levels of exposure (3000-50,000 ppm). Hematopoietic changes included bone marrow hypoplasia (12,000-50,000 ppm), increased splenic hematopoiesis (males only; 25,000 and 50,000 ppm), and an elevated incidence of micronucleated erythrocytes (6000-50,000 ppm). JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Dietz, D D AU - Elwell, M R AU - Chapin, R E AU - Shelby, M D AU - Thompson, M B AU - Filler, R AU - Stedham, M A AD - Division of Toxicology Research and Testing, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 48 EP - 58 VL - 18 IS - 1 SN - 0272-0590, 0272-0590 KW - Bile Acids and Salts KW - 0 KW - Phenolphthaleins KW - Phenolphthalein KW - 6QK969R2IF KW - Index Medicus KW - Eating -- drug effects KW - Animals KW - Bone Marrow -- pathology KW - Sex Characteristics KW - Reproduction -- drug effects KW - Testis -- pathology KW - Spleen -- pathology KW - Mice KW - Spermatogenesis -- drug effects KW - Biological Availability KW - Rats KW - Rats, Inbred F344 KW - Bile Acids and Salts -- blood KW - Micronucleus Tests KW - Body Weight -- drug effects KW - Female KW - Male KW - Organ Size -- drug effects KW - Phenolphthaleins -- toxicity KW - Phenolphthaleins -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72991040?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=Subchronic+%2813-week%29+toxicity+studies+of+oral+phenolphthalein+in+Fischer+344+rats+and+B6C3F1+mice.&rft.au=Dietz%2C+D+D%3BElwell%2C+M+R%3BChapin%2C+R+E%3BShelby%2C+M+D%3BThompson%2C+M+B%3BFiller%2C+R%3BStedham%2C+M+A&rft.aulast=Dietz&rft.aufirst=D&rft.date=1992-01-01&rft.volume=18&rft.issue=1&rft.spage=48&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-15 N1 - Date created - 1992-07-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Relationships between cdc2 kinase, DNA cross-linking, and cell cycle perturbations induced by nitrogen mustard. AN - 72990954; 1534688 AB - M phase-promoting factor (MPF) consists of a p34cdc2 (cdc2) kinase and cyclin B complex which in its active form promotes G2 to M transition. The role of MPF in G2 arrest following DNA damage, however, has remained largely uncharacterized. We have investigated whether nitrogen mustard (HN2) interfered with either the formation of MPF or its activation. For this purpose, we measured cdc2 kinase activity relative to cdc2 and cyclin B protein turnover and the phosphorylation status of cdc2. Studies were performed in two exceptional human lymphoma cell lines, which differed in HN2 sensitivity by 5-fold (CA46, 50% growth-inhibitory dose = 1.0 microM; JLP119, 50% growth-inhibitory dose = 0.2 microM) but exhibited virtually identical DNA interstrand and DNA-protein cross-link exposure. Following HN2 treatment, CA46 cells ceased to enter mitosis and exhibited a marked delay in G2 phase. Failure to enter mitosis paralleled inhibition of cdc2 kinase. Inhibition was not due to decreased levels of cdc2 or cyclin B protein; rather, G2 arrest correlated with the accumulation of both tyrosine-phosphorylated cdc2 and cyclin B. These findings implied that G2 arrest resulted from a down-regulation of the processes that activate MPF. We also found that JLP119 cells, within a few hours of mitosis at the time of drug treatment, evaded checkpoint control and continued cell division unabated by DNA damage. Furthermore, despite similar DNA cross-link exposure, JLP119 cells within the window of checkpoint control were more susceptible to S phase delay than CA46 cells. Altered cell cycle responses correlated with the greater susceptibility of JLP119 cells to the cytotoxic effects of HN2. JF - Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research AU - O'Connor, P M AU - Ferris, D K AU - White, G A AU - Pines, J AU - Hunter, T AU - Longo, D L AU - Kohn, K W AD - National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 43 EP - 52 VL - 3 IS - 1 SN - 1044-9523, 1044-9523 KW - Cross-Linking Reagents KW - 0 KW - Cyclins KW - Mechlorethamine KW - 50D9XSG0VR KW - CDC2 Protein Kinase KW - EC 2.7.11.22 KW - Index Medicus KW - Tumor Cells, Cultured KW - Phosphorylation KW - Humans KW - Cyclins -- metabolism KW - G2 Phase -- drug effects KW - CDC2 Protein Kinase -- drug effects KW - DNA Damage -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72990954?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell+growth+%26+differentiation+%3A+the+molecular+biology+journal+of+the+American+Association+for+Cancer+Research&rft.atitle=Relationships+between+cdc2+kinase%2C+DNA+cross-linking%2C+and+cell+cycle+perturbations+induced+by+nitrogen+mustard.&rft.au=O%27Connor%2C+P+M%3BFerris%2C+D+K%3BWhite%2C+G+A%3BPines%2C+J%3BHunter%2C+T%3BLongo%2C+D+L%3BKohn%2C+K+W&rft.aulast=O%27Connor&rft.aufirst=P&rft.date=1992-01-01&rft.volume=3&rft.issue=1&rft.spage=43&rft.isbn=&rft.btitle=&rft.title=Cell+growth+%26+differentiation+%3A+the+molecular+biology+journal+of+the+American+Association+for+Cancer+Research&rft.issn=10449523&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-10 N1 - Date created - 1992-07-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of cholera toxin by ADP-ribosylation factors, 20-kDa guanine nucleotide-binding proteins. AN - 72980806; 1600746 JF - Current topics in cellular regulation AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 49 EP - 72 VL - 32 SN - 0070-2137, 0070-2137 KW - Enterotoxins KW - 0 KW - Cholera Toxin KW - 9012-63-9 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - ADP-Ribosylation Factors KW - EC 3.6.5.2 KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Index Medicus KW - Enterotoxins -- metabolism KW - Sequence Homology, Nucleic Acid KW - Molecular Sequence Data KW - Adenylyl Cyclases -- metabolism KW - Amino Acid Sequence KW - GTP-Binding Proteins -- classification KW - GTP-Binding Proteins -- metabolism KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72980806?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+topics+in+cellular+regulation&rft.atitle=Activation+of+cholera+toxin+by+ADP-ribosylation+factors%2C+20-kDa+guanine+nucleotide-binding+proteins.&rft.au=Moss%2C+J%3BVaughan%2C+M&rft.aulast=Moss&rft.aufirst=J&rft.date=1992-01-01&rft.volume=32&rft.issue=&rft.spage=49&rft.isbn=&rft.btitle=&rft.title=Current+topics+in+cellular+regulation&rft.issn=00702137&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-13 N1 - Date created - 1992-07-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - EEG spectral power reduction and learning disability in rats exposed to lead through postnatal developing age. AN - 72968720; 1597338 AB - The present study was carried out to assess electrophysiological and behavioral changes in Wistar rats caused by consuming a daily dose of lead acetate (400 micrograms lead/g body weight/day, given by gastric intubation, from second day of birth to 60 days of age. At 60 days of age, the lead treated rats showed in both wakeful and slow wave sleep stages, a statistically significant reduction in the delta, theta, alpha and beta band EEG spectral power in motor cortex (MC) and hippocampus (HI) with the exception of the delta and beta bands power of MC in wakeful state (WA). Lead administration was discontinued after that age for allowing rehabilitation for 40 days. Then, operant behavioral assessment was done. Results revealed that the lead treated animals took significantly more time and sessions than control normal animals in attaining criterion of learning. Hence exposure to lead in early age could result in a learning disability persisting even after discontinuation of exposure. JF - Indian journal of physiology and pharmacology AU - Kumar, M V AU - Desiraju, T AD - Department of Neurophysiology, National Institute of Mental Health and Neurosciences, Bangalore. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 15 EP - 20 VL - 36 IS - 1 SN - 0019-5499, 0019-5499 KW - Lead KW - 2P299V784P KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Behavior, Animal -- drug effects KW - Animals KW - Time Factors KW - Male KW - Female KW - Discrimination Learning -- drug effects KW - Lead -- toxicity KW - Brain -- drug effects KW - Electroencephalography -- drug effects KW - Brain -- physiology KW - Brain -- growth & development KW - Learning Disorders -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72968720?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Indian+journal+of+physiology+and+pharmacology&rft.atitle=EEG+spectral+power+reduction+and+learning+disability+in+rats+exposed+to+lead+through+postnatal+developing+age.&rft.au=Kumar%2C+M+V%3BDesiraju%2C+T&rft.aulast=Kumar&rft.aufirst=M&rft.date=1992-01-01&rft.volume=36&rft.issue=1&rft.spage=15&rft.isbn=&rft.btitle=&rft.title=Indian+journal+of+physiology+and+pharmacology&rft.issn=00195499&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-08 N1 - Date created - 1992-07-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of N-methyl-N-nitrosourea on transcriptionally active and inactive nucleosomes: macromolecular damage and DNA repair. AN - 72967701; 1375028 AB - We previously reported a separation, on an organomercurial column, of transcriptionally inactive nucleosomes (class 1) from those containing active gene sequences (classes 2 and 3). In this paper, we analyzed nucleosomal damage caused by exposure of HeLa S3 cells in suspension culture to the directly alkylating carcinogen N-methyl-N-nitrosourea (MNU). The extent and site of methylation induced by the compound in nucleosomal DNA and RNA were determined by cell incubation in the presence of [3H]MNU. The highest amount of damage was detected in DNA of class 3 nucleosomes, while RNA alkylation was comparable in all nucleosomal classes. Cellular capacity for repair of MNU-induced DNA strand breaks (estimated after a short pulse with [3H]thymidine) was found to be higher in active nucleosomal fractions (classes 2 and 3) than in the inactive fraction (class 1). Our data support the postulate that chromatin primary structure plays a role in modulating carcinogen damage to chromosomal macromolecules and in DNA strand breakage and repair mechanisms. Some of these initial steps are believed to be critical in the process of carcinogenesis. JF - Molecular carcinogenesis AU - Boffa, L C AU - Mariani, M R AU - Carpaneto, E M AD - Department of Chemical Carcinogenesis, National Cancer Institute, IST., Genova, Italy. Y1 - 1992 PY - 1992 DA - 1992 SP - 174 EP - 177 VL - 5 IS - 3 SN - 0899-1987, 0899-1987 KW - Nucleosomes KW - 0 KW - Proteins KW - RNA KW - 63231-63-0 KW - Methylnitrosourea KW - 684-93-5 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Chromatography, Affinity KW - DNA -- isolation & purification KW - Transcription, Genetic -- drug effects KW - Proteins -- isolation & purification KW - HeLa Cells KW - Humans KW - RNA -- isolation & purification KW - Methylation KW - DNA Repair KW - Nucleosomes -- drug effects KW - Nucleosomes -- metabolism KW - Methylnitrosourea -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72967701?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Effects+of+N-methyl-N-nitrosourea+on+transcriptionally+active+and+inactive+nucleosomes%3A+macromolecular+damage+and+DNA+repair.&rft.au=Boffa%2C+L+C%3BMariani%2C+M+R%3BCarpaneto%2C+E+M&rft.aulast=Boffa&rft.aufirst=L&rft.date=1992-01-01&rft.volume=5&rft.issue=3&rft.spage=174&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-25 N1 - Date created - 1992-06-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immunological aspects of demyelinating diseases. AN - 72966944; 1375472 AB - Primary demyelination in the central nervous system results from damage to the myelin sheath or oligodendroglia and can be produced by a variety of mechanisms, including metabolic disturbances, toxicities, infection, and autoimmunity. The major human demyelinating disease affecting the central nervous system is multiple sclerosis (MS). Although the etiology of MS is not known, existing data indicate that both genetic and environmental factors contribute to pathogenesis. Experimental allergic encephalomyelitis (EAE) is induced by immunization of genetically susceptible animals with myelin proteins. This is mediated by autoimmune T cells. Characterization of MHC restriction, fine specificity of antigen recognition, and T cell receptor (TCR) usage by encephalitogenic T cells has resulted in highly specific immunotherapies. Both HLA and TCR genes have been linked to susceptibility for MS which is widely believed to be mediated by T cells that recognize an as yet unidentified autoantigen. Because of the advances in the understanding and treatment of EAE, recent research in MS has been focused on the characterization of cellular immune responses against myelin components. The results of these studies are reviewed and the potential implications of these findings for the pathogenesis and future therapy of MS are examined. JF - Annual review of immunology AU - Martin, R AU - McFarland, H F AU - McFarlin, D E AD - Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 153 EP - 187 VL - 10 SN - 0732-0582, 0732-0582 KW - Autoantigens KW - 0 KW - Myelin Basic Protein KW - Index Medicus KW - Animals KW - Encephalomyelitis, Autoimmune, Experimental -- immunology KW - Humans KW - Multiple Sclerosis -- immunology KW - T-Lymphocytes -- immunology KW - Myelin Basic Protein -- immunology KW - Demyelinating Diseases -- immunology KW - Demyelinating Diseases -- classification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72966944?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annual+review+of+immunology&rft.atitle=Immunological+aspects+of+demyelinating+diseases.&rft.au=Martin%2C+R%3BMcFarland%2C+H+F%3BMcFarlin%2C+D+E&rft.aulast=Martin&rft.aufirst=R&rft.date=1992-01-01&rft.volume=10&rft.issue=&rft.spage=153&rft.isbn=&rft.btitle=&rft.title=Annual+review+of+immunology&rft.issn=07320582&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-26 N1 - Date created - 1992-06-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Issues in AIDS training for substance abuse workers. AN - 72966648; 1593660 AB - Workers in drug treatment programs need specialized training concerning acquired immune deficiency syndrome (AIDS) to meet the demands of their expanding roles. Initially, the treatment community failed to anticipate training needs fully, but now, comprehensive and systematic AIDS training programs must be developed. This article discusses the five steps in developing and implementing such programs: (a) assessment and information gathering, (b) curriculum development, (c) training of instructors, (d) training delivery, and (e) evaluation. JF - Journal of substance abuse treatment AU - Ashery, R S AD - Alcohol, Drug Abuse, Mental Health Administration, National Institute on Drug Abuse, Rockville, Maryland 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 15 EP - 19 VL - 9 IS - 1 SN - 0740-5472, 0740-5472 KW - Index Medicus KW - AIDS/HIV KW - Risk Factors KW - Humans KW - Curriculum KW - Acquired Immunodeficiency Syndrome -- prevention & control KW - Inservice Training KW - Substance Abuse, Intravenous -- rehabilitation KW - Acquired Immunodeficiency Syndrome -- transmission KW - Substance Abuse, Intravenous -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72966648?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+substance+abuse+treatment&rft.atitle=Issues+in+AIDS+training+for+substance+abuse+workers.&rft.au=Ashery%2C+R+S&rft.aulast=Ashery&rft.aufirst=R&rft.date=1992-01-01&rft.volume=9&rft.issue=1&rft.spage=15&rft.isbn=&rft.btitle=&rft.title=Journal+of+substance+abuse+treatment&rft.issn=07405472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-01 N1 - Date created - 1992-07-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Recent advances in pharmacological research on alcohol. Possible relations with cocaine. AN - 72963838; 1350360 AB - Alcohol dependence is a major public health problem. Studies have shown that a person dependent on alcohol often coabuses other substances, such as cocaine. Cocaine is a powerful stimulant whereas ethanol is generally considered to be a depressant, with some stimulating properties. The subjective effects of these two substances in a dependent individual may often appear to be more similar than they are different. Animals also self-administer both substances. Basically, although both substances have anesthetic properties and both act to functionally increase catecholaminergic function, especially that of dopamine, there are some differences in their actions. Both alcohol and cocaine have various effects on several neurotransmitters and systems, which ultimately interact to produce the feeling of well-being avidly sought by many individuals today. This drive often eventually produces a dependence which has associated social and medical consequences. It seems likely that the neurochemical changes that ensue following abuse of these substances underlie the phenomena of dependence, tolerance, and subsequent withdrawal. The apparent similarities and differences between these two substances will be reviewed in this chapter. JF - Recent developments in alcoholism : an official publication of the American Medical Society on Alcoholism, the Research Society on Alcoholism, and the National Council on Alcoholism AU - Wozniak, K M AU - Linnoila, M AD - DICBR, National Institute on Alcohol Abuse and Alcoholism, Alcohol, Drug Abuse and Mental Health Administration (ADAMHA), Bethesda, Maryland 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 235 EP - 272 VL - 10 SN - 0738-422X, 0738-422X KW - Neurotransmitter Agents KW - 0 KW - Receptors, Neurotransmitter KW - Ethanol KW - 3K9958V90M KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Receptors, Neurotransmitter -- physiology KW - Animals KW - Neurotransmitter Agents -- metabolism KW - Synaptic Transmission -- drug effects KW - Humans KW - Receptors, Neurotransmitter -- drug effects KW - Synaptic Transmission -- physiology KW - Alcoholism -- rehabilitation KW - Substance-Related Disorders -- physiopathology KW - Brain -- drug effects KW - Arousal -- physiology KW - Substance-Related Disorders -- rehabilitation KW - Substance-Related Disorders -- psychology KW - Alcoholism -- psychology KW - Cocaine -- adverse effects KW - Brain -- physiopathology KW - Ethanol -- adverse effects KW - Ethanol -- pharmacokinetics KW - Arousal -- drug effects KW - Cocaine -- pharmacokinetics KW - Alcoholism -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72963838?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.atitle=Recent+advances+in+pharmacological+research+on+alcohol.+Possible+relations+with+cocaine.&rft.au=Wozniak%2C+K+M%3BLinnoila%2C+M&rft.aulast=Wozniak&rft.aufirst=K&rft.date=1992-01-01&rft.volume=10&rft.issue=&rft.spage=235&rft.isbn=&rft.btitle=&rft.title=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.issn=0738422X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-22 N1 - Date created - 1992-06-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular mechanisms associated with cocaine effects. Possible relationships with effects of ethanol. AN - 72960859; 1350361 AB - Cocaine has been shown to be a highly addictive and toxic drug. It produces these effects and a variety of other physiological and behavioral effects through its interactions with several distinct central nervous system receptor sites. We present the results of a series of studies that utilized multiple site analyses to elucidate which cocaine binding sites influence the reinforcing and toxic effects of cocaine and with what proportion of influence. The nature of cocaine interactions with monoamine transporters is also discussed, especially with the dopamine transporter, which has been shown to be the cocaine binding site that is primarily associated with the reinforcing effects of cocaine. We also provide evidence that vulnerability to both the toxic and addictive effects of cocaine may be significantly influenced by genetic differences in both humans and animals. In view of the fact that cocaine is commonly abused in a polydrug situation, we present the results of both behavioral and biochemical experiments which suggest that common biochemical pathways may mediate the reinforcing or addictive properties of drugs of abuse. Finally, we discuss research on the biochemical mechanisms associated with effects of ethanol, particularly those which may also influence cocaine self-administration and speculate on pharmacotherapeutic strategies for concurrent abuse of cocaine and ethanol. JF - Recent developments in alcoholism : an official publication of the American Medical Society on Alcoholism, the Research Society on Alcoholism, and the National Council on Alcoholism AU - Ritz, M C AU - Kuhar, M J AU - George, F R AD - Preclinical Pharmacology Branch, National Institute on Drug Abuse, Addiction Research Center, Baltimore, Maryland 21224. Y1 - 1992 PY - 1992 DA - 1992 SP - 273 EP - 302 VL - 10 SN - 0738-422X, 0738-422X KW - Neurotransmitter Agents KW - 0 KW - Receptors, Neurotransmitter KW - Ethanol KW - 3K9958V90M KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Animals KW - Risk Factors KW - Humans KW - Substance-Related Disorders -- physiopathology KW - Brain -- drug effects KW - Receptors, Neurotransmitter -- drug effects KW - Alcoholism -- genetics KW - Cocaine -- adverse effects KW - Brain -- physiopathology KW - Receptors, Neurotransmitter -- physiology KW - Ethanol -- adverse effects KW - Ethanol -- pharmacokinetics KW - Neurotransmitter Agents -- metabolism KW - Cocaine -- pharmacokinetics KW - Alcoholism -- physiopathology KW - Substance-Related Disorders -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72960859?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.atitle=Molecular+mechanisms+associated+with+cocaine+effects.+Possible+relationships+with+effects+of+ethanol.&rft.au=Ritz%2C+M+C%3BKuhar%2C+M+J%3BGeorge%2C+F+R&rft.aulast=Ritz&rft.aufirst=M&rft.date=1992-01-01&rft.volume=10&rft.issue=&rft.spage=273&rft.isbn=&rft.btitle=&rft.title=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.issn=0738422X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-22 N1 - Date created - 1992-06-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chronic treatment with meta-chlorophenylpiperazine (m-CPP) alters behavioral and cerebral metabolic responses to the serotonin agonists m-CPP and quipazine but not 8-hydroxy-2(di-N-propylamino)tetralin. AN - 72955915; 1534179 AB - The effects of the serotonin (5-HT) agonists meta-chlorophenylpiperazine (m-CPP), quipazine and 8-hydroxy-2(di-n-propylamino)tetralin (DPAT) on behavior and on regional cerebral metabolic rates for glucose (rCMRglc) were measured in control rats or in rats pretreated for 2 weeks with continuous infusion of saline or m-CPP (2.5 mg/kg/day, subcutaneously). rCMRglc was measured in 71 brain regions, using the quantitative autoradiographic [14C]2-deoxy-D-glucose technique, at 15 min after acute administration of m-CPP 2.5 mg/kg, 60 min after quipazine 20 mg/kg, or 10 min after DPAT 1 mg/kg. Behavioral effects were assessed for m-CPP with an activity monitor, for quipazine by counting head shakes and for DPAT by scoring the serotonin syndrome. Chronic m-CPP pretreatment produced tolerance to hypolocomotion induced by acute m-CPP and to head shakes caused by acute quipazine, but did not alter the serotonin syndrome produced by DPAT. m-CPP 2.5 mg/kg IP produced widespread rCMRglc reductions in control rats but failed to modify rCMRglc in any region after chronic m-CPP pretreatment. Quipazine increased rCMRglc in 4 regions in control rats, but reduced rCMRglc in 14 brain areas of chronically m-CPP-pretreated animals. DPAT altered rCMRglc to the same degree in control (25 regions affected) and in chronically m-CPP-pretreated rats (28 regions affected). Reduced behavioral and metabolic effects of acute m-CPP in chronically m-CPP-pretreated rats were not due to pharmacokinetic alterations. These results demonstrate that chronic administration of m-CPP produces behavioral and metabolic tolerance to acute administration of m-CPP, but not of DPAT.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Psychopharmacology AU - Freo, U AU - Holloway, H W AU - Greig, N H AU - Soncrant, T T AD - Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 30 EP - 38 VL - 107 IS - 1 SN - 0033-3158, 0033-3158 KW - Piperazines KW - 0 KW - Receptors, Serotonin KW - Tetrahydronaphthalenes KW - Quipazine KW - 4WCY05C0SJ KW - 8-Hydroxy-2-(di-n-propylamino)tetralin KW - 78950-78-4 KW - Deoxyglucose KW - 9G2MP84A8W KW - 1-(3-chlorophenyl)piperazine KW - REY0CNO998 KW - Index Medicus KW - Rats KW - Drug Tolerance KW - Animals KW - Rats, Inbred F344 KW - Drug Interactions KW - Motor Activity -- drug effects KW - Male KW - Deoxyglucose -- metabolism KW - Receptors, Serotonin -- drug effects KW - Piperazines -- pharmacokinetics KW - Behavior, Animal -- drug effects KW - Quipazine -- pharmacology KW - Tetrahydronaphthalenes -- pharmacology KW - Brain -- drug effects KW - Brain -- metabolism KW - Piperazines -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72955915?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychopharmacology&rft.atitle=Chronic+treatment+with+meta-chlorophenylpiperazine+%28m-CPP%29+alters+behavioral+and+cerebral+metabolic+responses+to+the+serotonin+agonists+m-CPP+and+quipazine+but+not+8-hydroxy-2%28di-N-propylamino%29tetralin.&rft.au=Freo%2C+U%3BHolloway%2C+H+W%3BGreig%2C+N+H%3BSoncrant%2C+T+T&rft.aulast=Freo&rft.aufirst=U&rft.date=1992-01-01&rft.volume=107&rft.issue=1&rft.spage=30&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology&rft.issn=00333158&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-24 N1 - Date created - 1992-06-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evidence that MEHP inhibits rat granulosa cell function by a protein kinase C-independent mechanism. AN - 72953835; 1317232 AB - We have recently shown that mono-(2-ethylhexyl) phthalate (MEHP), the active metabolite of the reproductive toxicant di-(ethylhexyl) phthalate (DEHP), inhibited FSH- but not forskolin-, isoproterenol-, or cholera toxin-stimulated granulosa cell cAMP accumulation in vitro. In addition, MEHP also inhibited FSH-stimulated progesterone production, a cAMP-dependent process. Similar to MEHP, the protein kinase C (PKC) activator, 12-0-tetradecanoyl-phorbol 13-acetate (TPA) has been shown to inhibit rat granulosa cell cAMP accumulation in a FSH-specific manner, and decrease FSH-stimulated progesterone production. Due to the similarity with respect to inhibition of cAMP accumulation, we conducted studies to determine if the inhibitory actions of MEHP on granulosa cell function are mediated via activation of PKC. Treatment of granulosa cells for 48 h with 100 microM MEHP produced no effect on forskolin- or isoproterenol-stimulated progesterone production, indicating that MEHP does not have a post-cyclic AMP site of action with respect to progesterone inhibition. Unlike the FSH-specific effect seen with MEHP, treatment with 10 nM TPA inhibited FSH-, forskolin-, and isoproterenol-stimulated progesterone production. In addition, maximally inhibitory concentrations of TPA and MEHP caused significantly greater inhibition of FSH-stimulated cAMP accumulation than either compound alone. Finally, addition of the progesterone precursor, pregnenolone, reversed the FSH-stimulated progesterone production inhibition by MEHP, but not that by TPA. Taken together, these data indicate that the inhibitory effects of MEHP on granulosa cell function are independent of phorbol ester-sensitive PKC activation. JF - Reproductive toxicology (Elmsford, N.Y.) AU - Treinen, K A AU - Heindel, J J AD - Developmental and Reproductive Toxicology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina. Y1 - 1992 PY - 1992 DA - 1992 SP - 143 EP - 148 VL - 6 IS - 2 SN - 0890-6238, 0890-6238 KW - Colforsin KW - 1F7A44V6OU KW - Progesterone KW - 4G7DS2Q64Y KW - Follicle Stimulating Hormone KW - 9002-68-0 KW - Diethylhexyl Phthalate KW - C42K0PH13C KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinase C KW - EC 2.7.11.13 KW - mono-(2-ethylhexyl)phthalate KW - FU2EWB60RT KW - Isoproterenol KW - L628TT009W KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Cyclic AMP -- biosynthesis KW - Follicle Stimulating Hormone -- antagonists & inhibitors KW - Isoproterenol -- pharmacology KW - Progesterone -- biosynthesis KW - Rats KW - Colforsin -- pharmacology KW - Rats, Inbred F344 KW - Cells, Cultured KW - Cyclic AMP -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Follicle Stimulating Hormone -- pharmacology KW - Female KW - Granulosa Cells -- drug effects KW - Diethylhexyl Phthalate -- toxicity KW - Protein Kinase C -- physiology KW - Diethylhexyl Phthalate -- analogs & derivatives KW - Granulosa Cells -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72953835?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.atitle=Evidence+that+MEHP+inhibits+rat+granulosa+cell+function+by+a+protein+kinase+C-independent+mechanism.&rft.au=Treinen%2C+K+A%3BHeindel%2C+J+J&rft.aulast=Treinen&rft.aufirst=K&rft.date=1992-01-01&rft.volume=6&rft.issue=2&rft.spage=143&rft.isbn=&rft.btitle=&rft.title=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.issn=08906238&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-26 N1 - Date created - 1992-06-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - AIDS and drug abuse in rural America. AN - 72953643; 10170975 AB - This paper reviews the nature and extent of drug abuse-related HIV disease services in the rural United States. Issues concerning the delivery of HIV disease and substance abuse health care services in rural settings are outlined and discussed. JF - The Journal of rural health : official journal of the American Rural Health Association and the National Rural Health Care Association AU - Steel, E AU - Haverkos, H W AD - Division of Applied Research, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 70 EP - 73 VL - 8 IS - 1 SN - 0890-765X, 0890-765X KW - Health administration KW - AIDS/HIV KW - Attitude to Health KW - Humans KW - United States -- epidemiology KW - Health Services Accessibility KW - Substance Abuse Treatment Centers -- supply & distribution KW - Rural Health -- trends KW - Acquired Immunodeficiency Syndrome -- epidemiology KW - HIV Infections -- transmission KW - Acquired Immunodeficiency Syndrome -- transmission KW - HIV Infections -- etiology KW - Substance-Related Disorders -- complications KW - Substance-Related Disorders -- rehabilitation KW - HIV Infections -- epidemiology KW - Acquired Immunodeficiency Syndrome -- etiology KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72953643?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+rural+health+%3A+official+journal+of+the+American+Rural+Health+Association+and+the+National+Rural+Health+Care+Association&rft.atitle=AIDS+and+drug+abuse+in+rural+America.&rft.au=Steel%2C+E%3BHaverkos%2C+H+W&rft.aulast=Steel&rft.aufirst=E&rft.date=1992-01-01&rft.volume=8&rft.issue=1&rft.spage=70&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+rural+health+%3A+official+journal+of+the+American+Rural+Health+Association+and+the+National+Rural+Health+Care+Association&rft.issn=0890765X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-24 N1 - Date created - 1992-06-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Alcohol and cocaine. Clinical and pharmacological interactions. AN - 72952145; 1317047 AB - Both clinical experience and epidemiological studies in community and specialized (e.g., treatment) populations indicate that the prevalence of co-use of alcohol and cocaine, and the comorbidity of alcoholism and cocaine addiction, are greater than would be expected from the chance occurrence of two independent conditions. Alcohol and cocaine have pharmacokinetic and pharmacodynamic interactions that may account for some of this co-use. While their reinforcing properties have neuropharmacological and behavioral differences, a unified theory of reinforcement by alcohol and cocaine has been proposed, involving dopamine activity in the ventral tegmental area-nucleus accumbens circuit. Regardless of their pharmacology, the prevalent co-use of alcohol and cocaine has important implications for drug abuse treatment and indicates the need for future research on this topic. JF - Recent developments in alcoholism : an official publication of the American Medical Society on Alcoholism, the Research Society on Alcoholism, and the National Council on Alcoholism AU - Gorelick, D A AD - Treatment and Early Intervention Branch, Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland. Y1 - 1992 PY - 1992 DA - 1992 SP - 37 EP - 56 VL - 10 SN - 0738-422X, 0738-422X KW - Receptors, Neurotransmitter KW - 0 KW - Ethanol KW - 3K9958V90M KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Drug Interactions KW - Humans KW - Brain -- drug effects KW - Receptors, Neurotransmitter -- drug effects KW - Comorbidity KW - Alcoholism -- rehabilitation KW - Substance-Related Disorders -- diagnosis KW - Ethanol -- pharmacokinetics KW - Substance-Related Disorders -- blood KW - Alcoholism -- epidemiology KW - Alcoholism -- diagnosis KW - Cocaine -- pharmacokinetics KW - Substance-Related Disorders -- rehabilitation KW - Substance-Related Disorders -- epidemiology KW - Alcoholism -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72952145?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.atitle=Alcohol+and+cocaine.+Clinical+and+pharmacological+interactions.&rft.au=Gorelick%2C+D+A&rft.aulast=Gorelick&rft.aufirst=D&rft.date=1992-01-01&rft.volume=10&rft.issue=&rft.spage=37&rft.isbn=&rft.btitle=&rft.title=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.issn=0738422X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-22 N1 - Date created - 1992-06-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A comparison of drug conditioning and craving for alcohol and cocaine. AN - 72950829; 1589599 AB - Craving is a potentially important concept that is difficult to define and study in the laboratory. Although alcohol and cocaine are very different pharmacologically, this discussion emphasizes common factors in addiction to these drugs, such as the tendency of alcoholics and cocaine abusers to crave these substances. I review commonalities in drug conditioning and cue reactivity to alcohol and cocaine. Both drugs support Pavlovian conditioning when they are presented as unconditioned stimuli, whether studied in rodents or humans. In addition, both drugs are craved when abusers are presented with stimuli associated with these drugs. Finally, I propose a theoretical definition of craving based on autoshaping and sign-tracking phenomena that suggests a common mechanism of addiction to these drugs. This model defines craving as a reflection of sign tracking to internal and external stimuli that have in the past reliably predicted presentation of these drugs. JF - Recent developments in alcoholism : an official publication of the American Medical Society on Alcoholism, the Research Society on Alcoholism, and the National Council on Alcoholism AU - Newlin, D B AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland 21224-2735. Y1 - 1992 PY - 1992 DA - 1992 SP - 147 EP - 164 VL - 10 SN - 0738-422X, 0738-422X KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Animals KW - Motivation KW - Humans KW - Association Learning KW - Conditioning, Classical KW - Substance-Related Disorders -- psychology KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72950829?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.atitle=A+comparison+of+drug+conditioning+and+craving+for+alcohol+and+cocaine.&rft.au=Newlin%2C+D+B&rft.aulast=Newlin&rft.aufirst=D&rft.date=1992-01-01&rft.volume=10&rft.issue=&rft.spage=147&rft.isbn=&rft.btitle=&rft.title=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.issn=0738422X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-22 N1 - Date created - 1992-06-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential induction of 15 and 16 kDa nuclear proteins in promotion sensitive and promotion resistant mouse JB6 cells. AN - 72949586; 1581616 AB - Gene expression relevant to promotion of neoplastic transformation was investigated by measuring proteins differentially synthesized in two mouse epidermal JB6 cell lines sensitive (P+) or resistant (P-) to tumor promoter induced transformation. One dimensional polyacrylamide gel electrophoresis of proteins from cells that had been pulse labeled with 35S-methionine after various times of exposure to the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) revealed two protein bands whose intensity increased after 20-24 hr exposure to TPA. Cell fractionation showed that these proteins of 15 and 16 kDa were localized in the nuclear, not the cytosolic, fraction. Parallel studies with 32P-labeled cells showed no evidence for phosphorylation of these proteins. Comparison of P- with P+ cells showed that the observed induction of p15/16 synthesis at 20 hr was specific for P+ cells, with little evidence for stimulated synthesis in P- cells during a 48 hr period. We thus conclude that the tumor promoter produces a late stimulation in the rate of synthesis of 15 and 16 kDa nuclear proteins preferentially in promotion sensitive cells. JF - Oncology research AU - Hirano, K AU - Smith, B M AU - Colburn, N H AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1992 PY - 1992 DA - 1992 SP - 17 EP - 21 VL - 4 IS - 1 SN - 0965-0407, 0965-0407 KW - Carcinogens KW - 0 KW - Nuclear Proteins KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - In Vitro Techniques KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - Molecular Weight KW - Cell Line KW - Cell Transformation, Neoplastic -- metabolism KW - Cell Transformation, Neoplastic -- drug effects KW - Nuclear Proteins -- chemistry KW - Nuclear Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72949586?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncology+research&rft.atitle=Differential+induction+of+15+and+16+kDa+nuclear+proteins+in+promotion+sensitive+and+promotion+resistant+mouse+JB6+cells.&rft.au=Hirano%2C+K%3BSmith%2C+B+M%3BColburn%2C+N+H&rft.aulast=Hirano&rft.aufirst=K&rft.date=1992-01-01&rft.volume=4&rft.issue=1&rft.spage=17&rft.isbn=&rft.btitle=&rft.title=Oncology+research&rft.issn=09650407&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-16 N1 - Date created - 1992-06-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of HMG chromosomal proteins during cell cycle and differentiation. AN - 72947484; 1581626 JF - Critical reviews in eukaryotic gene expression AU - Bustin, M AU - Crippa, M P AU - Pash, J M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 1992 PY - 1992 DA - 1992 SP - 137 EP - 143 VL - 2 IS - 2 SN - 1045-4403, 1045-4403 KW - High Mobility Group Proteins KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Gene Expression Regulation KW - High Mobility Group Proteins -- biosynthesis KW - High Mobility Group Proteins -- genetics KW - Cell Differentiation -- genetics KW - Cell Cycle -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72947484?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Critical+reviews+in+eukaryotic+gene+expression&rft.atitle=Expression+of+HMG+chromosomal+proteins+during+cell+cycle+and+differentiation.&rft.au=Bustin%2C+M%3BCrippa%2C+M+P%3BPash%2C+J+M&rft.aulast=Bustin&rft.aufirst=M&rft.date=1992-01-01&rft.volume=2&rft.issue=2&rft.spage=137&rft.isbn=&rft.btitle=&rft.title=Critical+reviews+in+eukaryotic+gene+expression&rft.issn=10454403&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-16 N1 - Date created - 1992-06-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Neurotransmitters as neurotrophic factors: a new set of functions. AN - 72944742; 1350276 AB - At the start of this review, factors were deemed trophic if they stimulated mitosis, permitted neural cell survival, promoted neurite sprouting and growth cone motility, or turned on a specific neuronal phenotype. The in vitro evidence from cell cultures is overwhelming that both neurotransmitters and neuropeptides can have such actions. Furthermore, the same chemical can exert several of these effects, either on the same or on different cell populations. Perhaps the most striking example is that of VIP, which can stimulate not only mitosis, but also survival and neurite sprouting of sympathetic ganglion neuroblasts (Pincus et al., 1990a,b). The in vivo data to support the in vitro experiments are starting to appear. A role for VIP in neurodevelopment is supported by in vivo studies that show behavioral deficits produced in neonatal rats by treatment with a VIP antagonist (Hill et al., 1991). The work of Shatz' laboratory (Chun et al., 1987; Ghosh et al., 1990) suggests that neuropeptide-containing neurons, transiently present, serve as guideposts for thalamocortical axons coming in to innervate specific cortical areas. Along similar lines, Wolff et al. (1979) demonstrated gamma-aminobutyric acid-accumulating glia in embryonic cortex that appeared to form axoglial synapses and suggested the possibility that gamma-aminobutyric acid released from the glia might play a role in synaptogenesis by increasing the number of postsynaptic thickenings. Meshul et al. (1987) have provided evidence that astrocytes can regulate synaptic density in the developing cerebellum. The work of Zagon and McLaughlin (1986a,b, 1987) has shown that naltrexone, an antagonist of the endogenous opioid peptides, affects both cell number and neuronal sprouting. Lauder's laboratory (Lauder et al., 1982) has shown a role for 5-HT in regulation of the proliferation of numerous cell types. These studies illustrate another important point, that neurotransmitters and neuropeptides function in communication not only between neurons, but also between neurons and glial cells, and between glial cells. Given that astrocytes can express virtually all of the neural receptors and can produce at least some of the neurotransmitters and neuropeptides, they must now be considered equal partners in the processes of intercellular communication in the nervous system, including the trophic responses. The actions of neurotransmitters and neuropeptides have to be considered in terms of a broad spectrum of actions that range from the trophic actions described in this review, to the classic transmitter actions, to potential roles in neurotoxicity.(ABSTRACT TRUNCATED AT 400 WORDS) JF - International review of neurobiology AU - Schwartz, J P AD - Unit on Growth Factors, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 1 EP - 23 VL - 34 SN - 0074-7742, 0074-7742 KW - Neuropeptides KW - 0 KW - Neurotransmitter Agents KW - Index Medicus KW - Phenotype KW - Neuroglia -- metabolism KW - Animals KW - Humans KW - Neuropeptides -- biosynthesis KW - Neurites -- physiology KW - Mitosis -- physiology KW - Cell Survival -- physiology KW - Neurons -- metabolism KW - Neurotransmitter Agents -- physiology KW - Neurons -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72944742?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+review+of+neurobiology&rft.atitle=Neurotransmitters+as+neurotrophic+factors%3A+a+new+set+of+functions.&rft.au=Schwartz%2C+J+P&rft.aulast=Schwartz&rft.aufirst=J&rft.date=1992-01-01&rft.volume=34&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=International+review+of+neurobiology&rft.issn=00747742&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-25 N1 - Date created - 1992-06-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Oxygen-derived free radical and active oxygen complex formation from cobalt(II) chelates in vitro. AN - 72934186; 1316186 AB - The electron paramagnetic resonance (EPR) spin trapping technique was used to study the generation of oxygen free radicals from the reaction of hydrogen peroxide with various Co(II) complexes in pH 7.4 phosphate buffer. The 5,5-dimethyl-1-pyrroline N-oxide (DMPO) spin trap was used in these experiments to detect superoxide and hydroxyl free radicals. Superoxide radical was generated from the reaction of H2O2 with Co(II), but was inhibited when Co(II) was chelated with adenosine 5'-diphosphate or citrate. Visible absorbance spectra revealed no change in the final oxidation state of the cobalt ion in these samples. The EDTA complex also prevented detectable free-radical formation when H2O2 was added, but visible absorbance data indicated oxidation of the Co(II) to Co(III) in this case. The amount of DMPO/.OOH adduct detected by EPR was greatly enhanced when H2O2 reacted with the nitrilotriacetate complex relative to Co(II) alone, and in addition, concurrent formation of the DMPO/.OH adduct due to slow oxidation of Co(II) was observed. The hydroxyl radical adduct formation was suppressed by ethanol, but not DMSO, indicating that free hydroxyl radical was not formed. The deferoxamine nitroxide radical was exclusively formed when H2O2 was added to the Co(II) complex of this ligand, most probably in a site-specific manner. In the presence of ethylenediamine, Co(II) bound molecular O2 and directly oxidized DMPO to its DMPO/.OH adduct without first forming free superoxide, hydroxyl radical, or hydrogen peroxide. An experiment using 17O-enriched water revealed that the Co(II)-ethylenediamine complex caused the DMPO to react with solvent water to form the DMPO/.OH adduct. The relevance of these results to toxicological studies of cobalt is discussed. JF - Chemical research in toxicology AU - Hanna, P M AU - Kadiiska, M B AU - Mason, R P AD - National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. PY - 1992 SP - 109 EP - 115 VL - 5 IS - 1 SN - 0893-228X, 0893-228X KW - Chelating Agents KW - 0 KW - Citrates KW - Cyclic N-Oxides KW - Ethylenediamines KW - Free Radicals KW - Cobalt KW - 3G0H8C9362 KW - 5,5-dimethyl-1-pyrroline-1-oxide KW - 7170JZ1QF3 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Edetic Acid KW - 9G34HU7RV0 KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Deferoxamine KW - J06Y7MXW4D KW - Nitrilotriacetic Acid KW - KA90006V9D KW - Oxygen KW - S88TT14065 KW - Index Medicus KW - Nitrilotriacetic Acid -- chemistry KW - Animals KW - Cattle KW - Electron Spin Resonance Spectroscopy KW - Citrates -- chemistry KW - Deferoxamine -- chemistry KW - Superoxide Dismutase -- chemistry KW - Cyclic N-Oxides -- chemistry KW - Ethylenediamines -- chemistry KW - Edetic Acid -- chemistry KW - Adenosine Triphosphate -- chemistry KW - Chelating Agents -- chemistry KW - Cobalt -- chemistry KW - Oxygen -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72934186?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=Oxygen-derived+free+radical+and+active+oxygen+complex+formation+from+cobalt%28II%29+chelates+in+vitro.&rft.au=Hanna%2C+P+M%3BKadiiska%2C+M+B%3BMason%2C+R+P&rft.aulast=Hanna&rft.aufirst=P&rft.date=1992-01-01&rft.volume=5&rft.issue=1&rft.spage=109&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-18 N1 - Date created - 1992-06-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Disorders of neuromuscular transmission due to natural environmental toxins. AN - 72932338; 1315843 AB - A variety of natural toxins of animal, plant, and bacterial origin are capable of causing disorders of neuromuscular transmission. Animal toxins include venomous snakes and arthropods, venoms of certain marine creatures, skin secretions of dart-poison frogs, and poisonous fish, shellfish, and crabs. There are plant poisons such as curare, and bacterial poisons such as botulinum toxin. These act at single or multiple sites of the neuromuscular apparatus interfering with voltage-gated ion channels, acetylcholine release, depolarization of the postsynaptic membrane, or generation and spread of the muscle action potential. The specific actions of these toxins are being widely exploited in the study of neuromuscular physiology and pathology. Some toxins have proved to be valuable pharmaceutical agents. Poisoning by natural neurotoxins is an important public health hazard in many parts of the world, particularly in the tropics. Poisoning may occur by a bite or a sting of a venomous animal, or by the ingestion of poisonous fish, shellfish or other marine delicacies. Contaminated food is a vehicle for poisons such as botulinum toxin. Clinically, a cardinal feature in the symptomatology is muscle paralysis with a distribution characteristic of myasthenia gravis, affecting muscles innervated by cranial nerves, neck flexors, proximal limb muscles, and respiratory muscles. Respiratory paralysis may end fatally. This paper reviews from the clinical and pathophysiologic viewpoints, naturally occurring environmental neurotoxins acting at the neuromuscular junction. JF - Journal of the neurological sciences AU - Senanayake, N AU - Román, G C AD - Neuroepidemiology Branch, NINDS, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 1 EP - 13 VL - 107 IS - 1 SN - 0022-510X, 0022-510X KW - Neurotoxins KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Synaptic Transmission -- drug effects KW - Nervous System Diseases -- physiopathology KW - Nervous System Diseases -- chemically induced KW - Neurotoxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72932338?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+neurological+sciences&rft.atitle=Disorders+of+neuromuscular+transmission+due+to+natural+environmental+toxins.&rft.au=Senanayake%2C+N%3BRom%C3%A1n%2C+G+C&rft.aulast=Senanayake&rft.aufirst=N&rft.date=1992-01-01&rft.volume=107&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+neurological+sciences&rft.issn=0022510X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-09 N1 - Date created - 1992-06-09 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Neurol Sci. 1993 Aug;118(1):101 [8229045] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Translational suppression in retroviral gene expression. AN - 72923788; 1575083 JF - Advances in virus research AU - Hatfield, D L AU - Levin, J G AU - Rein, A AU - Oroszlan, S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 193 EP - 239 VL - 41 SN - 0065-3527, 0065-3527 KW - RNA, Viral KW - 0 KW - Viral Proteins KW - Index Medicus KW - Viral Proteins -- genetics KW - Animals KW - Base Sequence KW - Molecular Sequence Data KW - Amino Acid Sequence KW - RNA, Viral -- genetics KW - Gene Expression Regulation, Viral -- physiology KW - Protein Biosynthesis -- physiology KW - Retroviridae -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72923788?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+virus+research&rft.atitle=Translational+suppression+in+retroviral+gene+expression.&rft.au=Hatfield%2C+D+L%3BLevin%2C+J+G%3BRein%2C+A%3BOroszlan%2C+S&rft.aulast=Hatfield&rft.aufirst=D&rft.date=1992-01-01&rft.volume=41&rft.issue=&rft.spage=193&rft.isbn=&rft.btitle=&rft.title=Advances+in+virus+research&rft.issn=00653527&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-04 N1 - Date created - 1992-06-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cholera and pertussis toxins modify regulation of glucose transport activity in rat adipose cells: evidence for mediation of a cAMP-independent process by G-proteins. AN - 72920046; 1315147 AB - Adenylyl cyclase in rat adipose cells is stimulated by ligands for Rs receptors (e.g. isoproterenol) and inhibited by ligands for Ri receptors (e.g. adenosine). In contrast, Rs receptors mediate inhibition and Ri receptors mediate augmentation of insulin-stimulated glucose transport activity by a process independent of changes in cellular cAMP-dependent protein kinase activity [Kuroda M., Honnor R. C., Cushman S. W., Londos C. and Simpson I. A. (1987) J. biol. Chem. 262, 245-253]. The present study examines the possible role of G-proteins in the regulation of insulin-stimulated glucose transport activity by Rs and Ri receptors. First, conditions were established that permit intoxication of isolated rat adipocytes by cholera and pertussis toxins without compromising cell integrity. Effectiveness of toxin treatment was monitored by examining adenylyl cyclase activity in isolated plasma membranes. Secondly, neither toxin interfered with the ability of a maximal concentration insulin to initiate the glucose transport response. Thirdly, pertussis toxin eliminated the augmenting effects of adenosine on insulin-stimulated glucose transport activity, but enhanced the inhibitory effects of isoproterenol. Findings with ligands for other Ri receptors (nicotinic acid and prostaglandin E2) mirrored those with adenosine. Finally, cholera toxin elicited a modest depression of transport activity, and only in the absence of an Ri ligand (e.g. adenosine). Furthermore, in contrast to the enhanced stimulation of adenylyl cyclase by isoproterenol and GTP, cholera toxin eliminated the inhibitory effect of isoproterenol on transport activity. The augmentative effects of adenosine on transport activity were unchanged. Measurements of (-/+cAMP) cAMP-dependent protein kinase activity ratios reinforce the notion that modulation of glucose transport activity is independent of changes in cAMP. We conclude that regulation of glucose transport activity by Rs and Ri receptors is mediated by the G-proteins, Gs and Gi (or other toxin substrates), respectively. Inasmuch as such regulation occurs at the plasma membrane and appears to be cAMP-independent, it is suggested that glucose transporters may be direct targets for receptor: G-protein interactions. JF - Cellular signalling AU - Honnor, R C AU - Naghshineh, S AU - Cushman, S W AU - Wolff, J AU - Simpson, I A AU - Londos, C AD - Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 87 EP - 98 VL - 4 IS - 1 SN - 0898-6568, 0898-6568 KW - Adenylate Cyclase Toxin KW - 0 KW - Ligands KW - Receptors, Cell Surface KW - Virulence Factors, Bordetella KW - Cholera Toxin KW - 9012-63-9 KW - Cyclic AMP KW - E0399OZS9N KW - Pertussis Toxin KW - EC 2.4.2.31 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Glucose KW - IY9XDZ35W2 KW - Index Medicus KW - Animals KW - Cell Membrane -- enzymology KW - Adenylyl Cyclases -- metabolism KW - Cholera Toxin -- pharmacology KW - Receptors, Cell Surface -- metabolism KW - Rats KW - Rats, Inbred Strains KW - Virulence Factors, Bordetella -- pharmacology KW - Cells, Cultured KW - Cyclic AMP -- metabolism KW - Biological Transport -- physiology KW - Adipose Tissue -- metabolism KW - Adipose Tissue -- cytology KW - Glucose -- metabolism KW - GTP-Binding Proteins -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72920046?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cellular+signalling&rft.atitle=Cholera+and+pertussis+toxins+modify+regulation+of+glucose+transport+activity+in+rat+adipose+cells%3A+evidence+for+mediation+of+a+cAMP-independent+process+by+G-proteins.&rft.au=Honnor%2C+R+C%3BNaghshineh%2C+S%3BCushman%2C+S+W%3BWolff%2C+J%3BSimpson%2C+I+A%3BLondos%2C+C&rft.aulast=Honnor&rft.aufirst=R&rft.date=1992-01-01&rft.volume=4&rft.issue=1&rft.spage=87&rft.isbn=&rft.btitle=&rft.title=Cellular+signalling&rft.issn=08986568&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-04 N1 - Date created - 1992-06-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cellular localization of flavin-containing monooxygenase in rabbit lung. AN - 72911215; 1572320 AB - A specific form of flavin monooxygenase has been identified in the lungs of a number of species. Distribution of the pulmonary flavin-containing monooxygenase (FMOp) is of interest because it oxidatively metabolizes a wide variety of nitrogen-, sulfur-, and phosphorous-containing xenobiotics, some of which form highly toxic reactive intermediates. We have identified the nonciliated bronchiolar epithelial (Clara) cell as the predominant location for this enzyme in rabbit lung. In addition, protein in ciliated, endothelial, type I, and type II cells and in tracheal lining layer reacted with antibodies to FMOp. In all these cell types antigen was found associated with cytoplasmic organelles, and in the Clara cell antigen was most concentrated in areas rich in smooth endoplasmic reticulum. Staining of ciliated surfaces was also observed at both the light and electron microscopy levels. Extracellular antigen was also apparent in tracheal lining layer smeared onto glass slides. We compared the location of the FMOp with that of two enzymes of the cytochrome P-450 monooxygenase system (studied here and elsewhere), cytochrome P450 IIB (P450 IIB), and NADPH cytochrome P450 reductase (reductase), and concluded that (1) FMOp is detected in all cells where P450 IIB and reductase are both present (Clara, type II, and ciliated); (2) FMOp and P450 IIB, but not reductase, are detected in endothelial cells; (3) P450 IIB alone is detected in the plasma membrane, cilia, and microvillae of ciliated cells and plasma membrane of endothelial cells; and (4) FMOp alone is detected in type I cells. JF - Experimental lung research AU - Overby, L AU - Nishio, S J AU - Lawton, M P AU - Plopper, C G AU - Philpot, R M AD - Laboratory of Cellular and Molecular Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709. PY - 1992 SP - 131 EP - 144 VL - 18 IS - 1 SN - 0190-2148, 0190-2148 KW - Antibodies, Monoclonal KW - 0 KW - Oxygenases KW - EC 1.13.- KW - dimethylaniline monooxygenase (N-oxide forming) KW - EC 1.14.13.8 KW - Index Medicus KW - Animals KW - Immunoblotting KW - Liver -- enzymology KW - Endothelium, Vascular -- enzymology KW - Endothelium, Vascular -- cytology KW - Rabbits KW - Bronchi -- enzymology KW - Epithelial Cells KW - Organ Specificity -- immunology KW - Antibody Specificity -- immunology KW - Microscopy, Immunoelectron KW - Trachea -- enzymology KW - Immunohistochemistry KW - Male KW - Oxygenases -- immunology KW - Oxygenases -- analysis KW - Lung -- cytology KW - Lung -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72911215?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Experimental+lung+research&rft.atitle=Cellular+localization+of+flavin-containing+monooxygenase+in+rabbit+lung.&rft.au=Overby%2C+L%3BNishio%2C+S+J%3BLawton%2C+M+P%3BPlopper%2C+C+G%3BPhilpot%2C+R+M&rft.aulast=Overby&rft.aufirst=L&rft.date=1992-01-01&rft.volume=18&rft.issue=1&rft.spage=131&rft.isbn=&rft.btitle=&rft.title=Experimental+lung+research&rft.issn=01902148&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-04 N1 - Date created - 1992-06-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Two dimensional gel electrophoresis of cellular and secreted proteins from rat alveolar macrophages after lipopolysaccharide treatment. AN - 72906175; 1567919 AB - Two dimensional gel electrophoresis (2-D PAGE) and automated image analysis were used to study the effects of bacterial lipopolysaccharide (LPS) activation on secreted and cellular rat alveolar macrophage proteins. Primary alveolar macrophages were cultured and exposed to LPS in the presence of [35S]-methionine for 24 h. Image analysis of 2-D PAGE revealed that LPS treatment primarily modulated the proportions of several alveolar macrophage cellular proteins versus control in addition to limited protein induction and repression. The differential effect of LPS was more pronounced on secreted proteins where qualitative and quantitative differences from control cells were found. Immunoblots of secreted proteins with anti-tumor necrosis factor alpha (TNF alpha) and anti-interleukin-1 alpha(IL-1 alpha) antibodies identified these monokines from protein fluorographic patterns. IL-1 alpha was detected as a single polypeptide of 17 kD at pI = 5. Use of recombinant TNF alpha and monoclonal and polyclonal antibodies for immunodetection revealed the 17 kD form of TNF alpha as well as higher molecular weight species at 18 kD and 22 kD. Thus, analysis of radiolabeled rat macrophages treated with LPS reveals quantitative modulation of several cellular proteins as well as a distinctive pattern of secreted proteins which contain multiple monokine forms resolvable by 2-D PAGE. JF - Applied and theoretical electrophoresis : the official journal of the International Electrophoresis Society AU - Merrick, B A AU - He, C Y AU - Craig, W A AU - Clark, G C AU - Corsini, E AU - Rosenthal, G J AU - Mansfield, B K AU - Selkirk, J K AD - Division of Toxicology Research and Testing, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 177 EP - 187 VL - 2 IS - 6 SN - 0954-6642, 0954-6642 KW - Lipopolysaccharides KW - 0 KW - Proteins KW - Index Medicus KW - Rats KW - Immunoblotting KW - Animals KW - Rats, Inbred F344 KW - Photofluorography KW - Electrophoresis, Gel, Two-Dimensional KW - Image Processing, Computer-Assisted KW - Female KW - Proteins -- secretion KW - Macrophages, Alveolar -- chemistry KW - Lipopolysaccharides -- toxicity KW - Macrophages, Alveolar -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72906175?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Applied+and+theoretical+electrophoresis+%3A+the+official+journal+of+the+International+Electrophoresis+Society&rft.atitle=Two+dimensional+gel+electrophoresis+of+cellular+and+secreted+proteins+from+rat+alveolar+macrophages+after+lipopolysaccharide+treatment.&rft.au=Merrick%2C+B+A%3BHe%2C+C+Y%3BCraig%2C+W+A%3BClark%2C+G+C%3BCorsini%2C+E%3BRosenthal%2C+G+J%3BMansfield%2C+B+K%3BSelkirk%2C+J+K&rft.aulast=Merrick&rft.aufirst=B&rft.date=1992-01-01&rft.volume=2&rft.issue=6&rft.spage=177&rft.isbn=&rft.btitle=&rft.title=Applied+and+theoretical+electrophoresis+%3A+the+official+journal+of+the+International+Electrophoresis+Society&rft.issn=09546642&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-22 N1 - Date created - 1992-05-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Epidemiologic studies on HIV/AIDS and drug abuse. AN - 72887265; 1562014 AB - The HIV and drug abuse epidemics are intertwined, and drug abusers make up a significant proportion of reported AIDS patients. For a variety of reasons, it is difficult to collect and interpret data about each epidemic. It is even more difficult to determine the relationships between the two. In this paper, various epidemiologic studies in both fields are reviewed. Some strengths and limitations of those studies are discussed, and possible methods for improvement are identified. JF - The American journal of drug and alcohol abuse AU - Steel, E AU - Haverkos, H W AD - AIDS Coordinating Office, National Institute on Drug Abuse, Rockville, Maryland 20857. Y1 - 1992 PY - 1992 DA - 1992 SP - 167 EP - 175 VL - 18 IS - 2 SN - 0095-2990, 0095-2990 KW - Index Medicus KW - AIDS/HIV KW - Sexual Behavior KW - Sex Factors KW - Humans KW - Health Surveys KW - Continental Population Groups KW - Adult KW - Aged KW - Middle Aged KW - Child KW - Adolescent KW - United States -- epidemiology KW - Male KW - Female KW - Acquired Immunodeficiency Syndrome -- epidemiology KW - HIV Seropositivity -- epidemiology KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72887265?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+drug+and+alcohol+abuse&rft.atitle=Epidemiologic+studies+on+HIV%2FAIDS+and+drug+abuse.&rft.au=Steel%2C+E%3BHaverkos%2C+H+W&rft.aulast=Steel&rft.aufirst=E&rft.date=1992-01-01&rft.volume=18&rft.issue=2&rft.spage=167&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+drug+and+alcohol+abuse&rft.issn=00952990&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-14 N1 - Date created - 1992-05-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Parenting difficulties among adult survivors of father-daughter incest. AN - 72873723; 1559172 AB - Women with a history of father-daughter incest as children often report difficulty in parenting their own children. This study examined the self-reported parenting experience and practices of women who were incest victims as children. Since many incest victims are also children of alcoholics, we compared their reports of parenting with those of women whose fathers were alcoholic but not sexually abusive, and to women who had no known risk during their childhood. The findigns were that incest survivors reported significantly less confidence and less sense of control as parents than nonrisk mothers. In addition, they reported significantly less support in the parental partnership with their spouses, and reported being less consistent and organized, and making fewer maturity demands on their children. The findings are discussed in terms of the incest survivor's sense of inefficacy and loss of control, the potential of the marital relationship to buffer the adverse effects of growing up in the dysfunctional, incestuous family, and future research directions. JF - Child abuse & neglect AU - Cole, P M AU - Woolger, C AU - Power, T G AU - Smith, K D AD - Laboratory of Developmental Psychology, NIMH, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 239 EP - 249 VL - 16 IS - 2 SN - 0145-2134, 0145-2134 KW - Index Medicus KW - Regression Analysis KW - Humans KW - Surveys and Questionnaires KW - Marriage KW - Child KW - Adolescent KW - Sexual Behavior -- psychology KW - Alcoholism -- psychology KW - Male KW - Female KW - Sexual Behavior -- statistics & numerical data KW - Child, Preschool KW - Child Abuse, Sexual -- psychology KW - Parenting -- psychology KW - Child Rearing -- psychology KW - Incest -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72873723?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Child+abuse+%26+neglect&rft.atitle=Parenting+difficulties+among+adult+survivors+of+father-daughter+incest.&rft.au=Cole%2C+P+M%3BWoolger%2C+C%3BPower%2C+T+G%3BSmith%2C+K+D&rft.aulast=Cole&rft.aufirst=P&rft.date=1992-01-01&rft.volume=16&rft.issue=2&rft.spage=239&rft.isbn=&rft.btitle=&rft.title=Child+abuse+%26+neglect&rft.issn=01452134&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-14 N1 - Date created - 1992-05-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Do quantitative exposure assessments improve risk estimates in occupational studies of cancer? AN - 72869762; 1553986 AB - Quantitative assessment of exposure intensity is a difficult process, particularly for jobs held long ago. Despite difficulties, the use of this approach is growing in occupational epidemiology because it is hoped that the estimates will more closely approximate delivered dose than more traditional measures such as duration of exposure. If this assumption is correct, development and use of quantitative exposure estimates should reduce nondifferential exposure misclassification, sharpen exposure-response gradients, and enhance interpretation of study results. In this report, we used two methods to assess the value of quantitative exposure assessments in cancer epidemiology. In one, we surveyed the literature for investigations on occupational cancer that included assessments of both duration and intensity of exposure. The results of this survey indicated that exposure measures based on some measure of intensity of exposure yielded monotonically increasing exposure-response gradients and larger relative risks more often than those based on duration of exposure. Duration of exposure, however, occasionally provided the larger relative risks. In another approach, we found that different measures of exposure to formaldehyde classified subjects quite differently. For example, duration of exposure was unrelated to average exposure and was only weakly associated with exposure intensity or peak exposure. Because different measures of exposure may classify subjects quite differently and because quantitative estimates usually, but not always, yield larger relative risks and sharper exposure-response gradients than other measures of exposure, we believe that the prudent approach in epidemiologic investigations would be to develop quantitative estimates of exposure and to conduct analyses using several different measures of exposure, or combinations such as duration by intensity. Multiple comparisons would, however, increase chance findings. The value of such an approach is twofold. When a true association exists, use of several different measures decreases the chances of an unfortunate selection of an exposure measure that is poorly related to delivered dose, which would tend to produce negative results, and increases the chances of uncovering sharper exposure-response gradients. Use of several exposure measures in investigations that fail to exhibit an association between exposure and disease would be of value because such an approach would provide greater confidence that negative findings were not simply due to exposure misclassification. JF - American journal of industrial medicine AU - Blair, A AU - Stewart, P A AD - Occupational Studies Section, National Cancer Institute, Rockville, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 53 EP - 63 VL - 21 IS - 1 SN - 0271-3586, 0271-3586 KW - Formaldehyde KW - 1HG84L3525 KW - Index Medicus KW - Risk KW - Humans KW - Time Factors KW - Occupational Exposure KW - Neoplasms -- chemically induced KW - Neoplasms -- epidemiology KW - Formaldehyde -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72869762?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+industrial+medicine&rft.atitle=Do+quantitative+exposure+assessments+improve+risk+estimates+in+occupational+studies+of+cancer%3F&rft.au=Blair%2C+A%3BStewart%2C+P+A&rft.aulast=Blair&rft.aufirst=A&rft.date=1992-01-01&rft.volume=21&rft.issue=1&rft.spage=53&rft.isbn=&rft.btitle=&rft.title=American+journal+of+industrial+medicine&rft.issn=02713586&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-28 N1 - Date created - 1992-04-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Arthritis in patients with psoriasis treated with gamma-interferon. AN - 72868464; 1556705 AB - We observed 3 patients with psoriasis who developed arthritis during treatment of psoriatic skin disease with intramuscular recombinant human gamma-interferon (IFN-gamma). Symptoms primarily involved the hands, feet, shoulders, and neck. One patient had acute plantar fasciitis. Routine laboratory studies were unrevealing. Patients presented with symptoms initially between the 10th and 12th weeks of treatment and the arthritis resolved after cessation of IFN-gamma. One patient was subsequently retreated with IFN-gamma for 4 weeks and had a temporary recurrence of arthritis with an associated rise and fall of his articular index. JF - The Journal of rheumatology AU - O'Connell, P G AU - Gerber, L H AU - Digiovanna, J J AU - Peck, G L AD - Department of Rehabilitation Medicine, Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 80 EP - 82 VL - 19 IS - 1 SN - 0315-162X, 0315-162X KW - Interferon-gamma KW - 82115-62-6 KW - Index Medicus KW - Humans KW - Injections, Intramuscular KW - Adult KW - Clinical Trials as Topic KW - Psoriasis -- drug therapy KW - Middle Aged KW - Male KW - Interferon-gamma -- therapeutic use KW - Arthritis, Psoriatic -- chemically induced KW - Interferon-gamma -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72868464?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+rheumatology&rft.atitle=Arthritis+in+patients+with+psoriasis+treated+with+gamma-interferon.&rft.au=O%27Connell%2C+P+G%3BGerber%2C+L+H%3BDigiovanna%2C+J+J%3BPeck%2C+G+L&rft.aulast=O%27Connell&rft.aufirst=P&rft.date=1992-01-01&rft.volume=19&rft.issue=1&rft.spage=80&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+rheumatology&rft.issn=0315162X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-07 N1 - Date created - 1992-05-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activating point mutation in Ki-ras codon 63 in a chemically induced rat renal tumor. AN - 72861750; 1554412 AB - Renal mesenchymal tumors induced in F344 rats with methyl(methoxymethyl)nitrosamine (DMN-OMe) have previously been shown by our laboratory to contain transforming Ki-ras sequences, activated most commonly by a variety of codon 12 mutations. Further sequence analysis of the one DMN-OMe-induced tumor with transforming Ki-ras sequences detected by NIH 3T3 transfection assay but with no mutation in codon 12 detected by selective oligonucleotide hybridization has now revealed an activating point mutation in codon 63. The observed GAG----AAG transition in codon 63, which replaces glutamic acid with lysine, was the only detectable mutation in exon 1 and 2 hotspot regions of Ki-ras in this tumor. The same mutation was also detected in Ki-ras sequences derived from first- and second-cycle transformants in NIH 3T3 transfection assays. Although random mutagenesis studies of cloned Ha-ras sequences by Fasano et al. (Proc Natl Acad Sci USA 81:4008-4012, 1984) had already indicated that GAG----AAG mutations in codon 63 of ras are transforming, this is the first demonstration of the natural occurrence of this particular activating mutation in a tumor. JF - Molecular carcinogenesis AU - Higinbotham, K G AU - Rice, J M AU - Perantoni, A O AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, Maryland. Y1 - 1992 PY - 1992 DA - 1992 SP - 136 EP - 139 VL - 5 IS - 2 SN - 0899-1987, 0899-1987 KW - Carcinogens KW - 0 KW - Codon KW - methyl(acetoxymethyl)nitrosamine KW - 56856-83-8 KW - Dimethylnitrosamine KW - M43H21IO8R KW - Index Medicus KW - Rats KW - Exons -- drug effects KW - Animals KW - 3T3 Cells KW - Rats, Inbred F344 KW - Base Sequence KW - Molecular Sequence Data KW - Mice KW - Mutation -- drug effects KW - Kidney Neoplasms -- genetics KW - Codon -- drug effects KW - Genes, ras -- drug effects KW - Kidney Neoplasms -- chemically induced KW - Dimethylnitrosamine -- analogs & derivatives KW - Gene Expression Regulation, Neoplastic -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72861750?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Activating+point+mutation+in+Ki-ras+codon+63+in+a+chemically+induced+rat+renal+tumor.&rft.au=Higinbotham%2C+K+G%3BRice%2C+J+M%3BPerantoni%2C+A+O&rft.aulast=Higinbotham&rft.aufirst=K&rft.date=1992-01-01&rft.volume=5&rft.issue=2&rft.spage=136&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-07 N1 - Date created - 1992-05-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Topical application of nitroxide protects radiation-induced alopecia in guinea pigs. AN - 72846827; 1544853 AB - We have recently found that treatment of Chinese hamster V79 cells with the stable nitroxide radical TEMPOL (4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl) afforded significant protection against superoxide, hydrogen peroxide, and X-ray mediated cytotoxicity. Radiation-induced alopecia is a common radiotherapeutic problem. Topical application of TEMPOL was evaluated for possible protective effects against radiation-induced alopecia using guinea pig skin as a model. For single acute X-ray doses up to 30 Gy, TEMPOL, when topically applied 15 min prior to irradiation provided a marked increase in the rate and extent of new hair recovery when compared to untreated skin. TEMPOL was detected in treated skin specimens with electron paramagnetic resonance (EPR) spectroscopy. Similar measurements of blood samples failed to show any signal resulting from topical application, nor could TEMPOL be detected in brain tissue after application on the scalp. TEMPOL represents a new class of compounds with potential for selective cutaneous radioprotection without systemic absorption. JF - International journal of radiation oncology, biology, physics AU - Goffman, T AU - Cuscela, D AU - Glass, J AU - Hahn, S AU - Krishna, C M AU - Lupton, G AU - Mitchell, J B AD - Radiation Oncology Branch, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 803 EP - 806 VL - 22 IS - 4 SN - 0360-3016, 0360-3016 KW - Cyclic N-Oxides KW - 0 KW - Radiation-Protective Agents KW - Spin Labels KW - tempol KW - U78ZX2F65X KW - Index Medicus KW - Animals KW - Skin -- radiation effects KW - Guinea Pigs KW - Radiation Injuries, Experimental -- prevention & control KW - Administration, Topical KW - Cyclic N-Oxides -- therapeutic use KW - Radiation-Protective Agents -- therapeutic use KW - Radiation-Protective Agents -- administration & dosage KW - Alopecia -- etiology KW - Cyclic N-Oxides -- administration & dosage KW - Alopecia -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72846827?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.atitle=Topical+application+of+nitroxide+protects+radiation-induced+alopecia+in+guinea+pigs.&rft.au=Goffman%2C+T%3BCuscela%2C+D%3BGlass%2C+J%3BHahn%2C+S%3BKrishna%2C+C+M%3BLupton%2C+G%3BMitchell%2C+J+B&rft.aulast=Goffman&rft.aufirst=T&rft.date=1992-01-01&rft.volume=22&rft.issue=4&rft.spage=803&rft.isbn=&rft.btitle=&rft.title=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.issn=03603016&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-14 N1 - Date created - 1992-04-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Salmonella mutagenicity tests: V. Results from the testing of 311 chemicals. AN - 72836806; 1541260 AB - 311 chemicals were tested under code, for mutagenicity, in Salmonella typhimurium; 35 of the chemicals were tested more than once in the same or different laboratories. The tests were conducted using a preincubation protocol in the absence of exogenous metabolic activation, and in the presence of liver S-9 from Aroclor-induced male Sprague-Dawley rats and Syrian hamsters. Some of the volatile chemicals were also tested in desiccators. A total of 120 chemicals were mutagenic or weakly mutagenic, 3 were judged questionable, and 172 were non-mutagenic. The remaining 16 chemicals produced different responses in the two or three laboratories in which they were tested. The results and data from these tests are presented. JF - Environmental and molecular mutagenesis AU - Zeiger, E AU - Anderson, B AU - Haworth, S AU - Lawlor, T AU - Mortelmans, K AD - Experimental Carcinogenesis and Mutagenesis Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC. Y1 - 1992 PY - 1992 DA - 1992 SP - 2 EP - 141 VL - 19 Suppl 21 SN - 0893-6692, 0893-6692 KW - Carcinogens KW - 0 KW - Mutagens KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Mesocricetus KW - Male KW - Cricetinae KW - Mutagenicity Tests KW - Carcinogens -- chemistry KW - Carcinogens -- toxicity KW - Mutagens -- toxicity KW - Salmonella typhimurium -- drug effects KW - Mutagens -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72836806?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+molecular+mutagenesis&rft.atitle=Salmonella+mutagenicity+tests%3A+V.+Results+from+the+testing+of+311+chemicals.&rft.au=Zeiger%2C+E%3BAnderson%2C+B%3BHaworth%2C+S%3BLawlor%2C+T%3BMortelmans%2C+K&rft.aulast=Zeiger&rft.aufirst=E&rft.date=1992-01-01&rft.volume=19+Suppl+21&rft.issue=&rft.spage=2&rft.isbn=&rft.btitle=&rft.title=Environmental+and+molecular+mutagenesis&rft.issn=08936692&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-09 N1 - Date created - 1992-04-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential c-jun expression in response to tumor promoters in JB6 cells sensitive or resistant to neoplastic transformation. AN - 72828208; 1543542 AB - The activity of AP-1, a trans-acting transcription factor, is stimulated by 12-O-tetradecanoylphorbol-13-acetate (TPA) and epidermal growth factor (EGF) in promotion-sensitive (P+) but not in promotion-resistant (P-) JB6 mouse epidermal cell lines. TPA and EGF also promote neoplastic transformation only in P+ cells. Thus, it has been proposed that AP-1-dependent gene expression is involved in determining sensitivity to tumor promotion. This paper explores the possible basis for the differential inducibility of AP-1 activity in P+ and P- JB6 cells, focusing in particular on the regulation of expression of the components of the AP-1 complex at the mRNA level. The expression of jun and fos gene family members, which make up the AP-1 complex, can be stimulated by serum and a number of growth factors, including EGF, and by TPA. Therefore, the possibility that differential expression of one or more forms of jun or fos contributes to the differential AP-1 activity was considered. The data presented here demonstrate both similarities and differences in the basal and TPA- or EGF-induced levels of fos and jun family members between P+ and P- cells. The most striking observation was that the overall TPA- and EGF-induced levels of jun but not fos expression were higher in P+ cells. This suggests that tumor promoter-regulated c-jun expression may contribute to the differential AP-1 activation observed in these cells and may be important in determining sensitivity to promotion of neoplastic transformation. JF - Molecular carcinogenesis AU - Ben-Ari, E T AU - Bernstein, L R AU - Colburn, N H AD - Cell Biology Section, National Cancer Institute, Frederick, MD 21702-1201. Y1 - 1992 PY - 1992 DA - 1992 SP - 62 EP - 74 VL - 5 IS - 1 SN - 0899-1987, 0899-1987 KW - Carcinogens KW - 0 KW - Proto-Oncogene Proteins c-jun KW - RNA, Messenger KW - Epidermal Growth Factor KW - 62229-50-9 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Neoplasm Transplantation KW - Gene Expression -- drug effects KW - Animals KW - Cells, Cultured KW - In Vitro Techniques KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - Epidermal Growth Factor -- pharmacology KW - RNA, Messenger -- genetics KW - Cell Transformation, Neoplastic -- genetics KW - Carcinogens -- pharmacology KW - Proto-Oncogene Proteins c-jun -- genetics KW - Genes, fos KW - Genes, jun UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72828208?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Differential+c-jun+expression+in+response+to+tumor+promoters+in+JB6+cells+sensitive+or+resistant+to+neoplastic+transformation.&rft.au=Ben-Ari%2C+E+T%3BBernstein%2C+L+R%3BColburn%2C+N+H&rft.aulast=Ben-Ari&rft.aufirst=E&rft.date=1992-01-01&rft.volume=5&rft.issue=1&rft.spage=62&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-16 N1 - Date created - 1992-04-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Conditions for detecting the mutagenicity of divalent metals in Salmonella typhimurium. AN - 72827200; 1541255 AB - The mutagenesis of metals in bacteria, as reported in the literature, can best be described as inconsistent. We report that cobalt chloride (Co++), ferrous sulfate (Fe++), manganese sulfate (Mn++), cadmium chloride (Cd++), and zinc chloride (Zn++) could be reproducibly detected as mutagens in Salmonella strain TA97 when preincubation exposures were made in sterile, distilled, deionized water, or in Hepes buffer in NaCl2/KCl2, rather than the standard sodium phosphate buffer. Co++ was also mutagenic under standard preincubation conditions. The individual components of Vogel-Bonner medium, i.e., potassium and ammonium phosphate, citrate, and magnesium sulfate, inhibit mutagenesis by these metals. The phosphates and the citrate probably inhibit by chelating the metals, while data are presented to suggest that Mg++ inhibition of metal mutagenesis is due to competitive inhibition for active transport via the magnesium active transport system in Salmonella. The chelator, diethyldithiocarbamate, inhibited the mutagenicity of Co++, Fe++, Zn++, and Mn++, but enhanced the mutagenicity of Cd++. The results presented show that divalent metals can be detected as mutagens in Salmonella, and that their lack of detection as mutagens is not due to an inherent insensitivity of Salmonella but to their interaction with media components and/or passive and active transport processes. JF - Environmental and molecular mutagenesis AU - Pagano, D A AU - Zeiger, E AD - Experimental Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 139 EP - 146 VL - 19 IS - 2 SN - 0893-6692, 0893-6692 KW - Cations, Divalent KW - 0 KW - Culture Media KW - Metals KW - Agar KW - 9002-18-0 KW - Index Medicus KW - Cations, Divalent -- toxicity KW - Species Specificity KW - Mutagenicity Tests KW - Salmonella typhimurium -- drug effects KW - Metals -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72827200?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+molecular+mutagenesis&rft.atitle=Conditions+for+detecting+the+mutagenicity+of+divalent+metals+in+Salmonella+typhimurium.&rft.au=Pagano%2C+D+A%3BZeiger%2C+E&rft.aulast=Pagano&rft.aufirst=D&rft.date=1992-01-01&rft.volume=19&rft.issue=2&rft.spage=139&rft.isbn=&rft.btitle=&rft.title=Environmental+and+molecular+mutagenesis&rft.issn=08936692&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-09 N1 - Date created - 1992-04-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of transforming growth factor-alpha in regenerating liver and during hepatic differentiation. AN - 72827130; 1543539 AB - Both the level of expression and cellular distribution of transcripts for transforming growth factor-alpha (TGF-alpha) were studied in adult rat liver after partial hepatectomy and during hepatic differentiation in fetal, neonatal, and adult livers by northern blot analysis and in situ hybridization. A marked increase in the expression of TGF-alpha was observed in neonatal livers and in adult livers after partial hepatectomy and during hepatic regeneration following modification of the Solt-Farber protocol. Quantitation of silver grains after in situ hybridization with a TGF-alpha riboprobe revealed a sixfold to eightfold increase in fetal and neonatal hepatocytes. Moreover, the expression of TGF-alpha in the liver 3 wk after birth was still fourfold higher than that of the adult quiescent liver. Both proliferating oval cells and basophilic foci of hepatocytes generated by modification of the Solt-Farber protocol were positive for TGF-alpha transcripts. The level of TGF-alpha transcripts was sixfold higher in the basophilic foci than in the surrounding liver. High concentrations of TGF-alpha transcripts were observed in the oval cells that lined pseudoducts and in the transitional cells proliferating within the ducts. The combination of in situ hybridization and immunocytochemistry using cell-specific antibodies revealed the presence of TGF-alpha transcripts in both oval cells and in perisinusoidal stellate cells. The observation that TGF-alpha transcripts were found both in primitive liver epithelial cells and perisinusoidal stellate cells suggests that this growth factor, in addition to its mitogenic action, may also have other important functions in the liver. JF - Molecular carcinogenesis AU - Evarts, R P AU - Nakatsukasa, H AU - Marsden, E R AU - Hu, Z AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 25 EP - 31 VL - 5 IS - 1 SN - 0899-1987, 0899-1987 KW - RNA, Messenger KW - 0 KW - Transforming Growth Factor alpha KW - Index Medicus KW - Rats KW - Animals KW - Blotting, Northern KW - Gene Expression KW - Cell Differentiation KW - Nucleic Acid Hybridization KW - RNA, Messenger -- genetics KW - Cell Division KW - Liver -- cytology KW - Transforming Growth Factor alpha -- genetics KW - Liver Regeneration KW - Liver -- physiology KW - Liver -- embryology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72827130?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Expression+of+transforming+growth+factor-alpha+in+regenerating+liver+and+during+hepatic+differentiation.&rft.au=Evarts%2C+R+P%3BNakatsukasa%2C+H%3BMarsden%2C+E+R%3BHu%2C+Z%3BThorgeirsson%2C+S+S&rft.aulast=Evarts&rft.aufirst=R&rft.date=1992-01-01&rft.volume=5&rft.issue=1&rft.spage=25&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-16 N1 - Date created - 1992-04-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of the SV40 large T antigen and EJ ras oncogene on fibronectin localization in human endometrial cells as viewed by confocal laser scanning microscopy. AN - 72826233; 1543549 AB - We utilized confocal laser scanning microscopy to examine the localization of fibronectin deposition in cultures of human endometrial stromal cells. We found that fibronectin in normal human endometrial stromal cell cultures was both intracellular, occurring in rough endoplasmic reticulum and in perinuclear regions, and extracellular, occurring diffusely over the entire cell surface. Endometrial stromal cells were transfected with a plasmid containing an origin-defective Simian Virus 40 (SV40) which codes for a temperature-sensitive large T antigen. When these cells were placed under temperature-restrictive conditions for large T-antigen function, they exhibited staining patterns similar to normal endometrial cells. Fibronectin deposition in cultures of partially or fully transformed endometrial cells was not intracellular as in normal cells, but was localized primarily between cells. Cells expressing the SV40 large T antigen deposited fibronectin mainly in parallel clumps between cells. Cells expressing both the SV40 large T antigen and the EJ ras oncogene, at high cell density, displayed networks of fibronectin arranged in matrix-like patterns between cells. The malignant cell line examined, sarcoma cells, also exhibited fibronectin networks between cells. Cell density affected fibronectin deposition in endometrial stromal cells expressing the EJ ras oncogene. At low density, cells expressing the SV40 large T antigen and the EJ ras oncogene displayed diffuse fibronectin patterns and, at high density, these cells formed colonies with networks of fibronectin between cells. JF - Pathobiology : journal of immunopathology, molecular and cellular biology AU - Carter, C A AU - Vollmer, G AU - Kaufman, D G AD - Experimental Carcinogenesis and Mutagenesis Branch, National Institute of Environmental Health Sciences, Research Triangle Park, N.C. 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 33 EP - 41 VL - 60 IS - 1 SN - 1015-2008, 1015-2008 KW - EJ ras KW - Antigens, Polyomavirus Transforming KW - 0 KW - Fibronectins KW - Index Medicus KW - Uterine Neoplasms -- genetics KW - Transfection KW - Cells, Cultured KW - Humans KW - Uterine Neoplasms -- metabolism KW - Female KW - Genes, ras KW - Fibronectins -- metabolism KW - Antigens, Polyomavirus Transforming -- genetics KW - Endometrium -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72826233?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pathobiology+%3A+journal+of+immunopathology%2C+molecular+and+cellular+biology&rft.atitle=Effects+of+the+SV40+large+T+antigen+and+EJ+ras+oncogene+on+fibronectin+localization+in+human+endometrial+cells+as+viewed+by+confocal+laser+scanning+microscopy.&rft.au=Carter%2C+C+A%3BVollmer%2C+G%3BKaufman%2C+D+G&rft.aulast=Carter&rft.aufirst=C&rft.date=1992-01-01&rft.volume=60&rft.issue=1&rft.spage=33&rft.isbn=&rft.btitle=&rft.title=Pathobiology+%3A+journal+of+immunopathology%2C+molecular+and+cellular+biology&rft.issn=10152008&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-13 N1 - Date created - 1992-04-13 N1 - Date revised - 2017-01-13 N1 - Gene symbol - EJ ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Oral contraceptives and primary liver cancer among young women. AN - 72823670; 1536912 AB - The association of oral contraceptive use with liver cancer was examined in a study of 76 deaths from primary liver cancer, 22 deaths from cancer of the intrahepatic bile ducts, and 629 controls among women aged 25 to 49 years. The subjects in the study are from the 1986 National Mortality Followback Survey, which included a questionnaire sent or administered to the next-of-kin of almost 20,000 deceased individuals in the United States. Information on a number of lifestyle factors was collected, including questions on oral contraceptive use. Increased risks of primary liver cancer were found for ever-users (odds ratio [OR] = 1.6, 95 percent confidence interval [CI] = 0.9-2.6), and for long-term (greater than or equal to 10 years) users (OR = 2.0, CI = 0.8-4.8) of oral contraceptives. When the analysis was restricted to subjects whose spouse or parent was the respondent, more pronounced risks were seen for ever-users (OR = 2.7, CI = 1.4-5.3) and long-term users (OR = 4.8, CI = 1.7-14.0). No clear excess risk was found for cancer of the intrahepatic bile ducts. This study, the largest to date, adds to the number of investigations demonstrating an increased risk of primary liver cancer with use, particularly long-term use, of oral contraceptives. JF - Cancer causes & control : CCC AU - Hsing, A W AU - Hoover, R N AU - McLaughlin, J K AU - Co-Chien, H T AU - Wacholder, S AU - Blot, W J AU - Fraumeni, J F AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 43 EP - 48 VL - 3 IS - 1 SN - 0957-5243, 0957-5243 KW - Contraceptives, Oral KW - 0 KW - Index Medicus KW - United States KW - Odds Ratio KW - Risk Factors KW - Humans KW - Health Surveys KW - Adult KW - Case-Control Studies KW - Confidence Intervals KW - National Center for Health Statistics (U.S.) KW - Middle Aged KW - Female KW - Contraceptives, Oral -- adverse effects KW - Bile Duct Neoplasms -- epidemiology KW - Bile Ducts, Intrahepatic KW - Bile Duct Neoplasms -- etiology KW - Liver Neoplasms -- epidemiology KW - Liver Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72823670?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+causes+%26+control+%3A+CCC&rft.atitle=Oral+contraceptives+and+primary+liver+cancer+among+young+women.&rft.au=Hsing%2C+A+W%3BHoover%2C+R+N%3BMcLaughlin%2C+J+K%3BCo-Chien%2C+H+T%3BWacholder%2C+S%3BBlot%2C+W+J%3BFraumeni%2C+J+F&rft.aulast=Hsing&rft.aufirst=A&rft.date=1992-01-01&rft.volume=3&rft.issue=1&rft.spage=43&rft.isbn=&rft.btitle=&rft.title=Cancer+causes+%26+control+%3A+CCC&rft.issn=09575243&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-30 N1 - Date created - 1992-03-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Cancer Causes Control. 1992 Jan;3(1):3-5 [1311211] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genotoxicity and cell proliferative activity of a nitrosated Oroxylum indicum Vent fraction in the pyloric mucosa of rat stomach. AN - 72819001; 1371592 AB - In vivo genotoxic activity and cell proliferative activity were examined in the stomach mucosa of male F344 rats by in vivo short-term methods after oral administration of a nitrosated Oroxylum indicum Vent (OiV) fraction, which had been found to be mutagenic without S9 mix to Salmonella typhimurium TA98 and TA100. Administration of the nitrosated OiV fraction at doses of 1 and 2 g/kg body weight induced dose-dependent DNA single-strand scission (p less than 0.02), determined by the alkaline elution method, in the stomach pyloric mucosa 2 h after its administration: a dose of 2 g/kg body weight induced an 18-fold increase in the DNA elution rate constant. Administration of the nitrosated OiV fraction at doses of 0.7-2.8 g/kg body weight also induced dose-dependent increases, up to 11-fold (p less than 0.05), in replicative DNA synthesis in the stomach pyloric mucosa 16 h after its administration. Moreover administration of the nitrosated OiV fraction at doses of 0.25-2.0 g/kg body weight induced dose-dependent increases, up to 100-fold, in ornithine decarboxylase activity in the stomach pyloric mucosa with a maximum 4 h after its administration. These results demonstrate that the nitrosated OiV fraction has genotoxic and cell proliferative activity in the pyloric mucosa of rat stomach in vivo. JF - Mutation research AU - Tepsuwan, A AU - Furihata, C AU - Rojanapo, W AU - Matsushima, T AD - Biochemistry and Chemical Carcinogenesis Section, Research Division, National Cancer Institute, Bangkok, Thailand. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 55 EP - 61 VL - 281 IS - 1 SN - 0027-5107, 0027-5107 KW - DNA, Single-Stranded KW - 0 KW - Plant Extracts KW - Ornithine Decarboxylase KW - EC 4.1.1.17 KW - Index Medicus KW - Rats KW - Administration, Oral KW - Animals KW - Rats, Inbred F344 KW - Mutagenicity Tests KW - DNA, Single-Stranded -- drug effects KW - Dose-Response Relationship, Drug KW - Ornithine Decarboxylase -- biosynthesis KW - Nitrosation KW - Plant Extracts -- adverse effects KW - Male KW - DNA Replication -- drug effects KW - Gastric Mucosa -- enzymology KW - DNA Damage KW - Plants, Medicinal KW - Cell Division -- drug effects KW - Gastric Mucosa -- drug effects KW - Gastric Mucosa -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72819001?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+research&rft.atitle=Genotoxicity+and+cell+proliferative+activity+of+a+nitrosated+Oroxylum+indicum+Vent+fraction+in+the+pyloric+mucosa+of+rat+stomach.&rft.au=Tepsuwan%2C+A%3BFurihata%2C+C%3BRojanapo%2C+W%3BMatsushima%2C+T&rft.aulast=Tepsuwan&rft.aufirst=A&rft.date=1992-01-01&rft.volume=281&rft.issue=1&rft.spage=55&rft.isbn=&rft.btitle=&rft.title=Mutation+research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-02 N1 - Date created - 1992-04-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Photodynamic therapy: the NCI experience and its nursing implications. AN - 72818764; 1538989 AB - Recent laboratory and clinical data have demonstrated encouraging results with a new treatment modality, photodynamic therapy (PDT). Initially used as a technique for tumor localization, PDT produces cytotoxic effects in superficial tumors such as those growing on the surfaces of the bladder, pleura, head and neck, bronchus, chest wall, and peritoneal cavity. PDT has three components: a light-sensitizing drug, light (generally from a laser), and oxygen. Initial results of phase I clinical trials conducted at the National Cancer Institute (NCI) are encouraging, and systemic toxicities have been minimal. Nursing intervention includes teaching, counseling, monitoring acute reactions, and follow-up care of these patients. This study outlines the results of experience with PDT at NCI and the nursing implications. JF - Oncology nursing forum AU - Dachowski, L J AU - DeLaney, T F AD - Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD. PY - 1992 SP - 63 EP - 67 VL - 19 IS - 1 SN - 0190-535X, 0190-535X KW - Index Medicus KW - Nursing KW - United States KW - Humans KW - National Institutes of Health (U.S.) KW - Decision Trees KW - Clinical Trials as Topic KW - Clinical Protocols KW - Neoplasms -- drug therapy KW - Photochemotherapy -- adverse effects KW - Neoplasms -- nursing KW - Photochemotherapy -- methods KW - Photochemotherapy -- nursing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72818764?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncology+nursing+forum&rft.atitle=Photodynamic+therapy%3A+the+NCI+experience+and+its+nursing+implications.&rft.au=Dachowski%2C+L+J%3BDeLaney%2C+T+F&rft.aulast=Dachowski&rft.aufirst=L&rft.date=1992-01-01&rft.volume=19&rft.issue=1&rft.spage=63&rft.isbn=&rft.btitle=&rft.title=Oncology+nursing+forum&rft.issn=0190535X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-01 N1 - Date created - 1992-04-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A prospective study of tobacco use and multiple myeloma: evidence against an association. AN - 72814591; 1536911 AB - The relationship between the use of cigarettes and other tobacco products and the risk of multiple myeloma was examined in a cohort of nearly 250,000 American veterans followed prospectively for 26 years. Compared with men who had never tobacco, the risk of death from myeloma was not increased among current (relative risk [RR] = 0.9, 95 percent confidence interval [CI] = 0.8-1.2) or former (RR = 1.0, CI = 0.8-1.3) cigarette smokers, nor among users of chewing tobacco or snuff (RR = 1.0, CI = 0.4-2.3). Risk was only slightly and nonsignificantly increased among pipe or cigar smokers (RR = 1.2, CI = 0.9-1.5). There was no indication of increasing risk with amount of tobacco used or earlier age at first use. With over 90 percent power to detect a 30 percent increased risk of this tumor occurring among current cigarette smokers, this study provides the strongest evidence to date against an association of cigarette smoking with multiple myeloma. JF - Cancer causes & control : CCC AU - Heineman, E F AU - Zahm, S H AU - McLaughlin, J K AU - Vaught, J B AU - Hrubec, Z AD - Epidemiology and Biometry Program, National Cancer Institute, Rockville, MD 20892. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 31 EP - 36 VL - 3 IS - 1 SN - 0957-5243, 0957-5243 KW - Index Medicus KW - Prospective Studies KW - Veterans -- statistics & numerical data KW - Aged, 80 and over KW - Risk Factors KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Male KW - Female KW - Plants, Toxic KW - Multiple Myeloma -- etiology KW - Multiple Myeloma -- epidemiology KW - Smoking -- epidemiology KW - Tobacco, Smokeless UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72814591?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+causes+%26+control+%3A+CCC&rft.atitle=A+prospective+study+of+tobacco+use+and+multiple+myeloma%3A+evidence+against+an+association.&rft.au=Heineman%2C+E+F%3BZahm%2C+S+H%3BMcLaughlin%2C+J+K%3BVaught%2C+J+B%3BHrubec%2C+Z&rft.aulast=Heineman&rft.aufirst=E&rft.date=1992-01-01&rft.volume=3&rft.issue=1&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=Cancer+causes+%26+control+%3A+CCC&rft.issn=09575243&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-30 N1 - Date created - 1992-03-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Cancer Causes Control. 1992 Jul;3(4):391-2 [1617129] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Geographic and gender variations in total tobacco use. AN - 72813790; 1536310 AB - This study is the first to provide complete information on prevalence rates by gender and geographic variation for each type of tobacco product used in the United States. Results indicate that, in nearly half of all states, total tobacco use in men exceeded 40% and, in four states, exceeded 50%. In women, only Nevada, Kentucky, and Michigan reported prevalence exceeding 33%. Results also indicate, however, that concurrent use of multiple tobacco forms is relatively rare. Substantial regional variation in male total tobacco use was evident, with southern males exhibiting the highest prevalence rate (44.6%). As a result, this region represents a target group in special need of comprehensive and effective tobacco use interventions. JF - American journal of public health AU - Shopland, D R AU - Niemcryk, S J AU - Marconi, K M AD - Cancer Control Sciences Program at the National Cancer Institute in Bethesda, Maryland 20892. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 103 EP - 106 VL - 82 IS - 1 SN - 0090-0036, 0090-0036 KW - Abridged Index Medicus KW - Index Medicus KW - Sex Factors KW - Humans KW - Adult KW - Surveys and Questionnaires KW - Confidence Intervals KW - United States -- epidemiology KW - Male KW - Female KW - Prevalence KW - Population Surveillance KW - Tobacco Use Disorder -- epidemiology KW - Tobacco Use Disorder -- etiology KW - Tobacco Use Disorder -- classification KW - Residence Characteristics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72813790?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+public+health&rft.atitle=Geographic+and+gender+variations+in+total+tobacco+use.&rft.au=Shopland%2C+D+R%3BNiemcryk%2C+S+J%3BMarconi%2C+K+M&rft.aulast=Shopland&rft.aufirst=D&rft.date=1992-01-01&rft.volume=82&rft.issue=1&rft.spage=103&rft.isbn=&rft.btitle=&rft.title=American+journal+of+public+health&rft.issn=00900036&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-20 N1 - Date created - 1992-03-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: JAMA. 1989 Jan 6;261(1):49-55 [2908994] NCI Monogr. 1989;(8):17-23 [2785646] J Natl Cancer Inst. 1989 Mar 15;81(6):409-14 [2783978] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Limited PCB antagonism of TCDD-induced malformations in mice. AN - 72813745; 1539179 AB - C57BL/6N mice used to model induction of cleft palate and kidney malformations in offspring following maternal treatment with TCDD, were dosed on gestation day (gd) 9 with 2,2',4,4',5,5'-hexachlorobiphenyl (HCB) (62.5, 125, 250, 500, 1000 mg/kg) and/or gd 10 with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (15 or 18 micrograms/kg) to investigate the potential protective effects of HCB against TCDD-induced teratogenicity. Maternal body weight gain was increased by combinations of 15 micrograms TCDD/kg and 125-500 mg HCB/kg and decreased at doses of 15 micrograms TCDD/kg + 1000 HCB mg/kg. At the doses used in this study, there was no effect of either compound on number of live or dead offspring. Fetal body weight was slightly decreased in all groups dosed with greater than or equal to 250 mg HCB/kg. HCB did not induce cleft palate at a dose of 1000 mg/kg, but did induce increases in hydronephrosis and hydroureter at 500 and 1000 mg/kg. Combinations of HCB and TCDD decreased the incidence of cleft palate induced by TCDD alone, but only at doses of 15 micrograms TCDD/kg combined with 125-500 mg HCB/kg. The antagonism of hydronephrosis (incidence and severity) appeared over a narrower dose range (15 micrograms TCDD/kg + 500 mg HCB/kg). HCB induced increases (3-fold) in ethoxyresorufin-O-deethylase (EROD) activity at doses of 500 and 1000 mg/kg, suggesting that the limited antagonism of TCDD teratogenicity by HCB could be under the control of the Ah-receptor. JF - Toxicology letters AU - Morrissey, R E AU - Harris, M W AU - Diliberto, J J AU - Birnbaum, L S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27711. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 19 EP - 25 VL - 60 IS - 1 SN - 0378-4274, 0378-4274 KW - Polychlorinated Dibenzodioxins KW - 0 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Polychlorinated Biphenyls KW - DFC2HB4I0K KW - Oxidoreductases KW - EC 1.- KW - Cytochrome P-450 CYP1A1 KW - EC 1.14.14.1 KW - 2,4,5,2',4',5'-hexachlorobiphenyl KW - ZRU0C9E32O KW - Index Medicus KW - Cytochrome P-450 Enzyme System -- analysis KW - Animals KW - Dose-Response Relationship, Drug KW - Mice, Inbred C57BL KW - Oxidoreductases -- analysis KW - Mice KW - Male KW - Female KW - Pregnancy KW - Polychlorinated Dibenzodioxins -- antagonists & inhibitors KW - Cleft Palate -- chemically induced KW - Polychlorinated Biphenyls -- pharmacology KW - Cleft Palate -- prevention & control KW - Hydronephrosis -- prevention & control KW - Abnormalities, Drug-Induced -- prevention & control KW - Hydronephrosis -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72813745?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+letters&rft.atitle=Limited+PCB+antagonism+of+TCDD-induced+malformations+in+mice.&rft.au=Morrissey%2C+R+E%3BHarris%2C+M+W%3BDiliberto%2C+J+J%3BBirnbaum%2C+L+S&rft.aulast=Morrissey&rft.aufirst=R&rft.date=1992-01-01&rft.volume=60&rft.issue=1&rft.spage=19&rft.isbn=&rft.btitle=&rft.title=Toxicology+letters&rft.issn=03784274&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-27 N1 - Date created - 1992-03-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - CONF T1 - Development shows some backbone. HFSP Workshop on Genetic Control of Vertebrate Development cosponsored by the Human Frontier Science Program, European Science Foundation, and European Molecular Biology Organization, Les Diablerets, Switzerland, May 26-30, 1991. AN - 72812557; 1346970 AB - This meeting aptly illustrated the power of a combined analysis of development in a range of vertebrate systems. Each system has its own inherent strengths: the mouse has gene transfer technology and targeted mutagenesis, the frog and chick have experimental embryology, and the zebrafish has genetics. It is the synergistic effect of considering all of these systems in combination that is without measure. In the past, the study of vertebrate development has been relegated to a largely descriptive phase. Initially, this was through analysis of morphological changes taking place during development. More recently, this has taken the form of cataloging the expression patterns of genes transcribed in development. It is clear that we are now entering an era when a functional analysis of development can get underway. JF - The New biologist AU - Mahon, K A AU - Dawid, I B Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 36 EP - 41 VL - 4 IS - 1 KW - Hox KW - Pax KW - Growth Substances KW - 0 KW - Tretinoin KW - 5688UTC01R KW - Index Medicus KW - Genes, Homeobox -- physiology KW - Tretinoin -- pharmacology KW - Animals KW - Neural Crest -- physiology KW - Extremities -- embryology KW - Embryonic Induction -- physiology KW - Embryonic and Fetal Development -- genetics KW - Mesoderm -- physiology KW - Nervous System -- embryology KW - Growth Substances -- physiology KW - Notochord -- physiology KW - Vertebrates -- genetics KW - Vertebrates -- embryology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72812557?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=The+New+biologist&rft.atitle=Development+shows+some+backbone.+HFSP+Workshop+on+Genetic+Control+of+Vertebrate+Development+cosponsored+by+the+Human+Frontier+Science+Program%2C+European+Science+Foundation%2C+and+European+Molecular+Biology+Organization%2C+Les+Diablerets%2C+Switzerland%2C+May+26-30%2C+1991.&rft.au=Mahon%2C+K+A%3BDawid%2C+I+B&rft.aulast=Mahon&rft.aufirst=K&rft.date=1992-01-01&rft.volume=4&rft.issue=1&rft.spage=36&rft.isbn=&rft.btitle=&rft.title=The+New+biologist&rft.issn=10434674&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-31 N1 - Date created - 1992-03-31 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Hox; Pax N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fifteen years of research of bioactive alkaloids. AN - 72810715; 1738243 JF - Medicinal research reviews AU - Brossi, A AD - Natural Products Section, National Institute of Diabetes, Digestive, and Kidney Diseases (NIDDK), National Institutes of Health, Bethesda, Maryland 20817. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 1 EP - 26 VL - 12 IS - 1 SN - 0198-6325, 0198-6325 KW - Alkaloids KW - 0 KW - Antimalarials KW - Morphinans KW - Morphine KW - 76I7G6D29C KW - Colchicine KW - SML2Y3J35T KW - Index Medicus KW - Antimalarials -- pharmacology KW - Animals KW - Colchicine -- pharmacology KW - MPTP Poisoning KW - Humans KW - Morphinans -- pharmacology KW - Structure-Activity Relationship KW - Morphine -- pharmacology KW - Alkaloids -- pharmacology KW - Alkaloids -- chemical synthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72810715?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Medicinal+research+reviews&rft.atitle=Fifteen+years+of+research+of+bioactive+alkaloids.&rft.au=Brossi%2C+A&rft.aulast=Brossi&rft.aufirst=A&rft.date=1992-01-01&rft.volume=12&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Medicinal+research+reviews&rft.issn=01986325&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-17 N1 - Date created - 1992-03-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The cloned promoter of the human DNA beta-polymerase gene contains a cAMP response element functional in HeLa cells. AN - 72806792; 1310859 AB - The mammalian DNA beta-polymerase (beta-pol) gene is constitutively expressed in cultured cells as a function of growth stage and DNA replication, but is expressed in rodents in a tissue-specific fashion. As revealed by transient expression experiments with wild-type and mutated beta-pol promoter fusion genes, the cloned human beta-pol promoter is transcriptionally regulated by signals acting through the single palindromic sequence (GT-GACGTCAC) known as an ATF/CRE-binding site centered at position -45 in the core promoter. Although the mere presence of the ATF/CRE palindromic sequence in a promoter does not always confer cAMP responsiveness or protein binding over and around the ATF/CRE sequence, we find that agents that increase cAMP levels (forskolin and IBMX) in HeLa cells activate the beta-pol promoter; activation also can be observed by coexpression of the protein kinase A catalytic subunit. Experiments with mutagenized beta-pol promoters indicate that the ATF/CRE-binding site mediates these effects. Thus, the ATF/CRE-binding site in the context of this TATA-less constitutive promoter is able to respond to the kinase A signal transduction pathway. JF - DNA and cell biology AU - Englander, E W AU - Wilson, S H AD - Laboratory of Biochemistry, National Cancer Institute, Bethesda, MD 20892. PY - 1992 SP - 61 EP - 69 VL - 11 IS - 1 SN - 1044-5498, 1044-5498 KW - Cyclic AMP Response Element-Binding Protein KW - 0 KW - DNA-Binding Proteins KW - Transcription Factors KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinases KW - EC 2.7.- KW - DNA Polymerase I KW - EC 2.7.7.- KW - Index Medicus KW - Base Sequence KW - Phosphorylation KW - Humans KW - Cyclic AMP -- pharmacology KW - Protein Kinases -- genetics KW - Molecular Sequence Data KW - Gene Expression Regulation KW - Transcription Factors -- genetics KW - Protein Binding KW - Cloning, Molecular KW - Promoter Regions, Genetic KW - HeLa Cells -- enzymology KW - DNA Polymerase I -- genetics KW - DNA-Binding Proteins -- genetics KW - HeLa Cells -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72806792?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=DNA+and+cell+biology&rft.atitle=The+cloned+promoter+of+the+human+DNA+beta-polymerase+gene+contains+a+cAMP+response+element+functional+in+HeLa+cells.&rft.au=Englander%2C+E+W%3BWilson%2C+S+H&rft.aulast=Englander&rft.aufirst=E&rft.date=1992-01-01&rft.volume=11&rft.issue=1&rft.spage=61&rft.isbn=&rft.btitle=&rft.title=DNA+and+cell+biology&rft.issn=10445498&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-26 N1 - Date created - 1992-03-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Muscarinic antagonists attenuate dizocilpine-induced hypermotility in mice. AN - 72805994; 1740967 AB - Pretreatment of mice with the muscarinic receptor antagonists scopolamine and atropine attenuated the hypermotility (but not the depression of rearing) induced by a low dose of dizocilpine maleate [(+)-MK-801; 0.1 mg/kg, i.p.], a non-competitive NMDA antagonist. In contrast, the muscarinic blockers failed to affect hypermotility induced by equieffective doses of phencyclidine (1 mg/kg, i.p.) or d-amphetamine (2 mg/kg, i.p.). These results suggest differences between the mechanism of behavioral activation produced by dizocilpine and phencyclidine, and demonstrate the potential of muscarinic blockade for diminishing the behavioral toxicity of NMDA antagonists. JF - Life sciences AU - Lapin, I P AU - Rogawski, M A AD - Neuronal Excitability Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - PL59 EP - PL64 VL - 50 IS - 9 SN - 0024-3205, 0024-3205 KW - Parasympatholytics KW - 0 KW - Scopolamine Hydrobromide KW - 451IFR0GXB KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - Atropine KW - 7C0697DR9I KW - Phencyclidine KW - J1DOI7UV76 KW - Dextroamphetamine KW - TZ47U051FI KW - Index Medicus KW - Animals KW - Scopolamine Hydrobromide -- pharmacology KW - Phencyclidine -- pharmacology KW - Mice KW - Atropine -- pharmacology KW - Male KW - Dextroamphetamine -- pharmacology KW - Dizocilpine Maleate -- antagonists & inhibitors KW - Parasympatholytics -- pharmacology KW - Motor Activity -- drug effects KW - Dizocilpine Maleate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72805994?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Life+sciences&rft.atitle=Muscarinic+antagonists+attenuate+dizocilpine-induced+hypermotility+in+mice.&rft.au=Lapin%2C+I+P%3BRogawski%2C+M+A&rft.aulast=Lapin&rft.aufirst=I&rft.date=1992-01-01&rft.volume=50&rft.issue=9&rft.spage=PL59&rft.isbn=&rft.btitle=&rft.title=Life+sciences&rft.issn=00243205&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-24 N1 - Date created - 1992-03-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ethanol inhibits mitogen-induced calcium mobilization in mouse splenocytes. AN - 72804763; 1346466 AB - Ethanol inhibited the mitogen-induced initial increase in cytoplasmic free-calcium [Ca2+]i in mouse splenocytes. This effect was concentration-dependent, reversible, and observed at pharmacologically relevant concentrations (24-166mM). Other short-chain alcohols such as propanol, butanol, and pentanol also inhibited this mitogen-induced increase in [Ca2+]i. The potencies of these alcohols to produce this effect were highly correlated (r = 0.98, p less than 0.001) with their membrane/buffer partition coefficients. Analysis of mouse splenocyte subpopulations demonstrated that this effect was manifest in both B and T lymphocytes. Within T lymphocyte subpopulations, both CD4+ and CD8+ T cells were affected. These results suggest that the inhibition of [Ca2+]i increase may be an early event mediating ethanol-induced immunosuppression and that this may be a predisposing factor to infection and malignancies associated with alcoholism. JF - Life sciences AU - Sei, Y AU - McIntyre, T AU - Skolnick, P AU - Arora, P K AD - Laboratory of Neuroscience, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 419 EP - 426 VL - 50 IS - 6 SN - 0024-3205, 0024-3205 KW - Concanavalin A KW - 11028-71-0 KW - Ethanol KW - 3K9958V90M KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - CD4-Positive T-Lymphocytes -- metabolism KW - Mice, Inbred C57BL KW - CD4-Positive T-Lymphocytes -- immunology KW - Mice KW - Flow Cytometry KW - Alcoholism -- immunology KW - CD4-Positive T-Lymphocytes -- drug effects KW - Concanavalin A -- pharmacology KW - Lymphocyte Activation -- drug effects KW - Calcium -- metabolism KW - B-Lymphocytes -- drug effects KW - T-Lymphocytes -- metabolism KW - Ethanol -- pharmacology KW - Spleen -- immunology KW - B-Lymphocytes -- immunology KW - T-Lymphocytes -- drug effects KW - B-Lymphocytes -- metabolism KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72804763?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Life+sciences&rft.atitle=Ethanol+inhibits+mitogen-induced+calcium+mobilization+in+mouse+splenocytes.&rft.au=Sei%2C+Y%3BMcIntyre%2C+T%3BSkolnick%2C+P%3BArora%2C+P+K&rft.aulast=Sei&rft.aufirst=Y&rft.date=1992-01-01&rft.volume=50&rft.issue=6&rft.spage=419&rft.isbn=&rft.btitle=&rft.title=Life+sciences&rft.issn=00243205&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-28 N1 - Date created - 1992-02-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - CONF T1 - Progress and prospects for human cancer vaccines. AN - 72804372; 1346654 JF - Journal of the National Cancer Institute AU - Cole, J S AU - Gruber, J Y1 - 1992/01/01/ PY - 1992 DA - 1992 Jan 01 SP - 18 EP - 23 VL - 84 IS - 1 KW - Vaccines KW - 0 KW - Index Medicus KW - Humans KW - Vaccines -- immunology KW - Neoplasms -- prevention & control KW - Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72804372?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Progress+and+prospects+for+human+cancer+vaccines.&rft.au=Cole%2C+J+S%3BGruber%2C+J&rft.aulast=Cole&rft.aufirst=J&rft.date=1992-01-01&rft.volume=84&rft.issue=1&rft.spage=18&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-13 N1 - Date created - 1992-03-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pharmacokinetic and dose tolerability study of ADD 94057 in comedicated patients with partial seizures. AN - 72793664; 1733743 AB - ADD 94057, a metabolite of fluzinamide, manufactured by the A. H. Robins Company, blocks chemically- and electrically-induced seizures in animals. The primary objective of this open add-on study was to evaluate patient tolerability of ADD 94057 at ascending target plasma concentrations. Nine subjects with medically refractory seizures were receiving phenytoin (PHT, 3), carbamazepine (CBZ, 3), or both (3). A pharmacokinetic profile after a single oral 400-mg dose of ADD 94057 was used to calculate ADD 94057 dosages. After a 4-week baseline period, patients were treated for 4 weeks with weekly ADD 94057 dosage escalations. Two patients completed the study at their assigned highest dosage level; the other patients finished the study at lower dosages. The patients receiving PHT (but not CBZ) tolerated higher plasma concentrations of ADD 94057 than did patients receiving CBZ, alone or in combination with PHT. Adverse experiences included headache, ataxia, blurred vision, diplopia, dizziness, lightheadedness, and mild confusion. Eight of nine patients had reductions in seizure frequency from baseline. JF - Epilepsia AU - Pledger, G W AU - Laxer, K D AU - Sahlroot, J T AU - Taylor, M R AU - Cereghino, J J AU - McCormick, C AU - Whitley, L AU - Manning, L W AD - Epilepsy Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 112 EP - 118 VL - 33 IS - 1 SN - 0013-9580, 0013-9580 KW - Anticonvulsants KW - 0 KW - Azetidines KW - Carbamazepine KW - 33CM23913M KW - Phenytoin KW - 6158TKW0C5 KW - AHR 11748 KW - 91077-32-6 KW - Index Medicus KW - Administration, Oral KW - Probability KW - Drug Administration Schedule KW - Drug Interactions KW - Dose-Response Relationship, Drug KW - Humans KW - Drug Therapy, Combination KW - Drug Tolerance KW - Phenytoin -- pharmacology KW - Adult KW - Carbamazepine -- pharmacology KW - Female KW - Male KW - Azetidines -- pharmacokinetics KW - Azetidines -- blood KW - Anticonvulsants -- pharmacokinetics KW - Epilepsies, Partial -- drug therapy KW - Azetidines -- administration & dosage KW - Anticonvulsants -- administration & dosage KW - Anticonvulsants -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72793664?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epilepsia&rft.atitle=Pharmacokinetic+and+dose+tolerability+study+of+ADD+94057+in+comedicated+patients+with+partial+seizures.&rft.au=Pledger%2C+G+W%3BLaxer%2C+K+D%3BSahlroot%2C+J+T%3BTaylor%2C+M+R%3BCereghino%2C+J+J%3BMcCormick%2C+C%3BWhitley%2C+L%3BManning%2C+L+W&rft.aulast=Pledger&rft.aufirst=G&rft.date=1992-01-01&rft.volume=33&rft.issue=1&rft.spage=112&rft.isbn=&rft.btitle=&rft.title=Epilepsia&rft.issn=00139580&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-28 N1 - Date created - 1992-02-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Anticonvulsant 1-phenylcycloalkylamines: two analogues with low motor toxicity when orally administered. AN - 72793010; 1531130 AB - 1-Phenylcyclohexylamine (PCA) and its analogues 1-phenylcyclopentylamine (PPA) and 1-(3-fluorophenyl)cyclohexylamine (3-F-PCA) are potent anticonvulsants in the mouse maximal electroshock (MES) seizure test. Unlike the structurally related dissociative anesthetic phencyclidine (PCP), however, which produces motor toxicity at anticonvulsant doses, PCA, PPA, and 3-F-PCA protect against MES seizures at 2.2- to 3.5-fold lower doses than those that cause motor toxicity when administered intraperitoneally (i.p.). In the present study, we evaluated the oral anticonvulsant activity of PCA, PPA, and 3-F-PCA in mice; we also examined 3-F-PCA in rats. All the compounds were orally active in the mouse MES seizure test (ED50 values 14.5, 53.4, and 26.7 mg/kg, respectively). Moreover, 3-F-PCA was especially potent in rats, either when administered i.p. (ED50 0.4 mg/kg vs. 9.4 mg/kg in mice) or orally (ED50 0.8 mg/kg). Surprisingly, however, oral PPA failed to cause motor toxicity in mice even at doses that were many times higher than those that were protective in the MES test (TD50 greater than 300 mg/kg). In rats, 3-F-PCA also showed a strikingly low oral toxicity (TD50 greater than 50 mg/kg) in relation to its potency as an anticonvulsant. Like PCP, PCA analogues block N-methyl-D-aspartate (NMDA)-induced behavioral effects and lethality in mice. Moreover, in vitro studies indicate that the compounds act as uncompetitive antagonists of the NMDA receptor-channel complex. Therefore, their anticonvulsant activity may, at least in part, relate to an interaction with NMDA receptors. JF - Epilepsia AU - Blake, P A AU - Yamaguchi, S AU - Thurkauf, A AU - Rogawski, M A AD - Neuronal Excitability Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 188 EP - 194 VL - 33 IS - 1 SN - 0013-9580, 0013-9580 KW - Amines KW - 0 KW - Anticonvulsants KW - Cyclohexylamines KW - Receptors, N-Methyl-D-Aspartate KW - 1-(3-fluorophenyl)cyclohexylamine KW - 125827-86-3 KW - 1-phenylcyclopentylamine KW - 17380-74-4 KW - N-Methylaspartate KW - 6384-92-5 KW - 1-phenylcyclohexylamine KW - HBO2D49I2S KW - Pentylenetetrazole KW - WM5Z385K7T KW - Index Medicus KW - Rats KW - Injections, Intraperitoneal KW - Administration, Oral KW - Animals KW - Receptors, N-Methyl-D-Aspartate -- drug effects KW - Dose-Response Relationship, Drug KW - N-Methylaspartate -- antagonists & inhibitors KW - Motor Activity -- drug effects KW - Mice KW - Electroshock KW - Male KW - Seizures -- chemically induced KW - Anticonvulsants -- pharmacology KW - Amines -- administration & dosage KW - Cyclohexylamines -- administration & dosage KW - Amines -- toxicity KW - Amines -- pharmacology KW - Cyclohexylamines -- toxicity KW - Anticonvulsants -- toxicity KW - Anticonvulsants -- administration & dosage KW - Seizures -- prevention & control KW - Cyclohexylamines -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72793010?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epilepsia&rft.atitle=Anticonvulsant+1-phenylcycloalkylamines%3A+two+analogues+with+low+motor+toxicity+when+orally+administered.&rft.au=Blake%2C+P+A%3BYamaguchi%2C+S%3BThurkauf%2C+A%3BRogawski%2C+M+A&rft.aulast=Blake&rft.aufirst=P&rft.date=1992-01-01&rft.volume=33&rft.issue=1&rft.spage=188&rft.isbn=&rft.btitle=&rft.title=Epilepsia&rft.issn=00139580&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-28 N1 - Date created - 1992-02-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 1,3-Butadiene: toxicity and carcinogenicity in laboratory animals and in humans. AN - 72789904; 1732994 AB - 1,3-Butadiene is a high production volume chemical used largely in the manufacture of synthetic rubber. The production and use of 1,3-butadiene increased dramatically during World War II with the development of the synthetic rubber industry. Before the 1980s, 1,3-butadiene was not considered to be particularly hazardous to human health; therefore, OSHA established a permissible limit of 1,000 ppm for occupational exposure to this chemical. Results of recent inhalation carcinogenicity studies have demonstrated clearly that 1,3-butadiene is a multiple-organ carcinogen in Sprague-Dawley rats and in B6C3F1 mice. Particularly noteworthy in mice were the early occurrences and extensive development of lymphomas, the induction of uncommon hemangiosarcomas of the heart, and the development of malignant lung tumors at exposure concentrations as low as 6.25 ppm. Because 6.25 ppm was the lowest concentration ever used in a long-term carcinogenicity of this gas, it is likely that lower exposure levels would also cause cancers in laboratory animals. In addition, multiple organ site neoplasia was induced in mice after only 13 weeks of exposure. Two reactive epoxides, 1,2-epoxy-3-butene and diepoxybutane, have been identified as intermediates in the biotransformation of 1,3-butadiene in rats and mice. Metabolism is probably an important factor in the carcinogenicity of 1,3-butadiene, because in vitro mutagenicity of 1,3-butadiene requires metabolic activation, whereas these epoxide intermediates are direct acting mutagens in bacteria and are carcinogens in rats and mice. The metabolism of 1,3-butadiene in rats and mice is linear up to concentrations of at least 1000 ppm. Pharmacokinetic studies on 1,3-butadiene and on 1,2-epoxy-3-butene have revealed certain quantitative differences in metabolic rates between Sprague-Dawley rats and B6C3F1 mice; however, these differences were not of sufficient magnitude to account for the reported different target site carcinogenic responses in these two strains of animals. Thus, additional factors must be involved in distinguishing site specificity in the carcinogenicity of 1,3-butadiene between species. In addition to its carcinogenic effects, 1,3-butadiene is a potent in vivo genotoxic agent to mouse bone marrow cells. Hematologic changes indicative of a partially regenerative anemia were induced in mice at 62.5 and higher concentrations. 1,3-Butadiene is also a reproductive and developmental toxicant. Epidemiology studies of workers employed in the production of 1,3-butadiene or of styrene-butadiene rubber have consistently revealed associations between occupational exposure to 1,3-butadiene and excess mortality due to lymphatic and hematopoietic cancers.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Reviews of environmental contamination and toxicology AU - Melnick, R L AU - Huff, J AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992 PY - 1992 DA - 1992 SP - 111 EP - 144 VL - 124 SN - 0179-5953, 0179-5953 KW - Butadienes KW - 0 KW - Carcinogens KW - Mutagens KW - 1,3-butadiene KW - JSD5FGP5VD KW - Index Medicus KW - Animals KW - Neoplasms, Experimental -- chemically induced KW - Biotransformation KW - Humans KW - Administration, Inhalation KW - Carcinogens -- metabolism KW - Butadienes -- toxicity KW - Mutagens -- metabolism KW - Carcinogens -- pharmacokinetics KW - Carcinogens -- toxicity KW - Mutagens -- toxicity KW - Mutagens -- pharmacokinetics KW - Butadienes -- metabolism KW - Butadienes -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72789904?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reviews+of+environmental+contamination+and+toxicology&rft.atitle=1%2C3-Butadiene%3A+toxicity+and+carcinogenicity+in+laboratory+animals+and+in+humans.&rft.au=Melnick%2C+R+L%3BHuff%2C+J&rft.aulast=Melnick&rft.aufirst=R&rft.date=1992-01-01&rft.volume=124&rft.issue=&rft.spage=111&rft.isbn=&rft.btitle=&rft.title=Reviews+of+environmental+contamination+and+toxicology&rft.issn=01795953&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-27 N1 - Date created - 1992-02-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lithium administration modulates platelet Gi in humans. AN - 72788575; 1731175 AB - Platelet G proteins were assessed in 7 normal volunteers before and after 14 days of lithium administration at therapeutic plasma levels. Cholera and pertussis toxin catalyzed ADP-ribosylation of platelet membrane proteins were measured by SDS-PAGE. Immunoblotting with specific antibodies was used to measure platelet membrane alpha i content. There was a statistically significant 37% increase in pertussis toxin mediated ADP-ribosylation of a 40,000 Mr protein in platelet membranes after lithium administration, but cholera toxin mediated ADP-ribosylation of a 45,000 Mr protein and alpha i immunoblotting were unchanged by lithium. Increased pertussis toxin stimulated ADP-ribosylation in the absence of changes in alpha i content could be explained by a shift in platelet Gi in favor of its undissociated, inactive form. This would be consistent with increased platelet adenylyl cyclase activity found in these same subjects after lithium. JF - Life sciences AU - Hsiao, J K AU - Manji, H K AU - Chen, G A AU - Bitran, J A AU - Risby, E D AU - Potter, W Z AD - Section on Clinical Pharmacology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 227 EP - 233 VL - 50 IS - 3 SN - 0024-3205, 0024-3205 KW - Adenylate Cyclase Toxin KW - 0 KW - Virulence Factors, Bordetella KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Cholera Toxin KW - 9012-63-9 KW - Lithium KW - 9FN79X2M3F KW - Pertussis Toxin KW - EC 2.4.2.31 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Index Medicus KW - Immunoblotting KW - Cell Membrane -- drug effects KW - Electrophoresis, Polyacrylamide Gel KW - Humans KW - Adenylyl Cyclases -- metabolism KW - Cholera Toxin -- pharmacology KW - Adenosine Diphosphate Ribose -- metabolism KW - Autoradiography KW - Molecular Weight KW - Virulence Factors, Bordetella -- pharmacology KW - Adult KW - Female KW - Male KW - GTP-Binding Proteins -- metabolism KW - Blood Platelets -- drug effects KW - Lithium -- administration & dosage KW - Blood Platelets -- metabolism KW - Lithium -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72788575?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Life+sciences&rft.atitle=Lithium+administration+modulates+platelet+Gi+in+humans.&rft.au=Hsiao%2C+J+K%3BManji%2C+H+K%3BChen%2C+G+A%3BBitran%2C+J+A%3BRisby%2C+E+D%3BPotter%2C+W+Z&rft.aulast=Hsiao&rft.aufirst=J&rft.date=1992-01-01&rft.volume=50&rft.issue=3&rft.spage=227&rft.isbn=&rft.btitle=&rft.title=Life+sciences&rft.issn=00243205&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-14 N1 - Date created - 1992-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antimutagenicity of a low molecular weight superoxide dismutase mimic against oxidative mutagens. AN - 72783938; 1310080 AB - A set of stable nitroxide free radicals that are used as spin labels have been shown to possess metal-independent superoxide dismutase-like activity. Unlike superoxide dismutase (SOD), these compounds are low molecular weight, and readily penetrate into the cell. A representative nitroxide, 4-hydroxy-2,2,6,6-tetramethylpiperidinyloxy (Tempol), was investigated for antimutagenic activity in the XPRT forward mutation assay in CHO AS52 cells. AS52 cells were exposed to hydrogen peroxide, or the hypoxanthine/xanthine oxidase superoxide generating system, in the presence or absence of 10 mM Tempol. Tempol itself was not mutagenic or toxic to AS52 cells. Tempol protected cells nearly completely from the cytotoxic and mutagenic effects of hydrogen peroxide and hypoxanthine/xanthine oxidase. We have previously shown that nitroxides do not alter the extracellular concentration of hydrogen peroxide, and that they are taken up by mammalian cells, suggesting that the antimutagenic activity of Tempol is an intracellular phenomenon. JF - Environmental and molecular mutagenesis AU - DeGraff, W G AU - Krishna, M C AU - Russo, A AU - Mitchell, J B AD - Radiobiology Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 21 EP - 26 VL - 19 IS - 1 SN - 0893-6692, 0893-6692 KW - Antimutagenic Agents KW - 0 KW - Cyclic N-Oxides KW - Spin Labels KW - Superoxides KW - 11062-77-4 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Catalase KW - EC 1.11.1.6 KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Xanthine Oxidase KW - EC 1.17.3.2 KW - Deferoxamine KW - J06Y7MXW4D KW - Nitrous Oxide KW - K50XQU1029 KW - tempol KW - U78ZX2F65X KW - Index Medicus KW - Xanthine Oxidase -- toxicity KW - Animals KW - Regression Analysis KW - Nitrous Oxide -- toxicity KW - Catalase -- pharmacology KW - Hydrogen Peroxide -- toxicity KW - Mutagenicity Tests KW - Deferoxamine -- pharmacology KW - Superoxide Dismutase -- pharmacology KW - Kinetics KW - Carcinogenicity Tests KW - CHO Cells KW - Superoxides -- toxicity KW - Cricetinae KW - Cyclic N-Oxides -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72783938?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+molecular+mutagenesis&rft.atitle=Antimutagenicity+of+a+low+molecular+weight+superoxide+dismutase+mimic+against+oxidative+mutagens.&rft.au=DeGraff%2C+W+G%3BKrishna%2C+M+C%3BRusso%2C+A%3BMitchell%2C+J+B&rft.aulast=DeGraff&rft.aufirst=W&rft.date=1992-01-01&rft.volume=19&rft.issue=1&rft.spage=21&rft.isbn=&rft.btitle=&rft.title=Environmental+and+molecular+mutagenesis&rft.issn=08936692&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-21 N1 - Date created - 1992-02-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of the amphiphilic peptides melittin and mastoparan on calcium influx, phosphoinositide breakdown and arachidonic acid release in rat pheochromocytoma PC12 cells. AN - 72776526; 1309880 AB - Two amphiphilic peptides from hymenopterid insects, melittin and mastoparan, stimulate secretion in a variety of cell types. In PC12 cells, both peptides stimulate calcium influx with melittin some 20-fold more potently than mastoparan. Melittin stimulates both breakdown of phosphoinositides (Pl) by phospholipase C to yield inositol phosphates and hydrolysis of phospholipids by phospholipase A2 to release arachidonic acid (AA). Mastoparan stimulates Pl breakdown, but has no effect on AA release. Maximal stimulation of Pl breakdown occurs at 1 to 2.5 micrograms/ml melittin and 30 micrograms/ml mastoparan, whereas maximal stimulation of AA release occurs at 2 to 5 micrograms/ml melittin. Organic calcium channel blockers (nifedipine, verapamil, diltiazem) have little or no effect on responses to the peptides. The influx of calcium elicited by melittin or mastoparan is completely or nearly completely blocked by inorganic calcium channel blockers (Co++, Mn++, Cd++). Mn++ and Cd++ inhibit melittin-induced Pl breakdown and AA release and mastoparan-induced Pl breakdown. Co++ has no effect on melittin-induced Pl breakdown and potentiates mastoparan-induced Pl breakdown. Pertussis toxin has no effect on the Pl breakdown induced by either peptide. The responses to melittin and mastoparan in PC12 cells are compared to those reported for maitotoxin. JF - The Journal of pharmacology and experimental therapeutics AU - Choi, O H AU - Padgett, W L AU - Daly, J W AD - Laboratory of Bioorganic Chemistry, National Institute of Diabetes, Digestive Disease, National Institutes of Health, Bethesda, Maryland. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 369 EP - 375 VL - 260 IS - 1 SN - 0022-3565, 0022-3565 KW - Calcium Channel Blockers KW - 0 KW - Marine Toxins KW - Oxocins KW - Peptides KW - Phosphatidylinositols KW - Virulence Factors, Bordetella KW - Wasp Venoms KW - Melitten KW - 20449-79-0 KW - Arachidonic Acid KW - 27YG812J1I KW - mastoparan KW - 72093-21-1 KW - maitotoxin KW - 9P59GES78D KW - Pertussis Toxin KW - EC 2.4.2.31 KW - Phospholipases A KW - EC 3.1.1.32 KW - Phospholipases A2 KW - EC 3.1.1.4 KW - Type C Phospholipases KW - EC 3.1.4.- KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Marine Toxins -- pharmacology KW - Animals KW - Phospholipases A -- drug effects KW - Type C Phospholipases -- drug effects KW - Type C Phospholipases -- metabolism KW - Rats KW - Virulence Factors, Bordetella -- pharmacology KW - Calcium Channel Blockers -- pharmacology KW - PC12 Cells KW - Phospholipases A -- metabolism KW - Calcium -- metabolism KW - Phosphatidylinositols -- metabolism KW - Calcium -- pharmacokinetics KW - Arachidonic Acid -- secretion KW - Melitten -- pharmacology KW - Wasp Venoms -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72776526?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.atitle=Effects+of+the+amphiphilic+peptides+melittin+and+mastoparan+on+calcium+influx%2C+phosphoinositide+breakdown+and+arachidonic+acid+release+in+rat+pheochromocytoma+PC12+cells.&rft.au=Choi%2C+O+H%3BPadgett%2C+W+L%3BDaly%2C+J+W&rft.aulast=Choi&rft.aufirst=O&rft.date=1992-01-01&rft.volume=260&rft.issue=1&rft.spage=369&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=00223565&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-18 N1 - Date created - 1992-02-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phase I/II trial and pharmacokinetics of intrathecal diaziquone in refractory meningeal malignancies. AN - 72760821; 1727916 AB - Because there is a compelling need to develop new agents for intrathecal use, we investigated the safety, efficacy, and CSF pharmacokinetics of diaziquone (AZQ) following intrathecal administration in patients with refractory meningeal malignancies. Thirty-nine patients received 45 courses of intrathecal AZQ. Two schedules were studied; twice-weekly administration of a 1- or 2-mg dose and "concentration times time" (C x T) administration of 0.5 mg every 6 hours for three doses, administered once weekly. Dose-limiting toxicity consisting of headache, nausea, or vomiting occurred in only three patients and only at the 2-mg, twice weekly dose. The schedules of 1 mg twice-weekly and 0.5 mg every 6 hours for three doses were well tolerated. Thirty-seven courses were assessable for response. The overall response rate was 62%. Complete responses (CRs) occurred in 14 of 37 courses (38%) and partial responses (PRs) occurred in nine of 37 courses (24%). Among patients with meningeal leukemia, CRs were observed in 11 of 26 courses (42%) and PRs in nine of 26 courses (35%). There was no difference in response rate related to dose or schedule. The pharmacokinetic behavior of intrathecally administered AZQ was characterized by biexponential disappearance from ventricular CSF, with mean half-lives of 18.2 and 78.6 minutes. The mean clearance rate was 0.37 mL/min. Intrathecal AZQ is safe, well tolerated, and highly active against refractory meningeal malignancies. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Berg, S L AU - Balis, F M AU - Zimm, S AU - Murphy, R F AU - Holcenberg, J AU - Sato, J AU - Reaman, G AU - Steinherz, P AU - Gillespie, A AU - Doherty, K AD - Pediatric Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 143 EP - 148 VL - 10 IS - 1 SN - 0732-183X, 0732-183X KW - Antineoplastic Agents KW - 0 KW - Aziridines KW - Benzoquinones KW - diaziquone KW - FQL5EUP13W KW - Index Medicus KW - Drug Evaluation KW - Drug Administration Schedule KW - Injections, Spinal KW - Humans KW - Adult KW - Child KW - Adolescent KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- drug therapy KW - Male KW - Female KW - Child, Preschool KW - Benzoquinones -- therapeutic use KW - Aziridines -- pharmacokinetics KW - Benzoquinones -- pharmacokinetics KW - Aziridines -- therapeutic use KW - Meningeal Neoplasms -- secondary KW - Meningeal Neoplasms -- drug therapy KW - Antineoplastic Agents -- pharmacokinetics KW - Antineoplastic Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72760821?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Phase+I%2FII+trial+and+pharmacokinetics+of+intrathecal+diaziquone+in+refractory+meningeal+malignancies.&rft.au=Berg%2C+S+L%3BBalis%2C+F+M%3BZimm%2C+S%3BMurphy%2C+R+F%3BHolcenberg%2C+J%3BSato%2C+J%3BReaman%2C+G%3BSteinherz%2C+P%3BGillespie%2C+A%3BDoherty%2C+K&rft.aulast=Berg&rft.aufirst=S&rft.date=1992-01-01&rft.volume=10&rft.issue=1&rft.spage=143&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=0732183X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-27 N1 - Date created - 1992-01-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Long term tolerance of thoracic organs to intraoperative radiotherapy. AN - 72759815; 1309205 AB - The tolerance of mediastinal structures to intraoperative radiotherapy (IORT) was investigated in 3 separate animals trials using 49 adult foxhounds and one limited Phase I trial in 4 patients with Stage II or III non-small cell lung cancer (NSCLC). The 1- to 2-year results of these trials have been previously reported with significant toxicity found at dose levels over 20 Gy. We now report the results of five dogs reserved for long term studies and one Stage II NSCLC patient alive at 5 years. Two dogs received 20 Gy IORT and one received 30 Gy IORT to the esophagus, all three to a single 6 cm field with 9 MeV electrons. One control dog underwent surgery without irradiation. One dog received 20 Gy IORT to a single 5 cm mediastinal field with 13 MeV electrons following left pneumonectomy. At 5 years, all five dogs reserved for a long term evaluation were alive and evaluable with minimal endoscopic and radiographic abnormalities. The one patient alive at 5 years for evaluation received 25 Gy IORT to two matched 6 cm fields with 13 MeV electrons. She has stable dyspnea on exertion and there is no evidence of cancer by endoscopy. We conclude, based on these limited data, that IORT in the mediastinum may be safe at dose levels that do not exceed 20 Gy, and further careful evaluation at these lower treatment doses is warranted to determine efficacy. JF - International journal of radiation oncology, biology, physics AU - Tochner, Z A AU - Pass, H I AU - Sindelar, W F AU - DeLuca, A M AU - Grisell, D L AU - Bacher, J D AU - Kinsella, T J AD - Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992 PY - 1992 DA - 1992 SP - 65 EP - 69 VL - 22 IS - 1 SN - 0360-3016, 0360-3016 KW - Index Medicus KW - Animals KW - Pneumonectomy KW - Bronchi -- radiation effects KW - Humans KW - Dogs KW - Follow-Up Studies KW - Intraoperative Period KW - Lung Neoplasms -- radiotherapy KW - Esophagus -- radiation effects KW - Mediastinum -- radiation effects KW - Lung -- radiation effects KW - Carcinoma, Non-Small-Cell Lung -- radiotherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72759815?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.atitle=Long+term+tolerance+of+thoracic+organs+to+intraoperative+radiotherapy.&rft.au=Tochner%2C+Z+A%3BPass%2C+H+I%3BSindelar%2C+W+F%3BDeLuca%2C+A+M%3BGrisell%2C+D+L%3BBacher%2C+J+D%3BKinsella%2C+T+J&rft.aulast=Tochner&rft.aufirst=Z&rft.date=1992-01-01&rft.volume=22&rft.issue=1&rft.spage=65&rft.isbn=&rft.btitle=&rft.title=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.issn=03603016&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-14 N1 - Date created - 1992-01-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The epithelial phenotype of human neuroblastoma cells express bradykinin, endothelin, and angiotensin II receptors that stimulate phosphoinositide hydrolysis. AN - 72755487; 1309239 AB - The neuroblastoma line SK-N-SH consists of distinct and interconverting cell types, which include a neuroblast phenotype (SH-SY5Y), an epithelial phenotype (SH-EP), and an intermediate cell type (SH-IN). In SH-SY5Y cells, only muscarinic receptor activation produced stimulation of phosphoinositide turnover, whereas in SH-EP cells, where muscarinic receptors are not present, the peptides bradykinin, endothelin, and angiotensin II stimulated phosphoinositide hydrolysis with EC50 values of 16, 6, and 0.7 nM, respectively, and a rank order of maximal effects of bradykinin greater than endothelin greater than angiotensin II. Fetal calf serum at concentrations between 1 and 10% was also a potent stimulator of phosphoinositide hydrolysis in SH-EP cells but not in SH-SY5Y cells. In the intermediate cell clone, SH-IN, phosphoinositide hydrolysis was stimulated not only by muscarinic receptors, but also by endothelin, bradykinin, and serum, an indication that this cell type harbors all the kinds of receptors that are differentially expressed in the other two cell types. The effects of the three peptides--bradykinin, endothelin, and angiotensin II--on phosphoinositide hydrolysis in SH-EP cells were additive, a result suggesting that the three kinds of receptors may activate distinct transducer proteins and/or phospholipase C subtypes. Pretreatment of intact SH-EP cells with pertussis toxin under conditions sufficient to ADP-ribosylate 90-95% of the endogenous guanine nucleotide regulatory protein substrates did not impair the ability of any of the receptors to stimulate phosphoinositide hydrolysis in any of the cell types. In contrast, short-term exposure to the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (1 microM) abolished the stimulation of phosphoinositide hydrolysis mediated by peptide receptors in SH-EP cells and partially inhibited that by muscarinic receptors in SH-SY5Y cells. Prolonged incubation of SH-EP cells with phorbol ester resulted in a recovery of receptor responsiveness, the extent and rate of which were different for each receptor type. In contrast, there was no recovery of responsiveness for muscarinic receptors in SH-SY5Y cells. The pattern of phorbol ester-mediated effects depended on the cell rather than on the receptor type. In fact, muscarinic receptor responsiveness in SH-IN, the intermediate cell type, was desensitized by and recovered from treatment with phorbol esters in a manner more similar to peptide receptors in SH-EP than to muscarinic receptors in SH-SY5Y. These data suggest that the transduction mechanisms by which distinct receptor types are coupled to phosphoinositide hydrolysis in the three cell phenotypes differ in sensitivity to feedback regulation by protein kinase C. JF - Journal of neurochemistry AU - Ogino, Y AU - Costa, T AD - Laboratory of Theoretical and Physical Biology, NICHD, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 46 EP - 56 VL - 58 IS - 1 SN - 0022-3042, 0022-3042 KW - Endothelins KW - 0 KW - Phosphatidylinositols KW - Receptors, Angiotensin KW - Receptors, Bradykinin KW - Receptors, Cell Surface KW - Receptors, Endothelin KW - Receptors, Neurotransmitter KW - Virulence Factors, Bordetella KW - Angiotensin II KW - 11128-99-7 KW - Pertussis Toxin KW - EC 2.4.2.31 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Bradykinin KW - S8TIM42R2W KW - Index Medicus KW - Humans KW - Hydrolysis KW - Epithelium -- physiopathology KW - Virulence Factors, Bordetella -- pharmacology KW - Angiotensin II -- metabolism KW - Endothelins -- metabolism KW - Tumor Cells, Cultured KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Epithelium -- pathology KW - Bradykinin -- metabolism KW - Receptors, Cell Surface -- metabolism KW - Neuroblastoma -- pathology KW - Phosphatidylinositols -- metabolism KW - Neuroblastoma -- genetics KW - Receptors, Neurotransmitter -- metabolism KW - Receptors, Angiotensin -- metabolism KW - Neuroblastoma -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72755487?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=The+epithelial+phenotype+of+human+neuroblastoma+cells+express+bradykinin%2C+endothelin%2C+and+angiotensin+II+receptors+that+stimulate+phosphoinositide+hydrolysis.&rft.au=Ogino%2C+Y%3BCosta%2C+T&rft.aulast=Ogino&rft.aufirst=Y&rft.date=1992-01-01&rft.volume=58&rft.issue=1&rft.spage=46&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-22 N1 - Date created - 1992-01-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immunotherapy with interleukin-2 and alpha-interferon in patients with metastatic renal cell cancer with in situ primary cancers: a pilot study. AN - 72753599; 1729540 AB - A total of 12 patients with stage 4 renal cell carcinoma and primary renal tumors in situ was entered into a pilot study using treatment with interleukin-2 and alpha-interferon followed by radical nephrectomy. Of the patients 11 underwent nephrectomy after an initial course of immunotherapy. Ten patients were able to receive a second course of immunotherapy given after nephrectomy. One patient achieved a complete response of lung and mediastinal metastases without any change in the primary renal tumor but after nephrectomy the patient remained in complete remission for greater than 11 months. A total of 3 patients achieved a partial response at some extrarenal sites but they had progression elsewhere. Toxicity was similar to previous experience with this immunotherapy regimen. Therefore, we demonstrated that metastatic tumor regression is possible with primary renal tumors in situ and that aggressive interleukin-2-based immunotherapy can be tolerated in the presence of a large renal tumor. JF - The Journal of urology AU - Spencer, W F AU - Linehan, W M AU - Walther, M M AU - Haas, G P AU - Lotze, M T AU - Topalian, S L AU - Yang, J C AU - Merino, M J AU - Lange, J R AU - Pockaj, B A AD - Division of Cancer Treatment, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1992/01// PY - 1992 DA - January 1992 SP - 24 EP - 30 VL - 147 IS - 1 SN - 0022-5347, 0022-5347 KW - Interferon-alpha KW - 0 KW - Interleukin-2 KW - Abridged Index Medicus KW - Index Medicus KW - Nephrectomy KW - Combined Modality Therapy KW - Humans KW - Adult KW - Pilot Projects KW - Middle Aged KW - Male KW - Female KW - Carcinoma, Renal Cell -- pathology KW - Kidney Neoplasms -- surgery KW - Kidney Neoplasms -- pathology KW - Interleukin-2 -- adverse effects KW - Interferon-alpha -- therapeutic use KW - Interferon-alpha -- adverse effects KW - Carcinoma, Renal Cell -- surgery KW - Carcinoma, Renal Cell -- therapy KW - Interleukin-2 -- therapeutic use KW - Immunotherapy KW - Carcinoma, Renal Cell -- secondary UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72753599?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+urology&rft.atitle=Immunotherapy+with+interleukin-2+and+alpha-interferon+in+patients+with+metastatic+renal+cell+cancer+with+in+situ+primary+cancers%3A+a+pilot+study.&rft.au=Spencer%2C+W+F%3BLinehan%2C+W+M%3BWalther%2C+M+M%3BHaas%2C+G+P%3BLotze%2C+M+T%3BTopalian%2C+S+L%3BYang%2C+J+C%3BMerino%2C+M+J%3BLange%2C+J+R%3BPockaj%2C+B+A&rft.aulast=Spencer&rft.aufirst=W&rft.date=1992-01-01&rft.volume=147&rft.issue=1&rft.spage=24&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+urology&rft.issn=00225347&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-10 N1 - Date created - 1992-02-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Specific binding to protein kinase C by ingenol and its induction of biological responses. AN - 72749754; 1727380 AB - We have examined the ability of ingenol to bind to and activate protein kinase C and to induce similar responses to the phorbol esters in biological systems. The rationale was that ingenol possesses the critical functionalities of the phorbol ester pharmacophore with the exception of the hydrophobic domain; it might therefore possess weak potency, although previous reports had indicated that ingenol was biologically inactive. Our data demonstrate that ingenol indeed binds to protein kinase C with a Ki of 30 microM and activates the enzyme. In addition, ingenol was biologically active in 3 separate cell systems, showing effects similar to the phorbol esters on morphological change, cell-cell communication, epidermal growth factor binding, arachidonic acid metabolite release, and ornithine decarboxylase activity. The 50% effective concentration values for the biological activity of ingenol were between 30 microM and 1 mM, varying somewhat with the cell system and type of response. The biological activity of ingenol in general supports the proposed models of the phorbol ester pharmacophore and imposes additional experimental constraints that the modeling must satisfy. JF - Cancer research AU - Hasler, C M AU - Acs, G AU - Blumberg, P M AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/01/01/ PY - 1992 DA - 1992 Jan 01 SP - 202 EP - 208 VL - 52 IS - 1 SN - 0008-5472, 0008-5472 KW - Diterpenes KW - 0 KW - Arachidonic Acid KW - 27YG812J1I KW - ingenol KW - 30220-46-3 KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Epidermal Growth Factor KW - 62229-50-9 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Ornithine Decarboxylase KW - EC 4.1.1.17 KW - Index Medicus KW - Animals KW - Phorbol 12,13-Dibutyrate -- metabolism KW - Cells, Cultured KW - Cell Communication -- drug effects KW - Keratinocytes -- drug effects KW - Enzyme Activation -- drug effects KW - Mice KW - Ornithine Decarboxylase -- biosynthesis KW - Mice, Inbred BALB C KW - Epidermal Growth Factor -- metabolism KW - Arachidonic Acid -- metabolism KW - Protein Kinase C -- metabolism KW - Diterpenes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72749754?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Specific+binding+to+protein+kinase+C+by+ingenol+and+its+induction+of+biological+responses.&rft.au=Hasler%2C+C+M%3BAcs%2C+G%3BBlumberg%2C+P+M&rft.aulast=Hasler&rft.aufirst=C&rft.date=1992-01-01&rft.volume=52&rft.issue=1&rft.spage=202&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-17 N1 - Date created - 1992-01-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Persistence of platinum-ammine-DNA adducts in gonads and kidneys of rats and multiple tissues from cancer patients. AN - 72749714; 1727376 AB - The persistence of platinum-DNA adducts was investigated using normal rats as well as tissues from cancer patients receiving either cisdiamminedichloroplatinum(II) (cisplatin) or diamminecyclobutanedicarboxylatoplatinum(II) (carboplatin) for cancer chemotherapy. These studies used an enzyme-linked immunosorbent assay, established with a rabbit anti-cisplatin-DNA that is specific for intrastrand platinum-DNA adducts. The gonads and kidneys of male and female rats, sites for antitumor activity and toxicity, respectively, were monitored for cisplatin-DNA adduct formation after a single dose of drug and during multiple-dose exposures (once a wk for 3 wk). DNA adducts were measured by enzyme-linked immunosorbent assay 4 h and 2, 4, 7, and 14 days after administering a single i.v. injection of 8 mg/kg of cisplatin. Adduct profiles in renal tissues were similar in both males and females with adduct levels increasing between 4 h and 2 days, decreasing between Days 2 and 7, and stable between Days 7 and 14. In both sexes, levels of kidney DNA adduct measured 7 to 14 days after cisplatin injection comprised about 30% of the highest (Day 2) value. In testes and ovaries, adduct removal was complete by 4 days, and 40 to 50% of adducts present at Day 2 persisted until Days 7 and 14. A study of multiple dosing showed that adducts in renal and testicular DNA from rats given three weekly doses of 5 mg/kg of cisplatin had different accumulation profiles. In the testis there was a 2-fold accumulation of adduct after the third dose, while in the kidney adducts dropped with repeated dosing. In humans, the persistence of platinum-DNA adducts was studied in tissues from eight cancer patients who received their last dose of cisplatin or carboplatin chemotherapy between 1 day and 15 mo before autopsy. The patients had either ovarian cancer, breast cancer, or lymphoma, and the tissues studied included ovarian tumor, bone marrow, kidney, liver, spleen, lymph node, peripheral nerve, and brain. When samples were available from tumor tissues and from bone marrow within the same patient, adduct levels were similar in the two tissues. In addition, adducts were persistent for many months, since half of the individuals received their most recent platinum-drug therapy 7 to 15 mo before death. Overall, these studies demonstrate a widespread distribution and high degree of platinum-DNA adduct persistence in both animal and human tissues subsequent to cisplatin or carboplatin treatment. JF - Cancer research AU - Poirier, M C AU - Reed, E AU - Litterst, C L AU - Katz, D AU - Gupta-Burt, S AD - Division of Cancer Etiology, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/01/01/ PY - 1992 DA - 1992 Jan 01 SP - 149 EP - 153 VL - 52 IS - 1 SN - 0008-5472, 0008-5472 KW - DNA Adducts KW - 0 KW - cisplatin-DNA adduct KW - DNA KW - 9007-49-2 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Rats KW - Enzyme-Linked Immunosorbent Assay -- methods KW - Animals KW - Sex Characteristics KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Tissue Distribution KW - Time Factors KW - Male KW - Female KW - Ovary -- metabolism KW - Ovary -- chemistry KW - Kidney -- metabolism KW - Testis -- metabolism KW - DNA -- administration & dosage KW - DNA -- metabolism KW - DNA -- analysis KW - Kidney -- chemistry KW - Cisplatin -- analysis KW - Testis -- chemistry KW - Cisplatin -- metabolism KW - Cisplatin -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72749714?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Persistence+of+platinum-ammine-DNA+adducts+in+gonads+and+kidneys+of+rats+and+multiple+tissues+from+cancer+patients.&rft.au=Poirier%2C+M+C%3BReed%2C+E%3BLitterst%2C+C+L%3BKatz%2C+D%3BGupta-Burt%2C+S&rft.aulast=Poirier&rft.aufirst=M&rft.date=1992-01-01&rft.volume=52&rft.issue=1&rft.spage=149&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-17 N1 - Date created - 1992-01-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of the gadd153 promoter by genotoxic agents: a rapid and specific response to DNA damage. AN - 72744912; 1727386 AB - Accumulation of gadd153 mRNA is strongly stimulated in mammalian cells by treatments which arrest growth or damage DNA (A. J. Fornace, Jr. et al., Mol. Cell. Biol., 9: 4196-4203, 1989). In previous studies, we demonstrated that the increased expression of gadd153 following treatment with several DNA-damaging agents was mediated transcriptionally (J. D. Luethy et al., J. Biol. Chem., 265: 16521-16526, 1990). To better define the specificity of this response, we have established a sensitive reporter system in which we have stably integrated a chimeric gene containing the gadd153 promoter linked to the coding region of the chloramphenicol acetyltransferase (CAT) gene into the genome of HeLa cells. Transcriptional activation from the gadd153 promoter was monitored by determining levels of CAT activity in cellular lysates prepared from gadd153CAT/HeLa cells treated with a variety of agents. The gadd153 promoter was strongly activated by a broad spectrum of genotoxic agents including UV-mimetic agents, DNA-cross-linking and alkylating agents, DNA intercalators, and topoisomerase inhibitors. Of the DNA-damaging agents tested, only X-irradiation and bleomycin treatments failed to induce gadd153 promoter activity. Agents which inhibit replication and cell division and agents which otherwise result in cytotoxicity or growth arrest also had little influence on gadd153 promoter activity. Expression of the gadd153CAT chimeric gene in xeroderma pigmentosum Group A cells, which are deficient in nucleotide excision DNA repair of pyrimidine dimers, was maximally induced at UV doses at least 6-fold lower than those required for similar induction in repair-proficient HeLa cells. However, the methyl methanesulfonate-induced gadd153 promoter activities were similar in both cell lines. Novobiocin pretreatment inhibited both UV- and methyl methanesulfonate-induced gadd153CAT expression. Collectively, these data indicate that: (a) the gadd153 promoter is activated rapidly and specifically by DNA damage; (b) the altered DNA structure is the inducing signal for the activation of the signal transduction pathway responsible for enhanced gadd153 expression; and (c) regulation of gadd153 by growth arrest is distinct from that of DNA damage. Thus, the gadd153CAT/HeLa cells are a useful model for examining the molecular mechanisms associated with the response to DNA damage and provide a reporter system for the screening of potential genotoxic agents. JF - Cancer research AU - Luethy, J D AU - Holbrook, N J AD - Laboratory of Molecular Genetics, Gerontology Research Center, National Institute on Aging, Baltimore, Maryland 21224. Y1 - 1992/01/01/ PY - 1992 DA - 1992 Jan 01 SP - 5 EP - 10 VL - 52 IS - 1 SN - 0008-5472, 0008-5472 KW - gadd153 KW - Mutagens KW - 0 KW - RNA, Messenger KW - Novobiocin KW - 17EC19951N KW - Dactinomycin KW - 1CC1JFE158 KW - DNA KW - 9007-49-2 KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - Dactinomycin -- toxicity KW - Enzyme Induction -- drug effects KW - HeLa Cells KW - Dose-Response Relationship, Drug KW - Humans KW - Novobiocin -- toxicity KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Chloramphenicol O-Acetyltransferase -- biosynthesis KW - DNA Damage KW - Mutagens -- toxicity KW - Gene Expression Regulation, Neoplastic -- radiation effects KW - DNA -- radiation effects KW - Gene Expression Regulation, Neoplastic -- drug effects KW - RNA, Messenger -- biosynthesis KW - Gene Expression Regulation, Neoplastic -- genetics KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72744912?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Activation+of+the+gadd153+promoter+by+genotoxic+agents%3A+a+rapid+and+specific+response+to+DNA+damage.&rft.au=Luethy%2C+J+D%3BHolbrook%2C+N+J&rft.aulast=Luethy&rft.aufirst=J&rft.date=1992-01-01&rft.volume=52&rft.issue=1&rft.spage=5&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-17 N1 - Date created - 1992-01-17 N1 - Date revised - 2017-01-13 N1 - Gene symbol - gadd153 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transfer of the bacterial gene for cytosine deaminase to mammalian cells confers lethal sensitivity to 5-fluorocytosine: a negative selection system. AN - 72744815; 1729703 AB - Expression of the bacterial gene for cytosine deaminase (CD; EC 3.5.4.1) in mammalian cells was evaluated as a negative selection system or suicide vector for potential use in gene transfer studies and therapies. Mammalian cells, unlike certain bacteria and fungi, do not contain the enzyme CD and do not ordinarily metabolize cytosine to uracil. Nor do they metabolize the innocuous compound 5-fluorocytosine to the highly toxic compound 5-fluorouracil. The Escherichia coli CD gene underwent PCR oligonucleotide-directed mutagenesis to enhance its expression in a eukaryotic system and it was then cloned into an expression vector, pLXSN, that also contains a neomycin-resistance gene. Murine fibroblast lines were transfected with the plasmid and subjected to brief selection in the neomycin analogue G418. Lysates from these cell populations exhibited significant CD activity detected by conversion of radiolabeled cytosine to uracil. In clonogenic assays transfected cells expressing CD were selectively killed by incubation in 5-fluorocytosine, whereas control cell lines were not. Dose-response studies evaluating [3H]thymidine incorporation or cloning efficiency demonstrated profound inhibition at and above 65 micrograms of 5-fluorocytosine per ml. Mixed cellular assays showed that CD-positive cells could be eliminated without bystander killing of other cells. Retrovirus-mediated CD gene transfer into various tissues was also demonstrated. Thus CD, with its ability to produce the toxic antimetabolite 5-fluorouracil from 5-fluorocytosine, may be useful as a negative selection system for studies and treatments employing gene transfer techniques. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Mullen, C A AU - Kilstrup, M AU - Blaese, R M AD - Cellular Immunology Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/01/01/ PY - 1992 DA - 1992 Jan 01 SP - 33 EP - 37 VL - 89 IS - 1 SN - 0027-8424, 0027-8424 KW - Oligodeoxyribonucleotides KW - 0 KW - Flucytosine KW - D83282DT06 KW - Nucleoside Deaminases KW - EC 3.5.4.- KW - Cytosine Deaminase KW - EC 3.5.4.1 KW - Index Medicus KW - Animals KW - Base Sequence KW - Transfection KW - Oligodeoxyribonucleotides -- chemistry KW - Genetic Vectors KW - DNA Mutational Analysis KW - In Vitro Techniques KW - Molecular Sequence Data KW - Escherichia coli -- genetics KW - Mice KW - Genetic Therapy KW - Cloning, Molecular KW - Nucleoside Deaminases -- genetics KW - Genes, Bacterial KW - Flucytosine -- toxicity KW - Cells, Cultured -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72744815?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Transfer+of+the+bacterial+gene+for+cytosine+deaminase+to+mammalian+cells+confers+lethal+sensitivity+to+5-fluorocytosine%3A+a+negative+selection+system.&rft.au=Mullen%2C+C+A%3BKilstrup%2C+M%3BBlaese%2C+R+M&rft.aulast=Mullen&rft.aufirst=C&rft.date=1992-01-01&rft.volume=89&rft.issue=1&rft.spage=33&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-12 N1 - Date created - 1992-02-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Mol Cell Biol. 1986 Aug;6(8):2895-902 [3785217] J Natl Cancer Inst. 1990 Feb 21;82(4):297-300 [2299679] J Mol Biol. 1981 Jul 25;150(1):1-14 [6271971] Chemotherapy. 1975;21(3-4):113-30 [1098864] Chemotherapy. 1976;22(3-4):137-53 [773604] Biochem Pharmacol. 1966 Apr;15(4):435-46 [5955812] J Bacteriol. 1989 Apr;171(4):2124-7 [2539360] Proc Natl Acad Sci U S A. 1988 Oct;85(20):7572-6 [2845412] Cell. 1986 Feb 14;44(3):419-28 [3002636] Annu Rev Genet. 1989;23:199-225 [2694931] Pharmacol Ther. 1989;43(2):155-85 [2675132] Arch Microbiol. 1989;152(2):115-8 [2673119] J Cell Biol. 1989 Feb;108(2):229-41 [2645293] Biotechniques. 1989 Oct;7(9):980-2, 984-6, 989-90 [2631796] J Virol Methods. 1989 Feb;23(2):187-94 [2786000] Protein Eng. 1986 Oct-Nov;1(1):67-74 [3507689] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of the antigen (CAK1) recognized by monoclonal antibody K1 present on ovarian cancers and normal mesothelium. AN - 72742877; 1727378 AB - K1 is a monoclonal antibody that reacts with a cell surface antigen (CAK1) found in human mesothelia and nonmucinous ovarian tumors. In this article, the characteristics of the CAK1 antigen have been examined in detail. Using immunofluorescence microscopy, we have found that the CAK1 signal is removed from the cell surface by treatment with proteases or by phosphatidylinositol-phospholipase C, but not by neuraminidase and beta-galactosidase. The phosphatidylinositol-phospholipase C-released material was found to contain the CAK1 antigen which was detected by a competition radioimmunoassay. The phosphatidylinositol-phospholipase C-released CAK1 antigen was examined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting and found to be approximately 40 kDa protein. The CAK1-K1 antibody complex remains on the cell surface and is poorly internalized, as shown by an acid wash immunofluorescence internalization assay. An immunotoxin composed of K1 and Lys-PE40, a mutant form of Pseudomonas exotoxin lacking the cell binding domain, was not cytotoxic, supporting the conclusion that the CAK1-K1 antibody complex is not internalized. However, an immunotoxin composed of K1 and native Pseudomonas exotoxin was selectively cytotoxic to cells expressing the CAK1 antigen. This cytotoxicity is due to the fact that domain I of Pseudomonas exotoxin promotes internalization of antigens which are not internalized or bound to antibody alone. Our results suggest that CAK1 is a polypeptide that is expressed on mesothelial cells and many ovarian cancers, and that K1 may be useful as a targeting agent for the immunotherapy of human ovarian cancer. JF - Cancer research AU - Chang, K AU - Pai, L H AU - Batra, J K AU - Pastan, I AU - Willingham, M C AD - Laboratory of Molecular Biology, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/01/01/ PY - 1992 DA - 1992 Jan 01 SP - 181 EP - 186 VL - 52 IS - 1 SN - 0008-5472, 0008-5472 KW - Antibodies, Monoclonal KW - 0 KW - Antigen-Antibody Complex KW - Antigens, Tumor-Associated, Carbohydrate KW - Immunotoxins KW - Phospholipases KW - EC 3.1.- KW - Index Medicus KW - Phospholipases -- pharmacology KW - Tumor Cells, Cultured -- immunology KW - Humans KW - Immunotoxins -- therapeutic use KW - Epithelium -- immunology KW - Antigen-Antibody Complex -- metabolism KW - Radioimmunoassay KW - Female KW - Ovarian Neoplasms -- metabolism KW - Antigens, Tumor-Associated, Carbohydrate -- metabolism KW - Antigens, Tumor-Associated, Carbohydrate -- analysis KW - Ovarian Neoplasms -- immunology KW - Antibodies, Monoclonal -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72742877?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Characterization+of+the+antigen+%28CAK1%29+recognized+by+monoclonal+antibody+K1+present+on+ovarian+cancers+and+normal+mesothelium.&rft.au=Chang%2C+K%3BPai%2C+L+H%3BBatra%2C+J+K%3BPastan%2C+I%3BWillingham%2C+M+C&rft.aulast=Chang&rft.aufirst=K&rft.date=1992-01-01&rft.volume=52&rft.issue=1&rft.spage=181&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-17 N1 - Date created - 1992-01-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutagenic specificities of four stereoisomeric benzo[c]phenanthrene dihydrodiol epoxides. AN - 72740874; 1729707 AB - The pS189 shuttle vector carrying a supF target gene was used to compare the mutagenic specificities of the four configurational isomers of benzo[c]phenanthrene 3,4-dihydrodiol 1,2-epoxide. One of these isomers is the most tumorigenic dihydrodiol epoxide tested to date and another is essentially inactive as a tumorigen. Overall mutagenicities were not correlated with tumorigenicities, but each configurational isomer induced a unique spectrum of mutational hot spots in the supF target gene, which monitors primarily point mutations. It is suggested that the demonstrated isomer-specific selectivity for mutation targets within the supF gene may be indicative of a similar selectivity for one gene versus another and that such selectivity may be one determinant of relative tumorigenicity. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Bigger, C A AU - St John, J AU - Yagi, H AU - Jerina, D M AU - Dipple, A AD - Chemistry of Carcinogenesis Laboratory, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1992/01/01/ PY - 1992 DA - 1992 Jan 01 SP - 368 EP - 372 VL - 89 IS - 1 SN - 0027-8424, 0027-8424 KW - supF KW - Mutagens KW - 0 KW - Phenanthrenes KW - 1,2-epoxy-3,4-dihydroxy-1,2,3,4-tetrahydrobenzo(c)phenanthrene KW - 111001-48-0 KW - RNA, Transfer KW - 9014-25-9 KW - Index Medicus KW - Stereoisomerism KW - Base Sequence KW - Cells, Cultured KW - Genetic Vectors KW - DNA Mutational Analysis KW - In Vitro Techniques KW - Molecular Sequence Data KW - Genes, Suppressor KW - Structure-Activity Relationship KW - Phenanthrenes -- toxicity KW - Mutagens -- toxicity KW - Phenanthrenes -- chemistry KW - Mutagenesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72740874?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Mutagenic+specificities+of+four+stereoisomeric+benzo%5Bc%5Dphenanthrene+dihydrodiol+epoxides.&rft.au=Bigger%2C+C+A%3BSt+John%2C+J%3BYagi%2C+H%3BJerina%2C+D+M%3BDipple%2C+A&rft.aulast=Bigger&rft.aufirst=C&rft.date=1992-01-01&rft.volume=89&rft.issue=1&rft.spage=368&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-12 N1 - Date created - 1992-02-12 N1 - Date revised - 2017-01-13 N1 - Gene symbol - supF N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1984 Mar;81(5):1494-8 [6369329] Cancer Res. 1984 Jun;44(6):2320-4 [6372992] Mol Carcinog. 1991;4(3):176-9 [2064722] Nature. 1964 May 23;202:781-4 [14187619] Nature. 1974 Nov 22;252(5481):326-8 [4473724] Cancer Res. 1990 Dec 1;50(23):7527-31 [2174727] Adv Cancer Res. 1985;45:45-105 [3911748] Nature. 1987 Jun 11-17;327(6122):535-6 [3587368] Nature. 1986 Jul 3-9;322(6074):78-80 [3014349] Proc Natl Acad Sci U S A. 1986 May;83(10):3402-6 [3010297] Mol Cell Biol. 1987 Jan;7(1):379-87 [3031469] Gene. 1985;38(1-3):233-7 [2998945] Carcinogenesis. 1986 Jul;7(7):1037-42 [3087641] Mutat Res. 1989 Mar-May;220(2-3):55-60 [2538741] Mutat Res. 1989 Mar-May;220(2-3):61-72 [2494447] Proc Natl Acad Sci U S A. 1989 Apr;86(7):2291-5 [2648399] Cancer Res. 1986 May;46(5):2257-61 [3697970] Carcinogenesis. 1990 Jan;11(1):165-8 [2295123] Proc Natl Acad Sci U S A. 1990 Jul;87(14):5464-8 [2371281] J Gen Virol. 1977 Jul;36(1):59-74 [886304] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The Contribution of French Jesuits to Chinese Science in the Seventeenth and Eighteenth Centuries AN - 61330294; 9403833 AB - The crucial role of the French Jesuits in the transfer of Western scientific knowledge to China in the seventeenth & eighteenth centuries is examined. A brief history of Sino-French contact is given, focusing on the role of the French Academie royale des sciences, which contributed to the establishment of science in China by providing Jesuit missionaries with scientific journals, books, instruments, & opportunities to correspond with academy members. Adapted from the source document. JF - Impact of Science on Society AU - Shi-ran, Du AU - Qi, Han AD - Instit History Natural Sciences Chinese Academy Sciences, Chao Nei Da Jie 137 100010 Beijing People's Republic China Y1 - 1992///0, PY - 1992 DA - 0, 1992 SP - 265 EP - 275 VL - 42 IS - 3 SN - 0019-2872, 0019-2872 KW - chinese scientific development, French Jesuits' role, 17th-18th centuries KW - Seventeenth Century KW - Scientific Knowledge KW - Jesuits KW - Scientific Development KW - China KW - Eighteenth Century KW - article KW - 1734: sociology of science; sociology of science UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/61330294?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocabs&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Impact+of+Science+on+Society&rft.atitle=The+Contribution+of+French+Jesuits+to+Chinese+Science+in+the+Seventeenth+and+Eighteenth+Centuries&rft.au=Shi-ran%2C+Du%3BQi%2C+Han&rft.aulast=Shi-ran&rft.aufirst=Du&rft.date=1992-01-01&rft.volume=42&rft.issue=3&rft.spage=265&rft.isbn=&rft.btitle=&rft.title=Impact+of+Science+on+Society&rft.issn=00192872&rft_id=info:doi/ LA - English DB - Sociological Abstracts N1 - Date revised - 2007-04-01 N1 - Last updated - 2016-09-28 N1 - CODEN - ISSOA8 N1 - SubjectsTermNotLitGenreText - Seventeenth Century; Eighteenth Century; China; Jesuits; Scientific Knowledge; Scientific Development ER - TY - JOUR T1 - Inactivated hepatitis A vaccine: Active and passive immunoprophylaxis in chimpanzees AN - 16937318; 3612034 AB - Studies of active and passive immunoprophylaxis were carried out in chimpanzees to determine whether a candidate hepatitis A virus (HAV) vaccine could stimulate antibody to HAV (anti-HAV) that was qualitatively similar to anti-HAV stimulated by natural infection. Normal immune globulin (Ig) was prepared from plasma obtained from human volunteers before and after vaccination with the HAV vaccine, and these preparations or commercially prepared Ig were administered to chimpanzees. Protective efficacy was compared to that obtained after vaccination of chimpanzees. As expected, pre-vaccination Ig did not protect chimpanzees against challenge with virulent hepatitis A. In contrast, chimpanzees were protected against hepatitis A by Ig prepared from volunteers who had received hepatitis A vaccine. The protection was qualitatively similar to that afforded by commercial normal Ig containing convalescent anti-HAV. The minimum protective dose of passively acquired anti-HAV was approximately the minimum dose detectable by serological means. This information will be useful in calculating minimum acceptable titres of anti-HAV in normal Ig. Whereas administration of Ig protected chimpanzees against hepatitis A pathology, it did not protect them from infection with HAV. Thus, these chimpanzees were protected by classical passive-active immunoprophylaxis. In contrast, chimpanzees actively immunized with HAV vaccine were apparently protected against both hepatitis A pathology and HAV infection. The mechanism of this complete protection is unknown but may simply represent the higher titre of anti-HAV in the vaccinated chimpanzees, compared to the passively protected animals. JF - Vaccine AU - Purcell, R H AU - D'Hondt, E AU - Bradbury, R AU - Emerson, SU AU - Govindarajan, S AU - Binn, L AD - Lab. Infect. Dis., NIAID/NIH, Build. 7, Rm. 202, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 VL - 10 SN - 0246-410X, 0246-410X KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology; Immunology Abstracts; Virology & AIDS Abstracts KW - vaccines KW - animal models KW - hepatitis A virus KW - immunization (passive) KW - Pan troglodytes KW - W3 33365:Vaccines (other) KW - F 06807:Active immunization KW - V 22097:Immunization: Vaccines & vaccination: Human KW - A 01097:Viruses KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16937318?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Vaccine&rft.atitle=Inactivated+hepatitis+A+vaccine%3A+Active+and+passive+immunoprophylaxis+in+chimpanzees&rft.au=Purcell%2C+R+H%3BD%27Hondt%2C+E%3BBradbury%2C+R%3BEmerson%2C+SU%3BGovindarajan%2C+S%3BBinn%2C+L&rft.aulast=Purcell&rft.aufirst=R&rft.date=1992-01-01&rft.volume=10&rft.issue=&rft.spage=no.+1+sul.&rft.isbn=&rft.btitle=&rft.title=Vaccine&rft.issn=0246410X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - vaccines; animal models; immunization (passive); hepatitis A virus; Pan troglodytes ER - TY - JOUR T1 - Synthesis of ligands related to the O-specific antigen of Shigella dysenteriae type 1. 4. Enhanced stereoselectivity of alpha -D-galactosylation in the synthesis of the sequence alpha -D-Galp-(1 arrow right 3)- alpha -D-GlcpNAc, allowing further extension of the chain at C-2' AN - 16928419; 3598846 AB - Stereoselective alpha -D-galactosylation at the position 3 of 4,6-O-substituted derivatives of methyl 2-acetamido-2-deoxy alpha -D-glucopyranoside is described. Glycosyl chlorides derived from 3,4,6-tri-O-acetyl-2-O-benzyl- and 2-O-(4-methoxybenzyl) D-galactopyranose have been used as glycosyl donors. Methyl 2-acetamido 4,6-di-O-acetyl-2-deoxy 3-O-(3,4,6-tri-O-acetyl alpha -D-galactopyranosyl) alpha -D-glucopyranoside and methyl 2-acetamido-4,6-di-O-benzyl 2-deoxy-3-O-(3,4,6-tri-O-acetyl alpha -D-galactopyranosyl) alpha -D-glucopyranoside have been prepared. JF - Journal of Carbohydrate Chemistry AU - Kovac, P AD - NIDDK/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 999 EP - 1014 VL - 11 IS - 8 SN - 0732-8303, 0732-8303 KW - O antigen KW - Microbiology Abstracts B: Bacteriology KW - chemical modification KW - ligands KW - stereoselectivity KW - Shigella dysenteriae KW - J 02832:Antigenic properties and virulence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16928419?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Carbohydrate+Chemistry&rft.atitle=Synthesis+of+ligands+related+to+the+O-specific+antigen+of+Shigella+dysenteriae+type+1.+4.+Enhanced+stereoselectivity+of+alpha+-D-galactosylation+in+the+synthesis+of+the+sequence+alpha+-D-Galp-%281+arrow+right+3%29-+alpha+-D-GlcpNAc%2C+allowing+further+extension+of+the+chain+at+C-2%27&rft.au=Kovac%2C+P&rft.aulast=Kovac&rft.aufirst=P&rft.date=1992-01-01&rft.volume=11&rft.issue=8&rft.spage=999&rft.isbn=&rft.btitle=&rft.title=Journal+of+Carbohydrate+Chemistry&rft.issn=07328303&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Shigella dysenteriae; ligands; chemical modification; stereoselectivity ER - TY - JOUR T1 - Genome sequence analysis: Scientific objectives and practical strategies AN - 16926365; 3602142 JF - Trends in Biotechnology AU - Venter, J C AU - Adams, MD AU - Martin-Gallardo, A AU - McCombie, W R AU - Fields, C AD - Sect. Receptor Biochem. and Mol. Biol., NINDS/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 8 EP - 11 VL - 10 IS - 1-2 SN - 0167-9430, 0167-9430 KW - Human Genome Project KW - Biotechnology and Bioengineering Abstracts; Genetics Abstracts; Medical and Pharmaceutical Biotechnology Abstracts KW - nucleotide sequence KW - reviews KW - gene mapping KW - genomes KW - analysis KW - G 07430:Chromosome studies/nucleotide sequence KW - W 30965:Miscellaneous, Reviews KW - W3 33055:Genetic engineering (general) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16926365?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Trends+in+Biotechnology&rft.atitle=Genome+sequence+analysis%3A+Scientific+objectives+and+practical+strategies&rft.au=Venter%2C+J+C%3BAdams%2C+MD%3BMartin-Gallardo%2C+A%3BMcCombie%2C+W+R%3BFields%2C+C&rft.aulast=Venter&rft.aufirst=J&rft.date=1992-01-01&rft.volume=10&rft.issue=1-2&rft.spage=8&rft.isbn=&rft.btitle=&rft.title=Trends+in+Biotechnology&rft.issn=01679430&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - nucleotide sequence; reviews; gene mapping; genomes; analysis ER - TY - JOUR T1 - Screening for chemopreventive (anticarcinogenic) compounds in rodents AN - 16920825; 3602340 AB - The Chemoprevention Branch is testing dozens of candidate chemopreventive compounds in the following rodent model carcinogenesis systems: mouse skin papillomas, DMBA/TPA induced, rat mammary adenocarcinoma, DMBA and MNU induced, hamster tracheal squamous cell carcinoma, MNU induced, and lung adenocarcinoma, DEN induced, rat and mouse colon adenocarcinoma, AOM and MAM acetate induced, respectively, and mouse bladder carcinoma, hydroxy BBN induced. Significant chemopreventive (i.e., anticancer) effects have been produced with 4-hydroxy-phenylretinamide, difluoromethylornithine, piroxicam, oltipraz (a dithiolthione), calcium glucarate, N-acetylcysteine, beta -carotene, ibuprofen, dehydroepiandrosterone (DHEA) and a 16-fluoro DHEA analog, 8354, tamoxifen, glycyrrhetinic acid, molybdate, selenite, curcumin, and fumaric acid. JF - Mutation Research AU - Boone, C W AU - Steele, V E AU - Kelloff, G J AD - Chemoprev. Branch, NCI/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 251 EP - 255 VL - 267 IS - 2 SN - 0027-5107, 0027-5107 KW - anticarcinogens KW - mice KW - chemoprevention KW - rats KW - piroxicam KW - ibuprofen KW - beta -carotene KW - oltipraz KW - calcium glucarate KW - Toxicology Abstracts; Genetics Abstracts KW - screening KW - compounds KW - Rodentia KW - X 24221:Toxicity testing KW - G 07221:Specific chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16920825?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+Research&rft.atitle=Screening+for+chemopreventive+%28anticarcinogenic%29+compounds+in+rodents&rft.au=Boone%2C+C+W%3BSteele%2C+V+E%3BKelloff%2C+G+J&rft.aulast=Boone&rft.aufirst=C&rft.date=1992-01-01&rft.volume=267&rft.issue=2&rft.spage=251&rft.isbn=&rft.btitle=&rft.title=Mutation+Research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Rodentia; compounds; screening ER - TY - JOUR T1 - Introduction of foreign DNA into the vaccinia virus genome by in vitro ligation: Recombination-independent selectable cloning vectors AN - 16876070; 3577361 AB - Homologous recombination has been the exclusive means of introducing foreign DNA into the genomes of large DNA viruses. We demonstrate that direct in vitro ligation can be used to efficiently insert DNA fragments of up to 26,000 bp into the genome of vaccinia virus modified to contain a single NotI site either in the Escherichia coli lacZ gene or in the vaccinia virus thymidine kinase gene. Viruses containing chimeric genomes can be identified by chromogenic screening or thymidine-kinase-negative selection. JF - Virology AU - Merchlinsky, M AU - Moss, B AD - Lab. Viral Dis., NIAID/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 522 EP - 526 VL - 190 IS - 1 SN - 0042-6822, 0042-6822 KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Virology & AIDS Abstracts KW - vaccinia virus KW - insertion KW - cloning vectors KW - recombination KW - genomes KW - DNA KW - ligation KW - N 14682:Cloning vectors KW - V 22050:Viral genetics including virus reactivation KW - W 30965:Miscellaneous, Reviews KW - W3 33055:Genetic engineering (general) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16876070?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Virology&rft.atitle=Introduction+of+foreign+DNA+into+the+vaccinia+virus+genome+by+in+vitro+ligation%3A+Recombination-independent+selectable+cloning+vectors&rft.au=Merchlinsky%2C+M%3BMoss%2C+B&rft.aulast=Merchlinsky&rft.aufirst=M&rft.date=1992-01-01&rft.volume=190&rft.issue=1&rft.spage=522&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=00426822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - insertion; cloning vectors; recombination; DNA; genomes; ligation; vaccinia virus ER - TY - JOUR T1 - Multiple myeloma among Danish women: Employment history and workplace exposures AN - 16868220; 3794845 AB - To investigate the role of employment history and workplace exposures as risk factors for multiple myeloma among women, a population-based case-control study using the Danish Cancer Registry data linkage system was conducted. All cases of myeloma diagnosed in Danish women between 1970 and 1984 (1,010 cases) and 4,040 age-matched women alive at the time of case-diagnosis were identified. Industrial histories from 1964 forward were obtained from the nationwide Pension Fund for 363 cases and 1,517 controls, and the most recent occupation on the tax record was available for 607 cases and 2,596 controls. Using industry/occupational-code combinations for the cases and controls who had industry employment, Danish industrial hygienists assessed the likelihood of exposure to 47 workplace substances. An increased myeloma risk was seen for women not in the Pension Fund, but who had an occupational title coded as 'Mrs/homemaker.' Nonsignificantly elevated risks of 1.3 or greater were observed for employment in: production of agricultural products; orchards/nurseries; spinning/weaving; other textile and plastics manufacturing; hotel, entertainment, and social services industries. Elevated, but nonsignificant risks were observed for possible and probable exposure to exhaust fumes, formaldehyde, wood dust, animals or animal products, and pesticides. The strongest association with myeloma was employment in the agricultural industry, however, the number of women who worked on family farms was unknown and could not be included in this risk estimate. JF - Cancer Causes & Control AU - Pottern, L M AU - Heineman, E F AU - Olsen, J H AU - Raffn, E AU - Blair, A AD - Occup. Stud. Sect., Environ. Epidemiol. Branch, NCI, EPN 418, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 427 EP - 432 VL - 3 IS - 5 SN - 0957-5243, 0957-5243 KW - multiple myeloma KW - Health & Safety Science Abstracts KW - agriculture KW - textile industry KW - Denmark KW - females KW - occupational exposure KW - H SM10.21:CANCER UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16868220?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Causes+%26+Control&rft.atitle=Multiple+myeloma+among+Danish+women%3A+Employment+history+and+workplace+exposures&rft.au=Pottern%2C+L+M%3BHeineman%2C+E+F%3BOlsen%2C+J+H%3BRaffn%2C+E%3BBlair%2C+A&rft.aulast=Pottern&rft.aufirst=L&rft.date=1992-01-01&rft.volume=3&rft.issue=5&rft.spage=427&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Denmark; females; occupational exposure; agriculture; textile industry ER - TY - JOUR T1 - Candidate biomarkers for application as intermediate end points of lung carcinogenesis AN - 16836083; 3567739 AB - The need for validated intermediate end point markers to facilitate lung cancer chemointervention research is compelling. Three major classes of lung markers are relevant for this application. Since lung cancer includes four distinct histologies, markers that map degrees of histologic differentiation are important. Many of the markers for squamous differentiation overlap with the candidates for application in the study of head and neck cancer. Production of tissue-specific cell products especially for surfactant or CEA is of interest, because the gene structure is known and many differentiation-related polymorphisms exist. This strategy would be useful for adenomatous type tissue. A second type of marker is the broad group of differentiation markers. The carbohydrate or blood group-like antigens comprise a representative example. Carbohydrate structures are expressed in a specific sequence during fetal processes, and this sequence appears to reverse with the development of a cancer. Retrodifferentiation of specific differentiation markers is the basis of a major effort to effect earlier lung cancer detection using sputum immunocytochemistry. The final class includes markers which affect either positive or negative aspects of growth. JF - Journal of Cellular Biochemistry AU - Mulshine, J L AU - Linnoila, R I AU - Treston, A M AU - Scott, F M AU - Quinn, K AU - Avis, I AU - Shaw, G L AU - Jensen, S M AU - Brown, P AD - Biomarkers and Prev. Res. Branch, Div. Cancer Prev. and Control, NCI, Bethesda, MD 20889, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 183 EP - 186 IS - Suppl. 16G SN - 0730-2312, 0730-2312 KW - biomarkers KW - Toxicology Abstracts KW - toxicity testing KW - lung KW - carcinogenesis KW - X 24221:Toxicity testing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16836083?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Cellular+Biochemistry&rft.atitle=Candidate+biomarkers+for+application+as+intermediate+end+points+of+lung+carcinogenesis&rft.au=Mulshine%2C+J+L%3BLinnoila%2C+R+I%3BTreston%2C+A+M%3BScott%2C+F+M%3BQuinn%2C+K%3BAvis%2C+I%3BShaw%2C+G+L%3BJensen%2C+S+M%3BBrown%2C+P&rft.aulast=Mulshine&rft.aufirst=J&rft.date=1992-01-01&rft.volume=&rft.issue=Suppl.+16G&rft.spage=183&rft.isbn=&rft.btitle=&rft.title=Journal+of+Cellular+Biochemistry&rft.issn=07302312&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - lung; carcinogenesis; toxicity testing ER - TY - JOUR T1 - Incorporation of radiophosphorus from labeled oligodeoxynucleotides into RNA of mycoplasma in cell cultures AN - 16802713; 3551219 AB - We have found that various mycoplasma species quickly and efficiently incorporate radiophosphorus into their RNA from labeled oligonucleotides added to the medium. The label can be in any of several positions in an oligodeoxynucleotide, and incorporation also occurs efficiently from labeled RNA. Mycoplasmas also incorporate the radiolabel when they infect a mammalian cell culture; the host cells do not. This incorporation presumably involves uptake of the oligodeoxynucleotide followed by digestion to mononucleotides, conversion to ribonucleotides, and incorporation in new RNA. We believe that the processing of oligodeoxynucleotides by mycoplasma could be a source of artifacts in antisense work in cell culture and could have implications for the development of antisense therapeutics. We also suggest ways to exploit the incorporation phenomenon in mycoplasma testing. JF - ANTISENSE RES. DEV. AU - Geselowitz, DA AU - Olson, L D AU - Neckers, L M AD - Clin. Pharmacol. Branch, NCI/NIH, Bethesda, MD, 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 41 EP - 49 VL - 2 IS - 1 SN - 1050-5261, 1050-5261 KW - phosphorus KW - oligodeoxyribonucleotides KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - antisense KW - RNA KW - radioactive labelling KW - incorporation KW - Mycoplasma KW - J 02726:RNA and ribosomes KW - N 14250:Biological properties UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16802713?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=ANTISENSE+RES.+DEV.&rft.atitle=Incorporation+of+radiophosphorus+from+labeled+oligodeoxynucleotides+into+RNA+of+mycoplasma+in+cell+cultures&rft.au=Geselowitz%2C+DA%3BOlson%2C+L+D%3BNeckers%2C+L+M&rft.aulast=Geselowitz&rft.aufirst=DA&rft.date=1992-01-01&rft.volume=2&rft.issue=1&rft.spage=41&rft.isbn=&rft.btitle=&rft.title=ANTISENSE+RES.+DEV.&rft.issn=10505261&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Mycoplasma; radioactive labelling; antisense; RNA; incorporation ER - TY - JOUR T1 - Genotoxicity of heated cooling oil vapors AN - 16784494; 3541216 AB - Epidemiological studies of lung cancer in Chinese women indicated that factors other than cigarette smoking are related to lung cancer risk. A case-control study suggested that indoor air pollution, particularly from cooking oil emissions, may be involved. Condensates of volatile emissions from rapeseed and soybean cooking oils were prepared and found to be genotoxic in short-term tests including the Salmonella mutation assay, SV50 forward-mutation assay, and sister-chromatid exchange assay, as well as the micronucleus assay in mouse bone marrow. In contrast, condensates from rapeseed oil with butylated hydroxyanisole or hydrogenated rapeseed oil were not mutagenic, implicating oxidation products as the cause for mutagenicity. Peanut oil and lard condensates were not mutagenic in any assay. The association of exposure to Chinese rapeseed cooking-oil emissions and lung-cancer risk may be related to the mutagenic component of these condensates. JF - Mutation Research AU - Qu, Y H AU - Xu, G X AU - Zhou, J Z AU - Chen, T D AU - Zhu, L F AU - Shields, P G AU - Wang, H W AU - Gao, Y T AD - NIH, NCI, DCE, Lab. Human Carcinog., Build. 37, Rm. 2C16, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 105 EP - 111 VL - 298 IS - 2 SN - 0921-8262, 0921-8262 KW - oils KW - cooking KW - man KW - vapor KW - lung cancer KW - Health & Safety Science Abstracts; Genetics Abstracts; Toxicology Abstracts KW - genotoxicity KW - lung KW - vapors KW - cancer KW - X 24120:Food, additives & contaminants KW - H SE4.20:POISONS AND POISONING KW - G 07221:Specific chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16784494?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+Research&rft.atitle=Genotoxicity+of+heated+cooling+oil+vapors&rft.au=Qu%2C+Y+H%3BXu%2C+G+X%3BZhou%2C+J+Z%3BChen%2C+T+D%3BZhu%2C+L+F%3BShields%2C+P+G%3BWang%2C+H+W%3BGao%2C+Y+T&rft.aulast=Qu&rft.aufirst=Y&rft.date=1992-01-01&rft.volume=298&rft.issue=2&rft.spage=105&rft.isbn=&rft.btitle=&rft.title=Mutation+Research&rft.issn=09218262&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - vapors; genotoxicity; lung; cancer; lung cancer; oils; cooking; man ER - TY - JOUR T1 - Adenovirus-mediated in vivo gene transfer and expression in normal rat liver AN - 16779263; 3540829 AB - Replication deficient, recombinant adenovirus (Ad) vectors do not require target cell replication for transfer and expression of exogenous genes and thus may be useful for in vivo gene therapy in hepatocytes. In vitro, primary cultures of rat hepatocytes infected with a recombinant Ad containing a human alpha 1-antitrypsin cDNA (Ad- alpha 1AT) synthesized and secreted human alpha 1AT for 4 weeks. In rats, in vivo intraportal administration of a recombinant Ad containing the E. coli lacZ gene, was followed by expression of beta -galactosidase in hepatocytes 3 days after infection. Intraportal infusion of Ad- alpha 1AT produced detectable serum levels of human alpha 1AT for 4 weeks. Thus, targeted gene expression has been achieved in the liver, albeit at low levels, suggesting that adenovirus vectors may be a useful means for in vivo gene therapy in liver disorders. JF - Nature Genetics AU - Jaffe, HA AU - Danel, C AU - Longenecker, G AU - Metzger, M AU - Setoguchi, Y AU - Rosenfeld, MA AU - Gant, T W AU - Thorgeirsson, S S AU - Crystal, R G AD - Pulm. Branch, Natl. Heart, Lung, and Blood Inst., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 372 EP - 378 VL - 1 IS - 5 SN - 1061-4036, 1061-4036 KW - rats KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Genetics Abstracts KW - gene transfer KW - gene therapy KW - adenovirus KW - cloning vectors KW - mediation KW - liver KW - gene expression KW - in vivo KW - G 07401:Rodentia (rats) KW - N 14671:Transduction KW - W 30965:Miscellaneous, Reviews KW - W3 33055:Genetic engineering (general) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16779263?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+Genetics&rft.atitle=Adenovirus-mediated+in+vivo+gene+transfer+and+expression+in+normal+rat+liver&rft.au=Jaffe%2C+HA%3BDanel%2C+C%3BLongenecker%2C+G%3BMetzger%2C+M%3BSetoguchi%2C+Y%3BRosenfeld%2C+MA%3BGant%2C+T+W%3BThorgeirsson%2C+S+S%3BCrystal%2C+R+G&rft.aulast=Jaffe&rft.aufirst=HA&rft.date=1992-01-01&rft.volume=1&rft.issue=5&rft.spage=372&rft.isbn=&rft.btitle=&rft.title=Nature+Genetics&rft.issn=10614036&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - gene therapy; gene transfer; cloning vectors; mediation; liver; gene expression; in vivo; adenovirus ER - TY - JOUR T1 - Structural features that influence the ability of lipid A and its analogs to abolish expression of suppressor T cell activity AN - 16767137; 3738450 AB - Lipid A preparations derived from the lipopolysaccharides of several gram-negative bacteria, as well as chemically defined synthetic lipid A's and their analogs (both glucosamine mono- and disaccharides), were used to establish the chemical structures required for (i) abolishing the expression of suppressor T cell (Ts) function and (ii) inducing polyclonal activation of B cells. Salmonella minnesota R595 lipid A (diphosphoryl lipid A) possesses both of these activities. Decreasing the number of phosphate groups in lipid A from two to one (monophosphoryl lipid A) as well as decreasing the fatty acyl content, primarily by removing the residue at the 3 position, resulted in a progressive reduction in toxicity; however, these structural modifications did not influence its ability to abolish the expression of Ts function. Reducing the fatty acyl content from five to four (lipid A precursor IV sub(A) or I sub(a)) eliminated the capacity to influence Ts function but not to induce polyclonal activation of B cells. None of the monosaccharide analogs of lipid A examined influenced the expression of Ts activity, although some were able to activate B cells polyclonally. Thus, in order to be able to abolish the expression of Ts function, lipid A (i) must be a glucosamine disaccharide, (ii) may have either one or two phosphate groups, and (iii) must have at least five fatty acyl groups. Also, the chain length of the nonhydroxylated fatty acid, as well as the location of acyloxyacyl groups (2' versus 3' position), may play an important role. These findings indicate that the chemical structures responsible for the toxicity of lipid A differ from those that influence its capacity to abolish the expression of Ts function and to induce polyclonal activation of B cells. JF - Infection and Immunity AU - Baker, P J AU - Hraba, T AU - Taylor, CE AU - Myers, K R AU - Takayama, K AU - Qureshi, N AU - Stuetz, P AU - Kusumoto, S AU - Hasegawa, A AD - Lab. Immunog., NIAID, Twinbrook-II Res. Fac., 12441 Parklawn Dr., Rockville, MD 20852, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 2694 EP - 2701 VL - 60 IS - 7 SN - 0019-9567, 0019-9567 KW - lipid A KW - Immunology Abstracts; Microbiology Abstracts B: Bacteriology KW - suppressor cells KW - Salmonella minnesota KW - lymphocytes T KW - analogs KW - activation KW - J 02731:Lipids KW - F 06757:NK cells UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16767137?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Structural+features+that+influence+the+ability+of+lipid+A+and+its+analogs+to+abolish+expression+of+suppressor+T+cell+activity&rft.au=Baker%2C+P+J%3BHraba%2C+T%3BTaylor%2C+CE%3BMyers%2C+K+R%3BTakayama%2C+K%3BQureshi%2C+N%3BStuetz%2C+P%3BKusumoto%2C+S%3BHasegawa%2C+A&rft.aulast=Baker&rft.aufirst=P&rft.date=1992-01-01&rft.volume=60&rft.issue=7&rft.spage=2694&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Salmonella minnesota; analogs; lymphocytes T; suppressor cells; activation ER - TY - JOUR T1 - Human neutrophil response to recombinant Neisserial Opa proteins AN - 16765718; 3738491 AB - Interactions of human neutrophils with recombinant Escherichia coli expressing gonococcal outer membrane Opa proteins were examined using chemiluminescent and biological assays. Seven opa loci from Neisseria gonorrhoeae MS11 4.8 were expressed as beta -lactamase-Opa fusion proteins that contained all but the mature N-terminal amino acid of the full-length Opa protein fused to three N-terminal amino acids derived from the mature beta -lactamase. The Opa fusion proteins were exported and assembled in the outer membrane of E. coli in a manner similar to that of Opa in N. gonorrhoeae, as evaluated by antibody binding and in situ proteolytic cleavage. All fusion proteins exhibited the characteristic heat-modifiable migration in SDS-polyacrylamide gel electrophoresis that typifies Opa proteins of neisseriae. Opa fusion proteins conferred on E. coli the ability to stimulate a chemiluminescent response from human neutrophils in the absence of antibody or complement. The nature of the response in terms of chemiluminescence, phagocytosis, and killing was in all cases analogous to that seen using N. gonorrhoeae expressing the equivalent Opa protein. Neither E. coli nor gonococci expressing OpaA elicited a response from neutrophils. Use of E. coli expressing Opa fusions should be useful in defining their biological activities and pathogenic roles. JF - Molecular Microbiology AU - Belland, R J AU - Chen, T AU - Swanson, J AU - Fischer, SH AD - Lab. Microbial Struct. and Funct., NIAID/NIH, Rocky Mountain Lab., Hamilton, MT 59840, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1729 EP - 1737 VL - 6 IS - 13 SN - 0950-382X, 0950-382X KW - opa protein KW - Immunology Abstracts; Microbiology Abstracts B: Bacteriology KW - immune response (cell-mediated) KW - fusion protein KW - leukocytes (neutrophilic) KW - Escherichia coli KW - Neisseria gonorrhoeae KW - F 06801:Bacteria KW - J 02833:Immune response and immune mechanisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16765718?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Microbiology&rft.atitle=Human+neutrophil+response+to+recombinant+Neisserial+Opa+proteins&rft.au=Belland%2C+R+J%3BChen%2C+T%3BSwanson%2C+J%3BFischer%2C+SH&rft.aulast=Belland&rft.aufirst=R&rft.date=1992-01-01&rft.volume=6&rft.issue=13&rft.spage=1729&rft.isbn=&rft.btitle=&rft.title=Molecular+Microbiology&rft.issn=0950382X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; Neisseria gonorrhoeae; fusion protein; immune response (cell-mediated); leukocytes (neutrophilic) ER - TY - JOUR T1 - Toxicological principles of metal carcinogenesis with special emphasis on cadmium AN - 16744370; 3723374 AB - Metals are an important and emerging class of carcinogens. At least three metals, specifically nickel, chromium, and arsenic, are confirmed human carcinogens, and several more are suspected to have carcinogenic potential in man. Considering that the list of known human carcinogens of any type is very small, it becomes clear that metals make up a substantial portion of the list. Furthermore, many metals are very potent carcinogens in laboratory animals. Despite this, relatively little attention has been given to the topic of metal carcinogenesis. The reasons for this relative lack of attention are not clear but perhaps are fostered by a perception that, because metals are the simplest of molecules, their mechanism of action must also be simple. This could not be farther from the truth and, although no clear mechanisms have emerged in the area of metal carcinogenesis, it has become apparent that they are anything but simple. Metal carcinogens possess several unique characteristics including a remarkable target site specificity. Detection of the mechanism, or mechanisms, of metal carcinogenesis has, however, proven elusive, in part because of a wide diversity of metallic carcinogenic agents and the intricate nature of metal interactions in biologic systems. The following review explores this broad topic, with special emphasis on toxicological principles including dose-response relationships and potential mechanisms, using cadmium as an example. (DBO) JF - Critical Reviews in Toxicology AU - Waalkes, M P AU - Coogan, T P AU - Barter, R A AD - Inorg. Carcinog. Sect., Lab. Comp. Carcino., Frederick Cancer Res. and Dev. Cent., NCI, Build. 538, Rm. 205E, Frederick, MD 21702-1201, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 175 EP - 201 VL - 22 IS - 3-4 SN - 1040-8444, 1040-8444 KW - cadmium KW - Toxicology Abstracts KW - reviews KW - carcinogenesis KW - metals KW - X 24250:Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16744370?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Critical+Reviews+in+Toxicology&rft.atitle=Toxicological+principles+of+metal+carcinogenesis+with+special+emphasis+on+cadmium&rft.au=Waalkes%2C+M+P%3BCoogan%2C+T+P%3BBarter%2C+R+A&rft.aulast=Waalkes&rft.aufirst=M&rft.date=1992-01-01&rft.volume=22&rft.issue=3-4&rft.spage=175&rft.isbn=&rft.btitle=&rft.title=Critical+Reviews+in+Toxicology&rft.issn=10408444&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - metals; carcinogenesis; reviews ER - TY - JOUR T1 - Isolation of multiple mouse cDNAs with coding homology to Saccharomyces cerevisiae CDC25: Identification of a region related to Bcr, Vav, Dbl and CDC24. AN - 16697243; 2981935 AB - In Saccharomyces cerevisiae , the product of the CDC25 gene is an essential Ras activator that appears to function by stimulating guanine nucleotide exchange on Ras. Using the ability of a mouse cDNA expression library to complement yeast cells lacking functional CDC25, Martegani et al. have identified a 1.7 kb partial cDNA from a gene, designated CDC25 super(Mm), with homology to CDC25. We have now screened a mouse brain cDNA library to identify full-length clones of CDC25 super(Mm). This cloning has led to the isolation of six distinct full-length cDNAs, each of which appear to be derived from the CDC25 super(Mm) gene, since their 3' 2 kb appear to be identical and to encode the same 661 C-terminal amino acids. Three cDNAs are predicted to encode protein products of 666 or 667 amino acids. The other three cDNAs encode products that are 836, 1120 and 1260 amino acids, respectively. A 241 amino acid region near the N-terminus of the two largest products was found to have homology to a domain shared by Bcr, Vav, Dbl and CDC24. Polyclonal antibodies raised to a peptide encoded by all the cDNAs have identified at least two protein products in NIH3T3 fibroblasts. Their apparent molecular weights are 75 and 95 kDa, which correspond closely to those predicted to be encoded, respectively, by the two shorter classes of cDNAs. In NIH3T3, the 95 kDa form is much more abundant than the 75 kDa form, while PC-12 pheochromocytoma cells contain relatively high levels of the 75 kDa form. We conclude that CDC25 super(Mm) is a complex gene whose protein products are regulated in a tissue-specific manner. JF - EMBO Journal AU - Cen, Hui AU - Papageorge, A G AU - Zippel, R AU - Lowy AU - Zhang, Ke AD - Lab. Cell. Oncol., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 4007 EP - 4015 VL - 11 IS - 11 SN - 0261-4189, 0261-4189 KW - CDC25 Mm gene KW - CDC25 gene KW - Saccharomyces cerevisiae KW - amino acid sequence KW - cDNA KW - gene products KW - genes KW - homology KW - mice KW - nucleotide sequence KW - predictions KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - G 07398:GENERAL KW - N 14640:Structure & sequence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16697243?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=EMBO+Journal&rft.atitle=Isolation+of+multiple+mouse+cDNAs+with+coding+homology+to+Saccharomyces+cerevisiae+CDC25%3A+Identification+of+a+region+related+to+Bcr%2C+Vav%2C+Dbl+and+CDC24.&rft.au=Cen%2C+Hui%3BPapageorge%2C+A+G%3BZippel%2C+R%3BLowy%3BZhang%2C+Ke&rft.aulast=Cen&rft.aufirst=Hui&rft.date=1992-01-01&rft.volume=11&rft.issue=11&rft.spage=4007&rft.isbn=&rft.btitle=&rft.title=EMBO+Journal&rft.issn=02614189&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - nucleotide sequence; cDNA; amino acid sequence; genes; homology; gene products ER - TY - JOUR T1 - Two-dimensional electrophoretic analysis of transformation-sensitive polypeptides during chemically, spontaneously, and oncogene-induced transformation of rat liver epithelial cells. AN - 16691523; 2976999 AB - Recently, we described the establishment of a computerized database of rat liver epithelial (RLE) cellular polypeptides. This database has now been expanded to include the analysis of cellular polypeptide alterations during chemically (aflatoxin B1; AFB), spontaneously, and oncogene (v-Ha-ras, v-raf, and v-myc/v-raf)-induced transformation of RLE cells. JF - Electrophoresis AU - Wirth, P J AU - Luo, Lin-di AU - Fujimoto, Y AU - Bisgaard, H C AD - Lab. Exp. Carcinog., NCI, Build. 37 Rm. 3C28, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 305 EP - 320 VL - 13 IS - 5 SN - 0170-0835, 0170-0835 KW - carcinogens KW - characterization KW - epithelium KW - liver KW - oncogenes KW - proteins KW - rats KW - treatment KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16691523?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Electrophoresis&rft.atitle=Two-dimensional+electrophoretic+analysis+of+transformation-sensitive+polypeptides+during+chemically%2C+spontaneously%2C+and+oncogene-induced+transformation+of+rat+liver+epithelial+cells.&rft.au=Wirth%2C+P+J%3BLuo%2C+Lin-di%3BFujimoto%2C+Y%3BBisgaard%2C+H+C&rft.aulast=Wirth&rft.aufirst=P&rft.date=1992-01-01&rft.volume=13&rft.issue=5&rft.spage=305&rft.isbn=&rft.btitle=&rft.title=Electrophoresis&rft.issn=01700835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - The prospects for domesticating milk protein genes AN - 16691286; 3053731 AB - It is possible to convert milk glands of transgenic animals into bioreactors producing heterologous proteins such as scarce human pharmaceuticals. To predictably and successfully engineer the milk gland, we will need a thorough understanding of its physiology. Expression studies in transgenic animals have located mammary specific and hormone inducible transcription elements in the promoter/upstream regions of milk protein genes, and transfection studies in cell lines or primary cells have identified constitutive and hormone inducible elements. Most importantly, it appears that in addition to individual promoter based transcription elements structural features of milk protein chromosomal loci may contribute to the tight developmental and hormonal regulation. I will discuss milk protein gene regulation with emphasis on regulatory differences between genes and species, and the possibility that transcription elements function only properly within genetically defined chromatin domains. Novel strategies to build mammary expression vectors and to test their functionality without pursuing the standard transgenic route will be presented. Finally, I will discuss homologous recombination with the goal to target milk protein genes. Only through the domestication of milk protein genes will we be able to use their full potential in the mammary bioreactor. JF - Journal of Cellular Biochemistry AU - Hennighausen, L AD - Lab. Biochem. Metab., NIDDK/NIH, Bldg. 10, Rm. 9N113, Bethesda, MD 20982, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 325 EP - 332 VL - 49 IS - 4 SN - 0730-2312, 0730-2312 KW - Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Medical and Pharmaceutical Biotechnology Abstracts KW - biotechnology KW - reviews KW - milk KW - genes KW - gene regulation KW - transgenic animals KW - proteins KW - pharmaceuticals KW - N 14100:Reviews KW - W 30965:Miscellaneous, Reviews KW - W3 33055:Genetic engineering (general) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16691286?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Cellular+Biochemistry&rft.atitle=The+prospects+for+domesticating+milk+protein+genes&rft.au=Hennighausen%2C+L&rft.aulast=Hennighausen&rft.aufirst=L&rft.date=1992-01-01&rft.volume=49&rft.issue=4&rft.spage=325&rft.isbn=&rft.btitle=&rft.title=Journal+of+Cellular+Biochemistry&rft.issn=07302312&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - biotechnology; reviews; genes; milk; gene regulation; transgenic animals; pharmaceuticals; proteins ER - TY - JOUR T1 - Development of polymerase chain reaction primer sets for diagnosis of Lyme disease and for species-specific identification of Lyme disease isolates by 16S rRNA signature nucleotide analysis AN - 16628440; 3659084 AB - We have determined and compared partial 16S rRNA sequences from 23 Lyme disease spirochete isolates and aligned these with 8 sequences previously presented. The 16S rRNA signature nucleotide compositions were defined for each isolate and compared with the genomic species signature nucleotide sets previously established. To identify positions truly indicative of species classification which could serve as targets for polymerase chain reaction species-specific identification primers, 16S rRNA-based phylogenetic analyses were conducted. On the basis of the identified signature nucleotides, we designed polymerase chain reaction primer sets which (i) amplify all spirochete species associated with Lyme disease and (ii) differentiate between these species. The primer sets were tested on 38 Borrelia isolates associated with Lyme disease and were found to be sensitive and specific. All Lyme disease isolates tested were amplification positive. These primers allow for the rapid species identification of Lyme disease isolates. (DBO) JF - Journal of Clinical Microbiology AU - Marconi, R T AU - Garon, C F AD - Lab. Vectors and Pathog., Rocky Mountain Lab., NIAID/NIH, Public Health Serv., U.S. DHHS, Hamilton, MT 59840, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 2830 EP - 2834 VL - 30 IS - 11 SN - 0095-1137, 0095-1137 KW - rRNA 16S KW - Microbiology Abstracts B: Bacteriology KW - nucleotide sequence KW - isolates KW - species KW - Borrelia burgdorferi KW - polymerase chain reaction KW - Lyme disease KW - J 02855:Human Bacteriology: Others UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16628440?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Microbiology&rft.atitle=Development+of+polymerase+chain+reaction+primer+sets+for+diagnosis+of+Lyme+disease+and+for+species-specific+identification+of+Lyme+disease+isolates+by+16S+rRNA+signature+nucleotide+analysis&rft.au=Marconi%2C+R+T%3BGaron%2C+C+F&rft.aulast=Marconi&rft.aufirst=R&rft.date=1992-01-01&rft.volume=30&rft.issue=11&rft.spage=2830&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Borrelia burgdorferi; Lyme disease; polymerase chain reaction; isolates; species; nucleotide sequence ER - TY - JOUR T1 - Current perspective on Lyme borreliosis. AN - 16626023; 2994470 JF - Journal of the American Medical Association AU - Kaslow, R A AD - Div. Microbiol. and Infect. Dis., NIAID/NIH, Solar Build. 3A24, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1381 EP - 1383 VL - 267 IS - 10 SN - 0098-7484, 0098-7484 KW - doxycycline KW - Microbiology Abstracts B: Bacteriology KW - injuries KW - Borrelia burgdorferi KW - treatment KW - infection KW - epidemiology KW - skin KW - J 02843:Skin UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16626023?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+American+Medical+Association&rft.atitle=Current+perspective+on+Lyme+borreliosis.&rft.au=Kaslow%2C+R+A&rft.aulast=Kaslow&rft.aufirst=R&rft.date=1992-01-01&rft.volume=267&rft.issue=10&rft.spage=1381&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+Medical+Association&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Borrelia burgdorferi; infection; injuries; skin; treatment; epidemiology ER - TY - JOUR T1 - Second primary cancers following anal and cervical carcinoma: Evidence of shared etiologic factors. AN - 16625044; 3007986 AB - The authors examined the incidence of second primary cancers occurring after cervical and anal cancer. Data from the Connecticut Tumor Registry for 1935-1988 and eight other US tumor registries for 1973-1988 were used. Women with primary invasive cervical cancer had a relative risk of 4.6 (95% confidence interval (CI) 2.4-8.1) for subsequent invasive anal cancer. Increased relative risks after cervical cancer were also found for cancers of the oral cavity (relative risk (RR) = 2.2), stomach (RR = 1.5), rectum (RR = 1.4), larynx (RR = 3.4), lung (RR = 3.0), vagina (RR = 5.6), bladder (RR = 2.7), and kidney (RR = 1.9); decreased relative risks were noted for melanoma (RR = 0.5) and breast cancer (RR = 0.8). Patients with a primary diagnosis of anal cancer had relative risks for subsequent invasive and in situ cervical cancer of 1.3 (95% CI 0.2-4.5) and 3.4 (95% CI 0.9-8.8), respectively. Anal cancer was also associated with increased relative risks of subsequent lung (RR = 2.5) and prostate (RR = 1.8) cancers, whereas the relative risk of uterine cancer was 0.2 (95% CI 0.0-0.9). JF - American Journal of Epidemiology AU - Rabkin, C S AU - Biggar, R J AU - Melbye, M AU - Curtis, R E AD - Viral Epidemiol. Sect., NCI, Executive Plaza N., Room 434, 6130 Executive Blvd., Rockville, MD 20852, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 54 EP - 58 VL - 136 IS - 1 SN - 0002-9262, 0002-9262 KW - secondary cancers KW - aetiology KW - papilloma virus (human) KW - Virology & AIDS Abstracts; Toxicology Abstracts KW - anorectal KW - cigarette smoking KW - cervix KW - man KW - carcinoma KW - V 22114:Human oncogenic viruses KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16625044?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Second+primary+cancers+following+anal+and+cervical+carcinoma%3A+Evidence+of+shared+etiologic+factors.&rft.au=Rabkin%2C+C+S%3BBiggar%2C+R+J%3BMelbye%2C+M%3BCurtis%2C+R+E&rft.aulast=Rabkin&rft.aufirst=C&rft.date=1992-01-01&rft.volume=136&rft.issue=1&rft.spage=54&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - cervix; anorectal; carcinoma; cigarette smoking; man ER - TY - JOUR T1 - Assessment of oxidative DNA damage in the oxyR-deficient SOS chromotest strain Escherichia coli PQ300. AN - 16624838; 2996414 AB - The SOS chromotest is a simple short-term genotoxicity assay measuring the induction of gene sfiA in Escherichia coli K-12. The recent availability of SOS tester strains with additional mutations in DNA repair or protection systems allows testing of DNA damaging compounds for genotoxic specificity. E. coli PQ300 differs from the standard SOS tester strain PQ37 in that it contains an additional mutation in gene oxyR that renders it more sensitive to oxidative genotoxins. The generation of reactive oxygen intermediates (ROI) by hydroperoxides (H sub(2)O sub(2), t-butyl hydroperoxide, cumene hydroperoxide), gamma -radiation, glucose oxidase, and xanthine oxidase resulted in a more vigorous SOS response in strain PQ300 compared to strain PQ37. PQ300 was also more sensitive than PQ37 for the detection of reducing agents such as ascorbic acid, cysteine, and glutathione, which also alter the redox status of the bacterial cells. JF - Environmental and Molecular Mutagenesis AU - Mueller, J AU - Janz, S AD - Lab. Genet., NCI, NIH, Bldg. 37, Rm. 2B09, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 297 EP - 306 VL - 20 IS - 4 SN - 0893-6692, 0893-6692 KW - Genetics Abstracts; Toxicology Abstracts KW - damage KW - SOS repair KW - free radicals KW - DNA KW - Escherichia coli KW - genotoxicity testing KW - G 07220:General theory/testing systems KW - X 24221:Toxicity testing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16624838?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+Molecular+Mutagenesis&rft.atitle=Assessment+of+oxidative+DNA+damage+in+the+oxyR-deficient+SOS+chromotest+strain+Escherichia+coli+PQ300.&rft.au=Mueller%2C+J%3BJanz%2C+S&rft.aulast=Mueller&rft.aufirst=J&rft.date=1992-01-01&rft.volume=20&rft.issue=4&rft.spage=297&rft.isbn=&rft.btitle=&rft.title=Environmental+and+Molecular+Mutagenesis&rft.issn=08936692&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; free radicals; DNA; damage; SOS repair; genotoxicity testing ER - TY - JOUR T1 - Is cigarette smoking a risk factor for non-Hodgkin's lymphoma or multiple myeloma? Results from the Lutheran Brotherhood cohort study. AN - 16623787; 3009329 AB - Among 17,633 U.S. white male insurance policy holders whose use of tobacco was characterized in a 1966 self-administered questionnaire, there were 49 deaths from non-Hodgkin's lymphoma (NHL) and 21 from multiple myeloma (MM) during a 20-year follow-up. Since this is the first cohort study suggesting a link between cigarette smoking and NHL and findings from case-control studies have been inconsistent, additional clarification should be sought from larger incidence-based cohort investigations. JF - Leukemia Research AU - Linet AU - McLaughlin, J K AU - Hsing, A W AU - Wacholder, S AU - Co Chien, HT AU - Schuman, L M AU - Bjelke, E AU - Blot, W J AD - AS/BB/EBP/DCE, NCI, Executive Plaza N., Suite 415B, Rockville, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 621 EP - 624 VL - 16 IS - 6-7 SN - 0145-2126, 0145-2126 KW - risk factors KW - lymphoma KW - multiple myeloma KW - man KW - Risk Abstracts; Immunology Abstracts KW - cigarette smoking KW - cigarettes KW - USA KW - smoking KW - R2 23060:Medical and environmental health KW - F 06866:Myeloma/plasmacytoma/thymoma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16623787?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Leukemia+Research&rft.atitle=Is+cigarette+smoking+a+risk+factor+for+non-Hodgkin%27s+lymphoma+or+multiple+myeloma%3F+Results+from+the+Lutheran+Brotherhood+cohort+study.&rft.au=Linet%3BMcLaughlin%2C+J+K%3BHsing%2C+A+W%3BWacholder%2C+S%3BCo+Chien%2C+HT%3BSchuman%2C+L+M%3BBjelke%2C+E%3BBlot%2C+W+J&rft.aulast=Linet&rft.aufirst=&rft.date=1992-01-01&rft.volume=16&rft.issue=6-7&rft.spage=621&rft.isbn=&rft.btitle=&rft.title=Leukemia+Research&rft.issn=01452126&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - USA; cigarette smoking; cigarettes; smoking; risk factors; lymphoma; multiple myeloma; man ER - TY - JOUR T1 - Failure of intragastrically administered Yersinia pestis capsular antigen to protect mice against challenge with virulent plague: Suppression of fraction 1-specific antibody response. AN - 16600077; 3008579 AB - We evaluated the Yersinia pestis capsular (fraction 1 (F1)) antigen as a potential oral immunogen in mice. We found that single doses of as much as 0.4 mg of F1, administered by intragastric (ig) intubation, were unprotective and did not stimulate production of detectable levels of specific antibody. Three weekly ig doses resulted in low serum antibody levels that also did not provide protection against challenge with virulent Y. pestis . Assays of type-specific antibody following intubation and subsequent challenge with a subcutaneous inoculation of F1 revealed that the quantity of antigen intubated and the secondary IgG2a antibody levels were inversely related, suggesting the induction of tolerance to intragastrically administered F1 antigen. Transfer of spleen cells from intubated mice to F1 immune recipients failed to demonstrate suppression of specific antibody, indicating that the immune tolerance observed in intubated mice was not due to a T suppressor cell-mediated effect. The results of this study indicate that Y. pestis F1 antigen is not likely to be an efficacious immunogen for oral vaccination of mice against plague. JF - American Journal of Tropical Medicine and Hygiene AU - Thomas, R E AU - Simpson, W J AU - Perry, L L AU - Schwan, T G AD - Lab. Vectors and Pathogens, NIAID/NIH, Rocky Mountain Lab., 903 S. 4th St., Hamilton, MT 59840, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 92 EP - 97 VL - 47 IS - 1 SN - 0002-9637, 0002-9637 KW - mice KW - Immunology Abstracts; Microbiology Abstracts B: Bacteriology KW - immunosuppression KW - antibodies KW - Yersinia pestis KW - immune response (humoral) KW - vaccination KW - J 02834:Vaccination and immunization KW - F 06807:Active immunization UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16600077?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.atitle=Failure+of+intragastrically+administered+Yersinia+pestis+capsular+antigen+to+protect+mice+against+challenge+with+virulent+plague%3A+Suppression+of+fraction+1-specific+antibody+response.&rft.au=Thomas%2C+R+E%3BSimpson%2C+W+J%3BPerry%2C+L+L%3BSchwan%2C+T+G&rft.aulast=Thomas&rft.aufirst=R&rft.date=1992-01-01&rft.volume=47&rft.issue=1&rft.spage=92&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Yersinia pestis; vaccination; immune response (humoral); immunosuppression; antibodies ER - TY - JOUR T1 - Gas chromatographic detection of cocaine and cocaethylene in hair of mice chronically injected with cocaine or cocaethylene and fed ethanol. AN - 16595221; 2989618 AB - GC and GC/MS analysis was used to detect cocaine and cocaethylene in hair extracts of mice injected with 20 mg/kg cocaine hydrochloride or an equivalent dose of cocaethylene fumarate twice daily for 3 weeks. Some mice were fed liquid Lieber-DeCarli diets containing ethanol (26% of total calories) and injected twice daily with the same doses of cocaine or cocaethylene or combination of cocaine and morphine (5 mg/kg). The average concentrations of cocaine in different experimental groups were in the range of 0.9-2.4 ng/mg of hair and for cocaethylene, 2.4-2.8 ng/mg of hair. There were no significant differences in hair concentrations of cocaine among groups receiving cocaine treatment, nor were there significant difference in cocaethylene concentration in hair in the two groups administered cocaethylene. In hair extracts of mice treated with cocaine and ethanol, levels of cocaethylene were below the limit of detection. JF - Forensic Science International AU - Pirozhkov, S V AU - Watson, R R AU - Eskelson, C D AD - Dep. Fam. and Community Med., NIAAA Alcohol Res. Cent., Univ. Arizona Health Sci. Cent., Tucson, AZ 85724, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 99 EP - 107 VL - 57 IS - 2 SN - 0379-0738, 0379-0738 KW - cocaine KW - cocaethylene KW - mice KW - Toxicology Abstracts KW - detection KW - hair KW - X 24222:Analytical procedures KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16595221?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Forensic+Science+International&rft.atitle=Gas+chromatographic+detection+of+cocaine+and+cocaethylene+in+hair+of+mice+chronically+injected+with+cocaine+or+cocaethylene+and+fed+ethanol.&rft.au=Pirozhkov%2C+S+V%3BWatson%2C+R+R%3BEskelson%2C+C+D&rft.aulast=Pirozhkov&rft.aufirst=S&rft.date=1992-01-01&rft.volume=57&rft.issue=2&rft.spage=99&rft.isbn=&rft.btitle=&rft.title=Forensic+Science+International&rft.issn=03790738&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - detection; hair ER - TY - JOUR T1 - Cell-mediated cleavage of Pseudomonas exotoxin between Arg super(279) and Gly super(280) generates the enzymatically active fragment which translocates to the cytosol. AN - 16590800; 3003802 AB - Pseudomonas exotoxin (PE) is a three-domain toxin which is cleaved by a cellular protease within cells and then reduced to generate two prominent fragments. The N-terminal fragment is 28 kDa in size and contains the binding domain. The 37-kDa C-terminal fragment, which translocates to the cytosol, contains the translocation domain and the ADP-ribosylation domain. Cleavage followed by reduction is essential for toxicity since mutant forms of the toxin that cannot be cleaved by cells are nontoxic. Previous results with these mutants suggested that cleavage occurred in an arginine-rich (arginine residues are at positions 274, 276, and 279) disulfide loop near the beginning of the translocation domain, but the exact site of cleavage was not determined. Since very few molecules of the 37-kDa fragment are generated within cells it was not possible to determine the site of cleavage by performing a conventional N-terminal sequence analysis of the 37-kDa fragment. Two experimental approaches were used to overcome this limitation. The results confirmed that cleavage was between Arg super(279) and Gly super(280). JF - Journal of Biological Chemistry AU - Ogata, M AU - Fryling, C M AU - Pastan, I AU - FitzGerald, D J AD - Lab. Mol. Biol., NCI, NIH, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 25396 EP - 25401 VL - 267 IS - 35 SN - 0021-9258, 0021-9258 KW - Microbiology Abstracts B: Bacteriology KW - sites KW - exotoxins KW - enzymatic activity KW - Pseudomonas KW - translocation KW - cytosol KW - cleavage KW - J 02822:Biosynthesis and physicochemical properties UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16590800?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Cell-mediated+cleavage+of+Pseudomonas+exotoxin+between+Arg+super%28279%29+and+Gly+super%28280%29+generates+the+enzymatically+active+fragment+which+translocates+to+the+cytosol.&rft.au=Ogata%2C+M%3BFryling%2C+C+M%3BPastan%2C+I%3BFitzGerald%2C+D+J&rft.aulast=Ogata&rft.aufirst=M&rft.date=1992-01-01&rft.volume=267&rft.issue=35&rft.spage=25396&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Pseudomonas; exotoxins; cleavage; cytosol; translocation; enzymatic activity; sites ER - TY - JOUR T1 - Induction of kinetochore positive and negative micronuclei in mouse bone marrow cells by salicylazosulfapyridine and sulfapyridine. AN - 16577513; 3008053 AB - Salicylazosulfapyridine (SASP) and its major metabolite sulfapyridine (SP) have been shown to induce chromosomal damage in vivo. Both chemicals were tested in the micronucleus (MN)/kinetochore (KC) staining test to gain insight into the question of whether chromosomal breakage, aneuploidy-inducing events, or both were important to the observed production of MN in bone marrow cells of mice. In this test, both SASP and SP were shown to be strong inducers of kinetochore positive (KC super(+)) MN. Although small increases in kinetochore negative (KC super(-)) MN were also observed in SP treated mice, as well as in mice receiving the highest dose of SASP tested, the results suggest that both chemicals induce predominantly aneuploidogenic type damage. JF - Mutation Research AU - Witt, K L AU - Gudi, R AU - Bishop, J B AD - NIEHS, P.O. Box 12233, MD-E403, RTP, NC 27709, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 53 EP - 57 VL - 283 IS - 1 SN - 0027-5107, 0027-5107 KW - salicylazosulfapyridine KW - sulfapyridine KW - mice KW - Genetics Abstracts; Toxicology Abstracts KW - induction KW - micronuclei KW - bone marrow KW - X 24117:Biochemistry KW - G 07221:Specific chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16577513?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+Research&rft.atitle=Induction+of+kinetochore+positive+and+negative+micronuclei+in+mouse+bone+marrow+cells+by+salicylazosulfapyridine+and+sulfapyridine.&rft.au=Witt%2C+K+L%3BGudi%2C+R%3BBishop%2C+J+B&rft.aulast=Witt&rft.aufirst=K&rft.date=1992-01-01&rft.volume=283&rft.issue=1&rft.spage=53&rft.isbn=&rft.btitle=&rft.title=Mutation+Research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - micronuclei; induction; bone marrow ER - TY - JOUR T1 - Regulation by proteolysis: Energy-dependent proteases and their targets. AN - 16575679; 3006511 AB - A number of critical regulatory proteins in both prokaryotic and eukaryotic cells are subject to rapid, energy-dependent proteolysis. Rapid degradation combined with control over biosynthesis provides a mechanism by which the availability of a protein can be limited both temporally and spatially. Highly unstable regulatory proteins are involved in numerous biological functions, particularly at the commitment steps in developmental pathways and in emergency responses. The proteases involved in energy-dependent proteolysis are large proteins with the ability to use ATP to scan for appropriate targets and degrade complete proteins in a processive manner. These cytoplasmic proteases are also able to degrade many abnormal proteins in the cell. JF - Microbiological reviews. Baltimore AU - Gottesman, S AU - Maurizi, M R AD - Lab. Mol. Biol., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 592 EP - 621 VL - 56 IS - 4 SN - 0146-0749, 0146-0749 KW - ATP KW - proteinase KW - proteins KW - proteolysis KW - regulation KW - reviews KW - Microbiology Abstracts B: Bacteriology; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - K 03020:Fungi KW - J 02727:Amino acids, peptides and proteins KW - J:20320 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16575679?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Microbiological+reviews.+Baltimore&rft.atitle=Regulation+by+proteolysis%3A+Energy-dependent+proteases+and+their+targets.&rft.au=Gottesman%2C+S%3BMaurizi%2C+M+R&rft.aulast=Gottesman&rft.aufirst=S&rft.date=1992-01-01&rft.volume=56&rft.issue=4&rft.spage=592&rft.isbn=&rft.btitle=&rft.title=Microbiological+reviews.+Baltimore&rft.issn=01460749&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - reviews; regulation; proteolysis; proteins ER - TY - JOUR T1 - Induction of hepatic CYP1A in male F344/NCr rats by dietary exposure to Aroclor 1254: Examination of immunochemical, RNA, catalytic, and pharmacokinetic endpoints. AN - 16575566; 2990071 AB - Male F344/NCr rats were exposed to low dietary concentrations of Aroclor 1254 (0-33 ppm) for 7 days, following which the induction of selected hepatic drug metabolizing enzymes was monitored. CYP1A1, measured indirectly by assaying the O-dealkylation of ethoxyresorufin in 9000 g supernatants, was increased 1.5-, 3-, 8-, and 37-fold following 7 days of exposure to 1.0, 3.3, 10, and 33 ppm Aroclor, respectively. In contrast, the O-dealkylation of benzyloxyresorufin, an indirect measure of CYP2B1 activity, was increased similar to 4-fold following exposure to 33 ppm dietary Aroclor. Measurement of the non-P450-mediated activities epoxide hydrolase, DT-diaphorase, and aldehyde dehydrogenase (NADP super(+), benzaldehyde) revealed < 4-fold inductions following feeding of 33 ppm Aroclor. JF - Environmental Research AU - Nims, R W AU - Beebe, LE AU - Dragnev, KH AU - Thomas, P E AU - Fox, S D AU - Issaq, HJ AU - Jones, C R AU - Lubet, R A AD - Lab. Comp. Carcinog., NCI-FCRDC, Build. 538, Rm. 205E, Frederick, MD 21702-1201, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 447 EP - 466 VL - 59 IS - 2 SN - 0013-9351, 0013-9351 KW - Aroclor 1254 KW - CYP1A KW - rats KW - PCB KW - Toxicology Abstracts KW - induction KW - liver KW - X 24153:Metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16575566?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Research&rft.atitle=Induction+of+hepatic+CYP1A+in+male+F344%2FNCr+rats+by+dietary+exposure+to+Aroclor+1254%3A+Examination+of+immunochemical%2C+RNA%2C+catalytic%2C+and+pharmacokinetic+endpoints.&rft.au=Nims%2C+R+W%3BBeebe%2C+LE%3BDragnev%2C+KH%3BThomas%2C+P+E%3BFox%2C+S+D%3BIssaq%2C+HJ%3BJones%2C+C+R%3BLubet%2C+R+A&rft.aulast=Nims&rft.aufirst=R&rft.date=1992-01-01&rft.volume=59&rft.issue=2&rft.spage=447&rft.isbn=&rft.btitle=&rft.title=Environmental+Research&rft.issn=00139351&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - induction; liver ER - TY - JOUR T1 - Induction of chromosomal damage in mammalian cells in vitro and in vivo by sulfapyridine or 5-aminosalicylic acid. AN - 16574689; 3008052 AB - Sulfapyridine (SP) and 5-aminosalicylic acid (5-ASA) are the two primary metabolites of the anti-inflammatory drug salicylazosulfapyridine (SASP). These two metabolites were studied for induction of chromosomal damage in mammalian cells, in vitro and in vivo, in an attempt to understand better the genetic effects produced by SASP in humans and laboratory mice. To this end, SP and 5-ASA were tested for induction of sister-chromatid exchanges (SCE) and chromosomal aberrations (Abs) in Chinese hamster ovary (CHO) cells in vitro. In addition, they were tested in vivo for induction of micronuclei (MN) in mouse bone marrow polychromatic erythrocytes (PCE). SP gave positive results in the in vitro SCE test and the in vivo MN test, and negative results in the in vitro Abs test. 5-ASA was negative in all three tests. These results indicate that it is the SP metabolite of SASP that is necessary for the induction of chromosomal damage reported to occur in humans and mice after treatment with SASP. JF - Mutation Research AU - Witt, K L AU - Bishop, J B AU - McFee, A F AU - Kumaroo, V AD - NIEHS, P.O. Box 12233, MDE403, RTP, NC 27709, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 59 EP - 64 VL - 283 IS - 1 SN - 0027-5107, 0027-5107 KW - sulfapyridine KW - 5-aminosalicylic acid KW - Genetics Abstracts; Toxicology Abstracts KW - chromosomes KW - damage KW - mammalian cells KW - X 24117:Biochemistry KW - G 07221:Specific chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16574689?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+Research&rft.atitle=Induction+of+chromosomal+damage+in+mammalian+cells+in+vitro+and+in+vivo+by+sulfapyridine+or+5-aminosalicylic+acid.&rft.au=Witt%2C+K+L%3BBishop%2C+J+B%3BMcFee%2C+A+F%3BKumaroo%2C+V&rft.aulast=Witt&rft.aufirst=K&rft.date=1992-01-01&rft.volume=283&rft.issue=1&rft.spage=59&rft.isbn=&rft.btitle=&rft.title=Mutation+Research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - chromosomes; damage; mammalian cells ER - TY - JOUR T1 - Recombinant inbred mouse strains: Models for disease study. AN - 16540842; 2966157 AB - Recombinant inbred (RI) strains of mice and the closely related recombinant congenic strains offer consideration promise for identifying and characterizing genes causally associated with many different diseases. Loci associated with diseases such as heart disease, autoimmune disease and leukemia have already been identified through the use of these unique strains. JF - Trends in Biotechnology AU - Justice, MJ AU - Jenkins, NA AU - Copeland, NG AD - Mammalian Genet. Lab., ABL-Basic Res. Program, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 120 EP - 126 VL - 10 IS - 4 SN - 0167-9430, 0167-9430 KW - mice KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts KW - reviews KW - inbreeding KW - genes KW - animal models KW - strains KW - recombinant KW - diseases KW - W 30965:Miscellaneous, Reviews KW - W3 33000:General topics and reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16540842?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Trends+in+Biotechnology&rft.atitle=Recombinant+inbred+mouse+strains%3A+Models+for+disease+study.&rft.au=Justice%2C+MJ%3BJenkins%2C+NA%3BCopeland%2C+NG&rft.aulast=Justice&rft.aufirst=MJ&rft.date=1992-01-01&rft.volume=10&rft.issue=4&rft.spage=120&rft.isbn=&rft.btitle=&rft.title=Trends+in+Biotechnology&rft.issn=01679430&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - reviews; genes; inbreeding; strains; animal models; recombinant; diseases ER - TY - JOUR T1 - Malaria transmission-blocking vaccines. AN - 16538800; 2965935 AB - Antibodies to surface proteins of the sexual stages of Plasmodium falciparum block completely the transmission of these malaria parasites. Transmission-blocking vaccines therefore represent a powerful and novel approach to controlling the spread of this lethal disease. JF - Trends in Biotechnology AU - Kaslow, D C AU - Bathurst, I C AU - Barr, P J AD - Mol. Vaccine Sect., Lab. Malaria Res., NIAID/NIH, Bethesda, MD, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 388 EP - 391 VL - 10 IS - 11 SN - 0167-9430, 0167-9430 KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts KW - vaccines KW - disease transmission KW - malaria KW - antibodies KW - Plasmodium falciparum KW - disease control KW - proteins KW - W3 33365:Vaccines (other) KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16538800?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Trends+in+Biotechnology&rft.atitle=Malaria+transmission-blocking+vaccines.&rft.au=Kaslow%2C+D+C%3BBathurst%2C+I+C%3BBarr%2C+P+J&rft.aulast=Kaslow&rft.aufirst=D&rft.date=1992-01-01&rft.volume=10&rft.issue=11&rft.spage=388&rft.isbn=&rft.btitle=&rft.title=Trends+in+Biotechnology&rft.issn=01679430&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - vaccines; disease transmission; malaria; antibodies; disease control; proteins; Plasmodium falciparum ER - TY - JOUR T1 - Reversible binding of platelet-derived growth factor-AA, -AB, and -BB isoforms to a similar site on the "slow" and "fast" conformations of alpha sub(2)-macroglobulin. AN - 16538690; 2972042 AB - The mechanism by which the platelet-derived growth factor (PDGF)-binding protein, alpha sub(2)-macroglobulin ( alpha sub(2)M), modulates PDGF bioactivity is unknown, but could involve reversible PDGF- alpha sub(2)M binding. We report that >70% of super(125)I-PDGF-BB or -AB complexed to alpha sub(2)M was dissociated by SDS-denaturation followed by SDS-polyacrylamide gel electrophoresis, i.e. most of the binding was noncovalent. Reduction of the PDGF. alpha sub(2)M complex following denaturation dissociated the cytokine from alpha sub(2)M by >90%, suggesting covalent disulfide bond formation. Approximately 50% of the growth factor was dissociated by lowering the pH from 7.5 to 4.0. super(125)I-PDGF-BB bound alpha sub(2)M in a time-dependent manner (t sub(1/2) = similar to 1 h), reaching equilibrium after 4 h. The super(125)I-PDGF.BB/ alpha sub(2)M complex dissociated more slowly (t sub(1/2) = similar to 2.5 h). "Slow" and "fast" alpha sub(2)M bound nearly equal amounts of PDGF-AB or -BB. Trypsin treatment converted PDGF-BB/ alpha sub(2)M complex to the fast conformation but did not release bound super(125)I-PDGF-BB. All PDGF-isoforms (AA, -AB, and -BB) competed for binding with super(125)I-PDGF-BB binding to slow alpha sub(2)M and fast alpha sub(2)M-methylamine by 65-80%. Other cytokines that bind alpha sub(2)M (transforming growth factor- beta 1 and - beta 2, tumor necrosis factor- alpha , basic fibroblast growth factor, interleukin-1 beta , and -6) did not compete for super(125)I-PDGF-BB binding slow alpha sub(2)M, but transforming growth factor- beta 1 and basic fibroblast growth factor inhibited super(125)I-PDGF-BB binding alpha sub(2)M-methylamine by 30-50%. The reversible nature of the PDGF- alpha sub(2)M complex could allow for targeted PDGF release near mesenchymal cells which possess PDGF receptors. JF - Journal of Biological Chemistry AU - Bonner, J C AU - Goodell, AL AU - Lasky, JA AU - Hoffman, M R AD - P. O. Box 12233, NIEHS, Research Triangle Park, NC 27709, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 12837 EP - 12844 VL - 267 IS - 18 SN - 0021-9258, 0021-9258 KW - alpha 2-macroglobulin KW - binding KW - conformation KW - disulfide bonds KW - isoforms KW - man KW - platelet-derived growth factor KW - reversible KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16538690?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Reversible+binding+of+platelet-derived+growth+factor-AA%2C+-AB%2C+and+-BB+isoforms+to+a+similar+site+on+the+%22slow%22+and+%22fast%22+conformations+of+alpha+sub%282%29-macroglobulin.&rft.au=Bonner%2C+J+C%3BGoodell%2C+AL%3BLasky%2C+JA%3BHoffman%2C+M+R&rft.aulast=Bonner&rft.aufirst=J&rft.date=1992-01-01&rft.volume=267&rft.issue=18&rft.spage=12837&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Bacterial expression, purification, and in vitro N-myristoylation of HIV-1 p17 super(gag). AN - 16538547; 2971627 AB - The coding region of the N-terminal 17-kDa portion of HIV-1 Pr55 super(gag) (p17 super(gag)) was cloned into the pET-3c expression vector and was used to overexpress HIV-1 p17 super(gag) in Escherichia coli . Induction of the transformed bacteria caused the accumulation of a 17-kDa polypeptide in the soluble cell fraction which was released by sonication in hypotonic nondetergent buffer. The 17-kDa polypeptide was purified by ammonium sulfate precipitation and successive chromatography on G-75 Sephadex, DEAE-Sephacel, and S-Sephadex. The final product was purified 12-fold with about a 16% recovery from the original soluble cell lysate and was judged to be 97+% pure by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Western blotting with two different antibodies confirmed the identity of the purified 17-kDa polypeptide as authentic p17 super(gag). In the presence of myristoyl-CoA and bovine brain N-myristoyl-transferase, p17 super(gag) was quantitatively N-myristoylated in vitro with a pseudo-first-order rate constant of 4.7 plus or minus 1.0 x 10 super(-3)/min, but with only about 3% of the catalytic efficiency of N-myristoylation of a 16-residue peptide homologous to the N-terminus of p17 super(gag). The myristate group in the N-myristoylated p17 super(gag) was stable to treatment with detergent and hydroxylamine consistent with a covalent N-acyl-amide linkage. The N-myristoylglycyl linkage was confirmed by partial acid hydrolysis and identification of the p-nitrobenzylazlactone derivative of the resulting N-myristoylglycine by high-performance liquid chromatography. JF - Protein Expression and Purification AU - Burnette, B AU - Kahn, R AU - Glover, C J AU - Felsted, RL AD - Lab. Biol. Chem., Div. Cancer Treat., NCI/NIH, Build. 37, Room 5D02, Bethesda, MD 20894, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 395 EP - 402 VL - 3 IS - 5 SN - 1046-5928, 1046-5928 KW - gag KW - p17 super(gag) KW - N-myristoylation KW - Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts KW - genes KW - purification KW - human immunodeficiency virus KW - Escherichia coli KW - overexpression KW - gene products KW - acquired immune deficiency syndrome KW - V 22002:AIDS: Molecular and in vitro aspects KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16538547?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Protein+Expression+and+Purification&rft.atitle=Bacterial+expression%2C+purification%2C+and+in+vitro+N-myristoylation+of+HIV-1+p17+super%28gag%29.&rft.au=Burnette%2C+B%3BKahn%2C+R%3BGlover%2C+C+J%3BFelsted%2C+RL&rft.aulast=Burnette&rft.aufirst=B&rft.date=1992-01-01&rft.volume=3&rft.issue=5&rft.spage=395&rft.isbn=&rft.btitle=&rft.title=Protein+Expression+and+Purification&rft.issn=10465928&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - human immunodeficiency virus; Escherichia coli; acquired immune deficiency syndrome; genes; overexpression; gene products; purification ER - TY - JOUR T1 - Assessment of a short-term reproductive and developmental toxicity screen. AN - 16534372; 2968550 AB - Short-term tests for reproductive and developmental toxicity are needed to provide preliminary data on the toxicity of chemicals about which little or no data exist. An ideal design would test all aspects of reproduction and identify the target process in a short time period. One potential design has been evaluated using four chemicals of varying reproductive/developmental toxicity. JF - Fundamental and Applied Toxicology AU - Harris, M W AU - Chapin, R E AU - Lockhart, A C AU - Jokinen, M P AD - Mail Drop El-02, NIEHS, P.O. Box 12233, RTP, NC 27709, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 186 EP - 196 VL - 19 IS - 2 SN - 0272-0590, 0272-0590 KW - Toxicology Abstracts KW - toxicity testing KW - development KW - tests KW - reproduction KW - evaluation KW - X 24221:Toxicity testing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16534372?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+Applied+Toxicology&rft.atitle=Assessment+of+a+short-term+reproductive+and+developmental+toxicity+screen.&rft.au=Harris%2C+M+W%3BChapin%2C+R+E%3BLockhart%2C+A+C%3BJokinen%2C+M+P&rft.aulast=Harris&rft.aufirst=M&rft.date=1992-01-01&rft.volume=19&rft.issue=2&rft.spage=186&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+Applied+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - toxicity testing; reproduction; tests; evaluation; development ER - TY - JOUR T1 - Thermodynamic effects of active-site ligands on the reversible, partial unfolding of dodecameric glutamine synthetase from Escherichia coli : Calorimetric studies. AN - 16525786; 2963414 AB - Dodecameric glutamine synthetase (GS) from Escherichia coli undergoes reversible, thermally induced partial unfolding without subunit dissociation. A single endotherm for Mn-GS ( plus or minus active-site ligands) in the presence of 1 Mn super(2+) and KCl at pH 7 is observed by differential scanning calorimetry (DSC). Previous deconvolutions of DSC data for Mn-GS showed only two two-state transitions. Ligand effects on T sub(m) values from DSC were similar to those from spectral measurements of Trp and Tyr exposures in two subunit domains. JF - Biochemistry (Washington) AU - Zolkiewski, M AU - Ginsburg, A AD - NHLBI/NIH, Build. 3, Rm. 208, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 11991 EP - 12000 VL - 31 IS - 48 SN - 0006-2960, 0006-2960 KW - glutamine synthase KW - effects on KW - Microbiology Abstracts B: Bacteriology KW - ligands KW - active sites KW - Escherichia coli KW - folding KW - J 02728:Enzymes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16525786?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry+%28Washington%29&rft.atitle=Thermodynamic+effects+of+active-site+ligands+on+the+reversible%2C+partial+unfolding+of+dodecameric+glutamine+synthetase+from+Escherichia+coli+%3A+Calorimetric+studies.&rft.au=Zolkiewski%2C+M%3BGinsburg%2C+A&rft.aulast=Zolkiewski&rft.aufirst=M&rft.date=1992-01-01&rft.volume=31&rft.issue=48&rft.spage=11991&rft.isbn=&rft.btitle=&rft.title=Biochemistry+%28Washington%29&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; active sites; ligands; folding ER - TY - JOUR T1 - Recombination between genes encoding major outer surface proteins A and B of Borrelia burgdorferi . AN - 16522912; 2962011 AB - Borrelia burgdorferi causes Lyme disease, a multisystem illness that can persist in humans for many years. We describe recombination between homologous genes encoding the major outer surface proteins (Osps) A and B of B. burgdorferi which both deletes osp gene sequences and creates chimaeric gene fusions. Recombinant osp genes occur in multiple strains and encode unique proteins that lack some characteristic Osp epitopes. Antigenic variation in Osp through recombination may be relevant to the persistence of B. burgdorferi in an infected host, and has important implications for the utility of OspA and OspB as diagnostic or vaccine candidates for Lyme diseases. We also describe Osp variation arising from nonsense mutations and sequence divergence, which may also represent significant sources of Osp polymorphism. JF - Molecular Microbiology AU - Rosa, P A AU - Schwan, T AU - Hogan, D AD - Lab. Microb. Struct. Funct., Rocky Mountain Lab., NIAID/NIH, Hamilton, MT 59840, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 3031 EP - 3040 VL - 6 IS - 20 SN - 0950-382X, 0950-382X KW - ospA gene KW - ospB gene KW - OspA protein KW - OspB protein KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology KW - membrane proteins KW - Borrelia burgdorferi KW - genes KW - recombination KW - outer membranes KW - Lyme disease KW - G 07320:Bacterial genetics KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16522912?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Microbiology&rft.atitle=Recombination+between+genes+encoding+major+outer+surface+proteins+A+and+B+of+Borrelia+burgdorferi+.&rft.au=Rosa%2C+P+A%3BSchwan%2C+T%3BHogan%2C+D&rft.aulast=Rosa&rft.aufirst=P&rft.date=1992-01-01&rft.volume=6&rft.issue=20&rft.spage=3031&rft.isbn=&rft.btitle=&rft.title=Molecular+Microbiology&rft.issn=0950382X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Borrelia burgdorferi; genes; recombination; outer membranes; membrane proteins; Lyme disease ER - TY - JOUR T1 - The neurotoxin 1-methyl-4-phenylpyridinium: A selective cytostatic agent in small-cell lung cancer cell lines with neuroendocrine properties. AN - 16518340; 2958638 AB - Purpose: We designed in vitro and in vivo studies to investigate whether the neuroendocrine features in classic SCLC cell lines were sufficient to make them sensitive to 1-methyl-4-phenylpyridinium (MPP super(+)), a known neurotoxin that destroys nigrostriatal dopaminergic neurons. Results: All four classic SCLC cell lines showed great sensitivity to MPP super(+), with detachment from laminin substrates and inhibition of DNA synthesis. MPP super(+) interfered with ( super(3)H)thymidine incorporation and, thus, with DNA synthesis in classic SCLC cell lines at low doses, whereas much higher doses (median, > 512 mu M) were required to inhibit ( super(3)H)thymidine incorporation in the variant lines. Treated cells excluded trypan blue dye, showing that inhibition of DNA synthesis was not due to cytotoxicity, and the cells incorporated ( super(3)H)thymidine when MPP super(+) was removed from the culture medium, demonstrating that the inhibition was reversible. JF - Journal of the National Cancer Institute AU - Marini, A M AU - Fridman, R AU - Kanemoto, T AU - Martin, G R AU - Guo, Y AU - Passaniti, A AD - NIMH, Build. 10, Rm. 3N 256, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1582 EP - 1587 VL - 84 IS - 20 SN - 0027-8874, 0027-8874 KW - 1-methyl-4-phenylpyridinium KW - CSA Neurosciences Abstracts; Toxicology Abstracts KW - tumor cell lines KW - neurotoxins KW - lung KW - cytotoxicity KW - antineoplastic drugs KW - N3 11101:General KW - X 24111:Acute exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16518340?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=The+neurotoxin+1-methyl-4-phenylpyridinium%3A+A+selective+cytostatic+agent+in+small-cell+lung+cancer+cell+lines+with+neuroendocrine+properties.&rft.au=Marini%2C+A+M%3BFridman%2C+R%3BKanemoto%2C+T%3BMartin%2C+G+R%3BGuo%2C+Y%3BPassaniti%2C+A&rft.aulast=Marini&rft.aufirst=A&rft.date=1992-01-01&rft.volume=84&rft.issue=20&rft.spage=1582&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - cytotoxicity; lung; tumor cell lines; antineoplastic drugs; neurotoxins ER - TY - JOUR T1 - Molecular cloning and expression of cDNA encoding the murine gonadotropin-releasing hormone receptor. AN - 16514613; 2954536 AB - The primary structure of the gonadotropin-releasing hormone (GnRH) receptor was determined by sequencing a functional receptor cDNA isolated by expression cloning from an immortalized murine gonadotroph ( alpha T3) cell line. Positive clone pools from a cDNA library were detected by screening expressed RNA in aequorin-injected Xenopus laevis oocytes, in which receptor-mediated calcium responses were monitored as light emission during stimulation by GnRH. The isolated receptor cDNA encodes a 327-amino acid protein that has seven putative transmembrane regions and is unique among G protein-coupled receptors in that the predicted sequence lacks a carboxyl-terminal cytoplasmic domain. COS-7 cells transfected with the receptor cDNA expressed high affinity binding sites for GnRH and its agonist and antagonist analogs and exhibited calcium responses to GnRH stimulation. These, and the prominent calcium responses of Xenopus oocytes injected with receptor RNA, were inhibited by GnRH antagonists. Northern blot analysis revealed two mRNAs (1.6 and 3.5 kilobases) in alpha T3 cells and in the mouse pituitary gland, and both transcripts were shown to encode functional GnRH receptors when expressed in Xenopus oocytes. A single 4.6-kilobase receptor mRNA was present in rat anterior pituitary gland, ovary, and Leydig cells. The absence of a carboxyl-terminal cytoplasmic domain indicates the importance of other regions of the GnRH receptor in agonist-induced signal transduction, and possibly in receptor desensitization and sequestration. JF - Journal of Biological Chemistry AU - Reinhart, J AU - Mertz, L M AU - Catt, K J AD - Endocrinol. and Reprod. Res. Branch, NICHD, Build. 10, Rm. B1-L400, NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 21281 EP - 21284 VL - 267 IS - 30 SN - 0021-9258, 0021-9258 KW - amino acid sequence KW - cDNA KW - calcium KW - cloning KW - expression KW - genes KW - gonadotropin-releasing hormone KW - mice KW - nucleotide sequence KW - predictions KW - receptors KW - response KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 1: Biological Membranes (till 1993); Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - G 07398:GENERAL KW - N 14640:Structure & sequence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16514613?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Molecular+cloning+and+expression+of+cDNA+encoding+the+murine+gonadotropin-releasing+hormone+receptor.&rft.au=Reinhart%2C+J%3BMertz%2C+L+M%3BCatt%2C+K+J&rft.aulast=Reinhart&rft.aufirst=J&rft.date=1992-01-01&rft.volume=267&rft.issue=30&rft.spage=21281&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - response; expression; nucleotide sequence; cloning; cDNA; amino acid sequence; genes; receptors ER - TY - JOUR T1 - Preclinical considerations for life-threatening illnesses. AN - 16489002; 2941469 AB - The implementation of the expedited development regulations in 1988 has had a significant impact on the development of products for serious and life-threatening illnesses. One important aspect of the development of a drug for any condition is the preclinical information about the product. The expedited rules have allowed for early decisions to be made concerning the development of drugs for diseases such as AIDS, cancer and Alzheimer's disease. JF - Clinical Research and Regulatory Affairs AU - Hamrell, M R AD - Regul. Compliance Sect., Pharm. and Regul. Affairs Branch, NIAID/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 225 EP - 232 VL - 9 IS - 4 SN - 1060-1333, 1060-1333 KW - expedited development regulations KW - monitoring KW - man KW - government policy KW - government policies KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts; Toxicology Abstracts KW - side effects KW - acquired immune deficiency syndrome KW - drugs KW - legislation KW - USA KW - H SE4.5:STANDARDS, LAWS, REGULATIONS, AND POLICY KW - V 22004:AIDS: Clinical aspects KW - X 24113:Side effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16489002?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Research+and+Regulatory+Affairs&rft.atitle=Preclinical+considerations+for+life-threatening+illnesses.&rft.au=Hamrell%2C+M+R&rft.aulast=Hamrell&rft.aufirst=M&rft.date=1992-01-01&rft.volume=9&rft.issue=4&rft.spage=225&rft.isbn=&rft.btitle=&rft.title=Clinical+Research+and+Regulatory+Affairs&rft.issn=10601333&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - USA; drugs; side effects; legislation; acquired immune deficiency syndrome; government policies; monitoring; man; government policy ER - TY - JOUR T1 - Inhibition of the relative movement of actin and myosin by caldesmon and calponin. AN - 16486165; 2936522 AB - Contractile activity of myosin II in smooth muscle and non-muscle cells requires phosphorylation of myosin by myosin light chain kinase. These cells have the potential for regulation at the thin filament level by caldesmon and calponin, both of which bind calmodulin. We have investigated this regulation using in vitro motility assays. Caldesmon completely inhibited the movement of actin filaments by either phosphorylated smooth muscle myosin or rabbit skeletal muscle heavy mermmyosin. The amount of caldesmon required for inhibition was decreased when tropomyosin is present. Calponin binding to actin resulted in inhibition of actin filament movement by both smooth muscle myosin and skeletal muscle heavy meromyosin. Tropomyosin had no effect on the amount of calponin needed for inhibition. High concentrations of calmodulin (10 mu m) in the presence of calcium completely reversed the inhibition. The nature of the inhibition by the two proteins was markedly different. Increasing caldesmon concentrations resulted in graded inhibition of the movement of actin filaments until complete inhibition of movement was obtained. JF - Journal of Biological Chemistry AU - Shirinsky, V P AU - Biryukov, K G AU - Hettasch, J M AU - Sellers, J R AD - Lab. Mol. Cardiol., NHLBI, NIH, Build. 10, Rm. 8N202, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 15886 EP - 15892 VL - 267 IS - 22 SN - 0021-9258, 0021-9258 KW - actin KW - caldesmon KW - calponin KW - contractility KW - inhibition KW - myosin KW - rabbits KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16486165?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Inhibition+of+the+relative+movement+of+actin+and+myosin+by+caldesmon+and+calponin.&rft.au=Shirinsky%2C+V+P%3BBiryukov%2C+K+G%3BHettasch%2C+J+M%3BSellers%2C+J+R&rft.aulast=Shirinsky&rft.aufirst=V&rft.date=1992-01-01&rft.volume=267&rft.issue=22&rft.spage=15886&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Cisplatin-DNA damage and repair in peripheral blood leukocytes in vivo and in vitro. AN - 16484106; 2934228 AB - We have extended our studies on the relationship between cisplatin/carboplatin-induced DNA damage in readily accessible tissue(s) and clinical response to therapy. Such an approach may assist in the study of cancer drug resistance and in establishing parameters for assessing human populations for sensitivity to DNA damaging agents in the environment. Platinum-DNA adduct levels were measured by atomic absorbance spectrometry. DNA repair capacity was assessed in human T-lymphocytes by the ability to repair cisplatin lesions in cellular DNA or in transfected plasmid DNA. In a "blinded" study of 21 patients receiving combination cisplatin/carboplatin drug therapy, there was a direct relationship between DNA damage in leukocytes and disease response. The cohort of patients had 15 different tumor types, suggesting that blood tissue and tumor tissue of an individual may process platinum-DNA damage similarly regardless of the orgin of the tumor. JF - Environmental Health Perspectives AU - Dabholkar, M AU - Bradshaw, L AU - Parker, R J AU - Gill, I AU - Bostick-Bruton, F AU - Muggia, F M AU - Reed, E AD - Med. Branch, NCI/NIH, Build. 10, Rm. 12N226, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 53 EP - 59 VL - 98 SN - 0091-6765, 0091-6765 KW - cisplatin KW - leucocytes KW - Biochemistry Abstracts 2: Nucleic Acids; Toxicology Abstracts KW - damage KW - DNA KW - blood KW - antineoplastic drugs KW - DNA repair KW - X 24117:Biochemistry KW - N 14652:DNA repair UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16484106?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Cisplatin-DNA+damage+and+repair+in+peripheral+blood+leukocytes+in+vivo+and+in+vitro.&rft.au=Dabholkar%2C+M%3BBradshaw%2C+L%3BParker%2C+R+J%3BGill%2C+I%3BBostick-Bruton%2C+F%3BMuggia%2C+F+M%3BReed%2C+E&rft.aulast=Dabholkar&rft.aufirst=M&rft.date=1992-01-01&rft.volume=98&rft.issue=&rft.spage=53&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - DNA; damage; DNA repair; blood; antineoplastic drugs ER - TY - JOUR T1 - Papillomavirus L1 major capsid protein self-assembles into virus-like particles that are highly immunogenic. AN - 16483902; 2931346 AB - Infection by certain human papillomavirus types is regarded as the major risk factor in the development of cervical cancer, one of the most common cancers of women worldwide. Analysis of the immunogenic and structural features of papillomavirus virions has been hampered by the inability to efficiently propagate the viruses in cultured cells. For instance, it has not been established whether the major capsid protein L1 alone is sufficient for virus particle assembly. The results indicate that L1 protein has the intrinsic capacity to assemble into empty capsid-like structures whose immunogenicity is similar to infectious virions. This type of L1 preparation might be considered as a candidate for a serological test to measure antibodies to conformational virion epitopes and for a vaccine to prevent papillomavirus infection. JF - Proceedings of the National Academy of Sciences, USA AU - Kirnbauer, R AU - Booy, F AU - Cheng, N AU - Lowy AU - Schiller, J T AD - Lab. Cell. Oncol., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 12180 EP - 12184 VL - 89 IS - 24 SN - 0027-8424, 0027-8424 KW - L1 protein KW - capsid protein KW - immunogenicity KW - papilloma virus (human) KW - self-assembly KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts KW - V 22092:Viral antigenic properties UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16483902?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=Papillomavirus+L1+major+capsid+protein+self-assembles+into+virus-like+particles+that+are+highly+immunogenic.&rft.au=Kirnbauer%2C+R%3BBooy%2C+F%3BCheng%2C+N%3BLowy%3BSchiller%2C+J+T&rft.aulast=Kirnbauer&rft.aufirst=R&rft.date=1992-01-01&rft.volume=89&rft.issue=24&rft.spage=12180&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - self-assembly; capsid protein; immunogenicity ER - TY - JOUR T1 - A 4-week feeding study of ground red chilli (Capsicum annuum ) in male B6C3F sub(1) mice. AN - 16482744; 2934261 AB - The toxicity of red chilli was examined in male B6C3F sub(1) mice fed a commercial meal diet mixed with ground Capsicum annuum) (Linn.) at levels of 0.5, 1.0, 2.5, 5.0, 7.5 and 10% by weight. Mice were offered control or test diet ad lib. starting at 6 wk of age. Food consumption was measured daily and individual body weights recorded weekly for the 4-wk feeding period. General health, body weight and food intake were apparently not adversely affected at any level of pepper consumption. Histopathological evaluation revealed slight glycogen depletion and anisocytosis of hepatocytes in the 10% group. However, other organs did not reveal any lesions attributable to the chilli exposure. It appears that red chilli is relatively non-toxic at the doses tested in male B6C3F sub(1) mice. JF - Food and Chemical Toxicology AU - Jang, J-J AU - Devor, DE AU - Logsdon, D L AU - Ward, J M AD - Tumor Pathol. and Pathog. Sect., Lab. Comp. Carcinog., NCI, Frederick, MD 21702-1201, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 783 EP - 787 VL - 30 IS - 9 SN - 0278-6915, 0278-6915 KW - mice KW - Toxicology Abstracts KW - Capsicum annuum KW - toxicity KW - X 24120:Food, additives & contaminants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16482744?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Food+and+Chemical+Toxicology&rft.atitle=A+4-week+feeding+study+of+ground+red+chilli+%28Capsicum+annuum+%29+in+male+B6C3F+sub%281%29+mice.&rft.au=Jang%2C+J-J%3BDevor%2C+DE%3BLogsdon%2C+D+L%3BWard%2C+J+M&rft.aulast=Jang&rft.aufirst=J-J&rft.date=1992-01-01&rft.volume=30&rft.issue=9&rft.spage=783&rft.isbn=&rft.btitle=&rft.title=Food+and+Chemical+Toxicology&rft.issn=02786915&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - Capsicum annuum; toxicity ER - TY - JOUR T1 - Bone-resorbing activity is expressed by rat macrophages in response to arthropathic streptococcal cell wall polymers. AN - 16482486; 2934197 AB - Rat peritoneal macrophages stimulated in vivo by group A streptococcal peptidoglycan-polysaccharide (PG-APS) resorb bone as measured by solubilization of super(45)Ca from radiolabeled, devitalized bone chips. Activity was strain-dependent and correlated with the susceptibility of rat strains to PG-APS-induced arthritis. PG-APS-stimulated macrophages from the resistant Buf rat strain were not induced to resorb bone, but ingested equivalent concentrations of PG-APS compared to bone-resorbing macrophages from the arthritis-susceptible Lew strain. These results indicate that expression of rat macrophage bone-resorbing activity reflects genetic regulation of the response to PG-APS rather than a defect in ingestion of these polymers and imply that PG-APS-stimulated, bone-resorbing macrophages may contribute to early, initial bone destruction that occurs in inflammatory arthritis. JF - Inflammation AU - Bristol-Rothstein, LA AU - Schwab, J H AD - NCI/NIH, Build. 10, Rm. 4B05, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 485 EP - 496 VL - 16 IS - 5 SN - 0360-3997, 0360-3997 KW - rats KW - Calcium & Calcified Tissue Abstracts; Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - cell walls KW - Streptococcus pyogenes KW - stimulation KW - macrophages KW - polymers KW - bone resorption KW - F 06801:Bacteria KW - J 02833:Immune response and immune mechanisms KW - F 06764:Function KW - T 20019:Cellular calcium, channels and currents UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16482486?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Inflammation&rft.atitle=Bone-resorbing+activity+is+expressed+by+rat+macrophages+in+response+to+arthropathic+streptococcal+cell+wall+polymers.&rft.au=Bristol-Rothstein%2C+LA%3BSchwab%2C+J+H&rft.aulast=Bristol-Rothstein&rft.aufirst=LA&rft.date=1992-01-01&rft.volume=16&rft.issue=5&rft.spage=485&rft.isbn=&rft.btitle=&rft.title=Inflammation&rft.issn=03603997&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - Streptococcus pyogenes; cell walls; polymers; stimulation; macrophages; bone resorption ER - TY - JOUR T1 - Naphthalene: A respiratory tract toxicant and carcinogen for mice. AN - 16482170; 2934085 AB - The toxicologic and carcinogenic potential of naphthalene was studied by exposing groups of males and female B6C3F sub(1) mice to atmospheres containing 0 (75 mice per sex), 10 ppm (75 mice per sex), or 30 ppm (150 mice per sex) of the chemical for 6 h daily, 5 days/wk for 103 wk. The final mean body weights of mice exposed to naphthalene were similar to those of the controls. The survival of control male mice was significantly lower than that of the exposed males. The lower survival was attributed to wound trauma and secondary infection related to fighting among the group-housed control animals. There was not significant difference in survival between control and exposed female mice. Under the conditions of this 2-yr study, naphthalene was not carcinogenic to male mice. In female mice it caused an increase in the incidence of pulmonary alveolar/bronchiolar adenomas. Naphthalene also caused an increase in the incidence and severity of chronic inflammation, olfactory epithelium metaplasia of hyperplasia of the nasal respiratory epithelium, and chronic nasal inflammation in the lung of mice of each sex. JF - Inhalation Toxicology AU - Abdo, K M AU - Eustis, S L AU - McDonald, M AU - Jokinen, M P AU - Adkins, B Jr AU - Haseman, J K AD - NIEHS, Research Triangle Park, NC 27709, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 393 EP - 409 VL - 4 IS - 4 SN - 0895-8378, 0895-8378 KW - naphthalene KW - mice KW - Toxicology Abstracts KW - carcinogenicity KW - toxicity KW - respiratory tract KW - X 24152:Chronic exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16482170?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Inhalation+Toxicology&rft.atitle=Naphthalene%3A+A+respiratory+tract+toxicant+and+carcinogen+for+mice.&rft.au=Abdo%2C+K+M%3BEustis%2C+S+L%3BMcDonald%2C+M%3BJokinen%2C+M+P%3BAdkins%2C+B+Jr%3BHaseman%2C+J+K&rft.aulast=Abdo&rft.aufirst=K&rft.date=1992-01-01&rft.volume=4&rft.issue=4&rft.spage=393&rft.isbn=&rft.btitle=&rft.title=Inhalation+Toxicology&rft.issn=08958378&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - toxicity; respiratory tract; carcinogenicity ER - TY - JOUR T1 - AIDS, the outcast is a risk. TT - Prevenire l'emarginazione per prevenire L'A.I.D.S. L'educazione e la sensibilizzazione sociale nella prevenzione dell'AIDS. Interventi integrati nell'USSL 60 di Vimercate (MI) AN - 16477704; 2932610 AB - The AIDS Prevention Operative Group of the USSL (National Health Service - Local Health) n. 60 - Lombardy (15 miles north of Milan) posed as a primary target a series of integrated prevention initiatives, based on health education and social sensitization, aimed to lessen fear by increasing the knowledge of the disease and the acceptance of the disease in the social context. The initial hypothesis was that an intolerant social environment brings about a high risk of infection. The target was to prevent the outcasting of serum positive people by increasing people's tolerance. JF - Igiene Moderna AU - Bianchi, S AU - Galbusera, A AU - Licini, M AU - Monaco, G AD - Serv. Ig. Pubblica Ambient. e Tutela Salute nei luoghi di lavoro USSL N. 60 Regione Lombardia, Vimercate-MI, Italy Y1 - 1992 PY - 1992 DA - 1992 SP - 59 EP - 67 VL - 98 IS - 1 SN - 0019-1655, 0019-1655 KW - infection KW - prevention KW - Italy, Lombardy KW - Risk Abstracts; Health & Safety Science Abstracts KW - sociology KW - Acquired Immune Deficiency Syndrome KW - education KW - risk assessment KW - R2 23060:Medical and environmental health KW - H SM10.7:HUMAN FACTORS UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16477704?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Igiene+Moderna&rft.atitle=AIDS%2C+the+outcast+is+a+risk.&rft.au=Bianchi%2C+S%3BGalbusera%2C+A%3BLicini%2C+M%3BMonaco%2C+G&rft.aulast=Bianchi&rft.aufirst=S&rft.date=1992-01-01&rft.volume=98&rft.issue=1&rft.spage=59&rft.isbn=&rft.btitle=&rft.title=Igiene+Moderna&rft.issn=00191655&rft_id=info:doi/ LA - Italian DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - Acquired Immune Deficiency Syndrome; risk assessment; education; sociology ER - TY - JOUR T1 - Spotted fever rickettsiae in ticks from the Northern Sinai Governate, Egypt. AN - 16461322; 2925144 AB - A field study was initiated in 1988 to investigate whether spotted fever group rickettsiae occur in geographic areas in Egypt that are adjacent to an area in the southern Israeli Negev that has a defined focus of spotted fever disease. Ticks were collected from dogs, sheep, and camels at four study sites in the northern Sinai. Tick hemolymph was processed for rickettsial detection by staining with fluorescein isothiocyanate-conjugated antibody to Rickettsia rickettsii . Of the 442 hemolymphs examined, 15 contained immunofluorescent rickettsiae. Eight hemolymph test-positive (HT+) ticks were Rhipicephalus sanguineus removed from dogs; the other HT+ ticks comprised three Hyalomma species, H. anatolicum, H. impeltatum , and H. dromedarii . Both HT+ and HT- ticks were tested for rickettsial DNA using the polymerase chain reaction (PCR). Eight of 10 HT+ field-collected ticks were PCR positive (PCR+). All laboratory colony R. rickettsii -infected ticks were PCR+. No HT- ticks from field or laboratory isolates were PCR+. JF - American Journal of Tropical Medicine and Hygiene AU - Lange, J V AU - El Dessouky, AG AU - Manor, E AU - Merdan, AI AU - Azad, A F AD - Off. Trop. Med. and Int. Res. NIAID/NIH, Build. CDB-3C25, 6003 Executive Blvd., Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 546 EP - 551 VL - 46 IS - 5 SN - 0002-9637, 0002-9637 KW - Egypt KW - Entomology Abstracts; Microbiology Abstracts B: Bacteriology KW - Ixodidae KW - spotted fevers KW - Hyalomma anatolicum KW - infection KW - Rickettsia rickettsii KW - Acari KW - Rhipicephalus sanguineus KW - J 02855:Human Bacteriology: Others KW - Z 05206:Medical & veterinary entomology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16461322?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.atitle=Spotted+fever+rickettsiae+in+ticks+from+the+Northern+Sinai+Governate%2C+Egypt.&rft.au=Lange%2C+J+V%3BEl+Dessouky%2C+AG%3BManor%2C+E%3BMerdan%2C+AI%3BAzad%2C+A+F&rft.aulast=Lange&rft.aufirst=J&rft.date=1992-01-01&rft.volume=46&rft.issue=5&rft.spage=546&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Rickettsia rickettsii; Rhipicephalus sanguineus; Hyalomma anatolicum; Ixodidae; Acari; infection; spotted fevers ER - TY - JOUR T1 - Characterization of ethanol's enhancement of tumorigenesis by N-nitrosodimethylamine in mice. AN - 16453819; 2917359 AB - The concentration-, time- and route-dependent effects of ethanol co-administration on tumorigenesis by N-nitrosodimethylamine (NDMA) were characterized in strain A male mice. With drinking-water administration, 1% ethanol was as effective as 5 or 10% in effecting a 4-fold enhancement of lung tumorigenesis by 5 p.p.m. NDMA. In a study of cumulative effects over time, 10% ethanol given with 1 p.p.m. NDMA resulted in a progressive increase in lung tumors from 16 to 72 weeks. In addition, at 72 weeks, the ethanol co-treatment resulted in a significant increase in kidney adenomas and possibly in vascular tumors of liver. A single i.g. dose of 5 mg/kg NDMA was significantly tumorigenic for lung, and the effect was dose-dependently increased by inclusion of ethanol, for up to a 9-fold enhancement with 20% ethanol. When 10% ethanol was given in the drinking water while NDMA was administered as 20 1 mg/kg doses by other routes--i.g., i.p., s.c. or i.v.--the ethanol treatment as without effect on lung tumor numbers. JF - Carcinogenesis AU - Anderson, L M AU - Carter, J P AU - Logsdon, D L AU - Driver, CL AU - Kovatch, R M AD - Lab. Comp. Carcinog., Natl. Cancer Inst., NCI, Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 2107 EP - 2111 VL - 13 IS - 11 SN - 0143-3334, 0143-3334 KW - N-nitrosodimethylamine KW - ethanol KW - mice KW - Toxicology Abstracts KW - tumorigenesis KW - X 24200:Nitrosamines & related compounds KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16453819?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Characterization+of+ethanol%27s+enhancement+of+tumorigenesis+by+N-nitrosodimethylamine+in+mice.&rft.au=Anderson%2C+L+M%3BCarter%2C+J+P%3BLogsdon%2C+D+L%3BDriver%2C+CL%3BKovatch%2C+R+M&rft.aulast=Anderson&rft.aufirst=L&rft.date=1992-01-01&rft.volume=13&rft.issue=11&rft.spage=2107&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - tumorigenesis ER - TY - JOUR T1 - Cadmium-induced DNA strand damage in cultured liver cells: Reduction in cadmium genotoxicity following zinc pretreatment. AN - 16449075; 2914841 AB - The effect of zinc pretreatment on cadmium-induced DNA strand damage was determined. Exposure of TRL-1215 cells to CdCl sub(2) for 1 hr at 37 degree C, using concentrations from 5 to 250 mu M, failed to induce detectable SSD in these cells; however, exposure to 500 mu M CdCl sub(2) resulted in significant SSD. A time-dependent increase in SSD was demonstrated following a 2 hr continuous exposure to 500 mu M CdCl sub(2). Pretreatment of cells with 80 mu M zinc acetate, 18 hr prior to exposure to 500 mu M CdCl sub(2), resulted in markedly reduced SSD when compared to non-pretreated cells. Zinc pretreatment increased the level of MT gene expression as well as MT protein production. The decrease in DNA strand damage associated with cadmium exposure was not due to a decrease in cadmium accumulation by zinc pretreated cells. In fact, cellular cadmium burden was increased over 2-fold following zinc pretreatment. JF - Toxicology and Applied Pharmacology AU - Coogan, T P AU - Bare, R M AU - Waalkes, M P AD - Inorg. Carcinog. Sect., Lab. Comp. Carcinog., NCI, Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 227 EP - 233 VL - 113 IS - 2 SN - 0041-008X, 0041-008X KW - cadmium KW - zinc KW - heavy metals KW - rats KW - Biochemistry Abstracts 2: Nucleic Acids; Toxicology Abstracts KW - damage KW - DNA KW - hepatocytes KW - tissue culture KW - N 14630:Chemical reactions & interactions, including effects of radiation KW - X 24165:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16449075?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+Applied+Pharmacology&rft.atitle=Cadmium-induced+DNA+strand+damage+in+cultured+liver+cells%3A+Reduction+in+cadmium+genotoxicity+following+zinc+pretreatment.&rft.au=Coogan%2C+T+P%3BBare%2C+R+M%3BWaalkes%2C+M+P&rft.aulast=Coogan&rft.aufirst=T&rft.date=1992-01-01&rft.volume=113&rft.issue=2&rft.spage=227&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+Applied+Pharmacology&rft.issn=0041008X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - DNA; damage; hepatocytes; tissue culture ER - TY - JOUR T1 - Risk factors for renal-cell cancer in Shanghai, China. AN - 16439242; 2914674 AB - A population-based case-control study of 154 histologically verified renal-cell cancer patients and 157 controls was performed in Shanghai, China, an area with low rates for this tumor. Elevated risks were observed for cigarette smoking, and for increasing categories of body weight and meat consumption, while reduced risks were seen for increasing categories of fruit and vegetable intake. An increased risk was also observed for regular use of phenacetin-containing analgesics. These findings are consistent with earlier studies in Western countries, and indicate that many of the same etiologic factors for renal-cell cancer operate in low- and high-risk societies. JF - International Journal of Cancer AU - McLaughlin, J K AU - Gao, Yu-Tang AU - Gao, Ru-Nie AU - Zheng, Wei AU - Ji, Bu-Tian AU - Blot, W J AU - Fraumeni, JF Jr AD - NCI-NIH, EPN/415, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 562 EP - 565 VL - 52 IS - 4 SN - 0020-7136, 0020-7136 KW - risk factors KW - man KW - China, Shanghai KW - Health & Safety Science Abstracts; Toxicology Abstracts KW - China, People's Rep., Shanghai KW - kidney KW - cancer KW - X 24240:Miscellaneous KW - H SM10.21:CANCER UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16439242?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Cancer&rft.atitle=Risk+factors+for+renal-cell+cancer+in+Shanghai%2C+China.&rft.au=McLaughlin%2C+J+K%3BGao%2C+Yu-Tang%3BGao%2C+Ru-Nie%3BZheng%2C+Wei%3BJi%2C+Bu-Tian%3BBlot%2C+W+J%3BFraumeni%2C+JF+Jr&rft.aulast=McLaughlin&rft.aufirst=J&rft.date=1992-01-01&rft.volume=52&rft.issue=4&rft.spage=562&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - China, People's Rep., Shanghai; kidney; cancer; risk factors; man ER - TY - JOUR T1 - A population-based case-control study of cancers of the nasal cavity and paranasal sinuses in Shanghai. AN - 16438985; 2914690 AB - A population-based case-control study of cancer of the nasal cavity and sinuses, involving interviews of 60 incident cases and 414 controls, was conducted in Shanghai, Cigarette smoking was associated with a mild elevation in risk of squamous-cell carcinoma but not cancers of other cell types. Occupational exposures to wood and silica dusts and to petroleum products, and the use of wood and straw as cooking fuel, were linked to moderate increases in risk, while 4-fold or greater increases were associated with a history of chronic nasal diseases, including those occurring 10 or more years prior to cancer diagnosis. Dietary analyses revealed a significant protective effect of consumption of allium vegetables, oranges and tangerines, with a 50% reduced risk of nasal cancer among individuals in the highest intake group of these foods. Consumption of salt-preserved vegetables, meat and fish was associated with a significantly increased risk of nasal cancer in a dose-response fashion. JF - International Journal of Cancer AU - Zheng, Wei AU - Blot, W J AU - Shu, Xiao-Ou AU - Diamond, EL AU - Gao, Yu-Tang AU - Ji, Bu-Tian AU - Fraumeni, JF Jr AD - NCI-NIH, Executive Pl. North, Rm. 431, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 557 EP - 561 VL - 52 IS - 4 SN - 0020-7136, 0020-7136 KW - nasal cavity KW - China, Shanghai KW - Toxicology Abstracts KW - paranasal sinus KW - nose KW - man KW - risk factors KW - cancer KW - X 24240:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16438985?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Cancer&rft.atitle=A+population-based+case-control+study+of+cancers+of+the+nasal+cavity+and+paranasal+sinuses+in+Shanghai.&rft.au=Zheng%2C+Wei%3BBlot%2C+W+J%3BShu%2C+Xiao-Ou%3BDiamond%2C+EL%3BGao%2C+Yu-Tang%3BJi%2C+Bu-Tian%3BFraumeni%2C+JF+Jr&rft.aulast=Zheng&rft.aufirst=Wei&rft.date=1992-01-01&rft.volume=52&rft.issue=4&rft.spage=557&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - paranasal sinus; cancer; risk factors; man; nose ER - TY - JOUR T1 - Clinical application of IL6 in cancer therapy. AN - 16435412; 2908844 AB - A variety of studies have suggested that IL6 may possess therapeutic activity against growing tumours in vivo. In vitro analyses of IL6 activities have demonstrated pleiotropic effects on host immune cells known to be important in anti-tumour responses, including NK/LAK cells, T cells, and monocytes/macrophages. Moreover, IL6 has been shown to have direct inhibitory effects on established tumor cell lines in vitro, although this area of study is rather controversial because some reports have shown either no effect or, in contrast, a stimulatory activity. In vivo, IL6 induction by cytokine administration has been demonstrated in cancer patients and in mice, as well as de novo synthesis and release of IL6 in tumour-bearing mice. Thus, collectively, these studies suggested that IL6 may be an important cytokine in the host's immune and metabolic responses to cancer. JF - Research in Immunology AU - Mule, J J AU - Marcus, S G AU - Yang, J C AU - Weber, J S AU - Rosenberg, SA AD - Surg. Branch, NCI/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 777 EP - 779 VL - 7 IS - 143 SN - 0923-2494, 0923-2494 KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Immunology Abstracts KW - reviews KW - interleukin 6 KW - cancer patients KW - immunotherapy KW - clinical trials KW - man KW - cancer KW - F 06818:Cancer immunotherapy KW - W3 33150:Cytokine based KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16435412?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Research+in+Immunology&rft.atitle=Clinical+application+of+IL6+in+cancer+therapy.&rft.au=Mule%2C+J+J%3BMarcus%2C+S+G%3BYang%2C+J+C%3BWeber%2C+J+S%3BRosenberg%2C+SA&rft.aulast=Mule&rft.aufirst=J&rft.date=1992-01-01&rft.volume=7&rft.issue=143&rft.spage=777&rft.isbn=&rft.btitle=&rft.title=Research+in+Immunology&rft.issn=09232494&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - reviews; cancer patients; interleukin 6; immunotherapy; clinical trials; cancer; man ER - TY - JOUR T1 - The use of nucleoside analogues in the treatment of HIV-infected children. AN - 16421196; 2903216 AB - Pediatric HIV disease is similar in many ways to the disease that occurs in HIV-infected adults, with progressive depletion of CD4 super(+) lymphocytes, immunosuppression, and resulting opportunistic and other infections. Many characteristics of pediatric HIV disease are distinctive, however, and are important considerations in undertaking and evaluating treatment of HIV infection in children. Most of these differences relate to the effects of HIV infection on growth and development at the cellular level, as well as at the level of the whole child. Of particular importance are the very rapid disease progression in many vertically infected infants, the high frequency of central nervous system involvement in children that is often expressed in the form of major as well as cognitive abnormalities, the high frequency of abnormal linear growth and poor weight gain, and the effects of HIV infection on the developing immune system. While further complicating the course of HIV-infected children, these features also have the potential to provide measurable clinical variables that may be useful to define treatment effects of antiretroviral drugs. JF - AIDS Research and Human Retroviruses AU - Husson, R N AU - Pizzo, P A AD - Infect. Dis. Sect., Pediatr. Branch, Build. 10, Rm. 13N240, NCI/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1059 EP - 1064 VL - 8 IS - 6 SN - 0889-2229, 0889-2229 KW - nucleosides KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Virology & AIDS Abstracts KW - antiviral agents KW - analogs KW - human immunodeficiency virus KW - treatment KW - infection KW - children KW - W3 33170:Cellular based KW - W 30965:Miscellaneous, Reviews KW - V 22004:AIDS: Clinical aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16421196?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+Research+and+Human+Retroviruses&rft.atitle=The+use+of+nucleoside+analogues+in+the+treatment+of+HIV-infected+children.&rft.au=Husson%2C+R+N%3BPizzo%2C+P+A&rft.aulast=Husson&rft.aufirst=R&rft.date=1992-01-01&rft.volume=8&rft.issue=6&rft.spage=1059&rft.isbn=&rft.btitle=&rft.title=AIDS+Research+and+Human+Retroviruses&rft.issn=08892229&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - antiviral agents; analogs; treatment; infection; children; human immunodeficiency virus ER - TY - JOUR T1 - Chemical mutagenesis testing in Drosophila : VIII. Reexamination of equivocal results. AN - 16419536; 2895446 AB - Twelve percent of the chemicals tested for mutagenicity by the National Toxicology Program (NTP) using the Drosophila sex-linked recessive lethal assay have been classified as producing equivocal results. We have reexamined the published data and the criteria used to determine mutagenicity in light of the historical distribution of the concurrent negative controls for this project. Many of the chemicals that originally produced equivocal results have been retested under code. As a result of changes to incorporate a comparison with the historical control in the algorithm used to determine mutagenicity and as a result of new data accumulated, 4 of the 25 chemicals that gave equivocal results are judged to be mutagenic, and 11 others are judged to be nonmutagenic under our test conditions. JF - Environmental and Molecular Mutagenesis AU - Mason, J M AU - Valencia, R AU - Zimmering, S AD - NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 227 EP - 234 VL - 19 IS - 3 SN - 0893-6692, 0893-6692 KW - Entomology Abstracts; Toxicology Abstracts; Genetics Abstracts KW - statistical analysis KW - mutagenicity testing KW - chemicals KW - Drosophila melanogaster KW - G 07220:General theory/testing systems KW - Z 05215:Mutation KW - X 24221:Toxicity testing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16419536?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+Molecular+Mutagenesis&rft.atitle=Chemical+mutagenesis+testing+in+Drosophila+%3A+VIII.+Reexamination+of+equivocal+results.&rft.au=Mason%2C+J+M%3BValencia%2C+R%3BZimmering%2C+S&rft.aulast=Mason&rft.aufirst=J&rft.date=1992-01-01&rft.volume=19&rft.issue=3&rft.spage=227&rft.isbn=&rft.btitle=&rft.title=Environmental+and+Molecular+Mutagenesis&rft.issn=08936692&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Drosophila melanogaster; mutagenicity testing; statistical analysis; chemicals ER - TY - JOUR T1 - Activity of diverse tumor promoters in a keratinocyte co-culture model of initiated epidermis. AN - 16418811; 2895602 AB - The suppression of focal growth of initiated mouse keratinocytes by co-culture with normal keratinocytes can be overcome by treatment of co-cultures with the phorbol ester tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). This keratinocyte co-culture model was developed as an analog of initiated mouse epidermis to facilitate the study of tumor promotion in cell culture. A number of promoters of TPA-type (those with protein kinase C (PKC) as receptor) were compared to non-TPA-type promoters for activity in the keratinocyte co-culture model. The TPA-type promoters teleocidin and aplysiatoxin show comparable activity to that of TPA. Exposure of co-cultures to oleoyl-2-acetylglycerol, a diacylglycerol activator of PKC, also induces focal outgrowth of initiated cells, suggesting that PKC is likely to be involved in the mechanisms of action of these compounds. JF - Carcinogenesis AU - Hennings, H AU - Lowry, D T AU - Robinson, V A AU - Morgan, D L AU - Fujiki, H AU - Yuspa, SH AD - Lab. Cell. Carcinog. and Tumor Promot., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 2145 EP - 2151 VL - 13 IS - 11 SN - 0143-3334, 0143-3334 KW - Toxicology Abstracts KW - keratinocytes KW - tumor-promoting agents KW - activity KW - tissue culture KW - X 24240:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16418811?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Activity+of+diverse+tumor+promoters+in+a+keratinocyte+co-culture+model+of+initiated+epidermis.&rft.au=Hennings%2C+H%3BLowry%2C+D+T%3BRobinson%2C+V+A%3BMorgan%2C+D+L%3BFujiki%2C+H%3BYuspa%2C+SH&rft.aulast=Hennings&rft.aufirst=H&rft.date=1992-01-01&rft.volume=13&rft.issue=11&rft.spage=2145&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - tumor-promoting agents; activity; tissue culture; keratinocytes ER - TY - JOUR T1 - A recombinant form of Pseudomonas exotoxin directed at the epidermal growth factor receptor that is cytotoxic without requiring proteolytic processing. AN - 16412807; 2894574 AB - Pseudomonas exotoxin A is composed of three structural domains that mediate cell recognition (I), membrane translocation (II), and ADP-ribosylation (III). Within the cell, the toxin is cleaved within domain II to produce a 37-kDa carboxyl-terminal fragment, containing amino acids 280-613, which is translocated to the cytosol and causes cell death. We constructed a mutant protein (PE37), composed of amino acids 280-613 of Pseudomonas exotoxin A, which does not require proteolysis to translocate. PE37 was targeted specifically to cells with epidermal growth factor receptors by inserting transforming growth factor- alpha (TGF- alpha ) after amino acid 607 near the carboxyl terminus of Pseudomonas exotoxin A. PE37/TGF- alpha was very cytotoxic to cells with epidermal growth factor receptors. It was severalfold more cytotoxic than a derivative of full-length Pseudomonas exotoxin A containing TGF- alpha in the same position, probably because the latter requires intracellular proteolytic processing to exhibit its cytotoxicity, and proteolytic processing is not 100% efficient. JF - Journal of Biological Chemistry AU - Theuer, C P AU - FitzGerald, D AU - Pastan, I AD - Lab. Mol. Biol., NCI, Div. Cancer Biol., Diagn. and Cent., NIH, 9000 Rockville Pike, Build. 37, Rm. 4E16, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 16872 EP - 16877 VL - 267 IS - 24 SN - 0021-9258, 0021-9258 KW - Pseudomonas KW - cytotoxicity KW - epidermal growth factor KW - exotoxin A KW - receptors KW - recombinants KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16412807?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=A+recombinant+form+of+Pseudomonas+exotoxin+directed+at+the+epidermal+growth+factor+receptor+that+is+cytotoxic+without+requiring+proteolytic+processing.&rft.au=Theuer%2C+C+P%3BFitzGerald%2C+D%3BPastan%2C+I&rft.aulast=Theuer&rft.aufirst=C&rft.date=1992-01-01&rft.volume=267&rft.issue=24&rft.spage=16872&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Modulation of tubulin-nucleotide interactions by metal ions: Comparison of beryllium with magnesium and initial studies with other cations. AN - 16412710; 2895226 AB - We have compared effects of beryllium and magnesium on tubulin-nucleotide interactions in both unpolymerized tubulin and in polymer. We postulate that enhanced polymer stability is a consequence of cation binding directly to tubulin and/or polymer while deficient GTP hydrolysis in the presence of beryllium, as well as aluminum and tin, is a consequence of tight binding of cation to GTP in the exchangeable site. JF - Archives of Biochemistry and Biophysics AU - Hamel, E AU - Lin, Chii M AU - Kenney, S AU - Skehan, P AU - Vaughns, J AD - Lab. Mol. Pharmacol., Dev. Ther. Program, Div. Cancer Treat., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 327 EP - 339 VL - 295 IS - 2 SN - 0003-9861, 0003-9861 KW - GTP KW - beryllium KW - hydrolysis KW - magnesium KW - modulation KW - nucleotides KW - tubulin KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16412710?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+Biochemistry+and+Biophysics&rft.atitle=Modulation+of+tubulin-nucleotide+interactions+by+metal+ions%3A+Comparison+of+beryllium+with+magnesium+and+initial+studies+with+other+cations.&rft.au=Hamel%2C+E%3BLin%2C+Chii+M%3BKenney%2C+S%3BSkehan%2C+P%3BVaughns%2C+J&rft.aulast=Hamel&rft.aufirst=E&rft.date=1992-01-01&rft.volume=295&rft.issue=2&rft.spage=327&rft.isbn=&rft.btitle=&rft.title=Archives+of+Biochemistry+and+Biophysics&rft.issn=00039861&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Non-promoting 12-deoxyphorbol 13-esters as potent inhibitors of phorbol 12-myristate 13-acetate-induced acute and chronic biological response in CD-1 mouse skin. AN - 16411546; 2896444 AB - In previous experiments, pretreatment of CD-1 mouse skin with prostatin (12-deoxyphorbol 13-acetate) inhibited hyperplasia, induction of ornithine decarboxylase and edema in response to acute treatment with phorbol 12-myristate 13-acetate (PMA). We report here that prostatin inhibits biological responses induced by multiple (chronic) PMA treatment. A typical chronic treatment schedule consisted of five applications of 3.2 nmol (2 mu g) PMA at 48 h intervals. Most effective inhibition could be achieved when the first PMA treatment was preceded 48 h before by a lower dose of prostratin (256 nmol = 100 mu g) and each PMA treatment was preceded 15 min before by a higher dose (2.56 mu mol = 1 mg) of prostatin. Under this schedule hyperplasia was completely blocked, as was keratin K6 expression (a marker of hyperproliferative epidermis), whereas myeloperoxidase activity (a marker of neutrophil granulocyte infiltration) was reduced to 36%. 12-Deoxyphorbol 13-phenylacetate (dPP), a non-promoting 12-deoxyphorbol derivative that binds to protein kinase C with two orders of magnitude higher potency than does prostatin, showed the same pattern of inhibition as did prostatin for a single PMA treatment by with a corresponding two orders of magnitude higher potency. JF - Carcinogenesis AU - Szallasi, Z AU - Krausz, K W AU - Blumberg, P M AD - Mol. Mechanisms Tumor Promot. Sect., Lab. Cell. Carcinog. and Tumor Promot., NCI, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 2161 EP - 2167 VL - 13 IS - 11 SN - 0143-3334, 0143-3334 KW - TPA KW - 12-deoxyphorbol 13-esters KW - biological response KW - mice KW - Toxicology Abstracts KW - skin KW - X 24172:Plants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16411546?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Non-promoting+12-deoxyphorbol+13-esters+as+potent+inhibitors+of+phorbol+12-myristate+13-acetate-induced+acute+and+chronic+biological+response+in+CD-1+mouse+skin.&rft.au=Szallasi%2C+Z%3BKrausz%2C+K+W%3BBlumberg%2C+P+M&rft.aulast=Szallasi&rft.aufirst=Z&rft.date=1992-01-01&rft.volume=13&rft.issue=11&rft.spage=2161&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - skin ER - TY - JOUR T1 - Inhibition of agonist-induced activation of phospholipase C following poxvirus infection. AN - 16397906; 2883461 AB - This study has examined the effects of vaccinia virus infection on phospholipase C activity. Infection of BS-C-1 cells, an African Green Monkey kidney cell line, or A431 cells, a human carcinoma cell line, with vaccinia virus inhibits receptor-mediated phospholipase C activation. As a consequence, agonist-mediated Ca super(2+) mobilization in BS-C-1 cells also was inhibited by vaccinia virus infection. Alleviation of the inhibition of phospholipase C activation was observed in vaccinia virus-infected cells treated with cycloheximide without influencing uninfected cells. Treatment of infected cells with alpha -amanitin, an inhibitor of host mRNA synthesis but not virus mRNA synthesis, failed to alleviate the inhibition of phospholipase C activation. Together these results suggest that a virus-encoded gene product mediates the inhibition of phospholipase C activation without the need of a virus-induced host factor. JF - Journal of Biological Chemistry AU - Oliver., KG AU - Buller, M L AU - Hughes, P J AU - Putney, JW Jr AU - Palumbo, G J AD - Calcium Regul. Sect., Mail Drop 7-10, Lab. Cell. and Mol. Pharmacol., NIEHS, NIH, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 25098 EP - 25103 VL - 267 IS - 35 SN - 0021-9258, 0021-9258 KW - activation KW - agonists KW - induction KW - infection KW - inhibition KW - man KW - monkeys KW - phospholipase C KW - poxvirus KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts KW - V 22032:Viral proteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16397906?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Inhibition+of+agonist-induced+activation+of+phospholipase+C+following+poxvirus+infection.&rft.au=Oliver.%2C+KG%3BBuller%2C+M+L%3BHughes%2C+P+J%3BPutney%2C+JW+Jr%3BPalumbo%2C+G+J&rft.aulast=Oliver.&rft.aufirst=KG&rft.date=1992-01-01&rft.volume=267&rft.issue=35&rft.spage=25098&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - agonists; inhibition; infection; induction; man; activation ER - TY - JOUR T1 - A yeast cyclophilin gene essential for lactate metabolism at high temperature. AN - 16395927; 2874598 AB - We have isolated a yeast cyclophilin gene, CPR3, which encodes a presumptive mitochondrial isoform. While CPR3 disruption mutants lack any phenotype at 30 degree C, they are unable to grow on L-lactate at 37 degree C. Disruptions of two other cyclophilin genes (CPR1, CPR2) and of FPR1, the gene encoding an FK506 binding protein with PPIase activity, do not affect growth on L-lactate at 37 degree C. L-Lactate metabolism requires transcriptional induction of CYB2, the gene encoding flavocytochrome b sub(2); cpr3 mutants induce transcription of this gene normally. This result demonstrates a conditional lethal phenotype for a cyclophilin mutation and presents a system for genetic and biochemical analysis of cyclophilin function. JF - Proceedings of the National Academy of Sciences, USA AU - Davis, E S AU - Becker, A AU - Heitman, J AU - Hall, M N AU - Brennan, M B AD - Unit Genomics, Clin. Neurogenet. Branch, NIMH/NIH, Build. 10, Rm. 4N320, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 11169 EP - 11173 VL - 89 IS - 23 SN - 0027-8424, 0027-8424 KW - CPR3 gene KW - Saccharomyces cerevisiae KW - amino acid sequence KW - cyclophilin KW - gene products KW - genes KW - lactic acid KW - metabolism KW - mutation KW - nucleotide sequence KW - predictions KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Microbiology Abstracts C: Algology, Mycology & Protozoology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - N 14640:Structure & sequence KW - G 07330:Fungal genetics KW - K 03079:Fungi UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16395927?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=A+yeast+cyclophilin+gene+essential+for+lactate+metabolism+at+high+temperature.&rft.au=Davis%2C+E+S%3BBecker%2C+A%3BHeitman%2C+J%3BHall%2C+M+N%3BBrennan%2C+M+B&rft.aulast=Davis&rft.aufirst=E&rft.date=1992-01-01&rft.volume=89&rft.issue=23&rft.spage=11169&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - nucleotide sequence; amino acid sequence; genes; metabolism; mutation; gene products ER - TY - JOUR T1 - Human liver cathepsin D. Purification, crystallization and preliminary X-ray diffraction analysis of a lysosomal enzyme. AN - 16395217; 2886755 AB - The two-chain form of active cathepsin D, a glycosylated, lysosomal aspartic proteinase, has been isolated from human liver. Isoelectric focusing revealed two major species of enzyme that differed by approximately 0.2 pI unit. Crystals suitable for X-ray diffraction analysis were prepared from acidic solutions using precipitation with ammonium sulfate. JF - Journal of Molecular Biology AU - Gulnik, S AU - Baldwin, E T AU - Tarasova, N AU - Erickson, J AD - Struct. Biochem. Program, Biomed. Supercomputing Cent. PRI/DynCorp, NCI-FCRDC, Frederick, MD 21702, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 265 EP - 270 VL - 227 IS - 1 SN - 0022-2836, 0022-2836 KW - X-ray diffraction KW - cathepsin D KW - liver KW - man KW - purification KW - structure KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16395217?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Molecular+Biology&rft.atitle=Human+liver+cathepsin+D.+Purification%2C+crystallization+and+preliminary+X-ray+diffraction+analysis+of+a+lysosomal+enzyme.&rft.au=Gulnik%2C+S%3BBaldwin%2C+E+T%3BTarasova%2C+N%3BErickson%2C+J&rft.aulast=Gulnik&rft.aufirst=S&rft.date=1992-01-01&rft.volume=227&rft.issue=1&rft.spage=265&rft.isbn=&rft.btitle=&rft.title=Journal+of+Molecular+Biology&rft.issn=00222836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Recombinant DNA approaches for the development of metabolic systems used in in vitro toxicology. AN - 16393183; 2873058 AB - The central theme of this review is the transfer of genetic information to improve the metabolic capability of cell systems used in genetic toxicology. However, a basic philosophy of the review is that genetic manipulation of cultured mammalian cells has the potential for developing systems to be used to better understand chemically induced toxicological effects. JF - Mutation Research AU - Langenbach, R AU - Smith, P B AU - Crespi, C AD - Exp. Carcinog. and Mutag. Branch, NIEHS (E4-05), P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 251 EP - 275 VL - 277 IS - 3 SN - 0027-5107, 0027-5107 KW - genetic information transfer KW - cytochrome P450 KW - Toxicology Abstracts; Genetics Abstracts KW - recombinants KW - reviews KW - toxicology KW - DNA KW - G 07220:General theory/testing systems KW - X 24250:Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16393183?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+Research&rft.atitle=Recombinant+DNA+approaches+for+the+development+of+metabolic+systems+used+in+in+vitro+toxicology.&rft.au=Langenbach%2C+R%3BSmith%2C+P+B%3BCrespi%2C+C&rft.aulast=Langenbach&rft.aufirst=R&rft.date=1992-01-01&rft.volume=277&rft.issue=3&rft.spage=251&rft.isbn=&rft.btitle=&rft.title=Mutation+Research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - reviews; recombinants; DNA; toxicology ER - TY - JOUR T1 - Isolation of rsp-1, a novel cDNA capable of suppressing v-Ras transformation. AN - 16390000; 2876133 AB - Using an expression cloning assay, we have isolated a novel cDNA, referred to as rsp-1, which suppresses the v-Ras-transformed phenotype. When introduced into NIH 3T3 fibroblasts under the control of a metallothionein promoter, rsp-1 confers resistance to v-Ras, but not to v-Mos or v-Src, and inhibits growth of the cells. The rsp-1 cDNA contains a 831-bp open reading frame encoding a 277-amino acid leucine-rich protein. The rsp-1 cDNA exhibits no significant homology to sequences in the DNA data bases. However, searches of the protein data bases revealed that it contains a series of leucine-based repeats which are homologous to the leucine repeats found in the regulatory region of the yeast adenylyl cyclase. rsp-1 specific RNA is detectable in a wide variety of cell lines and tissues, and the gene is conserved among eukaryotic species. These data suggest that rsp-1 plays a role in Ras signal transduction. JF - Molecular and Cellular Biology AU - Cutler, M L AU - Bassin, R H AU - Zanoni, L AU - Talbot, N AD - Lab. Tumor Immunol. and Biol., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 3750 EP - 3756 VL - 12 IS - 9 SN - 0270-7306, 0270-7306 KW - amino acid sequence KW - cDNA KW - genes KW - mice KW - nucleotide sequence KW - prediction KW - rsp-1 KW - rsp-1 gene KW - suppression KW - tumor suppressor genes KW - v-ras KW - v-ras gene KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Oncogenes & Growth Factors Abstracts; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - G 07398:GENERAL KW - N 14640:Structure & sequence KW - B 26410:Retinoblastoma gene (RB gene) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16390000?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+Cellular+Biology&rft.atitle=Isolation+of+rsp-1%2C+a+novel+cDNA+capable+of+suppressing+v-Ras+transformation.&rft.au=Cutler%2C+M+L%3BBassin%2C+R+H%3BZanoni%2C+L%3BTalbot%2C+N&rft.aulast=Cutler&rft.aufirst=M&rft.date=1992-01-01&rft.volume=12&rft.issue=9&rft.spage=3750&rft.isbn=&rft.btitle=&rft.title=Molecular+and+Cellular+Biology&rft.issn=02707306&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - suppression; nucleotide sequence; tumor suppressor genes; cDNA; amino acid sequence; genes; prediction ER - TY - JOUR T1 - Association of cyclic-AMP-dependent protein kinase with neurofilaments. AN - 16387316; 2878254 AB - Neurofilament preparations isolated from bovine spinal cord contain cyclic-AMP-dependent protein kinase (PKA) activity. Treatment of this preparation with cyclic AMP, to dissociate the regulatory subunit of the kinase from the catalytic subunit, resulted in retention of the kinase activity but loss of cyclic AMP regulation. This suggests that PKA is associated via its catalytic subunit with the neurofilament preparation. The association of exogenous PKA from bovine heart with the neurofilament preparation and with neurofilaments reconstituted from purified neurofilament proteins was also investigated. Either the free catalytic subunit or combinations of the catalytic and regulatory subunits of PKA were incubated with the preparations, and the degree of association was determined as the level of kinase activity that cosediments with neurofilaments. The results indicate that the free catalytic subunit of PKA co-sediments with neurofilaments reconstituted from purified proteins. JF - Biochemical Journal AU - Dosemeci, A AU - Pant, H C AD - Lab. Neurochem., NINDS/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 477 EP - 481 VL - 282 IS - 2 SN - 0264-6021, 0264-6021 KW - association KW - cattle KW - cyclic AMP KW - dependent KW - neurofilaments KW - protein kinase KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; CSA Neurosciences Abstracts KW - N3 11070:Neurochemistry and cellular biology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16387316?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+Journal&rft.atitle=Association+of+cyclic-AMP-dependent+protein+kinase+with+neurofilaments.&rft.au=Dosemeci%2C+A%3BPant%2C+H+C&rft.aulast=Dosemeci&rft.aufirst=A&rft.date=1992-01-01&rft.volume=282&rft.issue=2&rft.spage=477&rft.isbn=&rft.btitle=&rft.title=Biochemical+Journal&rft.issn=02646021&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - neurofilaments; association ER - TY - JOUR T1 - Carcinogenicity of oral cadmium in the male wister (WF/NCr) rat: Effect of chronic dietary zinc deficiency. AN - 16385810; 2860426 AB - The effect of chronic dietary zinc deficiency on the carcinogenic potential of dietary cadmium was assessed in male Wistar (WF/NCr) rats. Groups (n = 28) of rats were fed diets adequate (60 ppm) or marginally deficient (7 ppm) in zinc and containing cadmium at various levels (0, 25, 50, 100, or 200 ppm). Cadmium treatment did not reduce survival or food consumption and only at the highest doses of cadmium (100 and 200 ppm) was body weight reduced (maximum 17%). The incidence of prostatic proliferative lesions, both hyperplasias and adenomas, was increased over that seen in controls (1.8%) in both zinc-adequate (20%) and zinc-deficient rats (14%) fed 50 ppm cadmium. The overall incidence for prostatic lesions for all cadmium treatment groups was, however, much lower in zinc-deficient rats, possibly because of a marked increase in prostatic atrophy that was associated with reduced zinc intake. JF - Fundamental and Applied Toxicology AU - Waalkes, M P AU - Rehm, S AD - Lab. Comp. Carcinog., NCI-FCRDC, Build. 538, Rm. 205E, Frederick, MD 21702-1201, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 512 EP - 520 VL - 19 IS - 4 SN - 0272-0590, 0272-0590 KW - cadmium KW - zinc KW - rats KW - heavy metals KW - Toxicology Abstracts KW - carcinogenicity KW - deficiency KW - X 24162:Chronic exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16385810?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+Applied+Toxicology&rft.atitle=Carcinogenicity+of+oral+cadmium+in+the+male+wister+%28WF%2FNCr%29+rat%3A+Effect+of+chronic+dietary+zinc+deficiency.&rft.au=Waalkes%2C+M+P%3BRehm%2C+S&rft.aulast=Waalkes&rft.aufirst=M&rft.date=1992-01-01&rft.volume=19&rft.issue=4&rft.spage=512&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+Applied+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - deficiency; carcinogenicity ER - TY - JOUR T1 - Control of gal transcription through DNA looping: Inhibition of the initial transcribing complex. AN - 16385731; 2874656 AB - Involvement of DNA looping between two spatially separated gal operators, O sub(E) and O sub(I), in repression of the gal operon has been demonstrated in vivo. An in vitro transcription assay using a minicircle DNA containing the gal promoter region with lac operators was employed to elucidate the molecular mechanism of repression. Wild-type lac repressors (LacI super(+) protein molecules), which are capable of associating into a tetramer and forming a DNA loop, repressed transcription from promoter sites P1 and P2, whereas a non-looping lac repressor mutant (LacI super(adi)) failed to show normal repression of both of the gal promoters. Thus a DNA loop is also required for repression of transcription in vitro. Repression mediated by DNA looping resulted in the inhibition of the synthesis of complete as well as aborted transcripts, demonstrating that the repressive action was on the formation or activity of the initial transcribing complex. Under similar conditions, the gal repressor (GalR protein) did not repress the gal promoters effectively, apparently because it failed to loop DNA containing gal operators in the purified system. JF - Proceedings of the National Academy of Sciences, USA AU - Choy, HE AU - Adhya, S AD - Lab. Mol. Biol., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 11264 EP - 11268 VL - 89 IS - 23 SN - 0027-8424, 0027-8424 KW - looping KW - gal operator KW - Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts B: Bacteriology KW - repression KW - DNA KW - Escherichia coli KW - operators KW - transcription KW - J 02725:DNA KW - G 07320:Bacterial genetics KW - N 14555:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16385731?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Preferential+and+strand-specific+DNA+repair+of+%286-4%29+photoproducts+detected+by+a+photochemical+method+in+the+hamster+DHFR+gene.&rft.au=Link%2C+C+J%3BMitchell%2C+D+L%3BNairn%2C+R+S%3BBohr%2C+V+A&rft.aulast=Link&rft.aufirst=C&rft.date=1992-11-01&rft.volume=13&rft.issue=11&rft.spage=1975&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - Escherichia coli; DNA; operators; transcription; repression ER - TY - JOUR T1 - Crystal structure of human recombinant interleukin-4 at 2.25 angstrom resolution. AN - 16379745; 2858983 AB - The crystal structure of human recombinant interleukin-4 (IL-4) has been solved by multiple isomorphous replacement, and refined to an R factor of 0.218 at 2.25 angstrom resolution. The molecule is a left-handed four-helix bundle with a short stretch of beta sheet. The structure bears close resemblance to other cytokines such as granulocyte-macrophage colony stimulating factor (GM-CSF). Although no sequence similarity of IL-4 to GM-CSF and other related cytokines has been previously postulated, structure-based alignment of IL-4 and GM-CSF revealed that the core of the molecules, including large parts of all four helices and extending over half of the molecule, has 30% sequence identity. JF - FEBS Letters AU - Wlodaver, A AU - Pavlovsky, A AU - Gustchina, A AD - Macromol. Struct. Lab., NCI-Frederick Cancer Res. and Dev. Cent., ABL-Basic Res. Program, Frederick, MD 21702, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 59 EP - 64 VL - 309 IS - 1 SN - 0014-5793, 0014-5793 KW - crystal structure KW - interleukin 4 KW - man KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16379745?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+Letters&rft.atitle=Crystal+structure+of+human+recombinant+interleukin-4+at+2.25+angstrom+resolution.&rft.au=Wlodaver%2C+A%3BPavlovsky%2C+A%3BGustchina%2C+A&rft.aulast=Wlodaver&rft.aufirst=A&rft.date=1992-01-01&rft.volume=309&rft.issue=1&rft.spage=59&rft.isbn=&rft.btitle=&rft.title=FEBS+Letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Human immunodeficiency virus type 1 Vpu protein induces rapid degradation of CD4. AN - 16368467; 2859587 AB - CD4 is an integral membrane glycoprotein which is known as the human immunodeficiency virus (HIV) receptor for infection of human cells. We have recently demonstrated that the presence of the HIV-1-encoded integral membrane protein Vpu can reduce the formation of Env-CD4 complexes, resulting in increased gp160 processing and decreased CD4 stability. We have studied the effect of Vpu on CD4 stability and found that Vpu induces rapid degradation of CD4, reducing the half-life of CD4 from 6 h to 12 min. By using a CD4-binding mutant of gp160, we were able to show that this Vpu-induced degradation of CD4 requires retention of CD4 in the ER, which is normally accomplished through its binding to gp160. The involvement of gp160 in the induction of CD4 degradation is restricted to its function as a CD4 trap, since, in the absence of Env, an ER retention mutant of CD4, as well as wild-type CD4 in cultures treated with brefeldin A, a drug that blocks transport of proteins from the ER, is degraded in the presence of Vpu. JF - Journal of Virology AU - Willey, R L AU - Maldarelli, F AU - Martin, MA AU - Strebel, K AD - Lab. Mol. Microbiol., NIAID/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 7193 EP - 7200 VL - 66 IS - 12 SN - 0022-538X, 0022-538X KW - CD4 antigen KW - Vpu protein KW - degradation KW - human immunodeficiency virus 1 KW - immunoprecipitation KW - radioactive labelling KW - transfection KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts KW - V 22002:AIDS: Molecular and in vitro aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16368467?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=Human+immunodeficiency+virus+type+1+Vpu+protein+induces+rapid+degradation+of+CD4.&rft.au=Willey%2C+R+L%3BMaldarelli%2C+F%3BMartin%2C+MA%3BStrebel%2C+K&rft.aulast=Willey&rft.aufirst=R&rft.date=1992-01-01&rft.volume=66&rft.issue=12&rft.spage=7193&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - transfection; degradation; radioactive labelling; immunoprecipitation ER - TY - JOUR T1 - Synthesis and conformation of the trimeric coiled-coil segment of laminin. AN - 16367264; 2859681 AB - A disulfide linked 95-mer parallel hetero-trimeric active site segment of laminin was designed and synthesised. The three subunits, A (32-mer), B1 (30-mer) and B2 (33-mer), were prepared by Boc-based solid-phase peptide synthesis involving a two-step trimethylsilyl bromide-thioanisole and HF deprotection procedure. The interlinking of the three subunits was accomplished by the stepwise selective formation of two disulfide bridges using air-oxidation and thallium (III) trifluoroacetate oxidation. The conformations of the synthetic peptides were studied by circular dichroism (CD) spectroscopy, showing that the hetero-dimer, B1-B2, one of the homo-dimers, B1-B1, and the timer are 30 to 40% in the alpha -helical conformation in aqueous buffer. JF - International Journal of Peptide and Protein Reseach AU - Nomizu, M AU - Utani, A AU - Shiraishi, N AU - Yamada, Y AU - Roller, P P AD - Lab. Med. Chem., NCI, NIH, Build. 37, Rm 5C02, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 72 EP - 79 VL - 40 IS - 1 SN - 0367-8377, 0367-8377 KW - C.D. KW - active sties KW - conformation KW - laminin KW - peptide synthesis KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16367264?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Peptide+and+Protein+Reseach&rft.atitle=Synthesis+and+conformation+of+the+trimeric+coiled-coil+segment+of+laminin.&rft.au=Nomizu%2C+M%3BUtani%2C+A%3BShiraishi%2C+N%3BYamada%2C+Y%3BRoller%2C+P+P&rft.aulast=Nomizu&rft.aufirst=M&rft.date=1992-01-01&rft.volume=40&rft.issue=1&rft.spage=72&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Peptide+and+Protein+Reseach&rft.issn=03678377&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Incorporation of 2-fluorohistidine in murine protein in vivo. AN - 16365855; 2859534 AB - The tissue distribution and time course of incorporation into acid insoluble (bound) and acid soluble (free) fractions of ( super(3)H)2-fluorohistidine is compared to that of U( super(14)C)histidine in mouse tissues in vivo. The cycloheximide-sensitive incorporation of 2-FHis is between 9 and 17 percent of that of His. Unlike ( super(14)C)His a major fraction, approximately 90% at 72 hrs, of isotope derived from ( super(3)H)2-FHis remains in tissues for a prolonged period in an acid soluble form. The excretion of isotope from ( super(14)C)His (T sub(1/2) = 5 hr) is more rapid than from ( super(3)H)2-FHis (T sub(1/2) = 11.4 hrs). 2-FHis, at doses from 100 to 250 mg/kg produce a reversible inhibition of growth in mice. JF - Life Sciences AU - Creveling, C R AU - Padgett, W L AU - McNeal, E T AU - Cohen, LA AU - Kirk, K L AD - Lab. Bioorg. Chem., 8A/1A27, NIDDK, NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1197 EP - 1204 VL - 51 IS - 15 SN - 0024-3205, 0024-3205 KW - 2-fluorohistidine KW - incorporation KW - mice KW - proteins KW - Microbiology Abstracts B: Bacteriology KW - J:20320 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16365855?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Life+Sciences&rft.atitle=Incorporation+of+2-fluorohistidine+in+murine+protein+in+vivo.&rft.au=Creveling%2C+C+R%3BPadgett%2C+W+L%3BMcNeal%2C+E+T%3BCohen%2C+LA%3BKirk%2C+K+L&rft.aulast=Creveling&rft.aufirst=C&rft.date=1992-01-01&rft.volume=51&rft.issue=15&rft.spage=1197&rft.isbn=&rft.btitle=&rft.title=Life+Sciences&rft.issn=00243205&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Localization of neurokinin B in the central nervous system of the rat. AN - 16358580; 2855371 AB - The distribution of neurokinin B (NKB) was determined by immunocytochemistry with antisera directed toward its amino terminus. Immunoreactive perikarya were detected in the main and accessory olfactory bulbs, cortical regions, the olfactory tubercle, the bed nucleus of the stria terminalis, the diagonal band of Broca, the nucleus accumbens, the septum, the neostriatum, several hypothalamic nuclei, the superior colliculus, the central gray, the substantia nigra, the medullary reticular formation, and the external cuneate nucleus. The distribution of NKB-containing perikarya revealed by immunocytochemistry was similar to the distribution of protachykinin B-containing cells previously visualized by in situ hybridization. Immunoreactive nerve fibers and terminals were detected in all major subdivisions of the brain. JF - Peptides AU - Merchenthaler, I AU - Maderdrut, J L AU - O'Harte, F AU - Conlon, J M AD - Lab. Mol. and Integrative Neurosci., MD C4-07, NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 815 EP - 829 VL - 13 IS - 4 SN - 0196-9781, 0196-9781 KW - central nervous system KW - neurokinin B KW - rats KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; CSA Neurosciences Abstracts KW - N3 11080:Neuroendocrinology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16358580?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Peptides&rft.atitle=Localization+of+neurokinin+B+in+the+central+nervous+system+of+the+rat.&rft.au=Merchenthaler%2C+I%3BMaderdrut%2C+J+L%3BO%27Harte%2C+F%3BConlon%2C+J+M&rft.aulast=Merchenthaler&rft.aufirst=I&rft.date=1992-01-01&rft.volume=13&rft.issue=4&rft.spage=815&rft.isbn=&rft.btitle=&rft.title=Peptides&rft.issn=01969781&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - central nervous system ER - TY - JOUR T1 - Enhanced mutagenicity of anisidine isomers in bacterial strains containing elevated N-acetyltransferase activity. AN - 16357017; 2849847 AB - We show that both para- and ortho-anisidine isomers are mutagenic in a Salmonella typhimurium tester strain containing elevated levels of N-acetyltranferase (YG1029). p-Anisidine gave a positive mutagenic response using either hamster S9 or ram seminal vesicle microsomes (RSVM) as an activating system, while o-anisidine gave a positive response only with the hamster S9 fraction. The results demonstrate that both anisidine isomers are mutagenic and that N-acetyltransferase enzymes play an important role in/ their metabolism to mutagenic species. JF - Mutation Research AU - Thompson, D C AU - Josephy, P D AU - Chu, JWK AU - Eling, TE AD - Eicosanoid Biochem. Sect., NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 83 EP - 89 VL - 279 IS - 2 SN - 0027-5107, 0027-5107 KW - anisidine KW - N-acetyltransferase KW - Toxicology Abstracts; Genetics Abstracts KW - isomers KW - Salmonella typhimurium KW - mutagenicity KW - activity KW - X 24200:Nitrosamines & related compounds KW - G 07221:Specific chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16357017?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+Research&rft.atitle=Enhanced+mutagenicity+of+anisidine+isomers+in+bacterial+strains+containing+elevated+N-acetyltransferase+activity.&rft.au=Thompson%2C+D+C%3BJosephy%2C+P+D%3BChu%2C+JWK%3BEling%2C+TE&rft.aulast=Thompson&rft.aufirst=D&rft.date=1992-01-01&rft.volume=279&rft.issue=2&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=Mutation+Research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Salmonella typhimurium; isomers; mutagenicity; activity ER - TY - JOUR T1 - A comparative structural characterization of the human NSCL-1 and NSCL-2 genes: Two basic helix-loop-helix genes expressed in the developing nervous system. AN - 16356797; 2844854 AB - Human cDNA clones for NSCL-1 and NSCL-2, two basic domain helix-loop-helix (bHLH) genes expressed predominantly in the developing nervous system, were obtained from a fetal brain cDNA library. The full-length transcripts and the genomic structures were determined. The cDNAs for the two genes encode predicted proteins of similar size (133 and 135 amino acids for NSCL-1 and NSCL-2, respectively) and structure. The carboxyl-terminal 75 amino acids of the two proteins contain the bHLH motif and differ from each other by only three conservative amino acid changes, while the amino-terminal portions are markedly divergent from each other. The genes have a similar genomic organization, suggesting a close evolutionary relationship. JF - Journal of Biological Chemistry AU - Lipkowitz, S AU - Goebel, V AU - Varterasian, M L AU - Nakahara, K AU - Tchorz, K AU - Kirsch, IR AD - Navy Med. Oncol. Branch, NCI, Bethesda, MD 20889-5105, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 21065 EP - 21071 VL - 267 IS - 29 SN - 0021-9258, 0021-9258 KW - NSCL-1 gene KW - NSCL-2 gene KW - amino acid sequence KW - brain KW - cDNA KW - expression KW - gene products KW - genes KW - helix-loop-helix proteins KW - man KW - nucleotide sequence KW - predictions KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Human Genome Abstracts; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - N 14640:Structure & sequence KW - G 07430:Chromosome studies/nucleotide sequence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16356797?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=A+comparative+structural+characterization+of+the+human+NSCL-1+and+NSCL-2+genes%3A+Two+basic+helix-loop-helix+genes+expressed+in+the+developing+nervous+system.&rft.au=Lipkowitz%2C+S%3BGoebel%2C+V%3BVarterasian%2C+M+L%3BNakahara%2C+K%3BTchorz%2C+K%3BKirsch%2C+IR&rft.aulast=Lipkowitz&rft.aufirst=S&rft.date=1992-01-01&rft.volume=267&rft.issue=29&rft.spage=21065&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - expression; nucleotide sequence; cDNA; amino acid sequence; genes; brain; gene products; man ER - TY - JOUR T1 - Cellular proteins bound to immunodeficiency viruses: Implications for pathogenesis and vaccines. AN - 16354876; 2855110 AB - Cellular proteins associated with immunodeficiency viruses were identified by determination of the amino acid sequence of the proteins and peptides present in sucrose density gradient-purified human immunodeficiency virus (HIV)-1, HIV-2, and simian immunodeficiency virus (SIV). beta 2 microglobulin ( beta sub(2)m) and the alpha and beta chains of human lymphocyte antigen (HLA) DR were present in virus preparations at one-fifth the concentration of Gag on a molar basis. Antisera to HLA DR, beta sub(2)m, as well as HLA class I precipitated intact viral particles, suggesting that these cellular proteins were physically associated with the surface of the virus. Antisera to class I, beta sub(2)m, and HLA DR also inhibited infection of cultured cells by both HIV-1 and SIV. The specific, selective association of these cellular proteins in a physiologically relevant manner has major implications for our understanding of the infection process and the pathogenesis of immunodeficiency viruses and should be considered in the design of vaccines. JF - Science (Washington) AU - Arthur, LO AU - Bess, JW Jr AU - Sowder, RC II AU - Benveniste, R E AU - Mann, D L AU - Chermann, J-C AU - Henderson, LE AD - AIDS Vaccine Prog., Prog. Resources, Inc./DynCorp, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702 (USA) Y1 - 1992 PY - 1992 DA - 1992 SP - 1935 EP - 1938 VL - 258 IS - 5090 SN - 0036-8075, 0036-8075 KW - DR determinants KW - beta 2 microglobulin KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Immunology Abstracts; Virology & AIDS Abstracts KW - vaccines KW - histocompatibility antigen HLA KW - simian immunodeficiency virus KW - association KW - human immunodeficiency virus KW - amino acid sequence KW - binding KW - pathogenesis KW - W3 33365:Vaccines (other) KW - V 22002:AIDS: Molecular and in vitro aspects KW - W 30965:Miscellaneous, Reviews KW - F 06860:CMI UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16354876?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28Washington%29&rft.atitle=Cellular+proteins+bound+to+immunodeficiency+viruses%3A+Implications+for+pathogenesis+and+vaccines.&rft.au=Arthur%2C+LO%3BBess%2C+JW+Jr%3BSowder%2C+RC+II%3BBenveniste%2C+R+E%3BMann%2C+D+L%3BChermann%2C+J-C%3BHenderson%2C+LE&rft.aulast=Arthur&rft.aufirst=LO&rft.date=1992-01-01&rft.volume=258&rft.issue=5090&rft.spage=1935&rft.isbn=&rft.btitle=&rft.title=Science+%28Washington%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - vaccines; histocompatibility antigen HLA; association; amino acid sequence; binding; pathogenesis; simian immunodeficiency virus; human immunodeficiency virus ER - TY - JOUR T1 - A novel hypothalamic peptide, pituitary adenylate cyclase activating peptide, modulates Sertoli cell function in vitro. AN - 16347809; 2852604 AB - Pituitary adenylate cyclase-activating peptide (PACAP), a novel hypothalamic peptide that has been shown to exist in several tissues including the testis, was examined for its effects on cultured rat Sertoli cells. PACAP stimulates cAMP accumulation in Sertoli cells cultured from 15-day-old rats in the presence or absence of methylisobutylxanthine, a phosphodiesterase inhibitor, and in the presence of pertussis toxin, a blocker of the adenylate cyclase inhibitory pathway. Maximal stimulation, which is 20-40% of that attainable with FSH, occurs at PACAP concentrations of 10 nM: the ED sub(50) is approximately 100 pM. The ability of PACAP to stimulate Sertoli cell cAMP declines with increasing age of donor animals (15-60 days of age) in a fashion similar to the FSH effect. PACAP stimulation of Sertoli cell cAMP accumulation is additive with submaximal, but not maximal, concentrations of FSH or forskolin. PACAP also stimulates the secretion of lactate, estradiol, and inhibin in a concentration-dependent manner. JF - Biology of Reproduction AU - Heindel, J J AU - Powell, C J AU - Paschall, C S AU - Arimura, A AU - Culler, MD AD - NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 800 EP - 806 VL - 47 IS - 5 SN - 0006-3363, 0006-3363 KW - Sertoli cells KW - hypothalamus KW - modulation KW - peptides KW - pituitary KW - pituitary adenylate cyclase-activating polypeptide KW - rats KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; CSA Neurosciences Abstracts KW - N3 11210:HYPOTHALAMIC RELEASING HORMONES AND FACTORS UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16347809?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biology+of+Reproduction&rft.atitle=A+novel+hypothalamic+peptide%2C+pituitary+adenylate+cyclase+activating+peptide%2C+modulates+Sertoli+cell+function+in+vitro.&rft.au=Heindel%2C+J+J%3BPowell%2C+C+J%3BPaschall%2C+C+S%3BArimura%2C+A%3BCuller%2C+MD&rft.aulast=Heindel&rft.aufirst=J&rft.date=1992-01-01&rft.volume=47&rft.issue=5&rft.spage=800&rft.isbn=&rft.btitle=&rft.title=Biology+of+Reproduction&rft.issn=00063363&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - Sertoli cells; modulation; hypothalamus; peptides; pituitary ER - TY - JOUR T1 - Deficiencies in sex-regulated expression and levels of two hepatic sterol carrier proteins in a murine model of Niemann-Pick type C disease. AN - 16347307; 2848986 AB - Hepatic sterol carrier protein-2 (SCP sub(2)) and sterol carrier protein-X (SCP sub(x)) levels in normal and in mutant Niemann-Pick Type C mice were determined by immunoblotting with antiserum against rat SCP sub(2). JF - Journal of Biological Chemistry AU - Roff, C F AU - Pastuszyn, A AU - Strauss, JF III AU - Billheimer, J T AU - Vanier, M T AU - Brady, RO AU - Scallen, T J AU - Pentchev, P G AD - Build. 10/Rm. 3D12, DMN, NINDS, NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 15902 EP - 15908 VL - 267 IS - 22 SN - 0021-9258, 0021-9258 KW - Niemann-Pick disease KW - animal models KW - comparison KW - expression KW - females KW - males KW - mice KW - sterol carrier protein 2 KW - sterol carrier protein X KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16347307?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Deficiencies+in+sex-regulated+expression+and+levels+of+two+hepatic+sterol+carrier+proteins+in+a+murine+model+of+Niemann-Pick+type+C+disease.&rft.au=Roff%2C+C+F%3BPastuszyn%2C+A%3BStrauss%2C+JF+III%3BBillheimer%2C+J+T%3BVanier%2C+M+T%3BBrady%2C+RO%3BScallen%2C+T+J%3BPentchev%2C+P+G&rft.aulast=Roff&rft.aufirst=C&rft.date=1992-01-01&rft.volume=267&rft.issue=22&rft.spage=15902&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Dietary determinants of lung-cancer risk: Results from a case-control study in Yunnan Province, China. AN - 16346772; 2851909 AB - The relation between diet and lung cancer was studied among male residents of a mining community in Yunnan Province. After obtaining food frequency data from subjects or proxies, we compared diets of 428 cases, aged 35-74 years, and 1,011 age-matched controls. Cases tended to consume slightly more rice, but less protein-rich foods meat (i.e., bean curd, meat, eggs) and vegetable than did controls. The relative risks of lung cancer across increasing quartiles of (i.e., pork) consumption, for example, were 1.00 0.67, 0.72 and 0.46 (p for trend < 0.01). The relative risks of lung cancer across increasing quartiles of consumption of dark-green, leafy vegetables were 1.00, 0.62, 0.52 and 0.41 (p for trend < 0.01). JF - International Journal of Cancer AU - Swanson, CA AU - Mao, B L AU - Li, J Y AU - Lubin, J H AU - Yao, S X AU - Wang, J Z AU - Cai, S K AU - Hou, Y AU - Luo, Q S AU - Blot, W J AD - Epidemiol. and Biostat. Prog., DCE, NCI, NIH, 6130 Executive Blvd., EPN Rm. 430, Rockville, MD 20852, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 876 EP - 880 VL - 50 IS - 6 SN - 0020-7136, 0020-7136 KW - China, People's Rep., Yunnan Province KW - Risk Abstracts; Health & Safety Science Abstracts KW - lung cancer KW - diets KW - respiratory diseases KW - epidemiology KW - nutrition KW - risk assessment KW - R2 23060:Medical and environmental health KW - H SM3.8.6:DIET KW - H SM10.21:CANCER KW - H SM10.24:PULMONARY DISEASES UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16346772?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Cancer&rft.atitle=Dietary+determinants+of+lung-cancer+risk%3A+Results+from+a+case-control+study+in+Yunnan+Province%2C+China.&rft.au=Swanson%2C+CA%3BMao%2C+B+L%3BLi%2C+J+Y%3BLubin%2C+J+H%3BYao%2C+S+X%3BWang%2C+J+Z%3BCai%2C+S+K%3BHou%2C+Y%3BLuo%2C+Q+S%3BBlot%2C+W+J&rft.aulast=Swanson&rft.aufirst=CA&rft.date=1992-01-01&rft.volume=50&rft.issue=6&rft.spage=876&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - lung cancer; epidemiology; respiratory diseases; diets; risk assessment; nutrition ER - TY - JOUR T1 - Sequence and expression of caveolin, a protein component of caveolae plasma membrane domains phosphorylated on tyrosine in Rous sarcoma virus-transformed fibroblasts. AN - 16346094; 2844655 AB - We report the deduced protein sequence of chicken caveolin derived from cDNA PCR products and genomic DNA clones. Caveolin is a unique protein of 178 amino acids and displays little sequence similarity to other proteins in the GenBank data base. Hydrophobicity predictions indicate an unusual 40-amino acid hydrophobic region near the C terminus that may be used to anchor the protein to the membrane. When chicken caveolin was expressed in mouse 3T3 cells and detected by immunofluorescence microscopy, the typical caveolae pattern was observed. This includes brightly fluorescent membrane patches in many cases concentrated at the margin of cells and in arrays. Caveolae may be distinct from other membrane domains due at least in part to caveolin. JF - Proceedings of the National Academy of Sciences, USA AU - Glenney, JR Jr AU - Soppet, D AD - Lab. Mammalian Genet., NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 10517 EP - 10521 VL - 89 IS - 21 SN - 0027-8424, 0027-8424 KW - Rous sarcoma virus KW - amino acid sequence KW - cDNA KW - caveolin KW - chickens KW - expression KW - genes KW - nucleotide sequence KW - phosphorylation KW - predictions KW - transformation KW - tyrosine KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 1: Biological Membranes (till 1993); Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - N 14640:Structure & sequence KW - G 07380:GENERAL UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16346094?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=Sequence+and+expression+of+caveolin%2C+a+protein+component+of+caveolae+plasma+membrane+domains+phosphorylated+on+tyrosine+in+Rous+sarcoma+virus-transformed+fibroblasts.&rft.au=Glenney%2C+JR+Jr%3BSoppet%2C+D&rft.aulast=Glenney&rft.aufirst=JR&rft.date=1992-01-01&rft.volume=89&rft.issue=21&rft.spage=10517&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - expression; nucleotide sequence; cDNA; amino acid sequence; genes; phosphorylation; transformation ER - TY - JOUR T1 - Nonreplicating vaccinia vector efficiently expresses recombinant genes. AN - 16343834; 2848864 AB - We constructed an insertion plasmid with the Escherichia coli lacZ gene under the control of the vaccinia virus late promoter P11, flanked by sequences of MVA DNA, to allow homologous recombination at the site of naturally occurring 3500-based-pair deletion within the MVA genome. MVA recombinants were isolated and propagated in permissive avian cells and shown to express the enzyme beta -galactosidase upon infection of nonpermissive human cells. The amount of enzyme made was similar to that produced by a recombinant of vaccinia strain Western Reserve, which also had the lacZ gene under control of the P11 promoter, but multiplied to high titers. Since recombinant gene expression is unimpaired in nonpermissive human cells, MVA may serve as a highly efficient and exceptionally safe vector. JF - Proceedings of the National Academy of Sciences, USA AU - Sutter, G AU - Moss, B AD - Lab. Viral Dis., NIAID/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 10847 EP - 10851 VL - 89 IS - 22 SN - 0027-8424, 0027-8424 KW - Escherichia coli KW - cells KW - gene expression KW - genes KW - lacZ gene KW - man KW - recombinants KW - vaccinia virus KW - vectors KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Human Genome Abstracts; Genetics Abstracts; Virology & AIDS Abstracts KW - V 22050:Viral genetics including virus reactivation KW - G 07313:Viruses KW - W 30965:Miscellaneous, Reviews KW - W3 33180:Gene based (protocols, clinical trials, and animal models) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16343834?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=Nonreplicating+vaccinia+vector+efficiently+expresses+recombinant+genes.&rft.au=Sutter%2C+G%3BMoss%2C+B&rft.aulast=Sutter&rft.aufirst=G&rft.date=1992-01-01&rft.volume=89&rft.issue=22&rft.spage=10847&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - vectors; cells; recombinants; genes; gene expression; man; vaccinia virus; Escherichia coli ER - TY - JOUR T1 - In vivo gene transfer with retroviral vector-producer cells for treatment of experimental brain tumors. AN - 16342971; 2840454 AB - Direct in situ introduction of exogenous genes into proliferating tumors could provide an effective therapeutic approach for treatment of localized tumors. Rats with a cerebral glioma were given an intratumoral stereotaxic injection of murine fibroblasts that were producing a retroviral vector in which the herpes simplex thymidine kinase (HS-tk) gene had been inserted. After 5 days during which the HS-tk retroviral vectors that were produced in situ transduced the neighboring proliferating glioma cells, the rats were treated with the anti-herpes drug ganciclovir. Gliomas in the ganciclovir- and vector-treated rats regressed completely both macroscopically and microscopically. JF - Science (Washington) AU - Culver, K W AU - Ram, Z AU - Wallbridge, S AU - Ishii, H AU - Oldfield, E H AU - Blaese, R M AD - Cell. Immunol. Sect., Metab. Branch, NCI/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1550 EP - 1552 VL - 256 IS - 5063 SN - 0036-8075, 0036-8075 KW - fibroblasts KW - ganciclovir KW - gene expression KW - gene therapy KW - gene transfer KW - genes KW - glioma KW - herpes simplex virus KW - mice KW - regression KW - retrovirus KW - thymidine kinase KW - trans KW - treatment KW - vectors KW - Biotechnology and Bioengineering Abstracts; CSA Neurosciences Abstracts; Human Genome Abstracts; Genetics Abstracts; Medical and Pharmaceutical Biotechnology Abstracts KW - G 07480:Hematological disorders KW - W 30965:Miscellaneous, Reviews KW - N3 11124:Mammalian neuropathology (except primates) KW - W3 33180:Gene based (protocols, clinical trials, and animal models) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16342971?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28Washington%29&rft.atitle=In+vivo+gene+transfer+with+retroviral+vector-producer+cells+for+treatment+of+experimental+brain+tumors.&rft.au=Culver%2C+K+W%3BRam%2C+Z%3BWallbridge%2C+S%3BIshii%2C+H%3BOldfield%2C+E+H%3BBlaese%2C+R+M&rft.aulast=Culver&rft.aufirst=K&rft.date=1992-01-01&rft.volume=256&rft.issue=5063&rft.spage=1550&rft.isbn=&rft.btitle=&rft.title=Science+%28Washington%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - vectors; glioma; gene transfer; retrovirus; treatment; genes; fibroblasts; regression; gene expression; herpes simplex virus ER - TY - JOUR T1 - Research needs and opportunities related to respiratory health of women. AN - 16339524; 2851522 AB - To examine what is known about the respiratory biology and lung health and disease of women, the National Heart, Lung, and Blood Institute (NHLBI), the American Thoracic Society, and the American College of Chest Physicians sponsored a 2-day meeting on January 30 and 31, 1992, in Bethesda, Maryland. The topics included smoking-induced lung diseases; asthma; sarcoidosis and interstitial pulmonary fibrosis; cystic fibrosis; pulmonary thromboembolism; pulmonary infections; respiratory disorders of sleep; primary pulmonary hypertension; lung growth, development, and aging; critical care and adult respiratory distress syndrome; and occupational and environmental lung diseases. This summary of the workshop represents a broad assessment of the available information on each disease category. JF - American Journal of Respiratory and Critical Care Medicine AU - Bone, C R AU - Higgins, M W AU - Hurd, S S AU - Reynolds, HY AD - DLD, NHLBI, Westwood Build., Rm. 6A-15, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 528 EP - 535 VL - 146 IS - 2 SN - 0003-0805, 0003-0805 KW - biology KW - research and development KW - cystic fibrosis KW - Health & Safety Science Abstracts KW - lung KW - smoking KW - asthma KW - females KW - respiratory diseases KW - H SM10.24:PULMONARY DISEASES UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16339524?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Respiratory+and+Critical+Care+Medicine&rft.atitle=Research+needs+and+opportunities+related+to+respiratory+health+of+women.&rft.au=Bone%2C+C+R%3BHiggins%2C+M+W%3BHurd%2C+S+S%3BReynolds%2C+HY&rft.aulast=Bone&rft.aufirst=C&rft.date=1992-01-01&rft.volume=146&rft.issue=2&rft.spage=528&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Respiratory+and+Critical+Care+Medicine&rft.issn=00030805&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - respiratory diseases; lung; smoking; asthma; females ER - TY - JOUR T1 - The immunotherapy and gene therapy of cancer. AN - 16337113; 2838061 AB - In the last decade biologic therapy has emerged as a mode of treatment capable of mediating the regression of cancer in some patients. Biologic therapy differs conceptually from surgery, radiation therapy, or chemotherapy because it acts, not by directly attacking the tumor, but by stimulating natural host defense mechanisms to mediate cancer regression. The predominant natural host defense mechanism is the immune system. Studies with IL-2 attempting to isolate lymphocytes with the specific ability to recognize cancer but not normal cells led us to the description of lymphokine-activated killer (LAK) cells in 1980. A review is presented. JF - Journal of Clinical Oncology AU - Rosenberg, SA AD - Chief Surg., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 180 EP - 199 VL - 10 IS - 2 SN - 0732-183X, 0732-183X KW - lymphokine-activated KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Immunology Abstracts KW - gene therapy KW - reviews KW - cancer patients KW - killer cells KW - immunotherapy KW - cancer KW - man KW - F 06818:Cancer immunotherapy KW - W 30965:Miscellaneous, Reviews KW - W3 33180:Gene based (protocols, clinical trials, and animal models) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16337113?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Oncology&rft.atitle=The+immunotherapy+and+gene+therapy+of+cancer.&rft.au=Rosenberg%2C+SA&rft.aulast=Rosenberg&rft.aufirst=SA&rft.date=1992-01-01&rft.volume=10&rft.issue=2&rft.spage=180&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Oncology&rft.issn=0732183X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - gene therapy; reviews; cancer patients; killer cells; immunotherapy; man; cancer ER - TY - JOUR T1 - DnaJ, DnaK, and GrpE heat shock proteins are required in oriP1 DNA replication solely at the RepA monomerization step. AN - 16336545; 2845454 AB - We have found that three Escherichia coli heat shock proteins, DnaK (the hsp70 homolog), DnaJ, and GrpE, function in oriP1 DNA replication in vitro solely to activate DNA binding by the replication initiator protein RepA. Activation results from the conversion of P1 or P7 RepA dimers to monomers that bind with high affinity to the origin of replication of plasmid P1. Thus, the essential role of these three heat shock proteins in this replication system is to change the quaternary structure of a single protein, RepA. JF - Proceedings of the National Academy of Sciences, USA AU - Wickner, S AU - Skowyra, D AU - Hoskins, J AU - McKenney, K AD - Lab. Mol. Biol., NCI, NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 10345 EP - 10349 VL - 89 IS - 21 SN - 0027-8424, 0027-8424 KW - monomerization KW - DnaJ protein KW - DnaK protein KW - GrpE protein KW - replication origins KW - RepA protein KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - heat shock KW - DNA KW - Escherichia coli KW - role KW - J 02725:DNA KW - N 14930:Transcription factors KW - J 02727:Amino acids, peptides and proteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16336545?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=DnaJ%2C+DnaK%2C+and+GrpE+heat+shock+proteins+are+required+in+oriP1+DNA+replication+solely+at+the+RepA+monomerization+step.&rft.au=Wickner%2C+S%3BSkowyra%2C+D%3BHoskins%2C+J%3BMcKenney%2C+K&rft.aulast=Wickner&rft.aufirst=S&rft.date=1992-01-01&rft.volume=89&rft.issue=21&rft.spage=10345&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; heat shock; role; DNA ER - TY - JOUR T1 - The calanolides, a novel HIV-inhibitory class of coumarin derivatives from the tropical rainforest tree, Calophyllum lanigerum . AN - 16333892; 2842485 AB - Eight new coumarin compounds (1-8) were isolated by anti-HIV bioassay-guided fractionation of an extract of Calophyllum lanigerum . The structure of calanolide A (1), 12-acetoxycalanolide A (2), 12-methoxycalanolide A (3), calanolide B (4), 12-methoxycalanolide B (5), calanolide C (6) and related derivative 7 and 8 were solved by extensive spectroscopic analyses, particularly HMQC, HMBC and difference NOE NMR experiments. The absolute stereochemistry of calanolide A (1) and calanolide B (4) was established by a modified Mosher's method. Calanolides A (1) and B (4) were completely protective against HIV-1 replication and cytopathicity (EC sub(50) values of 0.1 mu M and 0.4 mu M, respectively), but were inactive against HIV-2. Some of the related compounds also showed evidence of anti-HIV-1 activity. Studies with purified bacterial recombinant reverse transcriptases (RT) revealed that the calanolides are HIV-1 specific RT inhibitors. The calanolides represent a substantial departure from the known class and therefore provide a novel new anti-HIV chemotype for drug development. JF - Journal of Medicinal Chemistry AU - Kashman, Y AU - Gustafson, K R AU - Fuller, R W AU - Cardellina, JH II AU - McMahon, J B AU - Currens, MJ AU - Buckheit, RW Jr AU - Hughes, SH AU - Cragg, G M AU - Boyd, M R AD - Lab. Drug Discovery Res. and Dev., NCI-FCRDC, Build. 1052, Room 121, Frederick, MD 21702-1201, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 2735 EP - 2743 VL - 35 IS - 15 SN - 0022-2623, 0022-2623 KW - calanolides KW - calophyllum lanigerum KW - coumarin KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Virology & AIDS Abstracts KW - human immunodeficiency virus 1 KW - analogs KW - inhibitors KW - reverse transcription KW - W 30965:Miscellaneous, Reviews KW - W3 33390:Products: Others KW - V 22004:AIDS: Clinical aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16333892?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Medicinal+Chemistry&rft.atitle=The+calanolides%2C+a+novel+HIV-inhibitory+class+of+coumarin+derivatives+from+the+tropical+rainforest+tree%2C+Calophyllum+lanigerum+.&rft.au=Kashman%2C+Y%3BGustafson%2C+K+R%3BFuller%2C+R+W%3BCardellina%2C+JH+II%3BMcMahon%2C+J+B%3BCurrens%2C+MJ%3BBuckheit%2C+RW+Jr%3BHughes%2C+SH%3BCragg%2C+G+M%3BBoyd%2C+M+R&rft.aulast=Kashman&rft.aufirst=Y&rft.date=1992-01-01&rft.volume=35&rft.issue=15&rft.spage=2735&rft.isbn=&rft.btitle=&rft.title=Journal+of+Medicinal+Chemistry&rft.issn=00222623&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - analogs; inhibitors; reverse transcription; human immunodeficiency virus 1 ER - TY - JOUR T1 - Allosteric changes in the cAMP receptor protein of Escherichia coli : Hinge reorientation. AN - 16331521; 2845839 AB - The cAMP receptor protein (CRP) of Escherichia coli is a dimer of a two-domain subunit. It requires binding of cAMP for a conformational change in order to function as a site-specific DNA-binding protein that regulates gene activity. The hinge region connecting the cAMP-binding domain to the DNA-binding domain is involved in the cAMP-induced allosteric change. We studied the structural changes in CRP that are required for gene regulation by making a large number of single and double amino acid substitutions at four different positions in or near the hinge. To achieve cAMP-independent transcription by CRP, amino acid residues 138 (located within the hinge region) and 141 (located in the D alpha -helix adjacent to the hinge) must be polar. This need for polar residues at positions 138 and 141 suggests an interaction that causes the C and D alpha -helices to come together. As a consequence, the F alpha -helix is released from the D alpha -helix and can interact with DNA. At position 144 in the D alpha -helix and within interacting distances of the F alpha -helix, replacement of alanine by an amino acid with a larger side chain, regardless of its nature, allows cAMP independence. JF - Proceedings of the National Academy of Sciences, USA AU - Kim, Jin AU - Adhya, S AU - Garges, S AD - Lab. Mol. Biol., NCI, NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 9700 EP - 9704 VL - 89 IS - 20 SN - 0027-8424, 0027-8424 KW - CRP protein KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - allosteric properties KW - gene regulation KW - Escherichia coli KW - conformation KW - N 14930:Transcription factors KW - J 02727:Amino acids, peptides and proteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16331521?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=Allosteric+changes+in+the+cAMP+receptor+protein+of+Escherichia+coli+%3A+Hinge+reorientation.&rft.au=Kim%2C+Jin%3BAdhya%2C+S%3BGarges%2C+S&rft.aulast=Kim&rft.aufirst=Jin&rft.date=1992-01-01&rft.volume=89&rft.issue=20&rft.spage=9700&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; allosteric properties; conformation; gene regulation ER - TY - JOUR T1 - Structural requirements for blockade of HIV infection, blockade of HIV-induced syncytium formation, and virostatic activity in vitro. AN - 16331361; 2843235 AB - CD4(81-92) peptides block human immunodeficiency virus (HIV) infection, virus-induced cell fusion, and antigen production by HIV-1-infected cells when derivatized on specific amino acid residues. An extensive series of structural variants of 1,4,5-tribenzyl-10-acetyl-CD4(81-92) were tested as anti-viral agents in an attempt to define the sequence and derivatization requirements for antiviral activity, and to maximize potency and stability for use as potential therapeutic agents. Alteration of the primary amino acid sequence of the stem compound 1,4,5-tribenzyl-CD4(81-92) diminished or abolished in parallel all three indices of anti-viral activity in a series of altered sequence compounds. Cyclization of the tribenzyl peptide to further conformationally restrict the molecule in a compound with anti-infection, anti-syncytial, and virostatic activity at submicromolar concentrations. JF - Biochemical Pharmacology AU - Rausch, D M AU - Lifson, J D AU - Padgett, M P AU - Chandresekhar, B AU - Lendvay, J AU - Hwang, K M AU - Eiden, LE AD - Lab. Cell Biol., NIMH/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1785 EP - 1796 VL - 43 IS - 8 SN - 0006-2952, 0006-2952 KW - amino acid sequence KW - antiviral agents KW - human immunodeficiency virus KW - infection KW - peptide synthesis KW - syncytia KW - treatment KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts KW - V 22004:AIDS: Clinical aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16331361?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+Pharmacology&rft.atitle=Structural+requirements+for+blockade+of+HIV+infection%2C+blockade+of+HIV-induced+syncytium+formation%2C+and+virostatic+activity+in+vitro.&rft.au=Rausch%2C+D+M%3BLifson%2C+J+D%3BPadgett%2C+M+P%3BChandresekhar%2C+B%3BLendvay%2C+J%3BHwang%2C+K+M%3BEiden%2C+LE&rft.aulast=Rausch&rft.aufirst=D&rft.date=1992-01-01&rft.volume=43&rft.issue=8&rft.spage=1785&rft.isbn=&rft.btitle=&rft.title=Biochemical+Pharmacology&rft.issn=00062952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - peptide synthesis; antiviral agents; treatment; amino acid sequence; infection; syncytia ER - TY - JOUR T1 - Modification of chromaffin cells with pertussis toxin or N-ethylmaleimide lowers cytoskeletal F-actin and enhances Ca super(2+)-dependent secretion. AN - 16329127; 2841954 AB - In an attempt to identify proteins involved in the secretory response, bovine chromaffin cells were modified with N-ethylmaleimide (NEM). NEM enhanced norepinephrine secretion evoked by nicotine or by K super(+) depolarization and increased Ca super(2+)-dependent secretion from digitonin-permeabilized cells. Higher concentrations of NEM inhibited secretion. The protein modified by NEM which was responsible for the enhancement of secretory activity appeared to rapidly diffuse out of the digitonin-permeabilized cells. JF - Journal of Biological Chemistry AU - Wu, You Neng AU - Yang, Yun Chung AU - Wagner, P D AD - Build. 37, Rm. 4C24, NCI/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 8396 EP - 8403 VL - 267 IS - 12 SN - 0021-9258, 0021-9258 KW - actin KW - cattle KW - chromaffin cells KW - effects on KW - guanine nucleotide-binding protein KW - norepinephrine KW - secretion KW - structure KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16329127?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Modification+of+chromaffin+cells+with+pertussis+toxin+or+N-ethylmaleimide+lowers+cytoskeletal+F-actin+and+enhances+Ca+super%282%2B%29-dependent+secretion.&rft.au=Wu%2C+You+Neng%3BYang%2C+Yun+Chung%3BWagner%2C+P+D&rft.aulast=Wu&rft.aufirst=You&rft.date=1992-01-01&rft.volume=267&rft.issue=12&rft.spage=8396&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - The carcinogenic effect of methapyrilene combined with nitrosodiethylamine given to rats in low doses. AN - 16327744; 2826467 AB - The carcinogenic effects of combinations of methapyrilene hydrochloride (MP), nitrosodiethylamine (NDEA), and phenobarbital (PB) or partial hepatectomy (PH) were examined following sequential treatment of rats. MP is a generally non-genotoxic liver carcinogen of moderate potency, NDEA is a genotoxic liver carcinogen, PB is primarily a liver tumor promoter and PH induces cell proliferation. The dose of each carcinogen was chosen to be below that causing significant liver tumor incidence when given singly. There were 12 protocols involving groups of 28 female rats each. Short treatments with NDEA and MP were followed by 60 weeks of PB promotion or by partial hepatectomy. Each treatment was given separately or in double combination as controls. Several animals of each group were killed at intervals during the experiment for examination of toxic effects and the presence of altered hepatic foci. In only 3 of 12 groups was there a significant incidence of rats with liver neoplasms: the two groups given three treatments: NDEA, MP and PB (86% tumors) or NDEA, MP and PH (33%), and the group receiving NDEA and MP without promotion (46%). JF - Carcinogenesis AU - Lijinsky, W AU - Kovatch, R M AU - Thomas, B J AD - ABL-Basic Res. Program, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1293 EP - 1297 VL - 13 IS - 7 SN - 0143-3334, 0143-3334 KW - methapyrilene KW - N-nitrosodiethylamine KW - rats KW - Toxicology Abstracts KW - carcinogenicity KW - X 24200:Nitrosamines & related compounds UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16327744?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=The+carcinogenic+effect+of+methapyrilene+combined+with+nitrosodiethylamine+given+to+rats+in+low+doses.&rft.au=Lijinsky%2C+W%3BKovatch%2C+R+M%3BThomas%2C+B+J&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1992-01-01&rft.volume=13&rft.issue=7&rft.spage=1293&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - carcinogenicity ER - TY - JOUR T1 - Human immunodeficiency virus type 1 gag-protease fusion proteins are enzymatically active. AN - 16327304; 2842916 AB - We have introduced mutations into the region of the genome of human immunodeficiency virus type 1 (HIV-1) that encodes the cleavage sites between the viral protease (PR) and the adjacent upstream region of the polyprotein precursor. Segments containing these mutations were introduced into plasmids, and the retroviral proteins were expressed in Escherichia coli . The mutations prevented cleavage between the PR and the adjacent polypeptide; however, other PR cleavage sites in the polyprotein were cleaved normally, showing that the release of free PR is not a prerequisite for the appropriate processing of HIV-1 precursors. JF - Journal of Virology AU - Kotler, M AU - Arad, G AU - Hughes, SH AD - NCI-Frederick Cancer Res. and Dev. Cent., P.O. Box B, Frederick, MD 21702-1201, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 6781 EP - 6783 VL - 66 IS - 11 SN - 0022-538X, 0022-538X KW - cleavage KW - enzymatic activity KW - fusion proteins KW - human immunodeficiency virus 1 KW - nucleotide sequence KW - plasmids KW - site-directed mutagenesis KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts KW - V 22002:AIDS: Molecular and in vitro aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16327304?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=Human+immunodeficiency+virus+type+1+gag-protease+fusion+proteins+are+enzymatically+active.&rft.au=Kotler%2C+M%3BArad%2C+G%3BHughes%2C+SH&rft.aulast=Kotler&rft.aufirst=M&rft.date=1992-01-01&rft.volume=66&rft.issue=11&rft.spage=6781&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - nucleotide sequence; site-directed mutagenesis; enzymatic activity; plasmids; cleavage ER - TY - JOUR T1 - Transplacental carcinogenic effects of nickel(II) acetate in the renal cortex, renal pelvis and adenohypophysis in F344/NCr rats. AN - 16325666; 2839357 AB - Nickel(II) acetate (NiAcet), a soluble nicked salt known to be an effective initiator of renal epithelial tumors in adult rats, was studied for possible transplacental carcinogenicity. Pregnant F344/NCr rats were given NiAcet i.p. either once a day on day 17 (90 mu mol/kg body wt; group 1) or twice on days 16 and 18 of gestation (45 mu mol/kg body wt/day; group 2). Offspring of these rats were further subdivided into groups 1A and B and 2A and B, respectively. Groups 1A and 2A received ordinary tap water while groups 1B and 2B received drinking water containing 500 p.p.m. sodium barbital (NaBB) during weeks 4-85 of age. Renal cortical epithelial and renal pelvic transitional epithelial tumors occurred in male offspring given NiAcet prenatally followed by NaBB postnatally (group 1B, 15 tumors in 8/15 rats; group 2B, 10 tumors in 7/15), but not in male offspring given NiAcet only (0/32) or in controls given prenatal sodium acetate (NaAcet) only (0/15) and rarely in males given NaAcet followed by the promoter NaBB (1/15). No renal tumors occurred in females. JF - Carcinogenesis AU - Diwan, BA AU - Kasprzak, K S AU - Rice, J M AD - Biol. Carcinog. and Dev. Program, PRI/DynCorp, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1351 EP - 1357 VL - 13 IS - 8 SN - 0143-3334, 0143-3334 KW - nickel acetate KW - rats KW - heavy metals KW - Toxicology Abstracts KW - pituitary (anterior) KW - kidney KW - transplacental carcinogenesis KW - X 24162:Chronic exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16325666?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Transplacental+carcinogenic+effects+of+nickel%28II%29+acetate+in+the+renal+cortex%2C+renal+pelvis+and+adenohypophysis+in+F344%2FNCr+rats.&rft.au=Diwan%2C+BA%3BKasprzak%2C+K+S%3BRice%2C+J+M&rft.aulast=Diwan&rft.aufirst=BA&rft.date=1992-01-01&rft.volume=13&rft.issue=8&rft.spage=1351&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - transplacental carcinogenesis; kidney; pituitary (anterior) ER - TY - JOUR T1 - Regulation of recombinant rat tyrosine hydroxylase by dopamine. AN - 16324710; 2841448 AB - Recombinant rat PC12 tyrosine hydroxylase, also called tyrosine 3-monooxygenase (L-tyrosine, tetrahydropteridine:oxygen oxidoreductase (3-hydroxylating), EC 1.14.16.2), purified from Escherichia coli is in an activated form with a low K sub(m) for the tetrahydrobiopterin cofactor and a pH optimum of 6.5. Pretreatment with low levels of the derived product, dopamine, inhibits catalytic activity, increases the K sub(m) for the cofactor, and shifts the pH curve towards a more acidic pH optimum. Labeled dopamine binds to tyrosine hydroxylase with high affinity (K sub(d) = 1 mu M) but low stoichiometry (r = 0.08 mol/mol of enzyme subunit). The binding of dopamine results in the appearance of a blue-green chromophore with lambda sub(max) at approximately equals 660 nm, which is consistent with the formation of a catecholamine-iron complex. In the absence of dopamine, the recombinant enzyme cannot be further activated by phosphorylation with cAMP-dependent protein kinase, although as much as 1 mol of phosphate is incorporated per mol of subunit. In contrast, the enzyme pretreated with dopamine is activated by phosphorylation in the same fashion and to the same extent as the native hydroxylase. JF - Proceedings of the National Academy of Sciences, USA AU - Ribeiro, P AU - Wang, Yuehua AU - Citron, BA AU - Kaufman, S AD - Lab. Neurochem., NIMH/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 9593 EP - 9597 VL - 89 IS - 20 SN - 0027-8424, 0027-8424 KW - dopamine KW - enzymatic activity KW - kinetics KW - rats KW - recombinants KW - regulation KW - tyrosine 3-monooxygenase KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16324710?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Electrophoresis&rft.atitle=Quantitative+two-dimensional+gel+electrophoresis+analysis+of+human+fibroblasts+transformed+by+ras+oncogenes.&rft.au=Miller%2C+M+J%3BMaher%2C+V+M%3BMcCormick%2C+J+J&rft.aulast=Miller&rft.aufirst=M&rft.date=1992-11-01&rft.volume=13&rft.issue=11&rft.spage=862&rft.isbn=&rft.btitle=&rft.title=Electrophoresis&rft.issn=01730835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Escherichia coli mutant SELD enzyme: The cysteine 17 residue is essential for selenophosphate formation from ATP and selenide. AN - 16322868; 2832059 AB - Synthesis of a labile selenium donor compound, selenophosphate, from selenide and ATP by the Escherichia coli SELD enzyme was reported previously from this laboratory. From the gene sequence, SELD is a 37-kDa protein that contains 7 cysteine residues, 2 of which are located at positions 17 and 19 in the sequence -Gly-Ala-Cys-Gly-Cys-Lys-Ile. Inactivation of the enzyme by alkylation with iodoacetamide indicated that at least 1 cysteine residue in the protein is essential for enzyme activity. To test the possibility that the Cys super(17) and/or Cys super(19) residue might be essential, these were changed to serine residues by site-specific mutagenesis. The results indicate that Cys super(17) has an essential role in the catalytic process that leads to the formation of selenophosphate from ATP and selenide. JF - Journal of Biological Chemistry AU - Kim, Ick Young AU - Veres, Z AU - Stadtman, T C AD - Lab. Biochem., NHLBI, NIH, Build. 3, Rm. 108, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 19650 EP - 19654 VL - 267 IS - 27 SN - 0021-9258, 0021-9258 KW - ATP KW - Escherichia coli KW - SELD protein KW - cysteine KW - enzymatic activity KW - formation KW - role KW - selenide KW - selenophosphate KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology KW - J 02728:Enzymes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16322868?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Escherichia+coli+mutant+SELD+enzyme%3A+The+cysteine+17+residue+is+essential+for+selenophosphate+formation+from+ATP+and+selenide.&rft.au=Kim%2C+Ick+Young%3BVeres%2C+Z%3BStadtman%2C+T+C&rft.aulast=Kim&rft.aufirst=Ick&rft.date=1992-01-01&rft.volume=267&rft.issue=27&rft.spage=19650&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - role; enzymatic activity; formation ER - TY - JOUR T1 - Crystal structure of a complex of HIV-1 protease with a dihydroxyethylene-containing inhibitor: Comparisons with molecular modeling. AN - 16320040; 2831005 AB - The structure of a crystal complex of recombinant human immunodeficiency virus type I (HIV-1) protease with a peptide-mimetic inhibitor containing a dihydroxyethylene isostere insert replacing the scissile bond has been determined. JF - Protein Science AU - Thanki, N AU - Rao, JKM AU - Foundling, SI AU - Howe, W J AU - Moon, J B AU - Hui, JO AU - Tomasselli, A G AU - Heinrikson, R L AU - Thaisrivongs, S AU - Wlodawer, A AD - Macromol. Struct. Lab., NCI-Frederick Cancer Res. and Dev. Cent., ABL-Basic Res. Program, Frederick, MD 21702, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1061 EP - 1072 VL - 1 IS - 8 SN - 0961-8368, 0961-8368 KW - complex KW - containing KW - crystal structure KW - dihydroxyethylene KW - human immunodeficiency virus 1 KW - inhibitors KW - peptidomimetic KW - proteinase KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts KW - V 22002:AIDS: Molecular and in vitro aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16320040?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Protein+Science&rft.atitle=Crystal+structure+of+a+complex+of+HIV-1+protease+with+a+dihydroxyethylene-containing+inhibitor%3A+Comparisons+with+molecular+modeling.&rft.au=Thanki%2C+N%3BRao%2C+JKM%3BFoundling%2C+SI%3BHowe%2C+W+J%3BMoon%2C+J+B%3BHui%2C+JO%3BTomasselli%2C+A+G%3BHeinrikson%2C+R+L%3BThaisrivongs%2C+S%3BWlodawer%2C+A&rft.aulast=Thanki&rft.aufirst=N&rft.date=1992-01-01&rft.volume=1&rft.issue=8&rft.spage=1061&rft.isbn=&rft.btitle=&rft.title=Protein+Science&rft.issn=09618368&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - complex; inhibitors; containing; crystal structure ER - TY - JOUR T1 - Construction and characterization of chimeric tick-borne encephalitis/dengue type 4 viruses. AN - 16318989; 2835614 AB - Dengue type 4 virus (DEN4) cDNA was used as a vector to express genes of the distantly related tick-borne encephalitis virus (TBEV). Full-length chimeric TBEV/DEN4 cDNAs were constructed by substituting TBEV genes coding for proteins such as capsid (C); pre-membrane, which is the precursor of membrane (M); envelope (E); or nonstructural protein NS1 for the corresponding DEN4 sequences. RNA transcripts prepared from cDNAs were used to transfect permissive simian cells. Two viable chimeric viruses that contained TBEV CME or ME genes were recovered. The findings indicate that (i) the TBEV M and E genes of the chimeric virus are major protective antigens and induce resistance to lethal TBEV challenge and (ii) other regions of the TBEV genome are essential for the ability of this virus to spread from a peripheral site to the brain. Success in constructing a viable TBEV/DEN4 chimera that retains the protective antigens of TBEV but lacks its peripheral invasiveness provides a strategy for the development of live attenuated TBEV vaccines. JF - Proceedings of the National Academy of Sciences, USA AU - Pletnev, A G AU - Bray, M AU - Huggins, J AU - Lai, Ching-Juh AD - Mol. Viral Biol. Sect., Lab. Infect. Dis., NIAID/NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 10532 EP - 10536 VL - 89 IS - 21 SN - 0027-8424, 0027-8424 KW - mice KW - pre-membrane protein KW - Biotechnology and Bioengineering Abstracts; Immunology Abstracts; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Virology & AIDS Abstracts; Medical and Pharmaceutical Biotechnology Abstracts KW - envelopes KW - chimeras KW - genes KW - immunogenicity KW - expression vectors KW - capsid protein KW - tick-borne encephalitis virus KW - encephalitis KW - virulence KW - gene expression KW - dengue virus 4 KW - proteins KW - antigens KW - V 22099:Immune response & immune mechanisms KW - V 22050:Viral genetics including virus reactivation KW - G 07313:Viruses KW - G 07120:Recombinant DNA/Genetic engineering KW - V 22150:Animal models & experimentally-induced viral infections KW - N 14684:Expression of cloned genes KW - W 30965:Miscellaneous, Reviews KW - F 06800:Viruses KW - W3 33055:Genetic engineering (general) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16318989?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=Construction+and+characterization+of+chimeric+tick-borne+encephalitis%2Fdengue+type+4+viruses.&rft.au=Pletnev%2C+A+G%3BBray%2C+M%3BHuggins%2C+J%3BLai%2C+Ching-Juh&rft.aulast=Pletnev&rft.aufirst=A&rft.date=1992-01-01&rft.volume=89&rft.issue=21&rft.spage=10532&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - capsid protein; envelopes; chimeras; genes; immunogenicity; encephalitis; virulence; gene expression; expression vectors; proteins; antigens; tick-borne encephalitis virus; dengue virus 4 ER - TY - JOUR T1 - Systemic and local carcinogenesis by directly acting N-nitroso compounds given to rats by intravesicular administration. AN - 16313837; 2826623 AB - A number of directly acting carcinogenic N-nitroso compounds were administered to female F344 rats intravesically, to assess their ability to induce tumors locally in the urinary bladder and systemically following absorption through the bladder mucosa. The compounds were alkylnitrosoureas and alkylnitrosocarbamates and could be formed by interaction of amides with bacterially produced nitrite in infected bladders. Methylnitrosourethane was very toxic: doses of 1-2 mg caused death of some rats. A total dose of 0.15 mmol of ethylnitrosourethane, which was much less toxic, was administered to each rat and almost all developed bladder tumors. Ethylnitrosourea also gave rise to bladder tumors following intravesical treatment, and induced some tumors systemically, whereas methylnitrosourea, 2-methoxyethylnitrosourea and 2-hydroxypropylnitrosourea induced bladder tumors in high incidence and few tumors systemically. Nitrosooxazolidone was quite toxic and induced few bladder tumors. JF - Carcinogenesis AU - Lijinsky, W AU - Thomas, B J AU - Kovatch, R M AD - ABL-Basic Res. Program, NCI-Frederick Cancer Res. and Dev., Frederick, MD 21702, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1101 EP - 1105 VL - 13 IS - 7 SN - 0143-3334, 0143-3334 KW - N-nitroso compounds KW - intravesicular administration KW - rats KW - Toxicology Abstracts KW - carcinogenesis KW - X 24200:Nitrosamines & related compounds UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16313837?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Systemic+and+local+carcinogenesis+by+directly+acting+N-nitroso+compounds+given+to+rats+by+intravesicular+administration.&rft.au=Lijinsky%2C+W%3BThomas%2C+B+J%3BKovatch%2C+R+M&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1992-01-01&rft.volume=13&rft.issue=7&rft.spage=1101&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - carcinogenesis ER - TY - JOUR T1 - CD4 and its role in infection of rabbit cell lines by human immunodeficiency virus type 1. AN - 16313621; 2833437 AB - Human CD4 (HuCD4) is the principal receptor for human immunodeficiency virus type 1 (HIV-1) in human cell infection. Susceptibility of rabbit cell lines to infection with HIV-1 raised questions concerning whether a CD4 homolog serves as HIV-1 receptor on rabbit cells. Sequence comparisons of rabbit CD4 (RbCD4) cloned from a rabbit thymus cDNA library showed that 6 of the 18 residues implicated in HIV-1 binding by CD4 differ between the human and rabbit proteins. No correlation between RbCD4 expression by rabbit cell lines and their ability to support HIV-1 infection was seen. Transfection of RbCD4-negative, HTLV-I-transformed cell lines with HuCD4 significantly enhanced HIV-1 infectivity, suggesting that these lines lack a receptor present on other RbCD4-negative lines that produce high levels of p24 in their native state. The results suggest that HIV-1 infection of the RbCD4-positive line proceeds through a receptor similar to HuCD4 but that an additional receptor or receptors may serve this purpose in RbCD4-negative lines. JF - Proceedings of the National Academy of Sciences, USA AU - Hague, B F AU - Sawasdikosol, S AU - Brown, T J AU - Lee, K AU - Recker, D P AU - Kindt, T J AD - Lab. Immunogenet., NIAID, Twinbrook II Fac., NIH, 12441 Parklawn Dr., Rockville, MD 20852, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 7963 EP - 7967 VL - 89 IS - 17 SN - 0027-8424, 0027-8424 KW - CD4 antigen KW - amino acid sequence KW - cDNA KW - cell lines KW - genes KW - human immunodeficiency virus KW - infection KW - nucleotide sequence KW - prediction KW - rabbits KW - role KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Virology & AIDS Abstracts; Immunology Abstracts KW - N 14640:Structure & sequence KW - G 07240:Immunogenetics KW - G 07394:GENERAL KW - V 22003:AIDS: Immunological aspects KW - F 06800:Viruses UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16313621?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=CD4+and+its+role+in+infection+of+rabbit+cell+lines+by+human+immunodeficiency+virus+type+1.&rft.au=Hague%2C+B+F%3BSawasdikosol%2C+S%3BBrown%2C+T+J%3BLee%2C+K%3BRecker%2C+D+P%3BKindt%2C+T+J&rft.aulast=Hague&rft.aufirst=B&rft.date=1992-01-01&rft.volume=89&rft.issue=17&rft.spage=7963&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - nucleotide sequence; cDNA; amino acid sequence; genes; infection; prediction; role; cell lines ER - TY - JOUR T1 - Effect of chronic consumption of ethanol and vitamin E on fatty acid composition and lipid peroxidation in rat heart tissue. AN - 16312600; 2830948 AB - Lipid peroxidation products and the fatty acid composition of phospholipids were studied in the hearts of rats chronically consuming ethanol supplemented with large amounts of vitamin E. Ethanol representing 36% of the total calories was ingested for 7 weeks in a modified Lieber-DeCarli liquid diet that contained vitamin E at 30 IU/L in the control or 172/L in the supplemental dietary group. Ethanol and/or vitamin E did not change the absolute content (kg per mg of phospholipids) of the main fatty acids (C sub(18:0), C sub(18:2), and C sub(20:4)) of heart phospholipids but increased the amount of the minor C sub(20)-C sub(22) fatty acids. Cardiac phospholipid levels increased in rats chronically consuming excess vitamin E and/or alcohol. Chronic ethanol consumption caused elevations of the relative content (percent of total fatty acids) of tri-, tetra-, and hexaenoic acids and peroxidizability index (PI) of the cardiac phospholipids. Supplementation with vitamin E blocked this ethanol-induced shift in the fatty acid profile toward unsaturation and decreased the PI. Ethanol enhanced accumulation of vitamin E in heart by 30% irrespective of the vitamin E content in the diet. Enrichment of the diet with vitamin E coincided with the low levels of fluorescent products in heart lipids. JF - Alcohol AU - Pirozhkov, S V AU - Eskelson, C D AU - Watson, R R AU - Hunter, G C AU - Piotrowski, J J AU - Bernhard, V AD - Dep. Surg. Biol., NIAAA Specialized Alcohol Res. Cent., Univ. Arizona Health Sci. Cent., Tucson, AZ 85724, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 329 EP - 334 VL - 9 IS - 4 SN - 0741-8329, 0741-8329 KW - ethanol KW - vitamin E KW - rats KW - Toxicology Abstracts KW - fatty acid composition KW - heart KW - lipid peroxidation KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16312600?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcohol&rft.atitle=Effect+of+chronic+consumption+of+ethanol+and+vitamin+E+on+fatty+acid+composition+and+lipid+peroxidation+in+rat+heart+tissue.&rft.au=Pirozhkov%2C+S+V%3BEskelson%2C+C+D%3BWatson%2C+R+R%3BHunter%2C+G+C%3BPiotrowski%2C+J+J%3BBernhard%2C+V&rft.aulast=Pirozhkov&rft.aufirst=S&rft.date=1992-01-01&rft.volume=9&rft.issue=4&rft.spage=329&rft.isbn=&rft.btitle=&rft.title=Alcohol&rft.issn=07418329&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - heart; fatty acid composition; lipid peroxidation ER - TY - JOUR T1 - Human macrophages convert L-tryptophan into the neurotoxin quinolinic acid. AN - 16311041; 2824910 AB - Substantial increases in the concentrations of the excitotoxin and N-methyl-D-aspartate-receptor agonist quinolinic acid (QUIN) occur in human patients and non-human primates with inflammatory diseases. Such increases were postulated to be secondary to induction of indoleamine 2,3-dioxygenase in inflammatory cells, particularly macrophages, by interferon- gamma . To test this hypothesis, human peripheral-blood macrophages were incubated with L-( super(13)C sub(6))tryptophan in the absence or presence of interferon- gamma . ( super(13)C sub(6))QUIN was quantified by gas chromatography and electron-capture negative-chemical-ionization mass spectrometry. Macrophages stimulated with interferon- gamma may be an important source of accelerated L-tryptophan conversion into QUIN in inflammatory diseases. JF - Biochemical Journal AU - Heyes, M P AU - Saito, K AU - Markey, S P AD - Sect. on Anal. Biochem., Lab. Clin. Sci., NIMH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 633 EP - 635 VL - 283 IS - 3 SN - 0264-6021, 0264-6021 KW - conversion KW - macrophages KW - man KW - production KW - quinolinic acid KW - tryptophan KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - F 06760:Biochemistry KW - J:20320 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16311041?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+Journal&rft.atitle=Human+macrophages+convert+L-tryptophan+into+the+neurotoxin+quinolinic+acid.&rft.au=Heyes%2C+M+P%3BSaito%2C+K%3BMarkey%2C+S+P&rft.aulast=Heyes&rft.aufirst=M&rft.date=1992-01-01&rft.volume=283&rft.issue=3&rft.spage=633&rft.isbn=&rft.btitle=&rft.title=Biochemical+Journal&rft.issn=02646021&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - conversion; macrophages; production; man ER - TY - JOUR T1 - Methods for assessing rat sperm motility. AN - 16309566; 2826883 AB - Computer-assisted sperm analysis (CASA) systems are becoming more widely used. With this spread of technology come more data from toxicology studies, designed to determine if treatment with putative toxicants affects sperm motion parameters. While these CASA methods provide us with more ways to evaluate toxicity and thus perhaps increase our chances of successfully protecting human health, there is also a greater likelihood that different laboratories will use different methods of collecting data on sperm motility. Different systems used with different methods in different laboratories will inevitably generate data that are difficult to compare. In a prospective attempt to address this issue of comparability and limit the problems, a group of individuals using CASA systems to analyze rat sperm motility convened to discuss methodologic issues, share data, and try to reach consensus about methods for performing these studies. This article shares those meeting and data in the hope that common methods will enhance interlaboratory comparisons. JF - Reproductive Toxicology AU - Chapin, R E AU - Filler, R S AU - Gulati, D AU - Heindel, J J AU - Katz, D F AU - Mebus, CA AU - Obasaju, F AU - Perreault, S D AU - Russell AD - Toxicol./Program NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 267 EP - 273 VL - 6 IS - 3 SN - 0890-6238, 0890-6238 KW - assessment KW - Toxicology Abstracts KW - toxicity testing KW - spermatozoa KW - motility KW - computer applications KW - methodology KW - X 24221:Toxicity testing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16309566?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reproductive+Toxicology&rft.atitle=Methods+for+assessing+rat+sperm+motility.&rft.au=Chapin%2C+R+E%3BFiller%2C+R+S%3BGulati%2C+D%3BHeindel%2C+J+J%3BKatz%2C+D+F%3BMebus%2C+CA%3BObasaju%2C+F%3BPerreault%2C+S+D%3BRussell&rft.aulast=Chapin&rft.aufirst=R&rft.date=1992-01-01&rft.volume=6&rft.issue=3&rft.spage=267&rft.isbn=&rft.btitle=&rft.title=Reproductive+Toxicology&rft.issn=08906238&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - toxicity testing; spermatozoa; motility; methodology; computer applications ER - TY - JOUR T1 - Pima Indians as a model to study the genetics of NIDDM. AN - 16305106; 2813591 AB - More than half the Pima Indians over 35 years of age have non-insulin dependent diabetes mellitus (NIDDM). They have been the focus of prospective epidemiologic and metabolic studies for over two decades and the data collected during these studies are now proving invaluable in efforts to find genetic markers for NIDDM in humans. The Pima Indian model of this disease affords two major advantages. The population is genetically homogeneous compared to Caucasian populations, and therefore the causes of NIDDM are less heterogeneous, simplifying genetic linkage studies. Equally important, based on results from metabolic studies, two pre-diabetic phenotypes have been identified in the Pimas: insulin resistance and a low metabolic rate. Use of these phenotypes in genetic linkage analyses should greatly improve chances of finding genetic markers for NIDDM since these phenotypes may be more closely related to be putative abnormal gene products, and actual disease genes, than is the hyperglycemia of the fully developed phenotype of NIDDM. JF - Journal of Cellular Biochemistry AU - Bogardus, C AU - Lillioja, S AD - Clin. Diabetes and Nutr. Sect., NIDDK, Natl. Inst. Health, 4212 N. Sixteenth St., Rm. 541, Phoenix, AZ 85016, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 337 EP - 343 VL - 48 IS - 4 SN - 0730-2312, 0730-2312 KW - Pima Indian KW - diabetes mellitus KW - genetics KW - insulin KW - man KW - resistance KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Human Genome Abstracts; Genetics Abstracts KW - W 30965:Miscellaneous, Reviews KW - G 07500:Miscellaneous KW - W3 33180:Gene based (protocols, clinical trials, and animal models) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16305106?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Cellular+Biochemistry&rft.atitle=Pima+Indians+as+a+model+to+study+the+genetics+of+NIDDM.&rft.au=Bogardus%2C+C%3BLillioja%2C+S&rft.aulast=Bogardus&rft.aufirst=C&rft.date=1992-01-01&rft.volume=48&rft.issue=4&rft.spage=337&rft.isbn=&rft.btitle=&rft.title=Journal+of+Cellular+Biochemistry&rft.issn=07302312&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - genetics; diabetes mellitus; resistance; man ER - TY - JOUR T1 - Organization and management of a plan aimed to recovery groundwater tables polluted by chlorinated solvents. TT - Organizzazione e gestione di un piano di recupero della falda acquifera inquinata da solventi clorurati AN - 16295941; 2821429 AB - The Service for Public Health and Environment of Health Unit 60 (USSL 60) of Lombardy, in accomplishment to the Regional Act 62/85 concerning the protection of ground waters from pollutants, located in its own territory point water sources polluted by chlorinated solvents. Policies of decontamination and the recovery of those financial burdens backed by the Public Administration vs. singled out responsibles have been projected and managed by the Service. JF - Igiene Moderna AU - Bianchi, S AU - Mantovani, A AU - Ghezzi, A AU - Cavallaro, A AU - Baiardi, G AU - Rossetti, F AU - Franzosi, C AD - Serv. Ig. Pubblica e Ambient., Tutela della Salute nei Luoghi di Lavoro, USSL 60 Regione Lombardia, Via G. Battisti, 23-20059 Vimercate, Italy Y1 - 1992 PY - 1992 DA - 1992 SP - 441 EP - 448 VL - 97 IS - 3 SN - 0019-1655, 0019-1655 KW - groundwater KW - ASFA 3: Aquatic Pollution & Environmental Quality; Pollution Abstracts KW - chlorinated hydrocarbons KW - pollution monitoring KW - Freshwater KW - environmental protection KW - Italy KW - groundwater pollution KW - pollution surveys KW - pollution control KW - P 2000:FRESHWATER POLLUTION KW - Q5 08505:Prevention and control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16295941?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Igiene+Moderna&rft.atitle=Organization+and+management+of+a+plan+aimed+to+recovery+groundwater+tables+polluted+by+chlorinated+solvents.&rft.au=Bianchi%2C+S%3BMantovani%2C+A%3BGhezzi%2C+A%3BCavallaro%2C+A%3BBaiardi%2C+G%3BRossetti%2C+F%3BFranzosi%2C+C&rft.aulast=Bianchi&rft.aufirst=S&rft.date=1992-01-01&rft.volume=97&rft.issue=3&rft.spage=441&rft.isbn=&rft.btitle=&rft.title=Igiene+Moderna&rft.issn=00191655&rft_id=info:doi/ LA - Italian DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2014-05-06 N1 - SubjectsTermNotLitGenreText - chlorinated hydrocarbons; pollution monitoring; groundwater pollution; pollution surveys; environmental protection; pollution control; groundwater; Italy; Freshwater ER - TY - JOUR T1 - The human loricrin gene. AN - 16292375; 2811122 AB - Loricrin is the major protein component of the cornified cell envelope of terminally differentiated mammalian epidermal (stratum corneum) cells. Using a specific human cDNA clone, we have isolated and characterized the human loricrin geen. We show that it has a very simple structure of a single intron of 1188 base pairs (bp) in the 5'-untranslated region; there are no introns in coding sequences. By use of rodent-human somatic cell hybrids, followed by in situ hybridization with a biotin-labeled genomic DNA clone, the single-copy gene maps to chromosome location 1q21. Polymerase chain reaction analyses of genomic DNAs from different individuals show that human loricrin consists of two allelic size variants, due to sequence variations in its second glycine loop domain, and these variants segregate in the human population by normal Mendelian mechanisms. There are multiple sequence variants within these two size class alleles due to various deletions of 12 bp (4 amino acids) in the major loop of this glycine loop domain. JF - Journal of Biological Chemistry AU - Yoneda, K AU - Hohl, d AU - McBride, O W AU - Wang, M AU - Cehrs, K U AU - Idler, W W AU - Steinert, P M AD - Lab. Skin Biol., NIAMS, Build. 10, Rm. 9N228, NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 18060 EP - 18066 VL - 267 IS - 25 SN - 0021-9258, 0021-9258 KW - amino acid sequence KW - cDNA KW - genes KW - loricrin KW - man KW - nucleotide sequence KW - predictions KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Human Genome Abstracts; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - N 14640:Structure & sequence KW - G 07430:Chromosome studies/nucleotide sequence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16292375?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=The+human+loricrin+gene.&rft.au=Yoneda%2C+K%3BHohl%2C+d%3BMcBride%2C+O+W%3BWang%2C+M%3BCehrs%2C+K+U%3BIdler%2C+W+W%3BSteinert%2C+P+M&rft.aulast=Yoneda&rft.aufirst=K&rft.date=1992-01-01&rft.volume=267&rft.issue=25&rft.spage=18060&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - nucleotide sequence; cDNA; amino acid sequence; genes; man ER - TY - JOUR T1 - Distribution of cytochrome P450 1A1 and NADPH-cytochrome P450 reductase in lungs of rabbits treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin: Ultrastructural immunolocalization and in situ hybridization. AN - 16278977; 2809639 AB - Induction of cytochrome P450 1A1 (P450 1A1) in a variety of tissues is a well established consequence of exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds. Although localization of the induced protein within the lung has been described, the precise intracellular distribution of the enzyme is not clear. Analysis of tissue sections, microsomal proteins, and mRNA from lungs of treated and untreated rabbits established that P450 1A1 had been induced by treatment with TCDD. Rabbit lungs from animals treated with TCDD were examined with immunocytochemistry and in situ hybridization, to identify the cell types that contain P450 1A1 and those that contain mRNA encoding P450 1A1. Endothelial cells of the entire vascular bed of rabbit lung reacted markedly with anti-P450 1A1. JF - Molecular Pharmacology AU - Overby, L H AU - Nishio, S AU - Weir, A AU - Carver, G T AU - Plopper, C G AU - Philpot, R M AD - NIEHS, P.O. Box 12233, MD 19-08, Research Triangle Park, NC 27709, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1039 EP - 1046 VL - 41 IS - 6 SN - 0026-895X, 0026-895X KW - cytochrome P450 KW - NADH-cytochrome P450 reductase KW - TCDD KW - rabbits KW - Toxicology Abstracts KW - lung KW - distribution KW - X 24155:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16278977?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Pharmacology&rft.atitle=Distribution+of+cytochrome+P450+1A1+and+NADPH-cytochrome+P450+reductase+in+lungs+of+rabbits+treated+with+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin%3A+Ultrastructural+immunolocalization+and+in+situ+hybridization.&rft.au=Overby%2C+L+H%3BNishio%2C+S%3BWeir%2C+A%3BCarver%2C+G+T%3BPlopper%2C+C+G%3BPhilpot%2C+R+M&rft.aulast=Overby&rft.aufirst=L&rft.date=1992-01-01&rft.volume=41&rft.issue=6&rft.spage=1039&rft.isbn=&rft.btitle=&rft.title=Molecular+Pharmacology&rft.issn=0026895X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - distribution; lung ER - TY - JOUR T1 - Smoking and risk of non-Hodgkin's lymphoma and multiple myeloma. AN - 16275543; 2802623 AB - Population-based case-control interview studies of 622 White men with non-Hodgkin's lymphoma and 820 controls from Iowa and Minnesota (United States) and 173 White men with multiple myeloma and 452 controls from Iowa offered the opportunity to investigate the relationship of these cancers with smoking. Risks were significantly elevated for all lymphoma (odds ratio (OR) = 1.4), high-grade lymphoma (OR = 2.3), and unclassified lymphoma (OR = 2.8) for cigarette smokers. Dose-response gradients were not seen with intensity of cigarette use, but risks for these subtypes were greatest for cigarette smokers of longest duration. Similar elevations in risks were seen for tobacco users. The risk of multiple myeloma was not significantly elevated for either tobacco users or cigarette smokers. The findings from this study confirm the lack of an association between smoking and multiple myeloma and provide some support for an association between tobacco use and certain subtypes of non-Hodgkin's lymphoma. JF - Cancer Causes & Control AU - Brown, L M AU - Everett, G D AU - Gibson, R AU - Burmeister, L F AU - Schuman, L M AU - Blair, A AD - Epidemiol. and Biostat. Program, NCI/NIH, Executive Plaza North, Rm. 415C, Bethesda MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 49 EP - 55 VL - 3 IS - 1 SN - 0957-5243, 0957-5243 KW - non-Hodgkin's KW - lymphoma KW - multiple myeloma KW - association KW - man KW - Health & Safety Science Abstracts; Toxicology Abstracts KW - smoke KW - smoking KW - tobacco KW - risk assessment KW - cancer KW - H SM3.8.4:DRUGS AND ALCOHOL KW - X 24180:Social poisons & drug abuse KW - H SM10.21:CANCER UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16275543?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Integrated+approach+for+evaluating+species+and+interindividual+differences+in+responsiveness+to+dioxins+and+structural+analogs.&rft.au=Clark%2C+G%3BTritscher%2C+A%3BBell%2C+D%3BLucier%2C+G&rft.aulast=Clark&rft.aufirst=G&rft.date=1992-11-01&rft.volume=98&rft.issue=&rft.spage=125&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - smoking; smoke; tobacco; cancer; risk assessment; lymphoma; multiple myeloma; association; man ER - TY - JOUR T1 - Morphological transformation of Syrian hamster embryo cells by mezerein. AN - 16271144; 2802956 AB - Mezerein (MEZ) has been described as a weak complete tumor promoter but an effective stage II promoter in the mouse skin initiation-promotion tumor model. In this study MEZ produced a strong transformation response when tested under code in the Syrian hamster embryo (SHE) clonal morphological transformation assay. Using a standard 7-day exposure protocol designed to detect complete carcinogens, MEZ was active at non-toxic concentrations, producing a linear response between 0.3-10 ng/ml in a log-log plot of transformation activity versus concentration. These concentrations were in the same range as those which had been shown to elicit promotion activity in several in vitro cell culture systems. Our data suggest that the SHE assay has the ability to detect some tumor promoters under the same conditions used to test for complete carcinogens. JF - Cancer Letters AU - Tu, A S AU - Tennant, R W AU - Spalding, J W AD - Exp. Carcinog. and Mutagenesis Branch, NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 159 EP - 165 VL - 62 IS - 2 SN - 0304-3835, 0304-3835 KW - mezerein KW - hamsters KW - Toxicology Abstracts KW - cell lines KW - transformation KW - X 24240:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16271144?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Letters&rft.atitle=Morphological+transformation+of+Syrian+hamster+embryo+cells+by+mezerein.&rft.au=Tu%2C+A+S%3BTennant%2C+R+W%3BSpalding%2C+J+W&rft.aulast=Tu&rft.aufirst=A&rft.date=1992-01-01&rft.volume=62&rft.issue=2&rft.spage=159&rft.isbn=&rft.btitle=&rft.title=Cancer+Letters&rft.issn=03043835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - transformation; cell lines ER - TY - JOUR T1 - Biochemical activities of the ParA partition protein of the P1 plasmid. AN - 16267216; 2792460 AB - The unit-copy P1 plasmid depends for stability on a plasmid-encoded partition region called par, consisting of the parA and parB genes and the parS site. ParA is absolutely required for partition, but its partition-critical role is not known. Purified ParA protein is shown to possess an ATPase activity in vitro which is specifically stimulated by purified ParB protein and by DNA. ParA is responsible for regulation of expression of parA and parB, and purified ParA has an ATP-dependent, site-specific DNA binding activity which recognizes a sequence that overlaps the parA promoter. The role of the ATP-dependence of the binding activity, as well as other possible functions of the ATPase activity in partition, is discussed. JF - Molecular Microbiology AU - Davis, MA AU - Martin, KA AU - Austin, S J AD - ABL-Basic Res. Program, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702-1201, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1141 EP - 1147 VL - 6 IS - 9 SN - 0950-382X, 0950-382X KW - DNA-binding protein KW - ParA protein KW - activity KW - adenosinetriphosphatase KW - bacteria KW - plasmid P1 KW - plasmids KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology KW - J 02760:Plasmids KW - J 02727:Amino acids, peptides and proteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16267216?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Microbiology&rft.atitle=Biochemical+activities+of+the+ParA+partition+protein+of+the+P1+plasmid.&rft.au=Davis%2C+MA%3BMartin%2C+KA%3BAustin%2C+S+J&rft.aulast=Davis&rft.aufirst=MA&rft.date=1992-01-01&rft.volume=6&rft.issue=9&rft.spage=1141&rft.isbn=&rft.btitle=&rft.title=Molecular+Microbiology&rft.issn=0950382X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - DNA-binding protein; bacteria; plasmids; activity ER - TY - JOUR T1 - Assembly of the active form of the transposase-Mu DNA complex: A critical control point in Mu transposition. AN - 16266287; 2797095 AB - Discovery and characterization of a new intermediate in Mu DNA transposition allowed assembly of the transposition machinery to be separated from the chemical steps of recombination. This stable intermediate, which accumulates in the presence of Ca super(2+), consists of the two ends of the Mu DNA synapsed by a tetramer of the Mu transposase. Within this stable synaptic complex (SSC), the recombination sites are engaged but not yet cleaved. The SSC is structurally related to both the cleaved donor and strand transfer complexes, but precedes them on the transposition pathway. Once the active protein-DNA complex is constructed, it is conserved throughout transposition. The participation of internal sequence elements and accessory factors exclusively during SSC assembly allows recombination to be controlled prior to the irreversible chemical steps. JF - Cell AU - Mizuuchi, M AU - Baker, T A AU - Mizuuchi, K AD - Lab. Mol. Biol., NIDDK, Natl. Inst. Health, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 303 EP - 311 VL - 70 IS - 2 SN - 0092-8674, 0092-8674 KW - stable synaptic complex KW - Biochemistry Abstracts 2: Nucleic Acids; Virology & AIDS Abstracts; Microbiology Abstracts B: Bacteriology KW - transposition KW - assembly KW - recombination KW - DNA KW - phage Mu KW - V 22050:Viral genetics including virus reactivation KW - N 14610:Occurrence, isolation & assay KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16266287?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell&rft.atitle=Assembly+of+the+active+form+of+the+transposase-Mu+DNA+complex%3A+A+critical+control+point+in+Mu+transposition.&rft.au=Mizuuchi%2C+M%3BBaker%2C+T+A%3BMizuuchi%2C+K&rft.aulast=Mizuuchi&rft.aufirst=M&rft.date=1992-01-01&rft.volume=70&rft.issue=2&rft.spage=303&rft.isbn=&rft.btitle=&rft.title=Cell&rft.issn=00928674&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - phage Mu; DNA; transposition; recombination; assembly ER - TY - JOUR T1 - Lack of renal tumour-initiating activity of a single dose of potassium bromate, a genotoxic renal carcinogen in male F344/NCr rats. AN - 16261437; 2795879 AB - The renal tumour-initiating activity of potassium bromate (KBrO sub(3)), a known genotoxic rat renal carcinogen, was investigated in male F344/NCr rats. 6-wk-old rats were given KBrO sub(3) intragastrically as a single dose of 300 mg/kg body weight, which was confirmed by our preliminary toxicity study as a maximum tolerated single dose for this strain of rat. Starting 2 wk after KBrO sub(3) treatment, groups of 39 rats received either a basal diet or a diet containing 4000 ppm barbital sodium (BBNa) as a promoting regimen and were killed at 30, 52, or 104 wk. Control rats received either dietary BBNa (4000 ppm) or the basal diet alone from wk 2 to 52 or 104 wk. Nephropathy was observed in all rats treated with KBrO sub(3) followed by BBNa at 30 wk and in rats receiving BBNa alone, but not in rats exposed to KBrO sub(3) alone. Dysplastic renal tubular cell foci (DTF), putative preneoplastic renal tubular cell lesions were found associated with nephropathy in rats exposed to KBrO sub(3) followed by BBNa from 47 wk. The incidences and multiplicities of DTF and renal tubular cell tumours observed from 31 to 104 wk revealed no initiating effect of KBrO sub(3) treatment. These results indicate that the KBrO sub(3) dose of 300 mg/kg did not initiate renal carcinogenesis. JF - Food and Chemical Toxicology AU - Kurata, Y AU - Diwan, BA AU - Ward, J M AD - Tumour Pathol. and Pathog. Sect., Lab. Comp. Carcinog., Div. Cancer Etiol., NCI, Frederick, MD 21702-1201, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 251 EP - 259 VL - 30 IS - 3 SN - 0278-6915, 0278-6915 KW - potassium bromate KW - rats KW - Toxicology Abstracts KW - carcinogenesis KW - food additives KW - kidney KW - X 24120:Food, additives & contaminants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16261437?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Food+and+Chemical+Toxicology&rft.atitle=Lack+of+renal+tumour-initiating+activity+of+a+single+dose+of+potassium+bromate%2C+a+genotoxic+renal+carcinogen+in+male+F344%2FNCr+rats.&rft.au=Kurata%2C+Y%3BDiwan%2C+BA%3BWard%2C+J+M&rft.aulast=Kurata&rft.aufirst=Y&rft.date=1992-01-01&rft.volume=30&rft.issue=3&rft.spage=251&rft.isbn=&rft.btitle=&rft.title=Food+and+Chemical+Toxicology&rft.issn=02786915&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - carcinogenesis; kidney; food additives ER - TY - JOUR T1 - A markedly diminished pleiotropic response to phenobarbital and structurally-related xenobiotics in Zucker rats in comparison with F344/Ncr or DA rats. AN - 16255371; 2785088 AB - Phenobarbital (PB) and certain structurally-related compounds induce a variety of hepatic drug-metabolizing enzymes in many strains of rats. Thus, following administration of BP (300, 500 ppm), barbital (BB, 1500 ppm) or 5-ethyl-5-phenylhydantoin (EPH, 500 ppm), CYP2B1-mediated benzyloxyresorufin O-dealkylase activity and epoxide hydrolase activity were profoundly induced in female DA and F344/NCr rats. In contrast, outbred female lean and obese Zucker rats showed markedly reduced CYP2B1 responses (< 15% and < 5% of those observed in the female DA or F344/NCr rat) to PB (doses less than or approximate to 300 ppm), BB (1500 ppm) or EPH (500 ppm). In parallel studies, profound increases in RNA levels coding for CYP2B1, glutathione S-transferases Ya/Yc ( alpha subclass), or epoxide hydrolase were detected in the female F344/NCr rat following treatment with PB (300 ppm), BB (1500 ppm) or EPH (500 ppm). In contrast, lean Zucker rats showed a strong response only to the highest dose of PB (500 ppm), implying that the diminished response in the Zucker rats may occur at some pretranslational level. JF - Biochemical Pharmacology AU - Lubet, R A AU - Nims, R W AU - Dragnev, KH AU - Jones, C R AU - Diwan, BA AU - Devor, DE AU - Ward, J M AU - Miller AU - Rice, J M AD - Lab. Comp. Carcinog., Build. 538, Rm. 205E, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1079 EP - 1087 VL - 43 IS - 5 SN - 0006-2952, 0006-2952 KW - phenobarbital KW - 5-ethyl-5-phenylhydantoin KW - rats KW - species differences KW - Toxicology Abstracts KW - induction KW - enzymes KW - X 24117:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16255371?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+Pharmacology&rft.atitle=A+markedly+diminished+pleiotropic+response+to+phenobarbital+and+structurally-related+xenobiotics+in+Zucker+rats+in+comparison+with+F344%2FNcr+or+DA+rats.&rft.au=Lubet%2C+R+A%3BNims%2C+R+W%3BDragnev%2C+KH%3BJones%2C+C+R%3BDiwan%2C+BA%3BDevor%2C+DE%3BWard%2C+J+M%3BMiller%3BRice%2C+J+M&rft.aulast=Lubet&rft.aufirst=R&rft.date=1992-01-01&rft.volume=43&rft.issue=5&rft.spage=1079&rft.isbn=&rft.btitle=&rft.title=Biochemical+Pharmacology&rft.issn=00062952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - enzymes; induction ER - TY - JOUR T1 - A pleiotropic response to phenobarbital-type enzyme inducers in the F344/NCr rat. Effects of chemicals of varied structure. AN - 16254186; 2784858 AB - The effects of a number of phenobarbital-type inducers on selected drug-metabolizing enzymes in male F344/NCr rats were determined by measuring specific catalytic activities and/or by measuring the levels of RNA which hybridize with specific probes for the corresponding genes. The effects on hepatic CYP2B1 were assessed by measuring the levels of CYP2B1-specific RNA and benzyloxyresorufin O-dealkylase and testosterone 16 beta -hydroxylase activities. When male F344/NCr rats were administered various doses of phenobarbital or dichlorodiphenyl-trichloroethane (DDT), strong correlations between the induction of CYP2B1 and the induction of epoxide hydrolase or UDP-glucuronyltransferase activities were observed. Treatment of rats with barbiturates, hydantoins, halogenated pesticides such as DDT or alpha -hexachlorocyclohexane, 2,4,5,2',4',5'-hexachlorobiphenyl, CYP2B1 inhibitors such as clotrimazole or clonazepam, or such structurally-diverse compounds as 2-hexanone or diallyl sulfide resulted in induction of CYP2B1-mediated enzyme activity and induction of certain other forms of cytochrome P450, microsomal epoxide hydrolase, at least one form of UDP-glucuronyltransferase, and multiple forms of glutathione S-transferase. JF - Biochemical Pharmacology AU - Lubet, R A AU - Dragnev, KH AU - Chauhan, D P AU - Nims, W R AU - Diwan, BA AU - Ward, J M AU - Jones, C R AU - Rice, J M AU - Miller AD - Lab. Comp. Carcinog., Build. 538, Rm. 205E, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1067 EP - 1078 VL - 43 IS - 5 SN - 0006-2952, 0006-2952 KW - phenobarbital KW - rats KW - Toxicology Abstracts KW - induction KW - structure-function relationships KW - derivatives KW - enzymes KW - X 24117:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16254186?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+Pharmacology&rft.atitle=A+pleiotropic+response+to+phenobarbital-type+enzyme+inducers+in+the+F344%2FNCr+rat.+Effects+of+chemicals+of+varied+structure.&rft.au=Lubet%2C+R+A%3BDragnev%2C+KH%3BChauhan%2C+D+P%3BNims%2C+W+R%3BDiwan%2C+BA%3BWard%2C+J+M%3BJones%2C+C+R%3BRice%2C+J+M%3BMiller&rft.aulast=Lubet&rft.aufirst=R&rft.date=1992-01-01&rft.volume=43&rft.issue=5&rft.spage=1067&rft.isbn=&rft.btitle=&rft.title=Biochemical+Pharmacology&rft.issn=00062952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - structure-function relationships; derivatives; enzymes; induction ER - TY - JOUR T1 - Human lipoprotein lipase. Analysis of the catalytic triad by site-directed mutagenesis of Ser-132, Asp-156, and His-241. AN - 16250566; 2784834 AB - Lipoprotein lipase (LPL) plays a central role in normal lipid metabolism as the key enzyme involved in the hydrolysis of triglycerides present in chylomicrons and very low density lipoproteins. LPL is a member of a family of hydrolytic enzymes that include hepatic lipase and pancreatic lipase. Based on primary sequence homology of LPL to pancreatic lipase, Ser-132, Asp-156, and His-241 have been proposed to be part of a domain required for normal enzymic activity. We have analyzed the role of these potential catalytic residues by site-directed mutagenesis and expression of the mutant LPL in human embryonic kidney-293 cells. JF - Journal of Biological Chemistry AU - Emmerich, J AU - Beg, OU AU - Peterson, J AU - Previato, L AU - Brunzell, J D AU - Brewer, HB Jr AU - Santamarina-Fojo, S AD - Mol. Dis. Branch, NHLBI, Build. 10, Rm. 7N117, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 4161 EP - 4165 VL - 267 IS - 6 SN - 0021-9258, 0021-9258 KW - aspartic acid KW - catalysis KW - histidine KW - lipoprotein lipase KW - man KW - requirements KW - serine KW - site-directed mutagenesis KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16250566?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Polycyclic+aromatic+hydrocarbon-DNA+adducts+and+the+CYP1A1+restriction+fragment+length+polymorphism.&rft.au=Shields%2C+P+G%3BSugimura%2C+H%3BCaporaso%2C+N+E%3BPetruzzelli%2C+S+F%3BBowman%2C+E+D%3BTrump%2C+B+F%3BWeston%2C+A%3BHarris%2C+C+C&rft.aulast=Shields&rft.aufirst=P&rft.date=1992-11-01&rft.volume=98&rft.issue=&rft.spage=191&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Characterization of a class 3 tyrosine kinase. AN - 16246270; 2773808 AB - We utilized polymerase chain reaction (PCR) technology and degenerate oligonucleotide primers to produce a cDNA library of kinase catalytic domains found in the human monocytic cell line AML-193. This search yielded a member of the class 3 tyrosine kinases closely related to the murine kinase FD-22. Previous work has identified this kinase as JAK1. This class of tyrosine kinases is characterized by being ubiquitously expressed, lacking both a ligand-binding domain and a SH2 domain, while containing a second domain similar to a degenerate kinase domain. Our studies focused on the further characterization of this class 3 tyrosine kinase using Northern blot analysis to demonstrate as increase in steady-state mRNA by interferon-gamma in human monocytes. A human-hamster somatic cell hybrid panel and linkage mapping was used to assign JAK1 (aml-116) to human chromosome 1. JF - Oncogene AU - Howard, OMZ AU - Dean, M AU - Young, H AU - Ramsburg, M AU - Turpin, JA AU - Michiel, D F AU - Kelvin, D J AU - Lee, L AU - Farrar, W L AD - Biol. Carcinog. and Dev. Program, Program Resour., Inc./DynCorp, NCI-Frederick Cancer Res. and Dev. Cent., P.O. Box B, Frederick, MD 21702, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 895 EP - 900 VL - 7 IS - 5 SN - 0950-9232, 0950-9232 KW - amino acid sequence KW - cDNA KW - chromosome 1 KW - genes KW - humans KW - man KW - mapping KW - nucleotide sequence KW - predictions KW - protein-tyrosine kinase KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Oncogenes & Growth Factors Abstracts; Human Genome Abstracts; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - N 14640:Structure & sequence KW - G 07430:Chromosome studies/nucleotide sequence KW - B 26400:HUMAN-RELATED ONCOGENES AND GROWTH FACTORS: CROSS REFERENCES KW - B 26120:Other oncogenes & GF's with tyrosine kinase activity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16246270?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=Characterization+of+a+class+3+tyrosine+kinase.&rft.au=Howard%2C+OMZ%3BDean%2C+M%3BYoung%2C+H%3BRamsburg%2C+M%3BTurpin%2C+JA%3BMichiel%2C+D+F%3BKelvin%2C+D+J%3BLee%2C+L%3BFarrar%2C+W+L&rft.aulast=Howard&rft.aufirst=OMZ&rft.date=1992-01-01&rft.volume=7&rft.issue=5&rft.spage=895&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=09509232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - nucleotide sequence; cDNA; amino acid sequence; genes; mapping; man ER - TY - JOUR T1 - Polynuclear ions in aluminum toxicity. AN - 16234897; 2776704 JF - Journal of Theoretical Biology AU - Flaten, T P AU - Garruto, R M AD - Natl. Inst. Neurol. Disorders and Stroke, NCI-FCRDC, Build. 376, P.O. Box B, Frederick, MD 21702-1201, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 129 EP - 132 VL - 156 IS - 7 SN - 0022-5193, 0022-5193 KW - aluminium KW - polynuclear ions KW - Toxicology Abstracts KW - toxicity KW - ions KW - X 24161:Acute exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16234897?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Theoretical+Biology&rft.atitle=Polynuclear+ions+in+aluminum+toxicity.&rft.au=Flaten%2C+T+P%3BGarruto%2C+R+M&rft.aulast=Flaten&rft.aufirst=T&rft.date=1992-01-01&rft.volume=156&rft.issue=7&rft.spage=129&rft.isbn=&rft.btitle=&rft.title=Journal+of+Theoretical+Biology&rft.issn=00225193&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - toxicity; ions ER - TY - JOUR T1 - The gene and cDNA for the human high affinity immunoglobulin E receptor beta chain and expression of the complete human receptor. AN - 16232537; 2755107 AB - The high affinity IgE receptor (Fc epsilon RI) is a tetrameric hetero-oligomer composed of an alpha chain, a beta chain, and two disulfide-linked gamma chains. The beta chain contains four transmembrane (TM) segments and long cytoplasmic domains that are thought to play an important role in intracellular signaling. We now report the structural characterization and the sequence of the complete human beta gene and cDNA. The gene spans similar to 10 kilobases and contains seven exons. There is a single transcription initiation site preceded by a TATA box. The first exon codes for the 5'-untranslated region and a portion of the N-terminal cytoplasmic tail. TM-1 is encoded in exons 2 and 3, TM-2 in exons 3 and 4, TM-3 in exon 5, and TM-4 in exon 6. The seventh and final exon encodes the end of the C-terminal cytoplasmic tail and the 3'-untranslated sequence. The human beta gene appears to be a single copy gene. JF - Journal of Biological Chemistry AU - Kuester, H AU - Zhang, Li AU - Brini, A T AU - MacGlashan, DWJ AU - Kinet, J-P AD - NIAID, NIH, Twinbrook II Build., 12441 Parklawn Dr., Rockville, MD 20852, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 12782 EP - 12787 VL - 267 IS - 18 SN - 0021-9258, 0021-9258 KW - Fc KW - amino acid sequence KW - beta chain KW - cDNA KW - genes KW - immunoglobulin E KW - man KW - mast cells KW - nucleotide sequence KW - predictions KW - receptors KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Human Genome Abstracts; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Immunology Abstracts KW - N 14640:Structure & sequence KW - G 07430:Chromosome studies/nucleotide sequence KW - F 06772:Other cells (leukocytes, eosinophils, basophils, neutrophils, platelets) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16232537?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=The+gene+and+cDNA+for+the+human+high+affinity+immunoglobulin+E+receptor+beta+chain+and+expression+of+the+complete+human+receptor.&rft.au=Kuester%2C+H%3BZhang%2C+Li%3BBrini%2C+A+T%3BMacGlashan%2C+DWJ%3BKinet%2C+J-P&rft.aulast=Kuester&rft.aufirst=H&rft.date=1992-01-01&rft.volume=267&rft.issue=18&rft.spage=12782&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - nucleotide sequence; Fc; cDNA; amino acid sequence; genes; immunoglobulin E; receptors; mast cells; man ER - TY - JOUR T1 - The bromodomain: A conserved sequence found in human, Drosophila and yeast proteins. AN - 16223940; 2755932 AB - Identification of conserved domains or motifs in proteins may aid in the localization and analysis of important structural and functional regions. We report here a protein sequence motif, called the bromodomain, that has been found in six genes from humans (CCG1 and RING3), Drosophila (fsh and brm), and yeast (SPT7 and SNF2). The fsh and brm genes are required maternally for proper expression fo certain homeotic genes. The SPT7 and SNF2 genes of Saccharomyces cerevisiae encode transcriptional activators. The SNF2 and brm proteins have extensive sequence homology. It is not clear whether the two human genes are involved in processes. CCG1 is a DNA-binding protein that complements temperature sensitive mutations that cause cell cycle arrest in G1. The RING3 gene is a newly identified human gene of unknown function, mapping to the class II region of the human major histocompatibility locus, that has substantial homology to the fsh gene. JF - Nucleic Acids Research AU - Haynes AU - Dollard, C AU - Winston, F AU - Beck, S AU - Trowsdale, J AU - Dawid, IB AD - Lab. Mol. Genet., NICHD, NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 2603 VL - 20 IS - 10 SN - 0305-1048, 0305-1048 KW - amino acid sequence KW - amphipathic KW - bromodomains KW - domains KW - helices KW - proteins KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16223940?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+Acids+Research&rft.atitle=The+bromodomain%3A+A+conserved+sequence+found+in+human%2C+Drosophila+and+yeast+proteins.&rft.au=Haynes%3BDollard%2C+C%3BWinston%2C+F%3BBeck%2C+S%3BTrowsdale%2C+J%3BDawid%2C+IB&rft.aulast=Haynes&rft.aufirst=&rft.date=1992-01-01&rft.volume=20&rft.issue=10&rft.spage=2603&rft.isbn=&rft.btitle=&rft.title=Nucleic+Acids+Research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Promotion of the in vitro renaturation of dodecameric glutamine synthetase from Escherichia coli in the presence of GroEL (chaperonin-60) and ATP. AN - 16222028; 2748851 AB - The folding and assembly of dodecameric glutamine synthetase (GS) from Escherichia coli was examined in the absence and presence of the E. coli heat shock protein, GroEL (chaperonin-60). At nonphysiological temperatures (15-20 degree C), unfolded GS spontaneously renatured to 80-90% of its original activity in the absence of GroEL. At near-physiological temperatures (37 degree C), only 20-40% of the original activity returns. Under the latter solution conditions, GroEL and ATP enhance the extent of GS renaturation to 70-80% of the original activity at 37 degree C. In the absence of ATP, GroEL arrests the renaturation of unfolded GS by forming a stable binary complex. The addition of ATP to this complex resulted in the release of GS subunits and formation of active dodecameric GS. The order of addition of ATP or unfolded GS to GroEL results in differences in the t sub(1/2) values where half-maximal GS activity is attained. At a constant GS concentration, the formation of the GroEL multiplied by GS complex followed by ATP addition resulted in approximately a 2-fold increase in the observed t sub(1/2) value compared to that observed when GroEL was preincubated with ATP before the GS renaturation reaction was initiated. JF - Biochemistry (Washington) AU - Fisher, M T AD - NHLBI/NIH, Build. 3, Rm. 207, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 3955 EP - 3963 VL - 31 IS - 16 SN - 0006-2960, 0006-2960 KW - ATP KW - Escherichia coli KW - GroEL protein KW - assembly KW - folding KW - glutamine synthase KW - renaturation KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology KW - J 02728:Enzymes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16222028?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry+%28Washington%29&rft.atitle=Promotion+of+the+in+vitro+renaturation+of+dodecameric+glutamine+synthetase+from+Escherichia+coli+in+the+presence+of+GroEL+%28chaperonin-60%29+and+ATP.&rft.au=Fisher%2C+M+T&rft.aulast=Fisher&rft.aufirst=M&rft.date=1992-01-01&rft.volume=31&rft.issue=16&rft.spage=3955&rft.isbn=&rft.btitle=&rft.title=Biochemistry+%28Washington%29&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - renaturation; assembly; folding ER - TY - JOUR T1 - The catecholic metal sequestering agent 1,2-dihydroxybenzene-3,5-disulfonate confers protection against oxidative cell damage. AN - 16219419; 2745965 AB - Tiron (1,2-dihydroxybenzene-3,5-disulfonate), a non-toxic chelator of a variety of metals, is used to alleviate acute metal overload in animals. Since Tiron reacts with potentially toxic intracellular species and is also a metal chelator, we evaluated its protective effects in V79 cells subjected to various types of oxidative damage and attempted to distinguish the protection due to direct detoxification of intracellular radicals from that resulting from chelation of redox-active transition metals. We found that Tiron protects Chinese hamster V79 cells against both superoxide free radicals-induced (and H sub(2)O sub(2) via dismutation of superoxide free radicals) and H sub(2)O sub(2)-induced cytotoxicity as measured by clonogenic assays. JF - Archives of Biochemistry and Biophysics AU - Krishna, C M AU - Liebmann, JE AU - Kaufman, D AU - DeGraff, W G AU - Hahn, S M AU - McMurry, T AU - Mitchell, J B AU - Russo, A AD - Radiat. Oncol. Branch/NCI, Build. 10, Rm. B3-B69, Bethesda, MD 20872, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 98 EP - 106 VL - 294 IS - 1 SN - 0003-9861, 0003-9861 KW - Toxicology Abstracts KW - tiron KW - toxicity KW - cell lines KW - free radicals KW - X 24240:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16219419?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+Biochemistry+and+Biophysics&rft.atitle=The+catecholic+metal+sequestering+agent+1%2C2-dihydroxybenzene-3%2C5-disulfonate+confers+protection+against+oxidative+cell+damage.&rft.au=Krishna%2C+C+M%3BLiebmann%2C+JE%3BKaufman%2C+D%3BDeGraff%2C+W+G%3BHahn%2C+S+M%3BMcMurry%2C+T%3BMitchell%2C+J+B%3BRusso%2C+A&rft.aulast=Krishna&rft.aufirst=C&rft.date=1992-01-01&rft.volume=294&rft.issue=1&rft.spage=98&rft.isbn=&rft.btitle=&rft.title=Archives+of+Biochemistry+and+Biophysics&rft.issn=00039861&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - tiron; free radicals; toxicity; cell lines ER - TY - JOUR T1 - Chronic lithium treatment prevents the dexamethasone-induced increase of brain polyamine metabolizing enzymes. AN - 16217223; 2744342 AB - The paper describes the effects of various regimens of lithium chloride treatment on dexamethasone-induced increases in brain polyamine metabolizing enzymes. In contrast to peripheral tissues where acute lithium treatment suppresses the increase in ornithine decarboxylase activity, in the brain only chronic treatment was effective in preventing this increase and also the increases in the activities of S-adenosylmethionine decarboxylase and spermidine/spermine N super(1)-acetyltransferase. This findings indicate a novel brain target for lithium's action and in turn provide new avenues for exploring polyamine function in the brain. JF - Life Sciences AU - Gilad, G M AU - Gilad, V H AU - Wyatt, R J AU - Casero, RA Jr AD - Neuropsychiatr. Branch, NIMH Neurosci. Cent., St. Elizabeths, Washington, DC 20032, USA Y1 - 1992 PY - 1992 DA - 1992 SN - 0024-3205, 0024-3205 KW - lithium KW - dexamethasone KW - increases KW - polyamines KW - rats KW - Toxicology Abstracts; CSA Neurosciences Abstracts KW - chronic effects KW - metabolism KW - induction KW - enzymes KW - prevention KW - brain KW - X 24117:Biochemistry KW - N3 11094:Central nervous system UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16217223?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Life+Sciences&rft.atitle=Chronic+lithium+treatment+prevents+the+dexamethasone-induced+increase+of+brain+polyamine+metabolizing+enzymes.&rft.au=Gilad%2C+G+M%3BGilad%2C+V+H%3BWyatt%2C+R+J%3BCasero%2C+RA+Jr&rft.aulast=Gilad&rft.aufirst=G&rft.date=1992-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Life+Sciences&rft.issn=00243205&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - chronic effects; prevention; induction; metabolism; enzymes; brain ER - TY - JOUR T1 - The folding and cell surface expression of CD4 requires glycosylation. AN - 16212937; 2755760 AB - To clarify the effect of glycosylation on surface expression, folding, and intracellular sorting of CD4, we generated a series of mutant cDNAs in which one, the other, or both glycosylation recognition sites were eliminated. Using in vitro transcription and translation we confirmed that both potential glycosylation sites of CD4 were utilized. Transient expression of the mutants in HeLa cells demonstrated that glycosylation at either site was necessary and sufficient for cell surface expression. We showed that unglycosylated CD4 produced in HeLa cells was incorrectly folded and retained intracellularly, probably in the endoplasmic reticulum. JF - Journal of Biological Chemistry AU - Tifft, C J AU - Proia, R L AU - Camerini-Otero, R D AD - Build. 10, Rm. 9D-15, Genet. and Biochem. Branch, NIDDK, NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 3268 EP - 3273 VL - 267 IS - 5 SN - 0021-9258, 0021-9258 KW - CD4 antigen KW - HeLa cells KW - expression KW - folding KW - glycosylation KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16212937?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=The+folding+and+cell+surface+expression+of+CD4+requires+glycosylation.&rft.au=Tifft%2C+C+J%3BProia%2C+R+L%3BCamerini-Otero%2C+R+D&rft.aulast=Tifft&rft.aufirst=C&rft.date=1992-01-01&rft.volume=267&rft.issue=5&rft.spage=3268&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Iron-catalyzed oxidative modification of glucose-6-phosphate dehydrogenase from Leuconostoc mesenteroides : Structural and functional changes. AN - 16212909; 2745194 AB - We report that Glu-6-PDH from Leuconostoc mesenteroides is rapidly inactivated by micromolar concentrations of Fe super(2+) and H sub(2)O sub(2). Our results demonstrate the inherent susceptibility of Glu-6-PDH from L. mesenteroides) to modification by an oxidation system known to exist in vivo. An assessment of the physiological significance of Fe super(2+)-catalyzed oxidation of Glu-6-PDH awaits extension of these studies to mammalian sources known to accumulate less active or inactive forms of the enzyme as a function of age. JF - Journal of Biological Chemistry AU - Szweda, LI AU - Stadtman, E R AD - NHLBI, NIH, Build. 3, Rm. 221, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 3096 EP - 3100 VL - 267 IS - 5 SN - 0021-9258, 0021-9258 KW - Leuconostoc mesenteroides KW - glucose-6-phosphate dehydrogenase KW - iron KW - oxidation KW - structure-activity relationships KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology KW - J 02728:Enzymes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16212909?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Iron-catalyzed+oxidative+modification+of+glucose-6-phosphate+dehydrogenase+from+Leuconostoc+mesenteroides+%3A+Structural+and+functional+changes.&rft.au=Szweda%2C+LI%3BStadtman%2C+E+R&rft.aulast=Szweda&rft.aufirst=LI&rft.date=1992-01-01&rft.volume=267&rft.issue=5&rft.spage=3096&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - structure-activity relationships; oxidation ER - TY - JOUR T1 - Cloning and expression of a novel angiotensin II receptor subtype. AN - 16211232; 2737973 AB - Angiotensin II (AII) is a major regulator of cardiovascular function and fluid homeostasis. To search for AII receptor subtypes, we amplified rat adrenal cortex cDNA by PCR using primers based on the AT sub(1) receptor. The product was distinct from the AT sub(1) receptor as indicated by restriction enzyme analysis and DNA sequencing. A full-length cDNA clone (2.2 kilobase pairs) encoding a novel AII receptor (AT sub(3)) was obtained by screening an adrenal cortex library. The AT sub(3) cDNA encodes a M sub(r) 40,959 protein with 95% amino acid identity to the rat smooth muscle receptor, but the overall nucleotide similarity is 71% due to low homology in the 5'- (58%) and 3'- (62%) untranslated regions. JF - Journal of Biological Chemistry AU - Sandberg, K AU - Ji, Hong AU - Clark, AJL AU - Shapira, H AU - Catt, K J AD - ERRB, NICHD, NIH, Build. 10, Rm. B1-L400, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 9455 EP - 9458 VL - 267 IS - 14 SN - 0021-9258, 0021-9258 KW - adrenal medulla KW - amino acid sequence KW - angiotensin II receptors KW - cDNA KW - genes KW - nucleotide sequence KW - predictions KW - rats KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - G 07402:GENERAL KW - N 14640:Structure & sequence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16211232?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Cloning+and+expression+of+a+novel+angiotensin+II+receptor+subtype.&rft.au=Sandberg%2C+K%3BJi%2C+Hong%3BClark%2C+AJL%3BShapira%2C+H%3BCatt%2C+K+J&rft.aulast=Sandberg&rft.aufirst=K&rft.date=1992-01-01&rft.volume=267&rft.issue=14&rft.spage=9455&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - nucleotide sequence; cDNA; amino acid sequence; genes; adrenal medulla ER - TY - JOUR T1 - Guanine nucleotide-binding proteins in the intestinal parasite Giardia lamblia . Isolation of a gene encoding an similar to 20-kDa ADP-ribosylation factor. AN - 16208528; 2735107 AB - To determine whether genes for guanine nucleotide-binding proteins are present in Giardia , genomic DNA and cDNA libraries were screened by polymerase chain reaction and by hybridization with mixed oligonucleotide probes complementary to sequences encoding conserved GTP-binding domains. A gene with a high degree of sequence identity with mammalian ADP-ribosylation factors (ARFs), believed to be important in vesicular transport, was identified. The Giardia ARF gene had a 573-base open reading frame encoding 191 amino acids which are 63-70% identical with known mammalian and yeast ARFs. Sequence conservation among ARFs was greatest in putative GTP-binding domains. A single ARF mRNA species of similar to 750 bases was found in two different Giardia isolates. JF - Journal of Biological Chemistry AU - Murtagh, JJ Jr AU - Mowatt, M R AU - Lee, Chii-Ming AU - Lee, Fang-Jen Scott AU - Mishima, K AU - Nash, TE AU - Moss, J AU - Vaughan, M AD - NHLBI, NIH, Build. 10/5N307, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 9654 EP - 9662 VL - 267 IS - 14 SN - 0021-9258, 0021-9258 KW - Giardia lamblia KW - amino acid sequence KW - cDNA KW - genes KW - guanine nucleotide-binding protein KW - nucleotide sequence KW - predictions KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - N 14640:Structure & sequence KW - G 07361:Protozoans/slime molds KW - K 03081:Protozoa UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16208528?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Guanine+nucleotide-binding+proteins+in+the+intestinal+parasite+Giardia+lamblia+.+Isolation+of+a+gene+encoding+an+similar+to+20-kDa+ADP-ribosylation+factor.&rft.au=Murtagh%2C+JJ+Jr%3BMowatt%2C+M+R%3BLee%2C+Chii-Ming%3BLee%2C+Fang-Jen+Scott%3BMishima%2C+K%3BNash%2C+TE%3BMoss%2C+J%3BVaughan%2C+M&rft.aulast=Murtagh&rft.aufirst=JJ&rft.date=1992-01-01&rft.volume=267&rft.issue=14&rft.spage=9654&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - nucleotide sequence; cDNA; amino acid sequence; genes ER - TY - JOUR T1 - Quinone induced stimulation of hexose monophosphate shunt activity in the guinea pig lens: Role of zeta-crystallin. AN - 16196178; 2741735 AB - The response of the hexose monophosphate shunt (HMS) in organ-cultured guinea pig lens to 1,2-naphthoquinone and 5-hydroxy-1,4-naphthoquinone (juglone) has been investigated. Both these compounds, which are substrates of guinea pig lens zeta-crystallin (NADPH:quinone oxidoreductase), were found to cause increases in the rate of super(14)CO sub(2) production from 1- super(14)C-labelled glucose. Exposure of lenses to 15 mu M 1,2-naphthoquinone or 20 mu M juglone yielded 5.9- and 7-fold stimulation of HMS activity, respectively. Unlike hydrogen peroxide-induced stimulation of HMS activity, these effects were not abolished by preincubation with the glutathione reductase inhibitor, 1,3-bis(2-chloroethyl)-1 nitrosourea (BCNU). While hydrogen peroxide produced substantial decrements in lens glutathione (GSH) levels, incubation with quinones was not associated with a similar reduction in GSH concentration. Protein-bound NADPH content in quinone-exposed guinea pig lenses was decreased, with a concomitant increase in the amounts of free NADP super(+). JF - BIOCHEM. BIOPHYS. ACTA. AU - Rao, P AU - Zigler, JS Jr AD - Build. 6, Rm. 237, NIH/NEI, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 75 EP - 81 VL - 1116 IS - 1 KW - eye lens KW - guinea-pigs KW - hexose monophosphate pathway KW - induction KW - quinone KW - role KW - stimulation KW - zeta-crystallin KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16196178?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BIOCHEM.+BIOPHYS.+ACTA.&rft.atitle=Quinone+induced+stimulation+of+hexose+monophosphate+shunt+activity+in+the+guinea+pig+lens%3A+Role+of+zeta-crystallin.&rft.au=Rao%2C+P%3BZigler%2C+JS+Jr&rft.aulast=Metz&rft.aufirst=D&rft.date=1992-11-01&rft.volume=103&rft.issue=5&rft.spage=1498&rft.isbn=&rft.btitle=&rft.title=Gastroenterology&rft.issn=00165085&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Insulin and isoproterenol induce phosphorylation of the particulate cyclic GMP-inhibited, low K sub(M) cyclic AMP phosphodiesterase (cGI PDE) in 3T3-L1 adipocytes. AN - 16195899; 2741673 AB - The cGI PDE in particulate fractions of differentiated adipocytes (but not control 3T3-L1 fibroblasts) was cross-reactive with a polyclonal antibody raised against the bovine adipose cGI PDE. The 3T3-L1 adipocyte cGI PDE is a 135 kDa protein which is phosphorylated in super(32)P-labeled cells in response to beta-agonist or insulin. The results indicate that the 3T3-L1 cGI PDE is similar in structure and hormonal regulation to the analogous enzyme in the rat adipocyte. JF - Biochemical and Biophysical Research Communications AU - Vasta, V AU - Smith, C J AU - Calvo, J AU - Belfrage, P AU - Manganiello, V C AD - Build. 10, Rm. 5N-307, NHLBI, NIH, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1070 EP - 1075 VL - 183 IS - 3 SN - 0006-291X, 0006-291X KW - 3',5'-cyclic-nucleotide phosphodiesterase KW - adipocytes KW - induction KW - insulin KW - isoproterenol KW - phosphorylation KW - rats KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16195899?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+Biophysical+Research+Communications&rft.atitle=Insulin+and+isoproterenol+induce+phosphorylation+of+the+particulate+cyclic+GMP-inhibited%2C+low+K+sub%28M%29+cyclic+AMP+phosphodiesterase+%28cGI+PDE%29+in+3T3-L1+adipocytes.&rft.au=Vasta%2C+V%3BSmith%2C+C+J%3BCalvo%2C+J%3BBelfrage%2C+P%3BManganiello%2C+V+C&rft.aulast=Vasta&rft.aufirst=V&rft.date=1992-01-01&rft.volume=183&rft.issue=3&rft.spage=1070&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+Biophysical+Research+Communications&rft.issn=0006291X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Toxicity of monochloroacetic acid administered by gavage to F344 rats and B6C3F1 mice for up to 13 weeks. AN - 16186925; 2721772 AB - Groups of 20 rats and 20 mice of each sex were administered monochloroacetic acid (MCAA) once daily, 5 days per week, in water by gavage for up to 13 weeks. Doses used were 0, 30, 60, 90, 120, or 150 mg/kg for rats and 0, 25, 50, 100, 150, or 200 mg/kg for mice. Compound-related deaths occurred at the four highest dose levels in rats and at the highest dose level in mice. Mean body weights of treated groups of rats and mice surviving until the end of study were similar to those of the controls. A dose-related increase in blood urea nitrogen, alanine aminotransferase, aspartate aminotransferase, as well as a dose-related increase in the relative liver and kidney weights was observed in rats but not in mice. A dose-related increase in the incidence and severity of cardiomyopathy occurred in rats. This lesion may be related to the inhibition of heart mitochondrial aconitase activity. No compound-related lesions were observed in mice. The results indicate that F344 rats are more sensitive than B6C3F1 mice; sexes within the species were equally sensitive. JF - Toxicology AU - Bryant, B J AU - Jokinen, M P AU - Eustis, S L AU - Thompson, M B AU - Abdo, K M AD - NIEHS, Mail Drop A0-01, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 77 EP - 87 VL - 72 IS - 1 SN - 0300-483X, 0300-483X KW - chloroacetic acid KW - rats KW - mice KW - Toxicology Abstracts KW - toxicity KW - herbicides KW - X 24132:Chronic exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16186925?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology&rft.atitle=Toxicity+of+monochloroacetic+acid+administered+by+gavage+to+F344+rats+and+B6C3F1+mice+for+up+to+13+weeks.&rft.au=Bryant%2C+B+J%3BJokinen%2C+M+P%3BEustis%2C+S+L%3BThompson%2C+M+B%3BAbdo%2C+K+M&rft.aulast=Bryant&rft.aufirst=B&rft.date=1992-01-01&rft.volume=72&rft.issue=1&rft.spage=77&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - toxicity; herbicides ER - TY - JOUR T1 - Detection by super(32)P-postlabelling of DNA adducts induced by free radicals and unsaturated aldehydes formed during the aerobic decomposition of fecapentaene-12. AN - 16186616; 2723162 AB - Fecapentaene-12 (fec-12), excreted in human faeces, is genotoxic to human cells and a known animal carcinogen. The mechanism of its genotoxicity is unknown but may involve direct alkylation and/or free-radical generation. The formation of reactive species during fec-12 aerobic degradation was thus investigated by electron paramagnetic resonance (EPR) and NMR spectroscopic techniques. Oxy- and alkyl-radicals were detected as the 5,5'-dimethyl-1-pyrroline-N-oxide spin-trap adducts at fec-12 concentrations of between 0.1 and 2.0 mM. Under anaerobic conditions no free-radical generation was observed. NMR spectroscopy indicated that fec-12 degraded at least initially into three unsaturated aldehydes. The co-formation of free-radicals and unsaturated aldehydes suggests that fec-12 decomposed aerobically via a process analogous to lipid peroxidation. JF - Carcinogenesis AU - Povey, A C AU - Wilson, V L AU - Zweier, J L AU - Kuppusamy, P AU - O'Neill, I K AU - Harris, C C AD - Lab. Human Carcinog., NCI, NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 395 EP - 401 VL - 13 IS - 3 SN - 0143-3334, 0143-3334 KW - fecapentaene-12 KW - Biochemistry Abstracts 2: Nucleic Acids; Toxicology Abstracts KW - decomposition KW - adducts KW - DNA KW - free radicals KW - N 14630:Chemical reactions & interactions, including effects of radiation KW - X 24240:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16186616?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Detection+by+super%2832%29P-postlabelling+of+DNA+adducts+induced+by+free+radicals+and+unsaturated+aldehydes+formed+during+the+aerobic+decomposition+of+fecapentaene-12.&rft.au=Povey%2C+A+C%3BWilson%2C+V+L%3BZweier%2C+J+L%3BKuppusamy%2C+P%3BO%27Neill%2C+I+K%3BHarris%2C+C+C&rft.aulast=Povey&rft.aufirst=A&rft.date=1992-01-01&rft.volume=13&rft.issue=3&rft.spage=395&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - free radicals; DNA; adducts; decomposition ER - TY - JOUR T1 - Molecular cloning and developmental analysis of a new glutamate receptor subunit isoform in cerebellum. AN - 16186386; 2721342 AB - The glutamate receptor gene GluR-4 is proposed to generate two spliced isoforms. Screening a rat cerebellar cDNA library, we have now identified a third type of transcript derived from GluR-4 gene by differential RNA processing. This transcript encodes a protein with a "flop" module between transmembrane regions 3 and 4, but with a C-terminus segment of 36 amino acids different from the previously described GluR-4 flip/flop cDNAs. This subunit was therefore designated as GluR-4c flop. Three transcripts of 6.2, 4.2, and 3.0 kilobases (kb) derived from the GluR-4 gene were much more abundant in the cerebellum than in other brain areas, and their levels increased during cerebellar development. In situ hybridization histochemistry revealed that the GluR-4c transcripts are preferentially expressed in cerebellar granule cells and Bergmann glial cells, whereas the expression of GluR-4 flip mRNAs is restricted to Bergmann glial cells. JF - Journal of Neuroscience AU - Gallo, V AU - Upson, L M AU - Hayes, W P AU - Vyklicky, L Jr AU - Winters, CA AU - Buonanno, A AD - Unit Mol. Neurobiol., Lab. Dev. Neurobiol., NICHD, Natl. Inst. Health, Build. 36, Rm. 2A-21, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1010 EP - 1023 VL - 12 IS - 3 SN - 0270-6474, 0270-6474 KW - amino acid sequence KW - cerebellum KW - developmental stages KW - expression KW - glutamic acid KW - isoforms KW - mRNA KW - predictions KW - rats KW - receptors KW - subunits KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids; CSA Neurosciences Abstracts KW - G 07402:GENERAL KW - N 14640:Structure & sequence KW - N3 11075:Molecular neurobiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16186386?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Neuroscience&rft.atitle=Molecular+cloning+and+developmental+analysis+of+a+new+glutamate+receptor+subunit+isoform+in+cerebellum.&rft.au=Gallo%2C+V%3BUpson%2C+L+M%3BHayes%2C+W+P%3BVyklicky%2C+L+Jr%3BWinters%2C+CA%3BBuonanno%2C+A&rft.aulast=Gallo&rft.aufirst=V&rft.date=1992-01-01&rft.volume=12&rft.issue=3&rft.spage=1010&rft.isbn=&rft.btitle=&rft.title=Journal+of+Neuroscience&rft.issn=02706474&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - cerebellum; mRNA ER - TY - JOUR T1 - Differentiation factor/leukemia inhibitory factor protection against lethal endotoxemia in mice: Synergistic effect with interleukin 1 and tumor necrosis factor. AN - 16176136; 2715875 AB - Differentiation factor (D factor), also called leukemia inhibitory factor (LIF), is a glycoprotein that has been increasingly recognized to possess a wide range of physiological activities. We examined the possibility that the administration of D factor may confer beneficial effects and enhance host resistance against lethal endotoxemia. A single intravenous dose of recombinant human D factor completely protected C57/BL6 mice from the lethal effect of Escherichia coli endotoxin (lipopolysaccharide (LPS)). The protective effects were dose dependent and observed when administered 2-24 h before LPS. Previous work has shown that interleukin 1 (IL-1) and tumor necrosis factor (TNF) also protect against a subsequent LPS challenge in a dose-dependent manner. When human D factor was combined with sub-protective doses of IL-1 beta or TNF- alpha , there was dramatic synergistic protection against a subsequent lethal LPS challenge. JF - Journal of Experimental Medicine AU - Alexander, H R AU - Wong, Grace GH AU - Doherty, G M AU - Venzon, D J AU - Fraker, D L AU - Norton, JA AD - Surg. Metab. Sect. Surg. Branch./NCI, Build. 10, Rm. 2B01, Natl. Inst. Health, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1139 EP - 1142 VL - 175 IS - 4 SN - 0022-1007, 0022-1007 KW - leukemia inhibitory factor KW - protection KW - synergism KW - mice KW - tumor necrosis factor KW - Toxicology Abstracts; Immunology Abstracts KW - endotoxins KW - interleukin 1 KW - Escherichia coli KW - endotoxemia KW - F 06774:Other cytokines (TNF, GM-CSF) KW - X 24171:Microbial UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16176136?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Experimental+Medicine&rft.atitle=Differentiation+factor%2Fleukemia+inhibitory+factor+protection+against+lethal+endotoxemia+in+mice%3A+Synergistic+effect+with+interleukin+1+and+tumor+necrosis+factor.&rft.au=Alexander%2C+H+R%3BWong%2C+Grace+GH%3BDoherty%2C+G+M%3BVenzon%2C+D+J%3BFraker%2C+D+L%3BNorton%2C+JA&rft.aulast=Alexander&rft.aufirst=H&rft.date=1992-01-01&rft.volume=175&rft.issue=4&rft.spage=1139&rft.isbn=&rft.btitle=&rft.title=Journal+of+Experimental+Medicine&rft.issn=00221007&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; endotoxemia; interleukin 1; endotoxins ER - TY - JOUR T1 - An efficient automated computer vision based technique for detection of three dimensional structural motifs in proteins. AN - 16174901; 2719732 AB - We present a method to overcome the limitations. The method discovers and ranks every piece of structural similarity between the structures compared thus allowing the simultaneous detection of real 3-D motifs in different domains, between domains, in active sites, surfaces etc. The method uses the Geometric Hashing Paradigm which is an efficient technique originally developed for Computer Vision. Computer Vision techniques are for the first time applied to molecular structure comparisons, resulting in an efficient, fully automated tool. The method has been tested in a number of cases, including comparisons of the haemoglobins, immunoglobulins, serine proteinases, calcium binding proteins, DNA binding proteins and others. JF - Journal of Biomolecular Structure and Dynamics AU - Fischer, D AU - Bachar, O AU - Nussinov, R AU - Wolfson, H AD - NCI-FCRF Build. 469, Rm. 151, Frederick, MD 21712, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 769 EP - 789 VL - 9 IS - 4 SN - 0739-1102, 0739-1102 KW - Computer vision KW - DNA binding protein KW - Geometric Hashing Paradigm KW - calcium-binding protein KW - computer programmes KW - detection KW - hemoglobin KW - immunoglobulins KW - machine vision KW - motif KW - pattern recognition KW - serine proteinase KW - structure KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16174901?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biomolecular+Structure+and+Dynamics&rft.atitle=An+efficient+automated+computer+vision+based+technique+for+detection+of+three+dimensional+structural+motifs+in+proteins.&rft.au=Fischer%2C+D%3BBachar%2C+O%3BNussinov%2C+R%3BWolfson%2C+H&rft.aulast=Fischer&rft.aufirst=D&rft.date=1992-01-01&rft.volume=9&rft.issue=4&rft.spage=769&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biomolecular+Structure+and+Dynamics&rft.issn=07391102&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Oxidative modification of Escherichia coli glutamine synthetase: Decreases in the thermodynamic stability of protein structure and specific changes in the active site conformation. AN - 16155759; 2698243 AB - Metal catalyzed oxidation of specific amino acid residues has been proposed to be an important physiological mechanism of marking proteins for proteolytic degradation. After initial oxidative inactivation of dodecameric Escherichia coli glutamine synthetase (GS), the integrity of the GS active site and protein structure was assessed by monitoring ATP binding, observing a susceptibility of GS to tryptic cleavage, and comparative thermodynamic analysis. The tryptic cleavage rates of an active site linked central loop were significantly accelerated for the oxidized conformer. This tryptic cleavage was essentially prevented in the presence of glutamate for native GS but not for the oxidized conformer. Our results suggest that small free energy decreases in GS protein structural stability of only 1-2 kcal/mol may be responsible for the selective proteolytic turnover of the oxidized GS. JF - Journal of Biological Chemistry AU - Fisher, M T AU - Stadtman, E R AD - NHLBI/NIH, Build. 3, Rm. 222, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1872 EP - 1880 VL - 267 IS - 3 SN - 0021-9258, 0021-9258 KW - ATP KW - Escherichia coli KW - active sites KW - binding KW - conformation KW - glutamine synthase KW - inactivation KW - oxidation KW - thermodynamics KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology KW - J 02728:Enzymes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16155759?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Oxidative+modification+of+Escherichia+coli+glutamine+synthetase%3A+Decreases+in+the+thermodynamic+stability+of+protein+structure+and+specific+changes+in+the+active+site+conformation.&rft.au=Fisher%2C+M+T%3BStadtman%2C+E+R&rft.aulast=Fisher&rft.aufirst=M&rft.date=1992-01-01&rft.volume=267&rft.issue=3&rft.spage=1872&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Peptide binding to HLA-A2 and HLA-B27 isolated from Escherichia coli . Reconstitution of HLA-A2 and HLA-B27 heavy chain/ beta sub(2)-microglobulin complexes requires specific peptides. AN - 16149629; 2691861 AB - The specificity of peptide binding by human leucocyte antigen (HLA) class I molecules was investigated in a cell-free direct-binding assay. Peptides were assessed for binding to HLA-A2 and HLA-B27 by measuring the formation of heterotrimeric HLA complexes that consisted of iodinated beta sub(2)-microglobulin, HLA heavy chain fragments isolated from the Escherichia coli) cytoplasm and peptide. In this system, no detectable HLA heavy chain- beta sub(2)-microglobulin complexes were formed unless appropriate peptides were intentionally added to the reconstitution solution. We conclude that HLA-A2 and HLA-B27 bind distinct but partially overlapping sets of peptides and that, at least in vitro, the assembly of HLA heavy chain- beta sub(2)-microglobulin complexes requires specific peptides. JF - Journal of Biological Chemistry AU - Parker, K C AU - Carreno, B M AU - Sestak, L AU - Utz, U AU - Biddison, W E AU - Coligan, JE AD - Biol. Resour. Branch, NIAID, Build. 4, Rm. 413, NIH, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 5451 EP - 5459 VL - 267 IS - 8 SN - 0021-9258, 0021-9258 KW - histocompatibility antigen HLA KW - A2 determinant KW - B27 determinant KW - heavy chains KW - complex KW - reconstitution KW - gene expression KW - man KW - beta 2-microglobulin KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Escherichia coli KW - F 06825:Human KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16149629?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Peptide+binding+to+HLA-A2+and+HLA-B27+isolated+from+Escherichia+coli+.+Reconstitution+of+HLA-A2+and+HLA-B27+heavy+chain%2F+beta+sub%282%29-microglobulin+complexes+requires+specific+peptides.&rft.au=Parker%2C+K+C%3BCarreno%2C+B+M%3BSestak%2C+L%3BUtz%2C+U%3BBiddison%2C+W+E%3BColigan%2C+JE&rft.aulast=Parker&rft.aufirst=K&rft.date=1992-01-01&rft.volume=267&rft.issue=8&rft.spage=5451&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli ER - TY - JOUR T1 - Cigarette smoking and cancers of the renal pelvis and ureter. AN - 16139924; 2688274 AB - A population-based case-control study of renal pelvis and ureter cancers (502 cases, 496 controls) conducted in three areas of the United States found cigarette smoking to be associated with a 3.1-fold increase in risk, with long-term (> 45 years) smokers having a 7.2-fold increased risk. Statistically significant dose-response associations were observed for both cancer sites and in both sexes regardless of the measure used: cigarettes per day, duration of use, or pack years. A significant decreasing trend in risk with increasing years quit smoking was also demonstrated for these cancers. Attributable risk estimates indicate that approximately 7 of 10 cancers of the renal pelvis and ureter among men and almost 4 of 10 among women are caused by smoking. The results of this study, the largest to date, confirm that cigarette smoking is the major cause of cancers of the renal pelvis and ureter, and that cessation of smoking could eliminate a large proportion of these tumors. JF - Cancer Research AU - McLaughlin, J K AU - Silverman, D T AU - Hsing, A W AU - Ross, R K AU - Schoenberg, J B AU - Yu, M C AU - Stemhagen, A AU - Lynch, C F AU - Blot, W J AU - Fraumeni, JF Jr AD - NCI, Executive Pl. North, Rm. 415, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 254 EP - 257 VL - 52 IS - 2 SN - 0008-5472, 0008-5472 KW - cigarette smoking KW - renal pelvis KW - ureter KW - man KW - Health & Safety Science Abstracts; Toxicology Abstracts KW - cigarettes KW - cancer KW - X 24180:Social poisons & drug abuse KW - H SM10.21:CANCER UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16139924?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Research&rft.atitle=Cigarette+smoking+and+cancers+of+the+renal+pelvis+and+ureter.&rft.au=McLaughlin%2C+J+K%3BSilverman%2C+D+T%3BHsing%2C+A+W%3BRoss%2C+R+K%3BSchoenberg%2C+J+B%3BYu%2C+M+C%3BStemhagen%2C+A%3BLynch%2C+C+F%3BBlot%2C+W+J%3BFraumeni%2C+JF+Jr&rft.aulast=McLaughlin&rft.aufirst=J&rft.date=1992-01-01&rft.volume=52&rft.issue=2&rft.spage=254&rft.isbn=&rft.btitle=&rft.title=Cancer+Research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - cancer; cigarettes; ureter; man ER - TY - JOUR T1 - Carbamazepine-induced neurotoxicity and its prevention by NMDA in cultured cerebellar granule cells. AN - 16129726; 2683392 AB - Long-term neurotoxicity of carbamazepine was studied in cultured cerebellar granule cells. Treatment of cells with carbamazepine for 3 days induced a dose-dependent neurotoxicity detected by a loss of ( super(3)H)ouabain binding to Na super(+),K super(+)-ATPase, and ( super(3)H)N-methyl scopolamine binding to muscarinic cholinergic receptors as well as by direct morphologic examination. NMDA protected against carbamazepine-induced toxicity and this protection was blocked by 2-amino-5-phosphono-valerate (APV). The neurotoxicity induced by carbamazepine may be involved in the teratogenic and adverse effects of overdose associated with the treatment of manic-depressive illness and seizures. JF - Neuroscience Letters AU - Gao, Xiao-Ming AU - Chuang, De-Maw AD - Biol. Psychiatr. Branch, NIMH, Build. 10, Rm. 3N212, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 159 EP - 162 VL - 135 IS - 2 SN - 0304-3940, 0304-3940 KW - carbamazepine KW - induction KW - prevention KW - rats KW - N-methyl-D-aspartic acid KW - Toxicology Abstracts; CSA Neurosciences Abstracts KW - granule cells KW - neurotoxicity KW - cerebellum KW - N3 11104:Mammals (except primates) KW - X 24111:Acute exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16129726?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+Letters&rft.atitle=Carbamazepine-induced+neurotoxicity+and+its+prevention+by+NMDA+in+cultured+cerebellar+granule+cells.&rft.au=Gao%2C+Xiao-Ming%3BChuang%2C+De-Maw&rft.aulast=Gao&rft.aufirst=Xiao-Ming&rft.date=1992-01-01&rft.volume=135&rft.issue=2&rft.spage=159&rft.isbn=&rft.btitle=&rft.title=Neuroscience+Letters&rft.issn=03043940&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - neurotoxicity; cerebellum; granule cells ER - TY - JOUR T1 - Locating essential Escherichia coli genes by using mini-Tn10 transposons: The pdxJ operon. AN - 16128150; 2680978 AB - The mini-Tn10 transposon ( Delta 16 Delta 17Tn10) confers tetracycline resistance. When inserted between a gene and its promoter, it blocks transcription and prevents expression of that gene. Tetracycline, in the medium induces divergent transcription of the tetA and tetR genes within the transposon, and this transcription extends beyond the transposon in both directions into the bacterial genes. If the mini-Tn10 inserts between an essential bacterial gene and its promoter, the insertion mutation can cause conditional growth which is dependent on the presence of tetracycline. Two essential genes in adjacent operons of Escherichia coli have been detected by screening for tetracycline dependence among tetracycline-resistant insertion mutants. These essential genes are the era gene in the rnc operon and the dpj gene in the adjacent pdxJ operon. The pdxJ operon has not been described previously. It consists of two genes, pdxJ and dpj. Whereas the dpj gene is essential for E. coli growth in all media tested, pdxJ is not essential. JF - Journal of Bacteriology AU - Takiff, HE AU - Baker, T AU - Copeland, T AU - Chen, S AU - Court, D L AD - Mol. Control and Genet. Sect., Lab. Chromosome Biol., ABL-Basic Res. Program, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 1544 EP - 1553 VL - 174 IS - 5 SN - 0021-9193, 0021-9193 KW - Escherichia coli KW - transposon Tn10 KW - era gene KW - dpj gene KW - characterization KW - tetracycline KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology KW - transposons KW - antibiotic resistance KW - genes KW - site-directed mutagenesis KW - G 07320:Bacterial genetics KW - J 02795:Antibiotic resistance KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16128150?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Bacteriology&rft.atitle=Locating+essential+Escherichia+coli+genes+by+using+mini-Tn10+transposons%3A+The+pdxJ+operon.&rft.au=Takiff%2C+HE%3BBaker%2C+T%3BCopeland%2C+T%3BChen%2C+S%3BCourt%2C+D+L&rft.aulast=Takiff&rft.aufirst=HE&rft.date=1992-01-01&rft.volume=174&rft.issue=5&rft.spage=1544&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - transposons; site-directed mutagenesis; genes; antibiotic resistance ER - TY - JOUR T1 - Characterization of a cellular protease that cleaves Pseudomonas exotoxin. AN - 16101459; 2655324 AB - Pseudomonas exotoxin (PE) is a 66-kDa bacterial toxin that is proteolytically cleaved by cells to produce an N-terminal fragment of 28 kDa and a C-terminal 37-kDa fragment which translocates to the cytosol and inhibits protein synthesis. When cells were broken by homogenization, the appropriate proteolytic activity was found associated with cellular membranes and not in soluble fraction. Proteolysis of PE by crude membranes was stimulated by divalent cations, was ATP independent, and had a pH optimum of 5.5. When cells were disrupted by nitrogen cavitation and fractionated on Percoll gradients, proteolytic activity was present in fractions corresponding to the density of plasma membranes or endosomes but not in fractions containing lysosomes. Proteolytic activity was recovered in detergent extracts after crude membranes were treated with Nonidet P-40 or octylglucoside. Proteolysis of PE by either crude membranes or detergent extracts generated fragments of 28 and 37 kDa. The sizes of these fragments resembled those produced by intact cells. JF - Infection and Immunity AU - Fryling, C AU - Ogata, M AU - Fitzgerald, D AD - Lab. Mol. Biol., Div. Cancer Biol., Diagn. and Cent., NCI, Bethesda, MD 20892, USA Y1 - 1992 PY - 1992 DA - 1992 SP - 497 EP - 502 VL - 60 IS - 2 SN - 0019-9567, 0019-9567 KW - proteinase KW - characterization KW - cleavage KW - cells KW - mice KW - Microbiology Abstracts B: Bacteriology KW - exotoxins KW - Pseudomonas KW - J 02823:In vitro and in vivo effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16101459?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Characterization+of+a+cellular+protease+that+cleaves+Pseudomonas+exotoxin.&rft.au=Fryling%2C+C%3BOgata%2C+M%3BFitzgerald%2C+D&rft.aulast=Fryling&rft.aufirst=C&rft.date=1992-01-01&rft.volume=60&rft.issue=2&rft.spage=497&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Pseudomonas; exotoxins ER - TY - JOUR T1 - Use of bipolar membranes for ion exchange resin regenerant production AN - 13709833; S199343613 AB - The capability of bipolar membranes for producing commercial regenerants (hydrochloric acid and sodium hydroxide from a sodium chloride solution as an example) was significant when considering the advantages that included on-site, on-demand production of regenerants without any transportation problems. The adoption of zero discharge conditions for water and the use of reclaimed water would require the availability and efficiency of bipolar membranes to counteract the combined effects of higher water costs and deteriorating potable and abstracted water quality. JF - Journal of Chemical Technology & Biotechnology AU - Bolton, H R AD - NEI Thompson Limited, Wolverhampton Y1 - 1992 PY - 1992 DA - 1992 SP - 341 EP - 347 VL - 54 IS - 4 KW - Aqualine Abstracts KW - AQ 00004:Water Treatment UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/13709833?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aaqualine&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Chemical+Technology+%26+Biotechnology&rft.atitle=Use+of+bipolar+membranes+for+ion+exchange+resin+regenerant+production&rft.au=Bolton%2C+H+R&rft.aulast=Bolton&rft.aufirst=H&rft.date=1992-01-01&rft.volume=54&rft.issue=4&rft.spage=341&rft.isbn=&rft.btitle=&rft.title=Journal+of+Chemical+Technology+%26+Biotechnology&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2000-09-01 N1 - Last updated - 2011-12-12 ER - TY - JOUR T1 - The pathobiology of asbestos-induced lung disease: a proposed role for macrophage-derived growth factors. AN - 72709055; 1809136 JF - Annals of the New York Academy of Sciences AU - Lasky, J A AU - Bonner, J C AU - Brody, A R AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/12/31/ PY - 1991 DA - 1991 Dec 31 SP - 239 EP - 244 VL - 643 SN - 0077-8923, 0077-8923 KW - Cytokines KW - 0 KW - Dust KW - Growth Substances KW - Peptides KW - alveolar macrophage growth factor KW - Asbestos KW - 1332-21-4 KW - Index Medicus KW - Animals KW - Cytokines -- biosynthesis KW - Macrophages, Alveolar -- metabolism KW - Lung Diseases -- etiology KW - Lung Diseases -- metabolism KW - Asbestos -- toxicity KW - Growth Substances -- metabolism KW - Asbestos -- metabolism KW - Macrophages, Alveolar -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72709055?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=The+pathobiology+of+asbestos-induced+lung+disease%3A+a+proposed+role+for+macrophage-derived+growth+factors.&rft.au=Lasky%2C+J+A%3BBonner%2C+J+C%3BBrody%2C+A+R&rft.aulast=Lasky&rft.aufirst=J&rft.date=1991-12-31&rft.volume=643&rft.issue=&rft.spage=239&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-15 N1 - Date created - 1992-05-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenicity of chrysotile asbestos: evidence from cohort studies. AN - 72706645; 1809127 JF - Annals of the New York Academy of Sciences AU - Dement, J M AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/12/31/ PY - 1991 DA - 1991 Dec 31 SP - 15 EP - 23 VL - 643 SN - 0077-8923, 0077-8923 KW - Carcinogens KW - 0 KW - Asbestos KW - 1332-21-4 KW - Mineral Oil KW - 8020-83-5 KW - Index Medicus KW - United States KW - Humans KW - Cohort Studies KW - Mineral Oil -- adverse effects KW - Environmental Exposure KW - Lung Neoplasms -- etiology KW - Lung Neoplasms -- epidemiology KW - Textiles KW - Asbestos -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72706645?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=Carcinogenicity+of+chrysotile+asbestos%3A+evidence+from+cohort+studies.&rft.au=Dement%2C+J+M&rft.aulast=Dement&rft.aufirst=J&rft.date=1991-12-31&rft.volume=643&rft.issue=&rft.spage=15&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-15 N1 - Date created - 1992-05-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Apoptosis and DNA degradation induced by 1-methyl-4-phenylpyridinium in neurons. AN - 72600205; 1764096 AB - Apoptosis is a prominent mechanism of programmed cell death in lymphocytes and in cancer cells not previously found in neurons. We have identified apoptosis and internucleosomal DNA degradation in cultures of cerebellar granule neurons. 1-methyl-4-phenylpyridinium, a selective neurotoxin that destroys the dopaminergic nigrostriatal pathway and results in a parkinsonian syndrome, increases the rate of apoptosis and kills cerebellar granule cells in culture via induction of programmed cell death. Inhibition of gene expression in granule cells with cycloheximide prevents the MPP(+)-induced apoptosis and the DNA fragmentation. Our findings demonstrate a new pathway of neuron death and suggest the possibility that neurodegenerative diseases may result from the inappropriate activation of programmed cell death by apoptosis. JF - Biochemical and biophysical research communications AU - Dipasquale, B AU - Marini, A M AU - Youle, R J AD - Biochemistry Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-0010. Y1 - 1991/12/31/ PY - 1991 DA - 1991 Dec 31 SP - 1442 EP - 1448 VL - 181 IS - 3 SN - 0006-291X, 0006-291X KW - DNA KW - 9007-49-2 KW - Cycloheximide KW - 98600C0908 KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Index Medicus KW - Rats KW - Animals KW - Cells, Cultured KW - Kinetics KW - Cycloheximide -- pharmacology KW - DNA -- isolation & purification KW - Cerebellum -- cytology KW - Neurons -- drug effects KW - Neurons -- cytology KW - Neurons -- physiology KW - Cell Death -- drug effects KW - Cerebellum -- physiology KW - DNA -- drug effects KW - 1-Methyl-4-phenylpyridinium -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72600205?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+biophysical+research+communications&rft.atitle=Apoptosis+and+DNA+degradation+induced+by+1-methyl-4-phenylpyridinium+in+neurons.&rft.au=Dipasquale%2C+B%3BMarini%2C+A+M%3BYoule%2C+R+J&rft.aulast=Dipasquale&rft.aufirst=B&rft.date=1991-12-31&rft.volume=181&rft.issue=3&rft.spage=1442&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+biophysical+research+communications&rft.issn=0006291X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-07 N1 - Date created - 1992-02-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dexamethasone prevents the growth inhibitory effects of recombinant tumor necrosis factor in a rat hepatoma cell line Reuber-RC-3: an association with the changes in the messenger RNA levels for multidrug resistance gene. AN - 72571375; 1722406 AB - Two days exposure to recombinant tumor necrosis factor (rTNF-alpha) produced a dose-dependent reduction in (methyl-3H) thymidine incorporation in RC-3 cells (ID50 = 25 units/ml). Prolonged treatment with rTNF-alpha further resulted in a significant reduction in colony formation (ID50 = 200 units/ml), which was reversed upon removal of the agent. Interferon levels were undetectable in the supernatants of the rTNF-alpha treated cells. Simultaneous exposure to dexamethasone prevented the growth inhibition in rTNF-alpha-treated RC-3 cells. Significant dose-dependent increase in the steady state levels of the mRNA for multidrug resistance (MDR1) gene was observed after rTNF-alpha treatment while simultaneous exposure to dexamethasone produced a substantial reduction in the mRNA levels for MDR1 gene. These data suggest that growth inhibitory effects of TNF are regulated by dexamethasone and are associated with changes in MDR1 mRNA levels in hepatoma-derived cells. JF - Biochemical and biophysical research communications AU - Chapekar, M S AU - Huggett, A C AU - Cheng, C AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/12/31/ PY - 1991 DA - 1991 Dec 31 SP - 1524 EP - 1531 VL - 181 IS - 3 SN - 0006-291X, 0006-291X KW - RNA, Messenger KW - 0 KW - Recombinant Proteins KW - Tumor Necrosis Factor-alpha KW - Dexamethasone KW - 7S5I7G3JQL KW - Interferons KW - 9008-11-1 KW - Thymidine KW - VC2W18DGKR KW - Index Medicus KW - Thymidine -- metabolism KW - Rats KW - Liver Neoplasms, Experimental KW - Animals KW - Recombinant Proteins -- pharmacology KW - Kinetics KW - Interferons -- analysis KW - Tumor Stem Cell Assay KW - Recombinant Proteins -- antagonists & inhibitors KW - DNA Replication -- drug effects KW - Cell Line KW - Drug Resistance -- genetics KW - RNA, Messenger -- metabolism KW - Dexamethasone -- pharmacology KW - Tumor Necrosis Factor-alpha -- pharmacology KW - RNA, Messenger -- drug effects KW - Cell Division -- drug effects KW - Tumor Necrosis Factor-alpha -- antagonists & inhibitors KW - RNA, Messenger -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72571375?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+biophysical+research+communications&rft.atitle=Dexamethasone+prevents+the+growth+inhibitory+effects+of+recombinant+tumor+necrosis+factor+in+a+rat+hepatoma+cell+line+Reuber-RC-3%3A+an+association+with+the+changes+in+the+messenger+RNA+levels+for+multidrug+resistance+gene.&rft.au=Chapekar%2C+M+S%3BHuggett%2C+A+C%3BCheng%2C+C&rft.aulast=Chapekar&rft.aufirst=M&rft.date=1991-12-31&rft.volume=181&rft.issue=3&rft.spage=1524&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+biophysical+research+communications&rft.issn=0006291X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-07 N1 - Date created - 1992-02-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of hair follicle cell proliferation and collagenolytic activity by specific growth factors. AN - 72711874; 1809087 JF - Annals of the New York Academy of Sciences AU - Weinberg, W C AU - Brown, P D AU - Stetler-Stevenson, W G AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20852. Y1 - 1991/12/26/ PY - 1991 DA - 1991 Dec 26 SP - 281 EP - 290 VL - 642 SN - 0077-8923, 0077-8923 KW - Growth Substances KW - 0 KW - Transforming Growth Factor alpha KW - Collagen KW - 9007-34-5 KW - Thymidine KW - VC2W18DGKR KW - Index Medicus KW - Thymidine -- metabolism KW - Animals, Newborn KW - Animals KW - Drug Interactions KW - Cells, Cultured KW - Kinetics KW - Cell Division -- drug effects KW - Transforming Growth Factor alpha -- pharmacology KW - Mice KW - Hair -- drug effects KW - Hair -- cytology KW - Collagen -- metabolism KW - Hair -- metabolism KW - Growth Substances -- pharmacology KW - DNA Replication -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72711874?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=Modulation+of+hair+follicle+cell+proliferation+and+collagenolytic+activity+by+specific+growth+factors.&rft.au=Weinberg%2C+W+C%3BBrown%2C+P+D%3BStetler-Stevenson%2C+W+G%3BYuspa%2C+S+H&rft.aulast=Weinberg&rft.aufirst=W&rft.date=1991-12-26&rft.volume=642&rft.issue=&rft.spage=281&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-19 N1 - Date created - 1992-05-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hair follicle transglutaminases. AN - 72701469; 1687305 JF - Annals of the New York Academy of Sciences AU - Lichti, U AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/12/26/ PY - 1991 DA - 1991 Dec 26 SP - 82 EP - 98; discussion 98-9 VL - 642 SN - 0077-8923, 0077-8923 KW - Detergents KW - 0 KW - Polyethylene Glycols KW - 30IQX730WE KW - Octoxynol KW - 9002-93-1 KW - Transglutaminases KW - EC 2.3.2.13 KW - Index Medicus KW - Animals KW - Electrophoresis, Polyacrylamide Gel KW - Mice KW - Chromatography, Ion Exchange KW - Mice, Inbred BALB C KW - Molecular Weight KW - Hair -- enzymology KW - Transglutaminases -- metabolism KW - Skin -- enzymology KW - Hair -- cytology KW - Transglutaminases -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72701469?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=Hair+follicle+transglutaminases.&rft.au=Lichti%2C+U&rft.aulast=Lichti&rft.aufirst=U&rft.date=1991-12-26&rft.volume=642&rft.issue=&rft.spage=265&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunotherapy+%3A+official+journal+of+the+Society+for+Biological+Therapy&rft.issn=10538550&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-19 N1 - Date created - 1992-05-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - An Alu polymorphism intragenic to the TP53 gene. AN - 72594698; 1762941 JF - Nucleic acids research AU - Futreal, P A AU - Barrett, J C AU - Wiseman, R W AD - Lab. of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709. Y1 - 1991/12/25/ PY - 1991 DA - 1991 Dec 25 SP - 6977 VL - 19 IS - 24 SN - 0305-1048, 0305-1048 KW - ALE3 KW - TP53 KW - Oligodeoxyribonucleotides KW - 0 KW - Index Medicus KW - Polymerase Chain Reaction KW - Base Sequence KW - Alleles KW - Sequence Homology, Nucleic Acid KW - Polymorphism, Genetic KW - Humans KW - Molecular Sequence Data KW - Oligodeoxyribonucleotides -- genetics KW - Introns -- genetics KW - Chromosomes, Human, Pair 17 KW - Genes, p53 KW - Repetitive Sequences, Nucleic Acid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72594698?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+acids+research&rft.atitle=An+Alu+polymorphism+intragenic+to+the+TP53+gene.&rft.au=Futreal%2C+P+A%3BBarrett%2C+J+C%3BWiseman%2C+R+W&rft.aulast=Futreal&rft.aufirst=P&rft.date=1991-12-25&rft.volume=19&rft.issue=24&rft.spage=6977&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-11 N1 - Date created - 1992-02-11 N1 - Date revised - 2017-01-13 N1 - Gene symbol - ALE3; TP53 N1 - SuppNotes - Cited By: J Neurochem. 1991 Mar;56(3):1024-9 [1825222] Am J Hum Genet. 1989 Nov;45(5):778-85 [2573278] Genomics. 1991 Jul;10(3):816-26 [1889821] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A sectored colony assay for monitoring mutagenesis by specific carcinogen-DNA adducts in Escherichia coli. AN - 72576963; 1751489 AB - To study the mutagenicity of various carcinogen-DNA adducts in Escherichia coli, a cassette plasmid was developed that permits positioning of specific carcinogen-modified bases within the ATG initiation codon of the lacZ' alpha-complementation gene. Adduct-induced mutations inactivate the gene and lead to formation of blue and white sectored colonies when transformants from an alpha-complementing version of E. coli strain AB1157 are grown on media containing 5-bromo-4-chloro-3-indolyl beta-D-galactoside. In the absence of mutation, blue colonies are produced. This system has been used to measure the mutagenicity of O6-methyl-, O6-ethyl-, and O6-benzyl-2'-deoxyguanosine residues incorporated in place of the normal 2'-deoxyguanosine of the ATG initiation codon. Although a low percentage of sectored colonies was produced in this repair-proficient strain, pretreatment of the bacteria with N-methyl-N'-nitro-N-nitrosoguanidine to disable DNA repair led to a dose-dependent increase in the percentage of sectored colonies. This percentage increased as a function of modified guanine in the order O6-benzyl- less than O6-methyl- less than O6-ethyl-2'-deoxy-guanosine. The only mutations detected at the site of incorporation of these O6-substituted guanines were G-to-A transitions. This sectored colony assay system permits convenient screening of large numbers of colonies and simplifies quantification of modified-base-induced mutations whether they be single-base changes, frameshifts, insertions, or deletions. JF - Biochemistry AU - Pauly, G T AU - Hughes, S H AU - Moschel, R C AD - Chemistry of Carcinogenesis Laboratory, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1991/12/17/ PY - 1991 DA - 1991 Dec 17 SP - 11700 EP - 11706 VL - 30 IS - 50 SN - 0006-2960, 0006-2960 KW - lacZ KW - Carcinogens KW - 0 KW - DNA, Bacterial KW - beta-Galactosidase KW - EC 3.2.1.23 KW - Deoxyguanosine KW - G9481N71RO KW - Index Medicus KW - Base Sequence KW - Phosphorylation KW - Molecular Sequence Data KW - Electrophoresis, Agar Gel KW - beta-Galactosidase -- genetics KW - Deoxyguanosine -- toxicity KW - Carcinogens -- pharmacology KW - Mutagenicity Tests KW - Plasmids KW - DNA, Bacterial -- drug effects KW - Deoxyguanosine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72576963?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=A+sectored+colony+assay+for+monitoring+mutagenesis+by+specific+carcinogen-DNA+adducts+in+Escherichia+coli.&rft.au=Pauly%2C+G+T%3BHughes%2C+S+H%3BMoschel%2C+R+C&rft.aulast=Pauly&rft.aufirst=G&rft.date=1991-12-17&rft.volume=30&rft.issue=50&rft.spage=11700&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-30 N1 - Date created - 1992-01-30 N1 - Date revised - 2017-01-13 N1 - Gene symbol - lacZ N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Changes in binding activity of luteinizing hormone receptors by site directed mutagenesis of potential glycosylation sites. AN - 72569922; 1755859 AB - Site directed mutagenesis of the rat ovarian luteinizing hormone (LH) receptor cDNA was performed at each of the six potential N-linked glycosylation sites to determine the effect of putative carbohydrate chains on the activity of the membrane receptor. The conversion of Asn173 to Gln resulted in the total loss of hormone binding to the surface of the transfected cell. Mutant receptors synthesized with substitutions at the remaining potential N-linked glycosylation positions of 77, 152, 269, 277 and 291 revealed no significant change in the hormone affinity. However Asn77Gln and Asn152Gln exhibited significant decreases (approximately 80%) in the number of high affinity hormone binding sites. The changes in hormone binding activity upon elimination of the potential glycosylation sites at 77, 152 and 173 indicate the presence of functional carbohydrate chains at these positions in the rat ovarian LH/hCG receptor. JF - Biochemical and biophysical research communications AU - Zhang, R AU - Tsai-Morris, C H AU - Kitamura, M AU - Buczko, E AU - Dufau, M L AD - Section on Molecular Endocrinology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/12/16/ PY - 1991 DA - 1991 Dec 16 SP - 804 EP - 808 VL - 181 IS - 2 SN - 0006-291X, 0006-291X KW - Receptors, LH KW - 0 KW - Glutamine KW - 0RH81L854J KW - Asparagine KW - 7006-34-0 KW - Index Medicus KW - Rats KW - Animals KW - Ovary -- chemistry KW - Transfection KW - Humans KW - Genetic Vectors KW - Glycosylation KW - Female KW - Cell Line KW - Protein Conformation KW - Carbohydrate Conformation KW - Binding Sites KW - Mutagenesis, Site-Directed KW - Receptors, LH -- chemistry KW - Receptors, LH -- genetics KW - Receptors, LH -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72569922?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+biophysical+research+communications&rft.atitle=Changes+in+binding+activity+of+luteinizing+hormone+receptors+by+site+directed+mutagenesis+of+potential+glycosylation+sites.&rft.au=Zhang%2C+R%3BTsai-Morris%2C+C+H%3BKitamura%2C+M%3BBuczko%2C+E%3BDufau%2C+M+L&rft.aulast=Zhang&rft.aufirst=R&rft.date=1991-12-16&rft.volume=181&rft.issue=2&rft.spage=804&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+biophysical+research+communications&rft.issn=0006291X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-24 N1 - Date created - 1992-01-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The JAM test. A simple assay for DNA fragmentation and cell death. AN - 72590879; 1765650 AB - Most current methods for measuring cell death are based on plasma membrane disintegration and the consequent release of cytoplasm. The relevant cells are usually loaded with a label (usually 51Cr or 125I), the release of which is measured. I describe here a method, based on the recent evidence that dying cells often degrade their DNA into small fragments, which measures the DNA retained by living cells rather than the cellular components lost by dying cells. The assay is set up essentially like the current cell lysis assays and harvested like a cell proliferation assay. It is faster, more sensitive, easier to set up, less expensive and safer than the current standard 51Cr release assay. JF - Journal of immunological methods AU - Matzinger, P AD - Laboratory for Cellular and Molecular Immunology, Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/12/15/ PY - 1991 DA - 1991 Dec 15 SP - 185 EP - 192 VL - 145 IS - 1-2 SN - 0022-1759, 0022-1759 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - In Vitro Techniques KW - DNA -- analysis KW - Mice KW - Mice, Inbred BALB C KW - Killer Cells, Natural -- immunology KW - DNA Damage KW - Cell Death KW - Cytotoxicity Tests, Immunologic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72590879?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunological+methods&rft.atitle=The+JAM+test.+A+simple+assay+for+DNA+fragmentation+and+cell+death.&rft.au=Matzinger%2C+P&rft.aulast=Matzinger&rft.aufirst=P&rft.date=1991-12-15&rft.volume=145&rft.issue=1-2&rft.spage=185&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunological+methods&rft.issn=00221759&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-14 N1 - Date created - 1992-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Relationship between DNA cross-links, cell cycle, and apoptosis in Burkitt's lymphoma cell lines differing in sensitivity to nitrogen mustard. AN - 72507199; 1742728 AB - We surveyed 11 Burkitt's lymphoma cell lines for chemosensitivity to nitrogen mustard (HN2) in order to determine whether any simple correlates to cytotoxic response might be revealed. The lines tested varied over a 5-fold range in concentration of HN2 required to inhibit tumor cell growth by 50%. Drug sensitivity correlated neither with continental origin of tumor, growth fraction, presence of Epstein-Barr virus, nor with the precise locations of (8;14) translocation breakpoints. Furthermore, contrary to experience with other cell lines, no simple correlation was found between the HN2 sensitivity of the four most divergent lines (low sensitivity, CA46 and MC116 cells; high sensitivity, Namalwa and JLP119 cells) and exposure to DNA cross-links (area under the DNA cross-linking-versus-time curve). In addition, we found similar extents of gene-specific HN2-induced damage in the native and translocated c-myc alleles of CA46 and JLP119 cells. At equimolar HN2 treatment, CA46 cells exhibited a profound arrest in G2M phase, while JLP119 cells exhibited prolonged S-phase delay. This suggested that despite similar DNA cross-link exposure, JLP119 cells were less able to complete DNA replication while repair was in progress. As cell cycle distribution returned to near normal, JLP119 cells exhibited DNA degradation characterized by oligonucleosome-sized DNA fragments prior to cell membrane disintegration. Our findings indicate that HN2-sensitive Burkitt's lymphoma cells may be more susceptible to delay in S phase for a given frequency of DNA cross-links and that prolongation of S phase correlated with apoptotic cell death. JF - Cancer research AU - O'Connor, P M AU - Wassermann, K AU - Sarang, M AU - Magrath, I AU - Bohr, V A AU - Kohn, K W AD - Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/12/15/ PY - 1991 DA - 1991 Dec 15 SP - 6550 EP - 6557 VL - 51 IS - 24 SN - 0008-5472, 0008-5472 KW - Cross-Linking Reagents KW - 0 KW - Mechlorethamine KW - 50D9XSG0VR KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Cross-Linking Reagents -- chemistry KW - DNA Repair KW - Tumor Cells, Cultured KW - Genes, myc KW - Humans KW - In Vitro Techniques KW - Drug Resistance KW - DNA -- chemistry KW - Alkylation KW - Mechlorethamine -- toxicity KW - DNA Damage KW - Burkitt Lymphoma -- physiopathology KW - Cell Death -- drug effects KW - Cell Cycle -- drug effects KW - Burkitt Lymphoma -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72507199?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Relationship+between+DNA+cross-links%2C+cell+cycle%2C+and+apoptosis+in+Burkitt%27s+lymphoma+cell+lines+differing+in+sensitivity+to+nitrogen+mustard.&rft.au=O%27Connor%2C+P+M%3BWassermann%2C+K%3BSarang%2C+M%3BMagrath%2C+I%3BBohr%2C+V+A%3BKohn%2C+K+W&rft.aulast=O%27Connor&rft.aufirst=P&rft.date=1991-12-15&rft.volume=51&rft.issue=24&rft.spage=6550&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-15 N1 - Date created - 1992-01-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanisms of hypoxic and aerobic cytotoxicity of mitomycin C in Chinese hamster V79 cells. AN - 72503754; 1660344 AB - Mitomycin C (MMC) induced aerobic and hypoxic cytotoxicity in Chinese hamster V79 cells was studied to evaluate the role of the 1-electron versus 2-electron reductive bioactivation. Superoxide dismutase, catalase, and desferal had no protective effects on the aerobic or hypoxic cytotoxicity of MMC, whereas Tempol and Tempol-H, which are known to interrupt and terminate radical reactions, provided partial protection under aerobic conditions. However, under hypoxic conditions, Tempol provided complete protection whereas Tempol-H was ineffective. Electron paramagnetic resonance and spin-trapping investigations, designed to study the mechanisms of such protective effects, confirmed that MMC is activated by the human NADPH:cytochrome P-450 oxidoreductase to its semiquinone radical and that, under aerobic conditions, the semiquinone radical reduces molecular oxygen. Under hypoxic conditions, the semiquinone of MMC reduces H2O2 to produce OH radicals as detected by electron paramagnetic resonance-spin trapping with 5,5-dimethyl-1-pyrroline N-oxide. The 1-electron reduced product of MMC was also found to reduce Tempol to the hydroxylamine, Tempol-H, whereas oxidation of Tempol-H by MMC-. was negligible. Cell survival studies and electron paramagnetic resonance observations indicate that the hypoxic cytotoxicity of MMC is mediated by 1-electron activation to its semiquinone intermediate. Under aerobic conditions, the steady state concentration of this intermediate is low due to the facile autooxidation of the semiquinone producing O2-. and H2O2 which are capable of causing oxidative cytotoxicity. Tempol, which can accept an electron from reducing radical species, completely inhibited the hypoxic cytotoxicity of MMC indicating MMC-., the semiquinone of MMC as the species responsible for DNA alkylation and selective hypoxic cytotoxicity of MMC. Our results also indicate that the aerobic cytotoxicity is mediated by other processes in addition to the 1-electron mediated activation. JF - Cancer research AU - Krishna, M C AU - DeGraff, W AU - Tamura, S AU - Gonzalez, F J AU - Samuni, A AU - Russo, A AU - Mitchell, J B AD - Radiation Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1991/12/15/ PY - 1991 DA - 1991 Dec 15 SP - 6622 EP - 6628 VL - 51 IS - 24 SN - 0008-5472, 0008-5472 KW - Alkylating Agents KW - 0 KW - Cyclic N-Oxides KW - Free Radicals KW - Spin Labels KW - Mitomycin KW - 50SG953SK6 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - tempol KW - U78ZX2F65X KW - Index Medicus KW - Animals KW - Superoxide Dismutase -- metabolism KW - Oxidation-Reduction KW - Cell Survival -- drug effects KW - Electron Spin Resonance Spectroscopy KW - Hypoxia KW - In Vitro Techniques KW - Alkylating Agents -- chemistry KW - Aerobiosis KW - Cell Line KW - Cricetinae KW - Hydrogen Peroxide -- chemistry KW - Cyclic N-Oxides -- pharmacology KW - Mitomycin -- toxicity KW - Cyclic N-Oxides -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72503754?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Mechanisms+of+hypoxic+and+aerobic+cytotoxicity+of+mitomycin+C+in+Chinese+hamster+V79+cells.&rft.au=Krishna%2C+M+C%3BDeGraff%2C+W%3BTamura%2C+S%3BGonzalez%2C+F+J%3BSamuni%2C+A%3BRusso%2C+A%3BMitchell%2C+J+B&rft.aulast=Krishna&rft.aufirst=M&rft.date=1991-12-15&rft.volume=51&rft.issue=24&rft.spage=6622&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-15 N1 - Date created - 1992-01-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of intravenous magnesium in suspected acute myocardial infarction: overview of randomised trials. AN - 72635270; 1838289 AB - To investigate the effect of intravenous magnesium on mortality in suspected acute myocardial infarction. Systematic overview of all available randomised trials in which patients were allocated to receive either intravenous magnesium or otherwise similar treatment without magnesium. Coronary care units of several hospitals. 1301 patients in seven randomised trials. Short term mortality. Considering the seven trials collectively there were 25 (3.8%) deaths among 657 patients allocated to receive magnesium and 53 (8.2%) deaths among 644 patients allocated control, generally during hospital follow up. This represents a 55% reduction in the odds of death (p less than 0.001) with 95% confidence intervals ranging from about one third to about two thirds. 70 of 648 patients allocated magnesium compared with 109 of 641 controls had serious ventricular arrhythmias, suggesting that magnesium reduces the incidence, though the definition varied among trials. Other adverse effects were rare in the limited number of patients for whom this data were available. Despite the limited number of patients randomised this overview suggests that intravenous magnesium therapy may reduce mortality in patients with acute myocardial infarction. Further large scale trials to confirm (or refute) these findings are desirable. JF - BMJ (Clinical research ed.) AU - Teo, K K AU - Yusuf, S AU - Collins, R AU - Held, P H AU - Peto, R AD - Division of Epidemiology and Clinical Applications, National Heart, Lung, and Blood Institute, Bethesda, Maryland. Y1 - 1991/12/14/ PY - 1991 DA - 1991 Dec 14 SP - 1499 EP - 1503 VL - 303 IS - 6816 SN - 0959-8138, 0959-8138 KW - Magnesium KW - I38ZP9992A KW - Abridged Index Medicus KW - Index Medicus KW - Single-Blind Method KW - Infusions, Intravenous KW - Hospitalization KW - Humans KW - Meta-Analysis as Topic KW - Myocardial Infarction -- mortality KW - Magnesium -- administration & dosage KW - Magnesium -- therapeutic use KW - Magnesium -- adverse effects KW - Myocardial Infarction -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72635270?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMJ+%28Clinical+research+ed.%29&rft.atitle=Effects+of+intravenous+magnesium+in+suspected+acute+myocardial+infarction%3A+overview+of+randomised+trials.&rft.au=Teo%2C+K+K%3BYusuf%2C+S%3BCollins%2C+R%3BHeld%2C+P+H%3BPeto%2C+R&rft.aulast=Teo&rft.aufirst=K&rft.date=1991-12-14&rft.volume=303&rft.issue=6816&rft.spage=1499&rft.isbn=&rft.btitle=&rft.title=BMJ+%28Clinical+research+ed.%29&rft.issn=09598138&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-16 N1 - Date created - 1992-03-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Rev Can Biol. 1960 Jun;19:122-35 [14422911] Br J Clin Pharmacol. 1991 Jul;32(1):3-10 [1888638] Am J Physiol. 1971 Apr;220(4):938-44 [4323905] Lancet. 1986 Feb 1;1(8475):234-6 [2868254] Lancet. 1986 Mar 8;1(8480):552-3 [2869274] Prog Cardiovasc Dis. 1985 Mar-Apr;27(5):335-71 [2858114] JAMA. 1988 Oct 7;260(13):1910-6 [3047448] Int J Cardiol. 1986 Aug;12(2):175-83 [2427458] JAMA. 1989 Dec 1;262(21):3037-40 [2509746] Arch Intern Med. 1989 Dec;149(12):2694-8 [2688587] Am Heart J. 1989 Dec;118(6):1333-4 [2589170] Clin Cardiol. 1988 Jun;11(6):377-81 [3396238] Am J Cardiol. 1988 Mar 1;61(8):515-8 [3344676] Magnesium. 1984;3(4-6):346-52 [6399346] Arch Intern Med. 1987 Apr;147(4):753-5 [3548627] Stat Med. 1987 Apr-May;6(3):245-54 [3616282] Stat Med. 1987 Apr-May;6(3):233-44 [3616281] Am Heart J. 1986 Oct;112(4):847-9 [3766386] Arch Intern Med. 1986 May;146(5):872-4 [3963976] J Am Coll Cardiol. 1985 Feb;5(2 Pt 1):280-9 [3968312] Am J Cardiol. 1990 Aug 1;66(3):271-4 [2195862] Lancet. 1980 Oct 4;2(8197):720-2 [6106829] S Afr Med J. 1983 Nov 5;64(20):775-6 [6635865] Acta Med Scand. 1980;207(1-2):59-66 [7368975] Science. 1980 Apr 11;208(4440):198-200 [7361117] Am Heart J. 1979 Jan;97(1):12-8 [83101] Am J Physiol. 1979 Oct;237(4):H413-23 [386807] Eur J Pharmacol. 1978 Dec 1;52(3-4):421-3 [729651] Am Heart J. 1977 Nov;94(5):600-2 [910698] Comment In: BMJ. 1992 Feb 15;304(6824):447-8 [1547408] BMJ. 1992 Jan 11;304(6819):119 [1737122] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differences in skin carcinogenesis by methylnitrosourea between mice of several strains. AN - 72609153; 1764693 AB - To compare the susceptibilities of the skin of different strains of mice to the carcinogenic effect of a directly acting alkylating agent, groups of 20 mice were treated twice a week with 25 microliters of a solution of methylnitrosourea in methanol. The solution was 0.04M and was applied to the shaved back of female BALB/c, Sencar, CD-1 and Swiss mice for 25 weeks. Four groups of 20 mice of each strain were 8 weeks old at the beginning of treatment. Another four groups were 58 weeks old when treatment began. More of the BALB/c mice developed skin tumors than the other three strains, the Sencar mice somewhat less. Few CD-1 mice developed skin tumors and about one third of the Swiss mice. In all four strains, there were fewer animals with skin tumors among those begun at 58 weeks than in the young mice, but the difference was small. Survival was poor among CD-1 mice, but there was not a large difference between the strains in time of appearance of first tumor, or in average latent period of skin tumors, almost all of which were carcinomas. The Sencar mice were not outstandingly more sensitive to skin carcinogenesis by MNU, as they were to UV radiation-induced skin carcinogenesis. In a comparable study in Swiss mice neither dimethylnitrosourea nor diethylnitrosourea induced skin tumors by painting and both showed only a weak systemic carcinogenic effect in the lungs, although they are directly acting mutagens. JF - Cancer letters AU - Lijinsky, W AU - Thomas, B J AU - Kovatch, R M AD - ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, MD 21702. Y1 - 1991/12/09/ PY - 1991 DA - 1991 Dec 09 SP - 1 EP - 5 VL - 61 IS - 1 SN - 0304-3835, 0304-3835 KW - Methylnitrosourea KW - 684-93-5 KW - Index Medicus KW - Animals KW - Neoplasms, Experimental -- chemically induced KW - Disease Models, Animal KW - Mice KW - Mice, Inbred BALB C KW - Female KW - Skin Neoplasms -- chemically induced KW - Mice, Inbred Strains -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72609153?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+letters&rft.atitle=Differences+in+skin+carcinogenesis+by+methylnitrosourea+between+mice+of+several+strains.&rft.au=Lijinsky%2C+W%3BThomas%2C+B+J%3BKovatch%2C+R+M&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1991-12-09&rft.volume=61&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Cancer+letters&rft.issn=03043835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-20 N1 - Date created - 1992-02-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The uptake of pristane (2,6,10,14-tetramethylpentadecane) into phospholipid bilayers as assessed by NMR, DSC, and tritium labeling methods. AN - 72588036; 1764453 AB - Unilamellar dioleoylphosphatidylcholine (DOPC) liposomes (250 microM) incorporated 2 mol% of [3H]pristane at 37 degrees C after addition of 50 microM pristane solubilized with beta-cyclodextrin. Conventional solubilization in dimethyl sulphoxide resulted in much lower uptake. Premixing of perdeuterated pristane with DOPC and dipalmitoylphosphatidylcholine (DPPC) prior to the formation of multilamellar liposomes resulted in homogeneous incorporation of up to 5 mol% pristane at 22 degrees C and 50 degrees C, respectively, as observed by 2H-NMR. Lipid order parameters measured by 31P and 2H-NMR remained unchanged after pristane uptake. Pristane induced the transformation of part of the dioleoylphosphatidylethanolamine (DOPE)/DOPC (3:1, mol/mol) liquid crystalline lamellar phase into an inverse hexagonal phase. 5 mol% pristane in DPPC bilayers decreased the midpoint of the main phase transition temperature of DPPC from 41.5 degrees C to 40.9 degrees C. Upon cooling in the temperature range from 41 degrees C to 36 degrees C, pristane was either displaced from the DPPC bilayer or the mode of incorporation changed. These results may aid in defining the mechanisms whereby pristane, an isoprenoid C19-isoalkane, induces plasmacytomagenesis in mice. JF - Biochimica et biophysica acta AU - Gawrisch, K AU - Janz, S AD - Division of Computer Research and Technology, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/12/09/ PY - 1991 DA - 1991 Dec 09 SP - 409 EP - 418 VL - 1070 IS - 2 SN - 0006-3002, 0006-3002 KW - Carcinogens KW - 0 KW - Lipid Bilayers KW - Phosphatidylcholines KW - Phosphatidylethanolamines KW - Phospholipids KW - Terpenes KW - Tritium KW - 10028-17-8 KW - 1,2-Dipalmitoylphosphatidylcholine KW - 2644-64-6 KW - pristane KW - 26HZV48DT1 KW - 1,2-dielaidoylphosphatidylethanolamine KW - 76391-83-8 KW - 1,2-oleoylphosphatidylcholine KW - H026DM5V6U KW - Index Medicus KW - Magnetic Resonance Spectroscopy -- methods KW - Radioisotope Dilution Technique KW - 1,2-Dipalmitoylphosphatidylcholine -- chemistry KW - Models, Biological KW - Phosphatidylethanolamines -- chemistry KW - Calorimetry, Differential Scanning -- methods KW - Phospholipids -- chemistry KW - Terpenes -- chemistry KW - Phosphatidylcholines -- chemistry KW - Carcinogens -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72588036?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.atitle=Role+of+nitric+oxide+in+antagonistic+effects+of+transforming+growth+factor-beta+and+interleukin-1+beta+on+the+beating+rate+of+cultured+cardiac+myocytes.&rft.au=Roberts%2C+A+B%3BVodovotz%2C+Y%3BRoche%2C+N+S%3BSporn%2C+M+B%3BNathan%2C+C+F&rft.aulast=Roberts&rft.aufirst=A&rft.date=1992-11-01&rft.volume=6&rft.issue=11&rft.spage=1921&rft.isbn=&rft.btitle=&rft.title=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.issn=08888809&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-14 N1 - Date created - 1992-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Isolation and characterization of the human gene for ADP-ribosylation factor 3, a 20-kDa guanine nucleotide-binding protein activator of cholera toxin. AN - 72514203; 1744102 AB - ADP-ribosylation factors (ARFs) are approximately 20-kDa guanine nucleotide-binding proteins that stimulate the ADP-ribosyltransferase activity of cholera toxin in vitro. Five different human ARFs have been identified by cDNA cloning. Northern analysis using ARF 3-specific oligonucleotides identified two mRNAs of 3.7 and 1.2 kilobases (kb). We report here the complete nucleotide sequence of the 3.7-kb ARF 3 mRNA derived from three overlapping cDNAs isolated from human hippocampus and fetal brain cDNA libraries, as well as the structure of human ARF 3 gene. Sequences of two overlapping genomic clones indicated that the ARF 3 gene spans approximately 18.3 kb and contains five exons and four introns. The conserved amino acid sequences involved in guanine nucleotide binding by ARF 3 are distributed among separate exons, as found in other GTP-binding protein genes. Translation initiates in exon 2 which includes the sequence GXXXXGK that probably participates in phosphate binding and GTP hydrolysis. The sequence DVGG in exon 3 coordinates binding of Mg2+ and the beta-phosphate of GDP. In the ARF 3 gene in contrast to those of other GTP-binding proteins, the sequence NKXD (which is thought to contribute to the specificity of interaction with the guanine ring) is divided between exons 4 and 5. The latter encodes the COOH-terminal 53 amino acids of ARF 3 and contains greater than 2500 base pairs of untranslated DNA. The sequence AATTAA is 19 bases 5' to the polyadenylation addition site of the 3.7-kb mRNA. Multiple transcription start sites were identified by primer extension and S1 and mung bean nuclease analyses. The 5'-flanking region of exon 1 contains neither a TATA nor a CAAT box, but is high in GC content (greater than 70%) and includes three potential Sp1-binding sites (GC box), consistent with the promoters described for several housekeeping genes. The 1.2-kb ARF 3 mRNA is shown to arise by use of an alternative polyadenylation signal (AACAAA) at nucleotide 1091 within the ARF 3 cDNA. JF - The Journal of biological chemistry AU - Tsai, S C AU - Haun, R S AU - Tsuchiya, M AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/12/05/ PY - 1991 DA - 1991 Dec 05 SP - 23053 EP - 23059 VL - 266 IS - 34 SN - 0021-9258, 0021-9258 KW - ARF 3 KW - Poly A KW - 24937-83-5 KW - DNA KW - 9007-49-2 KW - Cholera Toxin KW - 9012-63-9 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - ADP-Ribosylation Factors KW - EC 3.6.5.2 KW - Index Medicus KW - Blotting, Northern KW - Exons KW - Humans KW - Transcription, Genetic KW - Amino Acid Sequence KW - Poly A -- metabolism KW - Cloning, Molecular KW - Base Sequence KW - Restriction Mapping KW - Introns KW - Molecular Sequence Data KW - Gene Expression Regulation KW - Templates, Genetic KW - Cholera Toxin -- metabolism KW - GTP-Binding Proteins -- metabolism KW - GTP-Binding Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72514203?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Isolation+and+characterization+of+the+human+gene+for+ADP-ribosylation+factor+3%2C+a+20-kDa+guanine+nucleotide-binding+protein+activator+of+cholera+toxin.&rft.au=Tsai%2C+S+C%3BHaun%2C+R+S%3BTsuchiya%2C+M%3BMoss%2C+J%3BVaughan%2C+M&rft.aulast=Tsai&rft.aufirst=S&rft.date=1991-12-05&rft.volume=266&rft.issue=34&rft.spage=23053&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-13 N1 - Date created - 1992-01-13 N1 - Date revised - 2017-01-13 N1 - Gene symbol - ARF 3 N1 - Genetic sequence - M55199; GENBANK; S66610; S66768; M74491; S68759; M74492; M96682; M96681; M55201; M55200; M74992; M74993; S68763; S68761 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mouse pulmonary cytochrome P-450 naphthalene hydroxylase: cDNA cloning, sequence, and expression in Saccharomyces cerevisiae. AN - 72498257; 1742282 AB - We have isolated a cDNA clone, Nah-2, encoding the cytochrome P-450Nah (naphthalene hydroxylase) from a mouse lung lambda ZAP cDNA library using anti-cytochrome P-450Nah IgG as a probe. This same antibody selectively blocked [Nagata, K., Martin, B.M., Gillette, J.R., & Sasame, H.A. (1990) Drug Metab. Dispos. 18, 557-564] the cytochrome P-450 in mouse lung microsomes that catalyzed the conversion of naphthalene to (1R,2S)-naphthalene 1,2-oxide, which has been postulated as a causative agent in the naphthalene-induced tissue-specific necrosis of Clara cells in mouse lung. The toxic effect is seen in mouse and not in rat. The cDNA encodes a polypeptide of 491 amino acids with a molecular mass of 50 kDa. Northern blot analysis with an Nah-2-specific probe revealed that the mRNA is expressed in a species- and tissue-specific manner, present only in mouse lung and liver and not in that of rat. The mRNA encoding Nah-2 is constitutively expressed and is not induced by either phenobarbital, pyrazole, pregnenolone 16 alpha-carbonitrile, or 3-methylcholanthrene. Comparative amino acid sequence analyses with other documented members of the P-450 gene superfamily revealed that this encoded protein is in the IIF subfamily. To analyze its substrate specificity, the cDNA was inserted into the vector, pAAH5, and expressed in the Saccharomyces cerevisiae strain, AH22. The presence of cytochrome P-450Nah in the microsomes isolated from transformed cells and analyzed by Western blot was confirmed by immunocomplexing product with anti-cytochrome P450Nah IgG. Furthermore, activity toward naphthalene in the microsomes from the transformed cells established that this clone encodes a naphthalene hydroxylase.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Biochemistry AU - Ritter, J K AU - Owens, I S AU - Negishi, M AU - Nagata, K AU - Sheen, Y Y AU - Gillette, J R AU - Sasame, H A AD - Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/12/03/ PY - 1991 DA - 1991 Dec 03 SP - 11430 EP - 11437 VL - 30 IS - 48 SN - 0006-2960, 0006-2960 KW - RNA, Messenger KW - 0 KW - DNA KW - 9007-49-2 KW - Mixed Function Oxygenases KW - EC 1.- KW - naphthalene hydroxylase KW - Index Medicus KW - Rats KW - Animals KW - Liver -- enzymology KW - Blotting, Western KW - Base Sequence KW - Blotting, Northern KW - Transformation, Genetic KW - RNA, Messenger -- analysis KW - Molecular Sequence Data KW - Microsomes -- enzymology KW - Mice KW - Amino Acid Sequence KW - Male KW - Saccharomyces cerevisiae -- genetics KW - Mixed Function Oxygenases -- chemistry KW - Mixed Function Oxygenases -- metabolism KW - DNA -- genetics KW - Gene Expression KW - DNA -- chemistry KW - Lung -- enzymology KW - Saccharomyces cerevisiae -- enzymology KW - Mixed Function Oxygenases -- genetics KW - Cloning, Molecular UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72498257?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=Mouse+pulmonary+cytochrome+P-450+naphthalene+hydroxylase%3A+cDNA+cloning%2C+sequence%2C+and+expression+in+Saccharomyces+cerevisiae.&rft.au=Ritter%2C+J+K%3BOwens%2C+I+S%3BNegishi%2C+M%3BNagata%2C+K%3BSheen%2C+Y+Y%3BGillette%2C+J+R%3BSasame%2C+H+A&rft.aulast=Ritter&rft.aufirst=J&rft.date=1991-12-03&rft.volume=30&rft.issue=48&rft.spage=11430&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-14 N1 - Date created - 1992-01-14 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M82851; GENBANK; M82850; M82853; M82852; M82854; M82855; S69046; M77497; M82849; J05349; S62774 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Stretch sensitivity of the lateral wall of the auditory outer hair cell from the guinea pig. AN - 85260709; pmid-1726184 AB - The inner and outer hair cells of the mammalian hearing organ are mechano-transducer cells. Here we report evidence that the lateral wall of outer hair cells (OHCs) is a mechano-receptor. This mechano-sensitivity appears to complement that of the stereocilia. Patch clamping studies showed that stretching of the membrane patches by suction at the pipette activated potassium channels with 130 pS unit conductance specifically localized in the lateral wall. Application of an osmotic tension to the entire cell membrane under whole-cell recording produced a 10 mV hyperpolarization. The reversal potential and the magnitude of the macroscopic current under voltage clamp were consistent with the single-channel properties of stretch-activated potassium channels. The elongated cylindrical cell body of the OHC is optimally positioned in the cochlea to sense axial force due to the vibrations of the basilar membrane during sound stimulation. This sensitivity can explain the production of a predominantly hyperpolarizing response to sound stimuli, unique to the OHC. Coupled with voltage-dependent OHC motility, the stretch-activated channels may play an important role in producing a mechanical feedback, an indispensable element in cochlear tuning. JF - Neuroscience Letters AU - Iwasa, Kuni H AU - Li, M X AU - Jia, M AU - Kachar, B AD - National Institute on Deafness and Other Communication Disorders PY - 1991 SP - 171 EP - 174 VL - 133 IS - 2 SN - 0304-3940, 0304-3940 KW - Osmolar Concentration KW - Ion Channel Gating KW - Hair Cells KW - In Vitro KW - Mechanoreceptors KW - Guinea Pigs KW - Animal KW - Ion Channels KW - Membrane Potentials KW - Signal Transduction UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85260709?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+Letters&rft.atitle=Stretch+sensitivity+of+the+lateral+wall+of+the+auditory+outer+hair+cell+from+the+guinea+pig.&rft.au=Iwasa%2C+Kuni+H%3BLi%2C+M+X%3BJia%2C+M%3BKachar%2C+B&rft.aulast=Iwasa&rft.aufirst=Kuni&rft.date=1991-12-01&rft.volume=133&rft.issue=2&rft.spage=171&rft.isbn=&rft.btitle=&rft.title=Neuroscience+Letters&rft.issn=03043940&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - The role of sensorimotor experience in object recognition. A case of multimodal agnosia. AN - 85227081; pmid-1782531 AB - Object recognition was studied in a 19-yr-old male patient who presented severe multimodal amnesia and agnosia without significant intellectual, linguistic or perceptual deficits. Bilateral temporal lobe lesions involved medial, polar and anterior infero-temporal structures. Although visual recognition was impaired to various extents for all categories of objects, preservation of certain capacities were demonstrated. In particular, the patient was able to determine specifically how to manipulate certain objects, in spite of his incapacity to define their function or their context of utilization. It is argued that object recognition involves different processing modes such that when direct access to representations of an object is impaired, sensorimotor information activated via alternative cortical and subcortical pathways may provide a limited mechanism for recognition. JF - Brain AU - Sirigu, A AU - Duhamel, J R AU - Poncet, M AD - Cognitive Neuroscience Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 2555 EP - 2573 VL - 114 ( Pt 6) SN - 0006-8950, 0006-8950 KW - Cerebral Cortex KW - Verbal Learning KW - Agnosia KW - Memory KW - Human KW - Adult KW - Case Report KW - Neuropsychological Tests KW - Male KW - Visual Perception KW - Cognition UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85227081?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain&rft.atitle=The+role+of+sensorimotor+experience+in+object+recognition.+A+case+of+multimodal+agnosia.&rft.au=Sirigu%2C+A%3BDuhamel%2C+J+R%3BPoncet%2C+M&rft.aulast=Sirigu&rft.aufirst=A&rft.date=1991-12-01&rft.volume=114+%28+Pt+6%29&rft.issue=&rft.spage=2555&rft.isbn=&rft.btitle=&rft.title=Brain&rft.issn=00068950&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Alkylating agents and platinum: is clinical resistance simply a tumor cell phenomenon? AN - 72756043; 1843107 AB - Alkylating agents and platinum compounds comprise a large group of drugs that may exhibit marked differences in pharmacologic properties on the subcellular and clinical levels. Studies of the subcellular pharmacology of individual agents in this group suggest that cellular resistance to these drugs as a class may be modulated at three general levels: transmembrane drug accumulation, cytosolic inactivation of drug, and altered DNA repair. Traditionally, one unspoken assumption of cancer chemotherapy has been that in vitro tumor cell resistance equates with clinical resistance. Recent studies of platinum DNA adduct in nonmalignant tissues from cancer patients actively receiving therapy suggest that this assumption should be reassessed. In studies of platinum-DNA adduct from four different groups (using four different methods to assess adduct levels in nonmalignant tissues), the relationship between adduct level and disease response is a direct one; ie, the higher the adduct level, the better the clinical response to therapy. Here the data are reviewed that suggest that clinical resistance to DNA-damaging agents is not simply a tumor cell phenomenon and may represent the pharmacogenetic ability of individuals to protect cellular DNA. JF - Current opinion in oncology AU - Reed, E AD - Section of Genitourinary Cancer, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 1055 EP - 1059 VL - 3 IS - 6 SN - 1040-8746, 1040-8746 KW - Alkylating Agents KW - 0 KW - Platinum KW - 49DFR088MY KW - Index Medicus KW - Drug Resistance -- physiology KW - Humans KW - DNA Damage -- genetics KW - Leukocytes -- drug effects KW - Alkylating Agents -- pharmacology KW - Platinum -- pharmacology KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72756043?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+opinion+in+oncology&rft.atitle=Alkylating+agents+and+platinum%3A+is+clinical+resistance+simply+a+tumor+cell+phenomenon%3F&rft.au=Reed%2C+E&rft.aulast=Reed&rft.aufirst=E&rft.date=1991-12-01&rft.volume=3&rft.issue=6&rft.spage=1055&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+oncology&rft.issn=10408746&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-08 N1 - Date created - 1993-02-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Global atmospheric changes. AN - 72746969; 1820255 AB - Increasing concentrations of CO2 and other greenhouse gases in the atmosphere can be directly related to global warming. In terms of human health, because a major cause of increasing atmospheric concentrations of CO2 is the increased combustion of fossil fuels, global warming also may result in increases in air pollutants, acid deposition, and exposure to ultraviolet (UV) radiation. To understand better the impacts of global warming phenomena on human health, this review emphasizes the processes that are responsible for the greenhouse effect, air pollution, acid deposition, and increased exposure to UV radiation. JF - Environmental health perspectives AU - Piver, W T AD - Office of the Scientific Advisor to the Director, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 131 EP - 137 VL - 96 SN - 0091-6765, 0091-6765 KW - Acid Rain KW - 0 KW - Hydrocarbons, Halogenated KW - Carbon Dioxide KW - 142M471B3J KW - Ozone KW - 66H7ZZK23N KW - Index Medicus KW - Air Pollution KW - Environmental Health KW - Urban Health KW - Humans KW - Climate KW - Temperature KW - Periodicity KW - Forecasting KW - Energy-Generating Resources KW - Atmosphere UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72746969?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Global+atmospheric+changes.&rft.au=Piver%2C+W+T&rft.aulast=Piver&rft.aufirst=W&rft.date=1991-12-01&rft.volume=96&rft.issue=&rft.spage=131&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-04 N1 - Date created - 1992-08-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1990 Jul 6;249(4964):31-5 [17787623] Science. 1989 Feb 10;243(4892):771-81 [17820424] Science. 1989 Feb 10;243(4892):753-63 [17820422] Science. 1989 Feb 10;243(4892):745-52 [17820421] Am Rev Respir Dis. 1989 Mar;139(3):587-94 [2923355] Science. 1968 Dec 20;162(3860):1352-9 [5699650] Photochem Photobiol. 1989 Oct;50(4):507-13 [2687906] Am Rev Respir Dis. 1989 Sep;140(3 Pt 2):S49-55 [2782760] Health Phys. 1988 May;54(5):491-501 [3360603] Toxicol Appl Pharmacol. 1984 Oct;76(1):96-104 [6484996] Photochem Photobiol. 1989 Oct;50(4):515-24 [2687907] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Long-term chemical carcinogenesis experiments for identifying potential human cancer hazards: collective database of the National Cancer Institute and National Toxicology Program (1976-1991). AN - 72746406; 1820269 AB - The carcinogenicity database used for this paper originated in the late 1960s by the National Cancer Institute (NCI) and since 1978 has been continued and made more comprehensive by the National Toxicology Program (NTP). The extensive files contain, among other sets of information, detailed pathology data on more than 400 long-term (most often 24-month) chemical carcinogenesis studies, comprising nearly 1600 individual experiments having at least 10 million tissue sections that have been evaluated for toxicity and carcinogenicity.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Environmental health perspectives AU - Huff, J AU - Haseman, J AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 23 EP - 31 VL - 96 SN - 0091-6765, 0091-6765 KW - Carcinogens KW - 0 KW - Index Medicus KW - United States KW - Animals KW - Sex Factors KW - Humans KW - Mice KW - Organ Specificity KW - False Positive Reactions KW - Rats KW - False Negative Reactions KW - Rats, Inbred F344 KW - Mutagenicity Tests KW - Neoplasms, Experimental -- chemically induced KW - Risk Factors KW - National Institutes of Health (U.S.) KW - Carcinogenicity Tests KW - Mice, Inbred C3H KW - Mice, Inbred C57BL KW - Species Specificity KW - Databases, Factual KW - Carcinogens -- toxicity KW - Toxicology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72746406?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Long-term+chemical+carcinogenesis+experiments+for+identifying+potential+human+cancer+hazards%3A+collective+database+of+the+National+Cancer+Institute+and+National+Toxicology+Program+%281976-1991%29.&rft.au=Huff%2C+J%3BHaseman%2C+J&rft.aulast=Huff&rft.aufirst=J&rft.date=1991-12-01&rft.volume=96&rft.issue=&rft.spage=23&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-04 N1 - Date created - 1992-08-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Jpn J Cancer Res. 1989 Sep;80(9):795-807 [2513295] Environ Mol Mutagen. 1990;16 Suppl 18:15-31 [2091922] Cancer Metastasis Rev. 1989 Jun;8(1):1-22 [2667783] Cancer Res. 1989 Jul 15;49(14):3713-21 [2660980] Fundam Appl Toxicol. 1989 May;12(4):793-804 [2744280] Annu Rev Biochem. 1987;56:779-827 [3304147] Environ Mol Mutagen. 1990;16 Suppl 18:1-14 [2091921] Cancer Res. 1990 Oct 15;50(20):6441-8 [2208102] Science. 1987 May 22;236(4804):933-41 [3554512] Proc Natl Acad Sci U S A. 1989 May;86(9):3070-4 [2654935] Arch Toxicol Suppl. 1987;10:10-26 [3555413] Carcinogenesis. 1988 Nov;9(11):2045-52 [3052903] Ann N Y Acad Sci. 1988;534:1-30 [3291703] Environ Health Perspect. 1990 Jun;86:313-21 [2205492] Fundam Appl Toxicol. 1990 Jul;15(1):33-43 [2197145] Fundam Appl Toxicol. 1990 May;14(4):637-48 [2193843] Toxicol Pathol. 1990;18(1 Pt 1):71-7 [2362989] Toxicol Pathol. 1990;18(1 Pt 1):61-70 [2362988] Prog Clin Biol Res. 1984;141:43-64 [6718388] Fundam Appl Toxicol. 1983 Jul-Aug;3(4):334-9 [6628896] Toxicol Pathol. 1984;12(2):126-35 [11478313] Environ Health Perspect. 1987 Oct;74:229-35 [3691430] Cancer Lett. 1987 Oct 30;37(2):125-32 [3677049] Fundam Appl Toxicol. 1987 May;8(4):425-31 [3609532] Regul Toxicol Pharmacol. 1986 Jun;6(2):155-70 [3726178] J Natl Cancer Inst. 1985 Nov;75(5):975-84 [3863995] Environ Health Perspect. 1991 Dec;96:47-51 [1820276] Mol Carcinog. 1991;4(6):420-40 [1793481] Environ Health Perspect. 1991 Jun;93:247-70 [1773796] Annu Rev Pharmacol Toxicol. 1991;31:621-52 [2064387] Science. 1991 Jan 25;251(4992):387-8 [1989073] Toxicol Lett. 1989 Dec;49(2-3):267-81 [2690406] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The genetic toxicity database of the National Toxicology Program: evaluation of the relationships between genetic toxicity and carcinogenicity. AN - 72744083; 1820276 AB - The database of the U.S. National Toxicology Program has been developed over approximately two decades, principally focused on substances evaluated for carcinogenicity in rodent bioassays. These assays generally provide data on the relative toxicity and carcinogenicity of chemicals based upon discrete subchronic (13 week) and chronic (104 week) exposures. A major value of these data are that the assay protocols, rodent strains, and technical methodologies have been generally consistent, thus permitting comparisons between assays and chemicals. The genotoxicity data for many of the same chemicals have been developed also using standardized biological systems and protocols. Data for assays including mutagenicity in Salmonella and mouse lymphoma cells, chromosomal aberrations, and sister chromatid exchange in Chinese hamster ovary cells, transformation of Balb/c 3T3 cells, and in vivo cytogenetic effects in rodents have been compiled for many chemicals. The results of all of these assays provide a substantial database for evaluating chemical effects and for defining the complex relationships between mutagenicity and carcinogenicity. JF - Environmental health perspectives AU - Tennant, R W AD - Experimental Carcinogenesis and Mutagenesis Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 47 EP - 51 VL - 96 SN - 0091-6765, 0091-6765 KW - Carcinogens KW - 0 KW - Mutagens KW - Index Medicus KW - United States KW - Animals KW - Mutagenicity Tests KW - Drosophila melanogaster -- genetics KW - Dose-Response Relationship, Drug KW - National Institutes of Health (U.S.) KW - Drosophila melanogaster -- drug effects KW - Carcinogenicity Tests KW - Salmonella typhimurium -- drug effects KW - Structure-Activity Relationship KW - Carcinogens -- classification KW - Databases, Factual KW - Data Display KW - Toxicology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72744083?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=The+genetic+toxicity+database+of+the+National+Toxicology+Program%3A+evaluation+of+the+relationships+between+genetic+toxicity+and+carcinogenicity.&rft.au=Tennant%2C+R+W&rft.aulast=Tennant&rft.aufirst=R&rft.date=1991-12-01&rft.volume=96&rft.issue=&rft.spage=47&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-04 N1 - Date created - 1992-08-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Mutat Res. 1989 Jun;223(2):73-103 [2662004] Environ Mol Mutagen. 1989;14(4):238-44 [2511011] Environ Mutagen. 1987;9(3):235-50 [3569168] Environ Mutagen. 1985;7(5):677-702 [3930237] Environ Mutagen. 1985;7(3):349-67 [3930235] Environ Mutagen. 1985;7(3):325-48 [3930234] Environ Mutagen. 1985;7(1):87-100 [3917911] Environ Mutagen. 1985;7(2):213-32 [3971959] Mutagenesis. 1990 Jan;5(1):3-14 [2184307] Mutat Res. 1991 May;257(3):229-306 [1707500] Environ Mol Mutagen. 1991;17(3):196-219 [1902415] Environ Mol Mutagen. 1991;18(1):51-83 [1864269] Mutat Res. 1991 May;257(3):209-27 [2014033] Environ Mol Mutagen. 1990;16 Suppl 18:138-67 [2128695] Environ Mol Mutagen. 1990;16 Suppl 18:55-137 [2091924] Environ Mol Mutagen. 1990;16 Suppl 18:32-54 [2091923] Environ Mol Mutagen. 1989;13(1):60-94 [2642806] Mutat Res. 1989 Nov;224(3):347-50 [2811923] Environ Mol Mutagen. 1989;14(3):165-87 [2792092] Environ Mol Mutagen. 1989;13(4):339-42 [2737185] Environ Mol Mutagen. 1989;13(2):133-93 [2917552] Mutat Res. 1988 Jan;204(1):17-115 [3277047] Environ Mol Mutagen. 1988;12(1):85-154 [3383842] Environ Mol Mutagen. 1988;11(1):91-118 [3338442] Environ Mutagen. 1987;9 Suppl 9:1-109 [3552650] Mutagenesis. 1990 Jul;5(4):305-6 [2398815] Environ Mutagen. 1984;6(2):189-202 [6423381] Environ Mutagen. 1983;5 Suppl 1:1-142 [6365529] Environ Mol Mutagen. 1990;16 Suppl 18:1-14 [2091921] Environ Mol Mutagen. 1990;16(4):272-303 [2253606] Environ Mol Mutagen. 1988;12 Suppl 13:37-101 [3416841] Environ Mol Mutagen. 1988;12 Suppl 13:103-94 [3416838] Science. 1987 May 22;236(4804):933-41 [3554512] Environ Mol Mutagen. 1989;14(4):245-51 [2583131] Mutat Res. 1987 Mar;187(3):165-80 [3102959] Environ Mutagen. 1987;9(2):143-60 [3102223] Mutagenesis. 1988 Mar;3(2):141-6 [3288837] Environ Mutagen. 1986;8 Suppl 7:1-119 [3516675] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human immunodeficiency virus type 2 (HIV-2) gene expression: downmodulation by sequence elements downstream of the transcriptional initiation site. AN - 72705934; 1812941 AB - Human immunodeficiency virus type 2 (HIV-2) gene expression is downmodulated by sequence elements downstream of the transcriptional initiation site, corresponding to the U5 region of the long terminal repeat (LTR) and further downstream. This repression appeared to be related more to the length of the sequence intervening the transcriptional initiation site and the coding region than to a particular sequence content. The repressive effect of the downstream segment was not affected by HIV-2 and HIV-1 TAT or by the cytomegalovirus transactivator IE-2 gene. Nor was it affected by T-cell activation signals or by such cytokines as tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), interferon-gamma (IFN gamma), and interferon-alpha (IFN alpha). In contrast to HIV-1, HIV-2 LTR-directed gene expression was not modulated by TNF-alpha. A specific sequence element, located downstream of the TAR element in the R region, seemed to participate in modulation of gene expression. This element interacted with a nuclear protein with a mobility of about 26 kD. The repressive effect of the downstream sequence was to a certain extent cell type dependent, suggesting the involvement of cell type-specific factors. It was more effective in human lymphocytic CEM cells than in Jurkat cells. This may be relevant to the HIV-2 cell tropism (replication), latency, and virulence. JF - AIDS research and human retroviruses AU - Arya, S K AD - Laboratory of Tumor Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 1007 EP - 1014 VL - 7 IS - 12 SN - 0889-2229, 0889-2229 KW - Cytokines KW - 0 KW - Phytohemagglutinins KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - AIDS/HIV KW - Genes, pX KW - Animals KW - Cytokines -- pharmacology KW - Transcription, Genetic KW - Transcriptional Activation KW - Cloning, Molecular KW - Base Sequence KW - Down-Regulation KW - Transfection KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Genes, tat KW - Cell Line KW - T-Lymphocytes -- immunology KW - HIV Long Terminal Repeat KW - Gene Expression Regulation, Viral -- drug effects KW - HIV-2 -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72705934?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+research+and+human+retroviruses&rft.atitle=Human+immunodeficiency+virus+type+2+%28HIV-2%29+gene+expression%3A+downmodulation+by+sequence+elements+downstream+of+the+transcriptional+initiation+site.&rft.au=Arya%2C+S+K&rft.aulast=Arya&rft.aufirst=S&rft.date=1991-12-01&rft.volume=7&rft.issue=12&rft.spage=1007&rft.isbn=&rft.btitle=&rft.title=AIDS+research+and+human+retroviruses&rft.issn=08892229&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-12 N1 - Date created - 1992-06-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Obsessive-compulsive disorder. AN - 72705376; 1806635 AB - Within the past decade the field of psychiatry has rediscovered the neuropsychiatric syndrome of obsessive-compulsive disorder (OCD). Although excellently described over 150 years ago, for many years OCD was thought to be rare, untreatable, and to arise from hidden psychodynamic conflicts. All of these earlier ideas now appear to be wrong. Occurring in approximately 2% of adults, OCD consists of recurrent intrusive thoughts (obsessions) or senseless repetitive actions (compulsions). Although the aetiology of OCD remains unclear, recent neuro-imaging studies implicate the basal ganglia and frontal cortex as crucial structures in the pathogenesis of OCD. Genetic studies demonstrate a clear genetic component to OCD and an interesting link with chronic motor tics and the Gilles de la Tourette Syndrome. Although a true cure for the disorder remains elusive, most OCD symptoms respond well to treatment with 5HT reuptake inhibitors. The phenomenology and aetiology of OCD will be reviewed, with particular emphasis placed on the proper pharmacological treatment of this sometimes crippling disorder. JF - International clinical psychopharmacology AU - George, M S AD - NIMH, Bethesda, MD 20892. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 57 EP - 66; discussion 66-8 VL - 6 Suppl 3 SN - 0268-1315, 0268-1315 KW - Fluoxetine KW - 01K63SUP8D KW - Clomipramine KW - NUV44L116D KW - Fluvoxamine KW - O4L1XPO44W KW - Index Medicus KW - Fluoxetine -- adverse effects KW - Humans KW - Fluoxetine -- therapeutic use KW - Clomipramine -- adverse effects KW - Clomipramine -- therapeutic use KW - Fluvoxamine -- adverse effects KW - Obsessive-Compulsive Disorder -- psychology KW - Fluvoxamine -- therapeutic use KW - Obsessive-Compulsive Disorder -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72705376?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+clinical+psychopharmacology&rft.atitle=Obsessive-compulsive+disorder.&rft.au=George%2C+M+S&rft.aulast=George&rft.aufirst=M&rft.date=1991-12-01&rft.volume=6+Suppl+3&rft.issue=&rft.spage=57&rft.isbn=&rft.btitle=&rft.title=International+clinical+psychopharmacology&rft.issn=02681315&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-11 N1 - Date created - 1992-05-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pulse cyclophosphamide for severe neuropsychiatric lupus. AN - 72703397; 1808642 AB - We studied the effect of parenteral pulse cyclophosphamide therapy in nine patients with active systemic lupus erythematosus and severe central nervous system involvement. Seven patients had focal neurological deficits and/or seizures associated with abnormalities on cerebrospinal fluid analysis and/or magnetic resonance imaging. Two patients had organic brain syndrome with psychosis and normal cerebrospinal fluid and/or magnetic resonance imaging analysis. Six patients were unresponsive to treatment with high dose corticosteroid. Cyclophosphamide, 0.75-1.0 g/m2 body surface area, was administered intravenously every month for at least 2 months. Eight patients had a complete recovery or recovered with minor residuals. Cyclophosphamide was well tolerated with few side effects. We conclude that parenteral pulse cyclophosphamide is an effective adjunctive therapy for the management of patients with active systemic lupus erythematosus and central nervous system symptoms. JF - The Quarterly journal of medicine AU - Boumpas, D T AU - Yamada, H AU - Patronas, N J AU - Scott, D AU - Klippel, J H AU - Balow, J E AD - Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 975 EP - 984 VL - 81 IS - 296 SN - 0033-5622, 0033-5622 KW - Cyclophosphamide KW - 8N3DW7272P KW - Prednisolone KW - 9PHQ9Y1OLM KW - Methylprednisolone KW - X4W7ZR7023 KW - Index Medicus KW - Magnetic Resonance Imaging KW - Drug Therapy, Combination KW - Methylprednisolone -- therapeutic use KW - Drug Administration Schedule KW - Injections, Intravenous KW - Humans KW - Adult KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Prednisolone -- therapeutic use KW - Lupus Erythematosus, Systemic -- pathology KW - Cyclophosphamide -- administration & dosage KW - Central Nervous System Diseases -- pathology KW - Lupus Erythematosus, Systemic -- drug therapy KW - Central Nervous System Diseases -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72703397?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Quarterly+journal+of+medicine&rft.atitle=Pulse+cyclophosphamide+for+severe+neuropsychiatric+lupus.&rft.au=Boumpas%2C+D+T%3BYamada%2C+H%3BPatronas%2C+N+J%3BScott%2C+D%3BKlippel%2C+J+H%3BBalow%2C+J+E&rft.aulast=Boumpas&rft.aufirst=D&rft.date=1991-12-01&rft.volume=81&rft.issue=296&rft.spage=975&rft.isbn=&rft.btitle=&rft.title=The+Quarterly+journal+of+medicine&rft.issn=00335622&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-21 N1 - Date created - 1992-05-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Food allergy. AN - 72673402; 1793530 AB - Food allergy is now known to encompass a number of distinct clinical entities that follow the ingestion of specific food or food additives. Research continues to shed light on immediate reactions to foods and food protein-induced enterocolitis of newborns and infants. Adverse reactions to food additives remain an area of health concern. Studies of food allergies have entered an era in which improved clinical design is the hallmark of the research and conclusions may now be drawn reliably. JF - Current opinion in immunology AU - Metcalfe, D D AD - National Institutes of Health, Bethesda, Maryland. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 881 EP - 886 VL - 3 IS - 6 SN - 0952-7915, 0952-7915 KW - Food Additives KW - 0 KW - Index Medicus KW - Infant KW - Colitis -- etiology KW - Humans KW - Adult KW - Infant, Newborn KW - Child KW - Eczema -- etiology KW - Food Hypersensitivity -- etiology KW - Food Additives -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72673402?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+opinion+in+immunology&rft.atitle=Food+allergy.&rft.au=Metcalfe%2C+D+D&rft.aulast=Metcalfe&rft.aufirst=D&rft.date=1991-12-01&rft.volume=3&rft.issue=6&rft.spage=881&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+immunology&rft.issn=09527915&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-08 N1 - Date created - 1992-04-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cerebrospinal fluid variables among alcoholics lack seasonal variation. AN - 72668884; 1724338 AB - Seasonal influences on indices of serotonergic function, including cerebrospinal fluid (CSF) concentrations of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA), have been reported in psychiatric patients and healthy volunteers. We examined seasonal differences in CSF concentrations of 5-HIAA among 135 alcoholics admitted to a research ward who had a lumbar puncture. No significant seasonal differences were found for either CSF concentrations of 5-HIAA or CSF concentrations of other monoamine metabolites or peptides. The possible explanations for these negative findings are discussed. JF - Acta psychiatrica Scandinavica AU - Roy, A AU - Adinoff, B AU - DeJong, J AU - Linnoila, M AD - Laboratory of Clinical Studies, DICBR, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 579 EP - 582 VL - 84 IS - 6 SN - 0001-690X, 0001-690X KW - Neuropeptides KW - 0 KW - Serotonin KW - 333DO1RDJY KW - Methoxyhydroxyphenylglycol KW - 534-82-7 KW - Hydroxyindoleacetic Acid KW - 54-16-0 KW - Norepinephrine KW - X4W3ENH1CV KW - Homovanillic Acid KW - X77S6GMS36 KW - Index Medicus KW - Homovanillic Acid -- cerebrospinal fluid KW - Substance Abuse Treatment Centers KW - Methoxyhydroxyphenylglycol -- cerebrospinal fluid KW - Humans KW - Adult KW - Middle Aged KW - Norepinephrine -- cerebrospinal fluid KW - Male KW - Female KW - Alcoholism -- rehabilitation KW - Serotonin -- physiology KW - Neuropeptides -- cerebrospinal fluid KW - Seasons KW - Alcoholism -- cerebrospinal fluid KW - Hydroxyindoleacetic Acid -- cerebrospinal fluid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72668884?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Acta+psychiatrica+Scandinavica&rft.atitle=Cerebrospinal+fluid+variables+among+alcoholics+lack+seasonal+variation.&rft.au=Roy%2C+A%3BAdinoff%2C+B%3BDeJong%2C+J%3BLinnoila%2C+M&rft.aulast=Roy&rft.aufirst=A&rft.date=1991-12-01&rft.volume=84&rft.issue=6&rft.spage=579&rft.isbn=&rft.btitle=&rft.title=Acta+psychiatrica+Scandinavica&rft.issn=0001690X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-01 N1 - Date created - 1992-04-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The criteria of Cloninger et al. and von Knorring et al. for subgrouping alcoholics: a comparison in a clinical population. AN - 72668125; 1792921 AB - There is increasing evidence that meaningful subgroups of alcoholics may exist. Cloninger et al. and von Knorring et al. have developed criteria to delineate what both call type 1 and type 2 alcoholism. However, when we compared their criteria in a predominantly inpatient sample of male alcoholics, we found large differences between the approaches in identifying type 1 and type 2 alcoholism. Concordance was equally low in a subsample of 34 alcoholics exhibiting antisocial behavior and when subjects were divided by whether the first alcohol-related problem began before or after 20 years of age. Similar findings emerged when we limited our analyses to primary alcoholics and alcoholics with no other mental disorders. JF - Acta psychiatrica Scandinavica AU - Lamparski, D M AU - Roy, A AU - Nutt, D J AU - Linnoila, M AD - Laboratory of Clinical Studies, DICBR, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 497 EP - 502 VL - 84 IS - 6 SN - 0001-690X, 0001-690X KW - Index Medicus KW - Diagnosis, Differential KW - Risk Factors KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Alcoholism -- classification KW - Antisocial Personality Disorder -- genetics KW - Antisocial Personality Disorder -- classification KW - Personality Development KW - Antisocial Personality Disorder -- psychology KW - Alcoholism -- genetics KW - Alcoholism -- psychology KW - Social Environment UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72668125?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Public+health+reports+%28Washington%2C+D.C.+%3A+1974%29&rft.atitle=Estimating+the+prevalence+of+mental+disorders+in+U.S.+adults+from+the+Epidemiologic+Catchment+Area+Survey.&rft.au=Bourdon%2C+K+H%3BRae%2C+D+S%3BLocke%2C+B+Z%3BNarrow%2C+W+E%3BRegier%2C+D+A&rft.aulast=Bourdon&rft.aufirst=K&rft.date=1992-11-01&rft.volume=107&rft.issue=6&rft.spage=663&rft.isbn=&rft.btitle=&rft.title=Public+health+reports+%28Washington%2C+D.C.+%3A+1974%29&rft.issn=00333549&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-01 N1 - Date created - 1992-04-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Excitotoxicity in the embryonic chick spinal cord. AN - 72666806; 1686386 AB - Recent evidence implicates excitatory amino acids (EAAs), acting as excitotoxic agents, in the pathogenesis of neurological disorders involving the spinal cord. In this study, we used the chick embryo spinal cord as an in vitro model for studying the sensitivity of spinal neurons to the excitotoxic effects of EAA agonists. Compounds tested include the prototypic receptor-specific agonists, N-methyl-D-aspartate (NMDA), quisqualic acid (Quis), and kainic acid (KA), and the plant-derived excitotoxic food poisons, beta-N-oxalylamino-L-alanine, beta-N-methylamino-L-alanine, and domoic acid. Each agonist induced concentration-dependent acute degeneration of neurons distributed throughout the spinal cord. These cytopathological changes consisted of acute edematous degeneration of dendrosomal structures in the dorsal horn and intermediate zone, and dark cell changes with intracytoplasmic vacuolization of motor neurons; this damage is identical to that induced by excitotoxin agonists in other regions of the central nervous system. The NMDA receptor-specific antagonist MK-801 completely blocked toxicity of NMDA, and the nonNMDA antagonist CNQX preferentially blocked the toxicity of Quis- and KA-type agonists in the spinal cord. Our findings suggest that (1) the majority of spinal neurons have all three subtypes of EAA receptors, making them acutely vulnerable to excitotoxin exposure; and (2) EAA antagonists are effective in preventing excitotoxin-induced damage of the spinal cord. JF - Annals of neurology AU - Stewart, G R AU - Olney, J W AU - Pathikonda, M AU - Snider, W D AD - Laboratory of Neurophysiology, National Institute of Mental Health, NIH Animal Center, Poolesville, MD 20837. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 758 EP - 766 VL - 30 IS - 6 SN - 0364-5134, 0364-5134 KW - Amino Acids, Diamino KW - 0 KW - Glutamates KW - Neurotoxins KW - Quinoxalines KW - beta-N-methylamino-L-alanine KW - 108SA6URTV KW - beta-Alanine KW - 11P2JDE17B KW - Ibotenic Acid KW - 2552-55-8 KW - Glutamic Acid KW - 3KX376GY7L KW - N-Methylaspartate KW - 6384-92-5 KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - 6-Cyano-7-nitroquinoxaline-2,3-dione KW - 6OTE87SCCW KW - oxalyldiaminopropionic acid KW - 7554-90-7 KW - alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid KW - 77521-29-0 KW - Quisqualic Acid KW - 8OC22C1B99 KW - domoic acid KW - M02525818H KW - Kainic Acid KW - SIV03811UC KW - Index Medicus KW - Nerve Degeneration -- drug effects KW - Animals KW - beta-Alanine -- analogs & derivatives KW - Kainic Acid -- analogs & derivatives KW - Kainic Acid -- pharmacology KW - Chick Embryo KW - beta-Alanine -- pharmacology KW - Dizocilpine Maleate -- pharmacology KW - Ibotenic Acid -- pharmacology KW - Quisqualic Acid -- pharmacology KW - Motor Neurons -- pathology KW - Amino Acids, Diamino -- pharmacology KW - N-Methylaspartate -- pharmacology KW - Glutamates -- pharmacology KW - Ibotenic Acid -- analogs & derivatives KW - Quinoxalines -- pharmacology KW - Motor Neurons -- drug effects KW - Spinal Cord -- drug effects KW - Spinal Cord -- pathology KW - Neurotoxins -- pharmacology KW - Spinal Cord -- embryology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72666806?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+neurology&rft.atitle=Excitotoxicity+in+the+embryonic+chick+spinal+cord.&rft.au=Stewart%2C+G+R%3BOlney%2C+J+W%3BPathikonda%2C+M%3BSnider%2C+W+D&rft.aulast=Stewart&rft.aufirst=G&rft.date=1991-12-01&rft.volume=30&rft.issue=6&rft.spage=758&rft.isbn=&rft.btitle=&rft.title=Annals+of+neurology&rft.issn=03645134&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-26 N1 - Date created - 1992-03-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Attitudes toward problem drinkers, revisited: patient-therapist factors contributing to the differential treatment of patients with alcohol problems. AN - 72665032; 1665015 AB - Although there are many treatment alternative open to people with drinking problems, health professionals still exhibit negative attitudes towards alcoholics. In a previous study, the author demonstrated that those patients who were self-labelled alcoholics were treated in a less preferential manner than those who did not identify as such. This study used both overt and unobtrusive measures to determine whether negative attitudes of intake interviewers towards problem drinkers were elicited by the patients' self-label as an alcoholic or by other variables related to perceived treatment outcome. Pre- and postinterview data on patient likability, doctor's eagerness to work with the patient, interview content, treatment disposition, and patient compliance were collected from first-time patients, and from their interviewers, in the walk-in psychiatry and alcohol treatment units of a large, urban teaching hospital. The results elucidate how stereotypes interact with patient characteristics to influence both professional behavior and patient compliance. JF - Alcoholism, clinical and experimental research AU - Hanna, E Z AD - Division of Biometry and Epidemiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 927 EP - 931 VL - 15 IS - 6 SN - 0145-6008, 0145-6008 KW - Index Medicus KW - Stereotyping KW - Social Distance KW - Interview, Psychological KW - Substance Abuse Treatment Centers KW - Patient Compliance -- psychology KW - Humans KW - Alcohol Drinking -- psychology KW - Social Environment KW - Alcoholism -- rehabilitation KW - Attitude of Health Personnel KW - Psychotherapy KW - Physician-Patient Relations KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72665032?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%2C+clinical+and+experimental+research&rft.atitle=Attitudes+toward+problem+drinkers%2C+revisited%3A+patient-therapist+factors+contributing+to+the+differential+treatment+of+patients+with+alcohol+problems.&rft.au=Hanna%2C+E+Z&rft.aulast=Hanna&rft.aufirst=E&rft.date=1991-12-01&rft.volume=15&rft.issue=6&rft.spage=927&rft.isbn=&rft.btitle=&rft.title=Alcoholism%2C+clinical+and+experimental+research&rft.issn=01456008&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-20 N1 - Date created - 1992-03-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hyperalgesia and myoclonus with intrathecal infusion of high-dose morphine. AN - 72648848; 1784504 AB - We report the case of a patient who developed myoclonus and hyperalgesia following administration of high-dose subarachnoid morphine. This complication occurred with 40-80 mg/day continuous infusion. The pathophysiology of these side effects is discussed. JF - Pain AU - De Conno, F AU - Caraceni, A AU - Martini, C AU - Spoldi, E AU - Salvetti, M AU - Ventafridda, V AD - Pain Therapy and Palliative Care Division, National Cancer Institute of Milan, Italy. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 337 EP - 339 VL - 47 IS - 3 SN - 0304-3959, 0304-3959 KW - Morphine KW - 76I7G6D29C KW - Index Medicus KW - Drug Administration Schedule KW - Injections, Spinal KW - Humans KW - Middle Aged KW - Male KW - Myoclonus -- chemically induced KW - Morphine -- adverse effects KW - Morphine -- administration & dosage KW - Hyperalgesia -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72648848?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pain&rft.atitle=Hyperalgesia+and+myoclonus+with+intrathecal+infusion+of+high-dose+morphine.&rft.au=De+Conno%2C+F%3BCaraceni%2C+A%3BMartini%2C+C%3BSpoldi%2C+E%3BSalvetti%2C+M%3BVentafridda%2C+V&rft.aulast=De+Conno&rft.aufirst=F&rft.date=1991-12-01&rft.volume=47&rft.issue=3&rft.spage=337&rft.isbn=&rft.btitle=&rft.title=Pain&rft.issn=03043959&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-19 N1 - Date created - 1992-03-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Drug self-administration methods in abuse liability evaluation. AN - 72646416; 1786489 AB - The human drug self-administration paradigm is an extension of the animal model developed in the 1960s. The paradigm can be used to investigate the determinants and correlates of drug-seeking and drug-taking behavior and has proven useful in the development of medications for treating drug dependence. This paper describes the basic components of the human self-administration model and discusses studies that illustrate some of its applications, including assessment of the reinforcing effects of drugs, analysis of behavioral and pharmacological mechanisms of drug self-administration and measurement of the abuse liability, behavioral toxicity, and aversive effects of drugs. Some of the strengths and limitations of using the paradigm with human research subjects are also presented. It is concluded that the drug self-administration model should not replace other measures of abuse liability testing in humans, but should be incorporated into comprehensive programs of drug abuse assessment wherever possible. JF - British journal of addiction AU - Henningfield, J E AU - Cohen, C AU - Heishman, S J AD - Clinical Pharmacology Branch, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 1571 EP - 1577 VL - 86 IS - 12 SN - 0952-0481, 0952-0481 KW - Psychotropic Drugs KW - 0 KW - Index Medicus KW - Drug Evaluation -- methods KW - Risk Factors KW - Humans KW - Self Administration -- psychology KW - Substance-Related Disorders -- psychology KW - Psychotropic Drugs -- administration & dosage KW - Substance-Related Disorders -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72646416?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+addiction&rft.atitle=Drug+self-administration+methods+in+abuse+liability+evaluation.&rft.au=Henningfield%2C+J+E%3BCohen%2C+C%3BHeishman%2C+S+J&rft.aulast=Henningfield&rft.aufirst=J&rft.date=1991-12-01&rft.volume=86&rft.issue=12&rft.spage=1571&rft.isbn=&rft.btitle=&rft.title=British+journal+of+addiction&rft.issn=09520481&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-26 N1 - Date created - 1992-03-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular cloning, chromosomal assignment, and nucleotide sequence of the feline homeobox HOX3A. AN - 72642834; 1686012 AB - The feline homolog to the mammalian homeobox locus, HOX3A, was isolated by screening a domestic cat genomic library with the murine Hox-3.1 probe. The nucleotide sequence similarity of the feline homeobox was 96% to human HOX3A, 94% to mouse Hox-3.1, and 94% to rat R4. The deduced amino acid sequence (homeodomain) of this feline homeobox was identical to all homeodomains of these cognate genes. Using a panel of feline x rodent somatic cell hybrids, the HOX3A locus was assigned to feline chromosome B4. Human HOX3A and mouse Hox-3.1 have been mapped previously to human chromosome 12 and mouse chromosome 15, respectively, both of which share syntenic homology to feline chromosome B4. These data demonstrate evolutionary conservation of both HOX3A gene sequences and chromosomal location during mammalian evolution. JF - Genomics AU - Masuda, R AU - Yuhki, N AU - O'Brien, S J AD - Laboratory of Viral Carcinogenesis, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 1007 EP - 1013 VL - 11 IS - 4 SN - 0888-7543, 0888-7543 KW - HOX3A KW - DNA-Binding Proteins KW - 0 KW - HOX3A protein, Felis catus KW - Homeodomain Proteins KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Base Sequence KW - Sequence Homology, Nucleic Acid KW - Blotting, Southern KW - Humans KW - Restriction Mapping KW - Cats KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Chromosome Mapping KW - Cloning, Molecular KW - Genes, Homeobox KW - DNA-Binding Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72642834?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genomics&rft.atitle=Molecular+cloning%2C+chromosomal+assignment%2C+and+nucleotide+sequence+of+the+feline+homeobox+HOX3A.&rft.au=Masuda%2C+R%3BYuhki%2C+N%3BO%27Brien%2C+S+J&rft.aulast=Masuda&rft.aufirst=R&rft.date=1991-12-01&rft.volume=11&rft.issue=4&rft.spage=1007&rft.isbn=&rft.btitle=&rft.title=Genomics&rft.issn=08887543&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-13 N1 - Date created - 1992-03-13 N1 - Date revised - 2017-01-13 N1 - Gene symbol - HOX3A N1 - Genetic sequence - M59215; GENBANK; S56900; M59214; S56902; M59216; S56907; M62698; S56909; S56905; S80214 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The necessity and utility of abuse liability evaluations in human subjects. AN - 72638397; 1786484 AB - Assessments of the abuse potential of psychoactive drugs in preclinical and clinical studies are used in regulatory decision making process in the United States under the Controlled Substance Act (CSA) and the Federal Food, Drug, and Cosmetic Act (FD & C Act). Two types of drugs are evaluated in abuse potential studies, those being developed for a therapeutic indication by the pharmaceutical industry and illicitly manufactured 'street drugs' of abuse. Only the former will be considered here. In the case of drugs being pursued for marketing or are amendable to study in human subjects and are of scientific, medical, or regulatory interest, preclinical data may be inadequate for drug scheduling and marketing decisions. Preclinical data assessment can suggest hypotheses which must be validated in clinical studies. Moreover, there are limitations to the feasibility of evaluating certain drugs/dosage forms in preclinical studies. Thus, clinical studies are needed for the following scientific reasons: to validate preclinical hypotheses; to assess the time-course of subjective effects as a function of dose and route of administration; to evaluate the generalizability of drug liking in different human subject populations; and to evaluate the effects of drugs on cognitive and affective processes. Clinical studies are also needed if a claim is made regarding reduced or no abuse potential; and lack of additive or potentiative effects with alcohol. JF - British journal of addiction AU - Vocci, F J AD - Development Therapeutics Branch, National Institute on Drug Abuse, Rockville, Maryland 20857. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 1537 EP - 1542 VL - 86 IS - 12 SN - 0952-0481, 0952-0481 KW - Psychotropic Drugs KW - 0 KW - Index Medicus KW - United States KW - Risk Factors KW - Humans KW - Drug Evaluation -- trends KW - Drug and Narcotic Control -- legislation & jurisprudence KW - United States Food and Drug Administration -- legislation & jurisprudence KW - Substance-Related Disorders -- etiology KW - Substance-Related Disorders -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72638397?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+addiction&rft.atitle=The+necessity+and+utility+of+abuse+liability+evaluations+in+human+subjects.&rft.au=Vocci%2C+F+J&rft.aulast=Vocci&rft.aufirst=F&rft.date=1991-12-01&rft.volume=86&rft.issue=12&rft.spage=1537&rft.isbn=&rft.btitle=&rft.title=British+journal+of+addiction&rft.issn=09520481&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-26 N1 - Date created - 1992-03-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alcohol, the chloride ionophore and endogenous ligands for benzodiazepine receptors. AN - 72633581; 1723509 AB - Considerable evidence suggests that at least some of the effects of ethanol are mediated by an action on the GABAA receptor chloride channel complex. More speculative is the suggestion that ethanol might interact with endogenous ligands for the benzodiazepine receptor on the complex. This paper considers the evidence for such interactions. JF - Neuropharmacology AU - Lister, R G AU - Linnoila, M AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 1435 EP - 1440 VL - 30 IS - 12B SN - 0028-3908, 0028-3908 KW - Chloride Channels KW - 0 KW - Ion Channels KW - Ligands KW - Membrane Proteins KW - Receptors, GABA-A KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Animals KW - Humans KW - Receptors, GABA-A -- physiology KW - Ethanol -- pharmacology KW - Receptors, GABA-A -- drug effects KW - Membrane Proteins -- drug effects KW - Alcoholism -- physiopathology KW - Ion Channels -- physiology KW - Membrane Proteins -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72633581?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuropharmacology&rft.atitle=Alcohol%2C+the+chloride+ionophore+and+endogenous+ligands+for+benzodiazepine+receptors.&rft.au=Lister%2C+R+G%3BLinnoila%2C+M&rft.aulast=Lister&rft.aufirst=R&rft.date=1991-12-01&rft.volume=30&rft.issue=12B&rft.spage=1435&rft.isbn=&rft.btitle=&rft.title=Neuropharmacology&rft.issn=00283908&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-10 N1 - Date created - 1992-03-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of protein kinase C activating agents on respiratory glycoconjugate release from feline airways. AN - 72601416; 1767862 AB - Abnormal regulation of airway glycoprotein secretion may underlie many respiratory diseases. Experimental activation of the protein kinase C (PKC) family of cytosolic enzymes has been shown to induce a secretory response in many tissues. To estimate the effect of PKC activation on airway secretion, alteration in the amount of radiolabeled respiratory glycoconjugate (RGC) released into culture media was determined following feline airway explant exposure to PKC activating agents. Exposure to two known activators of PKC, phorbol 12-myristate 13-acetate (PMA) and mezerein (MEZ), resulted in profound increases in respiratory glycoconjugate release over a seven day experimental period. The response evolved over several hours and was dose dependent. Maximal RGC release, 90% above control, occurred 2 days after exposure to either PMA or MEZ. Pharmacological inhibition of the PKC effect using two PKC inhibitors, 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine and sphingosine, resulted in dose-dependent antagonism of the maximal PMA (10(-7) M)-stimulated RGC release, suggesting altered PKC activity was responsible for augmenting RGC release. Since altered arachidonic acid metabolism has been implicated in mediating some PKC effects, eicosanoids were assayed in airway explant supernatants following PMA exposure. Enhanced release of both cyclooxygenase and lipoxygenase pathway products was detected by radioimmunoassay. Cotreatment of explants with PMA and an inhibitor of oxidative arachidonic acid metabolism, nordihydroguaiaretic acid, blocked RGC release. These data demonstrate prolonged augmentation of respiratory glycoconjugate release from airway explants following exposure to PKC-activating agents. JF - The American journal of physiology AU - Rieves, R D AU - Lundgren, J D AU - Logun, C AU - Wu, T AU - Shelhamer, J H AD - Department of Critical Care Medicine, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - L415 EP - L423 VL - 261 IS - 6 Pt 1 SN - 0002-9513, 0002-9513 KW - Diterpenes KW - 0 KW - Eicosanoids KW - Glycoconjugates KW - Terpenes KW - mezerein KW - 34807-41-5 KW - Masoprocol KW - 7BO8G1BYQU KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Chromatography, Gel KW - Enzyme Activation KW - Kinetics KW - Eicosanoids -- metabolism KW - Cats KW - Organ Culture Techniques KW - Chromatography, High Pressure Liquid KW - Masoprocol -- pharmacology KW - Protein Kinase C -- metabolism KW - Tetradecanoylphorbol Acetate -- toxicity KW - Glycoconjugates -- metabolism KW - Lung -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Terpenes -- pharmacology KW - Lung -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72601416?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+physiology&rft.atitle=Effect+of+protein+kinase+C+activating+agents+on+respiratory+glycoconjugate+release+from+feline+airways.&rft.au=Rieves%2C+R+D%3BLundgren%2C+J+D%3BLogun%2C+C%3BWu%2C+T%3BShelhamer%2C+J+H&rft.aulast=Rieves&rft.aufirst=R&rft.date=1991-12-01&rft.volume=261&rft.issue=6+Pt+1&rft.spage=L415&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+physiology&rft.issn=00029513&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-14 N1 - Date created - 1992-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytotoxicity, genotoxicity and transforming activity of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in rat tracheal epithelial cells. AN - 72586412; 1722280 AB - The cytotoxicity, genotoxicity and transforming activity of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) were studied by the assays of colony-forming efficiency (CFE), micronucleus formation (MN), and cell transformation in rat tracheal epithelial (RTE) cells both in vitro and in vivo. Liver S9, primary hepatocytes and RTE cells from normal and Aroclor-1254 induced rats were compared for bioactivation of NNK using Salmonella mutagenesis as the endpoint. Results from the in vitro experiments indicated that low concentrations of NNK (0.01-25 micrograms/ml) caused from 15% to greater than 100% increases in CFE of RTE cells. At high concentrations (100-200 micrograms/ml), NNK was significantly toxic to RTE cells. NNK treatment in vitro (50-200 micrograms/ml) increased MN frequency as much as 3-fold above background and significantly increased the transformation frequency (TF) in 4/5 (50 micrograms/ml) and 6/8 (100 micrograms/ml) experiments. The in vivo exposure of rats to NNK (150-450 mg/kg, given i.p.) resulted in a 60-85% reduction in CFE and a 3-5-fold increase in MN formation in RTE cells. In vivo treatment with cumulative doses of 150 and 300 mg/kg of NNK produced significant increases in TF of tracheal cells from 3/3 and 2/3 rats, respectively. Without activation, NNK was not mutagenic in Salmonella TA1535. The bioactivation of NNK to a mutagenic metabolite was achieved by incubation of NNK with liver S9 fraction from Aroclor-1254 induced rats or primary hepatocytes from both untreated and Aroclor-1254 pretreated rats. RTE cells did not produce sufficient quantities of mutagenic NNK metabolites to be detected by the Salmonella assay. JF - Mutation research AU - Zhu, S Y AU - Cunningham, M L AU - Gray, T E AU - Nettesheim, P AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 249 EP - 259 VL - 261 IS - 4 SN - 0027-5107, 0027-5107 KW - Carcinogens KW - 0 KW - Mutagens KW - Nitrosamines KW - Smoke KW - 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone KW - 7S395EDO61 KW - Index Medicus KW - Smoke -- adverse effects KW - Animals KW - Liver -- cytology KW - Mutagenicity Tests -- methods KW - Salmonella typhimurium -- drug effects KW - Trachea -- cytology KW - Epithelium -- drug effects KW - Plants, Toxic KW - Rats KW - Micronucleus Tests KW - Cell Survival -- drug effects KW - Biotransformation KW - Cells, Cultured KW - Tobacco -- chemistry KW - Colony-Forming Units Assay KW - Nitrosamines -- toxicity KW - Carcinogens -- toxicity KW - Carcinogenicity Tests -- methods KW - Mutagens -- toxicity KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72586412?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+research&rft.atitle=Cytotoxicity%2C+genotoxicity+and+transforming+activity+of+4-%28methylnitrosamino%29-1-%283-pyridyl%29-1-butanone+%28NNK%29+in+rat+tracheal+epithelial+cells.&rft.au=Zhu%2C+S+Y%3BCunningham%2C+M+L%3BGray%2C+T+E%3BNettesheim%2C+P&rft.aulast=Zhu&rft.aufirst=S&rft.date=1991-12-01&rft.volume=261&rft.issue=4&rft.spage=249&rft.isbn=&rft.btitle=&rft.title=Mutation+research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-07 N1 - Date created - 1992-02-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The reinforcing and subjective effects of morphine in post-addicts: a dose-response study. AN - 72579779; 1762068 AB - The reinforcing and subjective effects of morphine were determined in five human volunteers with histories of i.v. heroin abuse. Subjects responded under a second-order schedule of i.m. injection. Under this schedule, every 100 lever presses produced a brief stimulus light [fixed ratio (FR) 100:s]; the 30th completion of the FR 100 requirement turned on the light for 15 min and the subject received an i.m. injection of morphine [FR 30 (FR 100:s)]. Once each weekday morphine or placebo was available under this schedule. Each drug dose was available for 1 week. Under these conditions placebo did not maintain responding; 3.75 mg of morphine maintained responding in four of five subjects, and higher morphine doses (7.5, 15 and 30 mg) maintained responding in all five subjects. Subjective effects were measured concurrently: these included measures of drug liking, the Morphine Benzedrine Group scale of the Addiction Research Center Inventory, drug detection and identification. Subjects did not report subjective effects different from placebo for the lowest dose of morphine; the intermediate doses of morphine produced inconsistent effects, and the highest dose of morphine occasioned reports of drug liking and "dope" identifications. These results indicate that there can be a significant dissociation of the reinforcing and the subjective effects of opioids, which has implications for theories of opioid abuse, particularly those assuming that the reinforcing effects are causally related to the euphoric effects of opioids. Furthermore, these results confirm that measures of reinforcing effects and measures of subjective effects do not necessarily lead to identical predictions when used to assess the liability for abuse of a substance. JF - The Journal of pharmacology and experimental therapeutics AU - Lamb, R J AU - Preston, K L AU - Schindler, C W AU - Meisch, R A AU - Davis, F AU - Katz, J L AU - Henningfield, J E AU - Goldberg, S R AD - Clinical Pharmacology Branch, National Institute on Drug Abuse, Baltimore, Maryland. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 1165 EP - 1173 VL - 259 IS - 3 SN - 0022-3565, 0022-3565 KW - Morphine KW - 76I7G6D29C KW - Index Medicus KW - Dose-Response Relationship, Drug KW - Humans KW - Analgesia, Patient-Controlled KW - Male KW - Reinforcement (Psychology) KW - Substance-Related Disorders -- rehabilitation KW - Substance-Related Disorders -- psychology KW - Morphine -- administration & dosage KW - Morphine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72579779?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.atitle=The+reinforcing+and+subjective+effects+of+morphine+in+post-addicts%3A+a+dose-response+study.&rft.au=Lamb%2C+R+J%3BPreston%2C+K+L%3BSchindler%2C+C+W%3BMeisch%2C+R+A%3BDavis%2C+F%3BKatz%2C+J+L%3BHenningfield%2C+J+E%3BGoldberg%2C+S+R&rft.aulast=Lamb&rft.aufirst=R&rft.date=1991-12-01&rft.volume=259&rft.issue=3&rft.spage=1165&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=00223565&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-07 N1 - Date created - 1992-02-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synexin: a target protein for toxic effects of cyclosporine and FK 506 in endocrine cells. AN - 72573660; 1721394 JF - Transplantation proceedings AU - Carroll, P B AU - Caohuy, H AU - Lee, G AU - De la Fuente, M AU - Pollard, H B AU - Atwater, I AD - Laboratory of Cell Biology and Genetics, NIDDK, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 3166 EP - 3168 VL - 23 IS - 6 SN - 0041-1345, 0041-1345 KW - Annexin A7 KW - 0 KW - Annexins KW - Calcium-Binding Proteins KW - Glycoproteins KW - Liposomes KW - Proteins KW - Cyclosporine KW - 83HN0GTJ6D KW - Tacrolimus KW - WM0HAQ4WNM KW - Index Medicus KW - Animals KW - Sequence Homology, Nucleic Acid KW - Dose-Response Relationship, Drug KW - Amino Acid Sequence KW - Glycoproteins -- genetics KW - Cattle KW - Lung KW - Kinetics KW - Molecular Sequence Data KW - Calcium-Binding Proteins -- genetics KW - Proteins -- drug effects KW - Chromaffin Granules -- drug effects KW - Tacrolimus -- toxicity KW - Chromaffin Granules -- ultrastructure KW - Tacrolimus -- pharmacology KW - Cyclosporine -- pharmacology KW - Adrenal Medulla -- ultrastructure KW - Cyclosporine -- toxicity KW - Proteins -- genetics KW - Proteins -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72573660?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Transplantation+proceedings&rft.atitle=Synexin%3A+a+target+protein+for+toxic+effects+of+cyclosporine+and+FK+506+in+endocrine+cells.&rft.au=Carroll%2C+P+B%3BCaohuy%2C+H%3BLee%2C+G%3BDe+la+Fuente%2C+M%3BPollard%2C+H+B%3BAtwater%2C+I&rft.aulast=Carroll&rft.aufirst=P&rft.date=1991-12-01&rft.volume=23&rft.issue=6&rft.spage=3166&rft.isbn=&rft.btitle=&rft.title=Transplantation+proceedings&rft.issn=00411345&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-22 N1 - Date created - 1992-01-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Glutathione S-transferase mu in human lymphocyte and liver: role in modulating formation of carcinogen-derived DNA adducts. AN - 72567442; 1747926 AB - Glutathione transferase (GT) activity towards trans-stilbene oxide (tSBO), benzo[a]pyrene-4,5-oxide (B[a]PO) and 1-chloro-2,4-dinitrobenzene (CDNB) was measured in human liver and lymphocytes. GT-tSBO activity is catalyzed by GT mu which has polymorphic expression in human lymphocytes. Our results show that activity of GT-tSBO in lymphocytes correlates with its activity in liver (r = 0.7, P less than 0.001). GT activity towards BPO (GT-BPO) also correlated with GT-tSBO in lymphocytes and liver. However, interindividual variation of GT-BPO is less than that of GT-tSBO, suggesting that BPO may not be as specific a substrate for GT mu and therefore other GT isozymes may contribute to BPO conjugation. Conjugation of CDNB by GT was not different using cytosols from either high or low GT mu individuals. The functional significance of the GT-mu polymorphism was evaluated by measuring its effect on benzo[a]pyrene (B[a]P)- and aflatoxin B1 (AFB1)-DNA adduct formation in vitro. Human liver cytosols prepared from persons having low or high GT-tSBO activity were incubated with human liver microsomes, calf thymus DNA and B[a]P or AFB1. HPLC analysis revealed that the major B[a]P adduct was dG(N2)-7 beta, 8 alpha-trihydroxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE-dG). BPDE-dG adducts were decreased equally by cytosols from either low or high conjugators. In contrast, AFB1-DNA binding was inhibited to a greater extent in high conjugators than low conjugators. HPLC analysis demonstrates that adducts formed were AFB1-FAPyr and AFB1-N7-Gua. The correlation between AFB1-DNA adduct concentrations and GT mu activity was highly significant with a correlation coefficient of r = 0.88 at P less than 0.001. These results suggest that GT mu plays an important role in detoxifying DNA reactive metabolites of AFB1 and this enzyme may be a susceptibility marker for AFB1 related liver cancer. Moreover, our data demonstrate that lymphocytes are a reliable surrogate tissue for detecting liver GT mu polymorphisms. JF - Carcinogenesis AU - Liu, Y H AU - Taylor, J AU - Linko, P AU - Lucier, G W AU - Thompson, C L AD - National Institute of Environmental Health Sciences, Laboratory of Biochemical Risk Analysis, Research Triangle Park, NC. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 2269 EP - 2275 VL - 12 IS - 12 SN - 0143-3334, 0143-3334 KW - Benzopyrenes KW - 0 KW - Carcinogens KW - Pyrimidines KW - Stilbenes KW - Benzo(a)pyrene KW - 3417WMA06D KW - benzo(a)pyrene 4,5-epoxide KW - 37574-47-3 KW - aflatoxin B1-formamidopyrimidine KW - 65386-83-6 KW - DNA KW - 9007-49-2 KW - Aflatoxin B1 KW - 9N2N2Y55MH KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Dinitrochlorobenzene KW - GE3IBT7BMN KW - stilbene oxide KW - L47V7XQ2XK KW - Index Medicus KW - Cytosol -- metabolism KW - Polymorphism, Genetic KW - Liver Neoplasms -- enzymology KW - Humans KW - Aged KW - Benzopyrenes -- metabolism KW - Stilbenes -- metabolism KW - Chromatography, High Pressure Liquid KW - Aflatoxin B1 -- metabolism KW - Aged, 80 and over KW - Dinitrochlorobenzene -- metabolism KW - Adult KW - Pyrimidines -- metabolism KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Benzo(a)pyrene -- metabolism KW - Glutathione Transferase -- physiology KW - Liver -- enzymology KW - Carcinogens -- metabolism KW - DNA -- metabolism KW - Glutathione Transferase -- metabolism KW - Lymphocytes -- enzymology KW - Glutathione Transferase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72567442?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+pharmacology&rft.atitle=Idazoxan+down-regulates+beta-adrenoceptors+on+C6+glioma+cells+in+vitro.&rft.au=Manji%2C+H+K%3BChen%2C+G%3BBitran%2C+J+A%3BGusovsky%2C+F%3BPotter%2C+W+Z&rft.aulast=Manji&rft.aufirst=H&rft.date=1992-11-02&rft.volume=227&rft.issue=3&rft.spage=275&rft.isbn=&rft.btitle=&rft.title=European+journal+of+pharmacology&rft.issn=00142999&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-22 N1 - Date created - 1992-01-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - FK 506 treatment of experimental autoimmune uveoretinitis in primates. AN - 72562518; 1721454 JF - Transplantation proceedings AU - Fujino, Y AU - Chan, C C AU - de Smet, M D AU - Hikita, N AU - Gery, I AU - Mochizuki, M AU - Nussenblatt, R B AD - Laboratory of Immunology, National Eye Institute, NIH, Bethesda, MD 20892. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 3335 EP - 3338 VL - 23 IS - 6 SN - 0041-1345, 0041-1345 KW - Tacrolimus KW - WM0HAQ4WNM KW - Index Medicus KW - Mycobacterium tuberculosis -- immunology KW - Animals KW - Liver -- pathology KW - Kidney -- pathology KW - Liver -- drug effects KW - Weight Loss KW - Kidney -- drug effects KW - Macaca mulatta KW - Liver Function Tests KW - Immunization KW - Retinitis -- drug therapy KW - Uveitis -- pathology KW - Retinitis -- pathology KW - Tacrolimus -- toxicity KW - Tacrolimus -- therapeutic use KW - Retinitis -- immunology KW - Autoimmune Diseases -- pathology KW - Autoimmune Diseases -- drug therapy KW - Uveitis -- immunology KW - Uveitis -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72562518?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Transplantation+proceedings&rft.atitle=FK+506+treatment+of+experimental+autoimmune+uveoretinitis+in+primates.&rft.au=Fujino%2C+Y%3BChan%2C+C+C%3Bde+Smet%2C+M+D%3BHikita%2C+N%3BGery%2C+I%3BMochizuki%2C+M%3BNussenblatt%2C+R+B&rft.aulast=Fujino&rft.aufirst=Y&rft.date=1991-12-01&rft.volume=23&rft.issue=6&rft.spage=3335&rft.isbn=&rft.btitle=&rft.title=Transplantation+proceedings&rft.issn=00411345&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-22 N1 - Date created - 1992-01-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Abnormal skeletal and cardiac muscle mitochondria induced by zidovudine (AZT) in human muscle in vitro and in an animal model. AN - 72556661; 1753716 AB - To examine the mechanism of mitochondrial myocytotoxicity caused by long-term administration of zidovudine (AZT) in human immunodeficiency virus-positive patients, we examined the effect of AZT in vitro on human muscle in tissue culture and in vivo in rats treated with daily intraperitoneal injections of AZT at doses equivalent to the total daily dose used in acquired immunodeficiency syndrome patients. After 19 days, the AZT-treated myotubes in tissue culture exhibited abnormal mitochondria characterized by proliferation (mean +/- SD, 27.5 +/- 8 mitochondria/16 microns2 surface area, compared with 12.8 +/- 4 in the control cultures (p less than 0.001], enlarged size, abnormal cristae and electron-dense deposits in their matrix. The changes were partially reversible after AZT withdrawal. Rats treated with AZT developed weight loss, 100-fold elevation of creatine kinase, and increased serum lactate and glucose. In tissues, AZT had its highest concentration in the skeletal muscle and the heart. Skeletal and heart muscles from the treated animals, but not the controls, showed enlarged mitochondria with disorganized or absent cristae and electron-dense deposits in their matrix. Study of the mitochondrial functions assessed by evaluating stimulated oxygen consumption rate, enzymatic activities of electron transport chain and coupling state of oxidative phosphorylation (respiratory control ratio) revealed a decrease in rotenone-sensitive NADH cytochrome C reductase (complex I + III) and an uncoupling effect demonstrated by decreased respiratory control ratio. We conclude that AZT, a DNA chain terminator, is a muscle mitochondrial toxin that affects the oxidation-phosphorylation coupling and the activity of complex I and III of the mitochondrial respiratory chain. JF - Laboratory investigation; a journal of technical methods and pathology AU - Lamperth, L AU - Dalakas, M C AU - Dagani, F AU - Anderson, J AU - Ferrari, R AD - National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 742 EP - 751 VL - 65 IS - 6 SN - 0023-6837, 0023-6837 KW - Zidovudine KW - 4B9XT59T7S KW - Index Medicus KW - AIDS/HIV KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Culture Techniques KW - Humans KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Zidovudine -- toxicity KW - Mitochondria, Muscle -- ultrastructure KW - Mitochondria, Heart -- drug effects KW - Mitochondria, Heart -- ultrastructure KW - Mitochondria, Muscle -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72556661?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Laboratory+investigation%3B+a+journal+of+technical+methods+and+pathology&rft.atitle=Abnormal+skeletal+and+cardiac+muscle+mitochondria+induced+by+zidovudine+%28AZT%29+in+human+muscle+in+vitro+and+in+an+animal+model.&rft.au=Lamperth%2C+L%3BDalakas%2C+M+C%3BDagani%2C+F%3BAnderson%2C+J%3BFerrari%2C+R&rft.aulast=Lamperth&rft.aufirst=L&rft.date=1991-12-01&rft.volume=65&rft.issue=6&rft.spage=742&rft.isbn=&rft.btitle=&rft.title=Laboratory+investigation%3B+a+journal+of+technical+methods+and+pathology&rft.issn=00236837&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-24 N1 - Date created - 1992-01-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Contingent tolerance to carbamazepine is associated with lowering of amygdala-kindled seizure thresholds. AN - 72550896; 1748204 AB - Amygdala-kindled seizure thresholds were studied in animals which were or were not tolerant to the anticonvulsant effects of carbamazepine. The seizure threshold was defined as the lowest current that elicited a major motor seizure (stage 3 or greater). Amygdala-kindled rats received carbamazepine, once daily, either before each electrical stimulation (carba-before) or after each stimulation (carba-after). The rats given carbamazepine before, but not after, each once-daily kindling stimulation became tolerant to its anticonvulsant effects. Following this manipulation, seizure thresholds were redetermined in both groups of animals while medication-free. The carba-before (i.e., tolerant) animals showed a decreased seizure threshold, while the carba-after (i.e., nontolerant) animals showed no change. Tolerance to carbamazepine was reversed by giving the rats kindled seizures for a period of 7 days without drug; nontolerant animals received the same stimulation and seizures. When seizure thresholds were reevaluated, the carba-before animals (now not tolerant) had returned to their pretolerance values, while the carba-after group again showed no change. This effect of carbamazepine tolerance and its reversal being associated with respective decreases and increases in basal seizure threshold was replicated two more times. In each case the change in the generalized seizure threshold mirrored the change in responsivity of the animals to carbamazepine. These findings, consistent with the formulations of Siegel regarding conditioned compensatory response mechanisms mediating contingent drug tolerance, may have important clinical and theoretical implications. JF - Experimental neurology AU - Weiss, S R AU - Haas, K AU - Post, R M AD - Biological Psychiatry Branch, NIMH, Bethesda, Maryland 20892. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 300 EP - 306 VL - 114 IS - 3 SN - 0014-4886, 0014-4886 KW - Carbamazepine KW - 33CM23913M KW - Index Medicus KW - Rats KW - Drug Tolerance KW - Animals KW - Male KW - Seizures -- chemically induced KW - Seizures -- physiopathology KW - Kindling, Neurologic KW - Carbamazepine -- pharmacology KW - Amygdala -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72550896?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Experimental+neurology&rft.atitle=Contingent+tolerance+to+carbamazepine+is+associated+with+lowering+of+amygdala-kindled+seizure+thresholds.&rft.au=Weiss%2C+S+R%3BHaas%2C+K%3BPost%2C+R+M&rft.aulast=Weiss&rft.aufirst=S&rft.date=1991-12-01&rft.volume=114&rft.issue=3&rft.spage=300&rft.isbn=&rft.btitle=&rft.title=Experimental+neurology&rft.issn=00144886&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-21 N1 - Date created - 1992-01-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cigarette smoking and addiction. AN - 72550096; 1747988 AB - Tobacco use is a form of drug addiction, as shown by studies assessing the abuse liability of tobacco and nicotine in humans and animals. Tobacco experimentation frequently leads to daily use, which is characterized by a highly consistent pattern of drug intake. Such a pattern is controlled by the biologic concentrations of nicotine, a psychoactive constituent of tobacco smoke. Nicotine is a euphoriant, self-administered by humans as well as by animals in laboratory settings. Nicotine controls smokers' behavior in such a way that reducing or suppressing tobacco consumption produces a withdrawal syndrome characterized by irritability, difficulty concentrating, cognitive impairments, and weight gain. Nonpharmacologic factors are also important determinants of tobacco addiction that interfere with successful cessation. Strategies to treat tobacco addiction are comparable to those developed for other drug addictions. For example, therapy may include the use of alternate forms of nicotine and possibly also nicotine antagonists and medications targeted to alleviate specific withdrawal symptoms, if such therapies become available. As in all drug addiction treatment strategies, behavioral intervention is important whether or not a medication is used. JF - Clinics in chest medicine AU - Cohen, C AU - Pickworth, W B AU - Henningfield, J E AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 701 EP - 710 VL - 12 IS - 4 SN - 0272-5231, 0272-5231 KW - Index Medicus KW - Animals KW - Substance Withdrawal Syndrome KW - Humans KW - Reinforcement (Psychology) KW - Tobacco Use Disorder -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72550096?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinics+in+chest+medicine&rft.atitle=Cigarette+smoking+and+addiction.&rft.au=Cohen%2C+C%3BPickworth%2C+W+B%3BHenningfield%2C+J+E&rft.aulast=Cohen&rft.aufirst=C&rft.date=1991-12-01&rft.volume=84&rft.issue=21&rft.spage=1638&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-23 N1 - Date created - 1992-01-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ernst Freese (1925-1990). AN - 72543906; 1720866 JF - Mutation research AU - Drake, J W AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 165 EP - 169 VL - 251 IS - 2 SN - 0027-5107, 0027-5107 KW - Index Medicus KW - History of medicine KW - Freese KW - United States KW - History, 20th Century KW - Mutagenesis KW - Molecular Biology -- history UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72543906?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+research&rft.atitle=Ernst+Freese+%281925-1990%29.&rft.au=Drake%2C+J+W&rft.aulast=Drake&rft.aufirst=J&rft.date=1991-12-01&rft.volume=251&rft.issue=2&rft.spage=165&rft.isbn=&rft.btitle=&rft.title=Mutation+research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-14 N1 - Date created - 1992-01-14 N1 - Date revised - 2017-01-13 N1 - People - Freese N1 - Last updated - 2017-01-17 N1 - SubjectsTermNotLitGenreText - Freese ER - TY - JOUR T1 - Interleukin 7 generates antitumor cytotoxic T lymphocytes against murine sarcomas with efficacy in cellular adoptive immunotherapy. AN - 72540891; 1744582 AB - Interleukin 7 (IL-7) is a 25-kD cytokine that was initially described as a pre-B cell growth factor. This cytokine has also been shown to have T cell proliferative and differentiation effects. In this report, we demonstrate that antitumor cytotoxic T lymphocytes (CTL) generated by secondary in vitro sensitization of draining lymph node cells in IL-7 are effective in treating 3-day syngeneic methylcholanthrene (MCA) sarcoma pulmonary metastases in mice. In vivo titrations comparing IL-7 to IL-2 antitumor CTL show that they have equivalent potency in adoptive immunotherapy. IL-7 antitumor CTL generated against MCA sarcomas of weak immunogeneity are also tumor specific in their in vivo efficacy. This study represents the first successful use of a cytokine other than IL-2 for the generation of cells with in vivo efficacy in cellular adoptive transfer. JF - The Journal of experimental medicine AU - Jicha, D L AU - Mulé, J J AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/12/01/ PY - 1991 DA - 1991 Dec 01 SP - 1511 EP - 1515 VL - 174 IS - 6 SN - 0022-1007, 0022-1007 KW - Interleukin-2 KW - 0 KW - Interleukin-7 KW - Methylcholanthrene KW - 56-49-5 KW - Index Medicus KW - Interleukin-2 -- pharmacology KW - Animals KW - Mice, Inbred C57BL KW - Mice KW - Female KW - Sarcoma, Experimental -- therapy KW - Sarcoma, Experimental -- chemically induced KW - Immunotherapy, Adoptive KW - T-Lymphocytes, Cytotoxic -- immunology KW - Interleukin-7 -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72540891?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+experimental+medicine&rft.atitle=Interleukin+7+generates+antitumor+cytotoxic+T+lymphocytes+against+murine+sarcomas+with+efficacy+in+cellular+adoptive+immunotherapy.&rft.au=Jicha%2C+D+L%3BMul%C3%A9%2C+J+J%3BRosenberg%2C+S+A&rft.aulast=Jicha&rft.aufirst=D&rft.date=1991-12-01&rft.volume=174&rft.issue=6&rft.spage=1511&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+experimental+medicine&rft.issn=00221007&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-15 N1 - Date created - 1992-01-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Immunol. 1987 Jul 1;139(1):295-304 [2953816] J Exp Med. 1988 Apr 1;167(4):1417-27 [2965738] J Exp Med. 1989 Mar 1;169(3):707-16 [2522498] Proc Natl Acad Sci U S A. 1989 Jan;86(1):302-6 [2643102] J Immunol. 1989 Aug 15;143(4):1215-22 [2787360] Proc Natl Acad Sci U S A. 1989 Aug;86(15):5923-7 [2788279] Blood. 1989 Sep;74(4):1368-73 [2788467] Nature. 1988 Jun 9;333(6173):571-3 [3259677] J Exp Med. 1988 Mar 1;167(3):988-1002 [3258354] J Immunol. 1987 Feb 15;138(4):1121-9 [3543122] Nature. 1987 Apr 23-29;326(6115):795-8 [3494950] J Exp Med. 1987 Sep 1;166(3):792-7 [3498002] Science. 1986 Sep 19;233(4770):1318-21 [3489291] J Immunol. 1990 Apr 15;144(8):3015-20 [1969881] J Immunol. 1990 Sep 15;145(6):1706-12 [2118152] J Immunol. 1989 Nov 1;143(9):2917-22 [2572646] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tumor necrosis factor-alpha alters response of lung cancer cells to oxidative stress. AN - 72511437; 1960995 AB - Selected immunotherapies (tumor necrosis factor, interleukin-1, interleukin-2, and gamma interferon), chemotherapeutic agents (mitomycin, platinum, doxorubicin [Adriamycin], and bleomycin), and radiation therapy have been described to exert cytotoxicity through the generation of reactive oxygen species, including superoxide and hydrogen peroxide. Tumor necrosis factor, however, has been shown to impart increased resistance in vitro and in vivo against reactive oxygen species stress, including radiation therapy and oxygen toxicity, possibly because of the induction of increased cellular buffering capacities. It is unknown whether the sensitivity of a lung cancer cell to reactive oxygen species therapy is altered by tumor necrosis factor through the induction of free radical scavenging enzymes such as manganese superoxide dismutase. This question was investigated as follows: A549 lung adenocarcinoma cells, exposed for 24 hours to 0, 0.1, 1.0, or 10 micrograms/ml concentrations of tumor necrosis factor, were exposed to hypoxanthine plus xanthine oxidase, a superoxide generating system, for varying intervals. The number of cells surviving 5 days after the stress was determined, and cells exposed to tumor necrosis factor were examined by Northern Blot analysis for induction of the manganese superoxide dismutase gene. The hypoxanthine-xanthine oxidase stress alone caused a time-dependent decrease in survival; however, pretreatment with tumor necrosis factor increased cell survival significantly. Moreover, the cells exposed to tumor necrosis factor had a fivefold increase in the number of manganese superoxide dismutase transcripts. These findings suggest that tumor necrosis factor may confer resistance of lung cancer cells to subsequent reactive oxygen species-based therapies, and the resistance of these cells may be due to increased expression of manganese superoxide dismutase. Clinical treatment failures may result, especially if tumor necrosis factor is given concurrently with other therapies. JF - The Journal of thoracic and cardiovascular surgery AU - Pogrebniak, H W AU - Prewitt, T W AU - Matthews, W A AU - Pass, H I AD - Thoracic Oncology Section, National Cancer Institute, National Institutes of Health, Bethesda, Md., 20892. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 904 EP - 907 VL - 102 IS - 6 SN - 0022-5223, 0022-5223 KW - Tumor Necrosis Factor-alpha KW - 0 KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Xanthine Oxidase KW - EC 1.17.3.2 KW - Abridged Index Medicus KW - Index Medicus KW - Tumor Cells, Cultured KW - Enzyme Induction -- drug effects KW - Humans KW - Cell Division -- drug effects KW - Superoxide Dismutase -- biosynthesis KW - Adenocarcinoma -- metabolism KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Xanthine Oxidase -- pharmacology KW - Lung Neoplasms -- pathology KW - Lung Neoplasms -- metabolism KW - Adenocarcinoma -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72511437?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+thoracic+and+cardiovascular+surgery&rft.atitle=Tumor+necrosis+factor-alpha+alters+response+of+lung+cancer+cells+to+oxidative+stress.&rft.au=Pogrebniak%2C+H+W%3BPrewitt%2C+T+W%3BMatthews%2C+W+A%3BPass%2C+H+I&rft.aulast=Pogrebniak&rft.aufirst=H&rft.date=1991-12-01&rft.volume=102&rft.issue=6&rft.spage=904&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+thoracic+and+cardiovascular+surgery&rft.issn=00225223&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-09 N1 - Date created - 1992-01-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Clinical evaluation of intraperitoneal Pseudomonas exotoxin immunoconjugate OVB3-PE in patients with ovarian cancer. AN - 72507184; 1960550 AB - OVB3-PE is an immunotoxin composed of a murine monoclonal antibody reactive with human ovarian cancer and conjugated to Pseudomonas exotoxin (PE). Twenty-three patients with refractory ovarian cancer were treated intraperitoneally (IP) with escalating doses of OVB3-PE to study toxicity, pharmacokinetics, antiimmunotoxin antibody formation, and antitumor response. Dose-limiting CNS toxicity occurred after repeated doses at 5 and 10 micrograms/kg. Other non-dose-limiting toxicities included transient elevation of liver enzymes, fever, and gastrointestinal toxicity. Pharmacokinetics of IP and serum OVB3-PE were determined in 16 patients. Peak peritoneal fluid levels exceeded the in vitro median effective dose at all doses tested. At doses of 1 to 2 micrograms/kg, the immunotoxin concentration in the peritoneal fluid remained constant for up to 8 hours and dropped to negligible levels after 12 hours. At the 5 and 10 micrograms/kg doses, levels remained high for up to 24 hours (greater than 100 ng/mL) and then gradually decreased and became undetectable (less than 4 ng/mL) after 72 hours. Serum levels of OVB3-PE were also analyzed in 16 patients. At doses of 1 micrograms/kg and 2 micrograms/kg, serum levels were not detectable (less than 5 ng/mL). However, after doses of 5 or 10 micrograms/kg, peak serum level occurred at 24 hours after each dose and dropped to negligible levels by 72 hours. Sera from 12 patients were analyzed for anti-PE antibodies and antibodies to mouse immunoglobulin (HAMA). All patients developed antibodies against PE within 14 days of therapy. Domain II of PE appeared to be the most immunogenic portion of the PE molecule. HAMA was detected on day 14 of therapy in nine patients, on day 21 in two, and on day 28 in one patient. No clinical antitumor responses were observed. We conclude that IP OVB3-PE at dose levels of 5 micrograms/kg (x 3) and 10 micrograms/kg (x 2) is accompanied by dose-limiting toxic encephalopathy. Neurologic toxicity is likely to be due to crossreactivity of OVB3 to normal human brain tissue, which was not appreciated during preclinical screening. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Pai, L H AU - Bookman, M A AU - Ozols, R F AU - Young, R C AU - Smith, J W AU - Longo, D L AU - Gould, B AU - Frankel, A AU - McClay, E F AU - Howell, S AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 2095 EP - 2103 VL - 9 IS - 12 SN - 0732-183X, 0732-183X KW - Antibodies, Monoclonal KW - 0 KW - Bacterial Toxins KW - Exotoxins KW - Immunotoxins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Neoplasm Invasiveness KW - Drug Evaluation KW - Drug Administration Schedule KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Infusions, Parenteral KW - Female KW - Antibodies, Monoclonal -- therapeutic use KW - Immunotoxins -- adverse effects KW - Exotoxins -- adverse effects KW - Ovarian Neoplasms -- therapy KW - Exotoxins -- pharmacokinetics KW - Bacterial Toxins -- adverse effects KW - Carcinoma -- therapy KW - Carcinoma -- pathology KW - Bacterial Toxins -- pharmacokinetics KW - Ovarian Neoplasms -- pathology KW - Bacterial Toxins -- therapeutic use KW - Immunotoxins -- therapeutic use KW - Pseudomonas aeruginosa KW - Exotoxins -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72507184?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Clinical+evaluation+of+intraperitoneal+Pseudomonas+exotoxin+immunoconjugate+OVB3-PE+in+patients+with+ovarian+cancer.&rft.au=Pai%2C+L+H%3BBookman%2C+M+A%3BOzols%2C+R+F%3BYoung%2C+R+C%3BSmith%2C+J+W%3BLongo%2C+D+L%3BGould%2C+B%3BFrankel%2C+A%3BMcClay%2C+E+F%3BHowell%2C+S&rft.aulast=Pai&rft.aufirst=L&rft.date=1991-12-01&rft.volume=9&rft.issue=12&rft.spage=2095&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=0732183X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-09 N1 - Date created - 1992-01-09 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Clin Oncol. 1991 Dec;9(12):2088-90 [1960548] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ascorbic acid and oxidative inactivation of proteins. AN - 72498091; 1962558 AB - A number of active oxygen species are likely implicated in the etiology or manifestation of several pathological conditions, including aging, arthritis, carcinogenesis, atherosclerosis, and muscular dystrophy. Ascorbate plays a key role in protecting cells against oxidative damage. Paradoxically, in the presence of Fe3+ or Cu2+, ascorbate can promote the generation of the same reactive oxygen species (.OH, O2-, H2O2, and ferryl ion) it is known to destroy. This prooxidant activity derives from the ability of ascorbate to reduce Fe3+ or Cu2+ to Fe2+ or Cu+, respectively, and to reduce O2 to O2-. and H2O2. Damage to nucleic acid and proteins results from the binding of either Fe2+ or Cu+ to metal binding sites on these macromolecules followed by reaction of the metal complexes with H2O2; this leads to the production of active oxygen species that attack functional groups at or near the metal binding sites. JF - The American journal of clinical nutrition AU - Stadtman, E R AD - Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 1125S EP - 1128S VL - 54 IS - 6 Suppl SN - 0002-9165, 0002-9165 KW - Antioxidants KW - 0 KW - Ions KW - Metals KW - Proteins KW - Ascorbic Acid KW - PQ6CK8PD0R KW - Abridged Index Medicus KW - Index Medicus KW - Oxidation-Reduction KW - Antioxidants -- pharmacology KW - Humans KW - Metals -- metabolism KW - Proteins -- metabolism KW - Catalysis KW - Ascorbic Acid -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72498091?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+clinical+nutrition&rft.atitle=Ascorbic+acid+and+oxidative+inactivation+of+proteins.&rft.au=Stadtman%2C+E+R&rft.aulast=Stadtman&rft.aufirst=E&rft.date=1991-12-01&rft.volume=54&rft.issue=6+Suppl&rft.spage=1125S&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+clinical+nutrition&rft.issn=00029165&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-06 N1 - Date created - 1992-01-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activating and inactivating mutations of the alpha subunit of Gi2 protein have opposite effects on proliferation of NIH 3T3 cells. AN - 72492155; 1660138 AB - Previous studies have demonstrated that mutations of highly conserved residues in the alpha subunit of Gs (alpha s) can inhibit either the intrinsic GTPase activity (glutamine-227 to leucine, Q227L) or the ability of the protein to be activated by GTP (glycine-226 to alanine, G226A). We stably transfected NIH 3T3 cells with cDNAs encoding Gi2 alpha subunit (alpha i2) containing either wild-type sequence or the homologous mutations Q205L and G204A. High expression of wild-type alpha i2, Q205L alpha i2, and G204A alpha i2 was confirmed in transfected cells by immunoblot analysis. The overexpression of all three alpha i2 proteins was accompanied by an increase in beta-subunit expression. Q205L alpha i2 was a poor substrate for ADP-ribosylation by pertussis toxin as compared with wild-type alpha i2. Expression of Q205L alpha i2 markedly decreased forskolin- or cholera toxin-stimulated intracellular cAMP levels in intact cells, confirming the constitutively activated state of the protein. In contrast, G204A alpha i2 increased intracellular cAMP and was resistant to guanosine 5'-[gamma-thio]triphosphate-induced inhibition of ADP-ribosylation by pertussis toxin, as expected for an inactive alpha i2. Transfection of wild-type, Q205L, or G204A alpha i2 cDNA did not induce focus formation of NIH 3T3 cells. However, overexpression of Q205L alpha i2 induced a decreased serum requirement, a reduced doubling time, and an 8- to 10-fold increase in [3H]thymidine incorporation. Q205L alpha i2 cells formed small colonies in soft agar, demonstrating some degree of anchorage-independent proliferation. Expression of G204A alpha i2 slowed the growth of NIH 3T3 cells. We conclude that alpha i2 plays an important role in regulation of fibroblast growth. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Hermouet, S AU - Merendino, J J AU - Gutkind, J S AU - Spiegel, A M AD - Molecular Pathophysiology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/12/01/ PY - 1991 DA - 1991 Dec 01 SP - 10455 EP - 10459 VL - 88 IS - 23 SN - 0027-8424, 0027-8424 KW - Macromolecular Substances KW - 0 KW - Oligodeoxyribonucleotides KW - Cyclic AMP KW - E0399OZS9N KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Gene Expression KW - Mice KW - Cloning, Molecular KW - Rats KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Transfection KW - Kinetics KW - Molecular Sequence Data KW - DNA Replication KW - Cyclic AMP -- metabolism KW - GTP-Binding Proteins -- physiology KW - GTP-Binding Proteins -- genetics KW - Cell Division UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72492155?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Activating+and+inactivating+mutations+of+the+alpha+subunit+of+Gi2+protein+have+opposite+effects+on+proliferation+of+NIH+3T3+cells.&rft.au=Hermouet%2C+S%3BMerendino%2C+J+J%3BGutkind%2C+J+S%3BSpiegel%2C+A+M&rft.aulast=Hermouet&rft.aufirst=S&rft.date=1991-12-01&rft.volume=88&rft.issue=23&rft.spage=10455&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-09 N1 - Date created - 1992-01-09 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1991 Aug 5;266(22):14193-7 [1907271] J Biol Chem. 1987 Apr 25;262(12):5522-9 [3032936] Proc Natl Acad Sci U S A. 1991 Aug 15;88(16):7031-5 [1651490] Nature. 1991 May 2;351(6321):63-5 [1851251] Nature. 1991 Jan 10;349(6305):117-27 [1898771] Nucleic Acids Res. 1986 Dec 22;14(24):9679-98 [3027659] Nature. 1988 Sep 15;335(6187):254-6 [3045568] J Biol Chem. 1984 Dec 25;259(24):15320-3 [6439719] Annu Rev Biochem. 1987;56:779-827 [3304147] Science. 1990 Aug 10;249(4969):655-9 [2116665] Biochem Biophys Res Commun. 1990 May 16;168(3):1184-93 [2161217] Annu Rev Pharmacol Toxicol. 1990;30:675-705 [2111655] Mol Cell Biol. 1990 Jun;10(6):2931-40 [1692962] EMBO J. 1990 Aug;9(8):2423-8, 2389 [2196173] Cell. 1984 Jul;37(3):1053-62 [6331674] Cell. 1977 May;11(1):223-32 [194704] J Virol. 1969 Nov;4(5):549-53 [4311790] J Cyclic Nucleotide Res. 1975;1(4):207-18 [177461] Anal Biochem. 1976 May 7;72:248-54 [942051] Nature. 1990 Nov 8;348(6297):125-32 [2122258] J Biol Chem. 1991 Mar 15;266(8):4673-6 [1848223] Cell. 1990 Nov 16;63(4):697-706 [2121366] J Biol Chem. 1990 Oct 15;265(29):17456-62 [2170379] Cell Growth Differ. 1990 Jan;1(1):9-15 [2150330] FEBS Lett. 1989 Jun 5;249(2):189-94 [2500363] Nature. 1989 Aug 31;340(6236):692-6 [2549426] Mol Cell Biol. 1989 Dec;9(12):5434-9 [2511433] J Biol Chem. 1989 Sep 15;264(26):15475-82 [2549065] J Biol Chem. 1989 Sep 15;264(26):15467-74 [2549064] Biochem Biophys Res Commun. 1989 Oct 16;164(1):46-53 [2508638] Proc Natl Acad Sci U S A. 1989 Oct;86(20):7809-13 [2510151] Nature. 1987 Apr 23-29;326(6115):800-3 [3033510] J Biol Chem. 1987 Oct 15;262(29):14241-9 [2820999] J Biol Chem. 1987 Oct 25;262(30):14683-8 [3117789] J Biol Chem. 1987 Sep 15;262(26):12463-7 [3040750] J Biol Chem. 1988 May 15;263(14):6476-9 [3129425] FEBS Lett. 1986 Dec 15;209(2):352-6 [3466805] Nature. 1988 Aug 25;334(6184):712-5 [3137475] J Biol Chem. 1985 Jun 25;260(12):7226-33 [2860111] Science. 1991 May 10;252(5007):802-8 [1902986] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A minimal lentivirus Tat. AN - 72456047; 1658392 AB - Transcriptional regulatory mechanisms found in lentiviruses employ RNA enhancer elements called trans-activation responsive (TAR) elements. These nascent RNA stem-loops are cis-acting targets of virally encoded Tat effectors. Interactions between Tat and TAR increase the processivity of transcription complexes and lead to efficient copying of viral genomes. To study essential elements of this trans activation, peptide motifs from Tats of two distantly related lentiviruses, equine infectious anemia virus (EIAV) and human immunodeficiency virus type 1 (HIV-1), were fused to the coat protein of bacteriophage R17 and tested on the long terminal repeat of EIAV, where TAR was replaced by the R17 operator, the target of the coat protein. This independent RNA-tethering mechanism mapped activation domains of Tats from HIV-1 and EIAV to 47 and 15 amino acids and RNA-binding domains to 10 and 26 amino acids, respectively. Thus, a minimal lentivirus Tat consists of 25 amino acids, of which 15 modify viral transcription and 10 bind to the target RNA stem-loop. JF - Journal of virology AU - Derse, D AU - Carvalho, M AU - Carroll, R AU - Peterlin, B M AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, Maryland 21702-1201. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 7012 EP - 7015 VL - 65 IS - 12 SN - 0022-538X, 0022-538X KW - Tat KW - RNA, Viral KW - 0 KW - Index Medicus KW - AIDS/HIV KW - Base Sequence KW - Sequence Homology, Nucleic Acid KW - Capsid -- genetics KW - Molecular Sequence Data KW - Transcription, Genetic KW - Amino Acid Sequence KW - RNA, Viral -- genetics KW - Repetitive Sequences, Nucleic Acid KW - Plasmids KW - Binding Sites KW - HIV-1 -- genetics KW - Gene Expression Regulation, Viral KW - Enhancer Elements, Genetic KW - Infectious Anemia Virus, Equine -- genetics KW - Lentivirus -- genetics KW - Genes, tat KW - Transcriptional Activation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72456047?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=A+minimal+lentivirus+Tat.&rft.au=Derse%2C+D%3BCarvalho%2C+M%3BCarroll%2C+R%3BPeterlin%2C+B+M&rft.aulast=Derse&rft.aufirst=D&rft.date=1991-12-01&rft.volume=65&rft.issue=12&rft.spage=7012&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-26 N1 - Date created - 1991-12-26 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Tat N1 - SuppNotes - Cited By: J Virol. 1991 Mar;65(3):1053-6 [1995941] J Mol Biol. 1981 Mar 25;147(1):11-23 [6455533] Genes Dev. 1990 Aug;4(8):1365-73 [2227414] Cell. 1990 Nov 16;63(4):791-802 [2225077] Cell. 1990 Nov 16;63(4):655-7 [2225069] Biochemistry. 1987 Mar 24;26(6):1563-8 [3297131] Proc Natl Acad Sci U S A. 1988 Apr;85(8):2494-8 [2965813] Genes Dev. 1989 Apr;3(4):547-58 [2470647] Science. 1988 Feb 19;239(4842):910-3 [3277284] Nature. 1987 Dec 3-9;330(6147):489-93 [2825027] Cell. 1988 Jan 15;52(1):5-6 [2449971] Virology. 1987 Jun;158(2):300-12 [3035786] J Virol. 1989 Dec;63(12):5501-4 [2479775] Proc Natl Acad Sci U S A. 1989 Oct;86(19):7397-401 [2552444] EMBO J. 1990 Dec;9(12):4145-53 [2249668] J Virol. 1991 Jul;65(7):3468-74 [1645778] J Virol. 1991 Jul;65(7):3460-7 [1645777] Genes Dev. 1991 Feb;5(2):201-10 [1899841] Trends Genet. 1991 Jan;7(1):9-14 [2003337] Proc Natl Acad Sci U S A. 1989 Jul;86(13):4858-62 [2544877] Cell. 1989 Jul 14;58(1):215-23 [2752420] Nature. 1988 Jul 14;334(6178):165-7 [3386755] J Virol. 1990 Apr;64(4):1616-24 [2157047] Cell. 1990 Aug 24;62(4):769-76 [2117500] Science. 1990 Sep 14;249(4974):1281-5 [2205002] Proc Natl Acad Sci U S A. 1990 May;87(9):3624-8 [2333305] New Biol. 1990 Jan;2(1):20-31 [2078551] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Analysis of cis-acting elements present in the CD20/B1 antigen promoter. AN - 72452971; 1719097 AB - A genomic clone spanning a large portion of the 5' untranscribed region of the CD20 gene was isolated. Deletion analysis of subcloned fragments identified several regulatory elements. A major positive cis-acting element was localized between base pairs -290/-186. A second positive regulatory element was localized between -454/-280 and negative regulatory elements were present in the region between bp -828/-454. The sequence -280/-186 conferred B cell-specific expression on a heterologous, TATA box containing c-fos promoter. Electrophoretic mobility shift assays with overlapping oligonucleotide probes spanning -280/-186 revealed that a 25-bp probe (-225/-201) bound a nuclear protein present in B cell lines expressing the CD20/B1 antigen but not in Jurkat (T cell), U937 (promonocytic), U251 (glioma), or HeLa cells. To confirm the functional significance of this sequence, a trimer of this region was subcloned into the c-fos promoter containing CAT plasmid. Expression was observed only in BJA-B and HS-Sultan cells but not in CD20/B1- cell lines. This sequence element is also important in phorbol ester-induced CD20 expression in the pre-B cell line BP-697. These results partially characterize several regulatory elements present in the CD20 promoter that are likely important in the B cell-specific expression of the CD20 gene. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Rieckmann, P AU - Wilson, G L AU - Thevenin, C AU - Hong, J X AU - Kehrl, J H AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/12/01/ PY - 1991 DA - 1991 Dec 01 SP - 3994 EP - 3999 VL - 147 IS - 11 SN - 0022-1767, 0022-1767 KW - Antigens, CD KW - 0 KW - Antigens, CD20 KW - Antigens, Differentiation, B-Lymphocyte KW - DNA-Binding Proteins KW - Oligonucleotides KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Genes KW - Oligonucleotides -- chemistry KW - Humans KW - Enhancer Elements, Genetic KW - DNA Mutational Analysis KW - Restriction Mapping KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Gene Expression Regulation -- drug effects KW - DNA-Binding Proteins -- physiology KW - Promoter Regions, Genetic KW - Antigens, Differentiation, B-Lymphocyte -- genetics KW - Antigens, CD -- genetics KW - B-Lymphocytes -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72452971?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Analysis+of+cis-acting+elements+present+in+the+CD20%2FB1+antigen+promoter.&rft.au=Rieckmann%2C+P%3BWilson%2C+G+L%3BThevenin%2C+C%3BHong%2C+J+X%3BKehrl%2C+J+H&rft.aulast=Rieckmann&rft.aufirst=P&rft.date=1991-12-01&rft.volume=147&rft.issue=11&rft.spage=3994&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-18 N1 - Date created - 1991-12-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The intragenic enhancer of human immunodeficiency virus type 1 contains functional AP-1 binding sites. AN - 72451510; 1942259 AB - An intragenic enhancer in the pol gene of human immunodeficiency virus type 1 has previously been identified (Verdin et al., Proc. Natl. Acad. Sci. USA 87:4874-4878, 1990). This element is composed of two subdomains both exhibiting phorbol ester-inducible enhancing activity on the viral thymidine kinase promoter in HeLa cells. Examination of the nucleotide sequence of one of these domains (nucleotides 4079 to 4342, HXB2 isolate) revealed the presence of three short DNA regions highly homologous to the recognition site for cellular transcription factor AP-1. Two short oligonucleotides containing these AP-1 sites each functioned as a phorbol ester-inducible enhancer when cloned upstream of the thymidine kinase promoter and transfected into HeLa cells. Gel mobility shift assays and competition experiments using the same two oligonucleotides demonstrated that they bound affinity-purified AP-1 or AP-1 present in uninduced and 12-O-tetradecanoylphorbol-13-acetate-induced HeLa nuclear extracts. Footprinting experiments confirmed that all three predicted sites bound purified AP-1. These results suggest that the AP-1 factor could play a role in the transcriptional regulation of human immunodeficiency virus type 1 gene expression. JF - Journal of virology AU - Van Lint, C AU - Burny, A AU - Verdin, E AD - Laboratory of Viral and Molecular Pathogenesis, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 7066 EP - 7072 VL - 65 IS - 12 SN - 0022-538X, 0022-538X KW - DNA, Viral KW - 0 KW - Oligodeoxyribonucleotides KW - Proto-Oncogene Proteins c-jun KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - AIDS/HIV KW - Base Sequence KW - Transcription, Genetic -- drug effects KW - Transfection KW - HeLa Cells KW - Humans KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Nucleus -- physiology KW - Cell Nucleus -- drug effects KW - Plasmids KW - Binding Sites KW - HIV-1 -- genetics KW - Enhancer Elements, Genetic KW - Introns KW - Proto-Oncogene Proteins c-jun -- metabolism KW - Genes, Viral KW - DNA, Viral -- genetics KW - Genes, pol KW - DNA, Viral -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72451510?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=The+intragenic+enhancer+of+human+immunodeficiency+virus+type+1+contains+functional+AP-1+binding+sites.&rft.au=Van+Lint%2C+C%3BBurny%2C+A%3BVerdin%2C+E&rft.aulast=Van+Lint&rft.aufirst=C&rft.date=1991-12-01&rft.volume=65&rft.issue=12&rft.spage=7066&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-26 N1 - Date created - 1991-12-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1989 Apr 25;264(12):7025-32 [2540170] Methods Enzymol. 1980;65(1):499-560 [6246368] J Virol. 1989 Jul;63(7):3001-15 [2542608] Mol Cell Biol. 1989 May;9(5):2247-50 [2501665] Cell. 1989 Jul 14;58(1):1-4 [2665940] Cell. 1989 Jul 28;58(2):227-9 [2665943] Science. 1989 Jul 28;245(4916):371-8 [2667136] J Virol. 1989 Sep;63(9):4115-9 [2760991] Mol Cell Biol. 1989 Jun;9(6):2728-33 [2548087] Annu Rev Biochem. 1989;58:799-839 [2673023] J Virol. 1989 Nov;63(11):4919-24 [2795721] EMBO J. 1989 Dec 1;8(12):3825-32 [2511003] Cell. 1989 Dec 1;59(5):827-36 [2512012] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] Science. 1983 May 20;220(4599):868-71 [6189183] Science. 1984 May 4;224(4648):500-3 [6200936] Science. 1984 Aug 24;225(4664):840-2 [6206563] Science. 1984 Dec 7;226(4679):1165-71 [6095449] J Immunol. 1985 Nov;135(5):3151-62 [2995487] Science. 1986 Feb 21;231(4740):850-3 [2418502] J Immunol. 1986 Jun 1;136(11):4049-53 [2422271] Science. 1986 Oct 3;234(4772):47-52 [3529394] Virology. 1986 Oct 30;154(2):249-58 [3639669] Nature. 1987 Jan 22-28;325(6102):368-72 [3027570] Nature. 1987 Apr 16-22;326(6114):711-3 [3031512] Cell. 1987 Jun 19;49(6):729-39 [3034432] Cell. 1987 Jun 19;49(6):741-52 [3034433] Mol Cell Biol. 1987 Jun;7(6):2256-66 [3037355] Nucleic Acids Res. 1987 Jul 10;15(13):5490 [3037497] Nature. 1987 Oct 15-21;329(6140):648-51 [2821407] Cell. 1987 Oct 23;51(2):251-60 [2822255] Science. 1988 Mar 4;239(4844):1150-3 [2964084] Nature. 1988 Mar 17;332(6161):275-8 [2831462] Nature. 1988 Apr 7;332(6164):557-61 [2833704] Genes Dev. 1988 Mar;2(3):267-81 [3288540] Science. 1988 Jul 8;241(4862):202-5 [3260404] Cell. 1988 Jul 29;54(3):325-34 [2840203] Nature. 1988 Aug 11;334(6182):535-7 [3136397] Nature. 1988 Aug 18;334(6183):629-31 [2457172] Proc Natl Acad Sci U S A. 1988 Aug;85(16):5839-43 [2842750] Proc Natl Acad Sci U S A. 1988 Sep;85(17):6267-71 [3166139] Cell. 1988 Nov 4;55(3):395-7 [3141060] Proc Natl Acad Sci U S A. 1988 Nov;85(22):8464-7 [3186736] Cell. 1988 Dec 2;55(5):917-24 [3142692] EMBO J. 1988 Aug;7(8):2475-83 [3142763] Genes Dev. 1988 Sep;2(9):1055-62 [2847958] Science. 1988 Dec 9;242(4884):1418-20 [3201230] EMBO J. 1988 Nov;7(11):3389-95 [2463158] Nature. 1989 Feb 16;337(6208):661-3 [2537468] Science. 1989 Mar 31;243(4899):1689-94 [2494701] Nature. 1990 May 24;345(6273):361-4 [2160609] Annu Rev Immunol. 1990;8:453-75 [2188670] Proc Natl Acad Sci U S A. 1990 Jun;87(12):4874-8 [2352955] Genes Dev. 1990 Jun;4(6):993-1006 [2116990] EMBO J. 1990 Dec;9(13):4417-23 [2124973] Nature. 1990 May 24;345(6273):359-61 [2188137] Virology. 1973 Apr;52(2):456-67 [4705382] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Genes Dev. 1989 Feb;3(2):173-84 [2497053] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - IL-4 inhibits the costimulatory activity of IL-2 or picolinic acid but not of lipopolysaccharide on IFN-gamma-treated macrophages. AN - 72451370; 1940368 AB - We reported previously that IL-2 induces tumoricidal activity in IFN-gamma-treated murine macrophages. The present study was performed to investigate the regulation of IL-2-dependent tumoricidal activity in murine macrophage cell lines. The v-raf/v-myc-immortalized murine macrophage cell lines ANA-1, GG2EE, and HEN-CV did not express constitutive levels of cytotoxic activity against P815 mastocytoma cells. Moreover, these macrophage cell lines did not become tumoricidal after exposure to IL-4, IFN-gamma, IL-2 or LPS. However, these macrophages developed cytotoxic capabilities after incubation with either IFN-gamma plus IL-2 or IFN-gamma plus LPS. IL-4 inhibited IFN-gamma plus IL-2- but not IFN-gamma plus LPS-induced tumoricidal activity. This effect of IL-4 was not restricted to v-raf/v-myc-immortalized macrophage cell lines because similar results were obtained by using a macrophage cell line that was established from a spontaneous histiocytic sarcoma. The suppressive activity of IL-4 on the ANA-1 macrophage cell line was dose-dependent (approximately 12-200 U/ml) and was neutralized by the addition of anti-IL-4 mAb. IL-4 decreased the IFN-gamma-induced expression of mRNA for the p55 (alpha) subunit of the IL-2R in ANA-1 macrophages. Therefore, at least one mechanism by which IL-4 may have inhibited IFN-gamma plus IL-2-induced tumoricidal activity was by reducing macrophage IL-2R alpha mRNA expression. We have previously reported that picolinic acid, a tryptophan metabolite, is a costimulator of macrophage tumoricidal activity. We now report that IL-4 also inhibited IFN-gamma plus picolinic acid-induced cytotoxicity in ANA-1 macrophages. We propose that IL-2 and picolinic acid may have a common mechanism of action that is susceptible to IL-4 suppression. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Cox, G W AU - Chattopadhyay, U AU - Oppenheim, J J AU - Varesio, L AD - Laboratory of Molecular Immunoregulation, National Cancer Institute-Frederick Cancer Research and Development Center, National Institutes of Health, MD 21702-1201. Y1 - 1991/12/01/ PY - 1991 DA - 1991 Dec 01 SP - 3809 EP - 3814 VL - 147 IS - 11 SN - 0022-1767, 0022-1767 KW - Interleukin-2 KW - 0 KW - Lipopolysaccharides KW - Picolinic Acids KW - Receptors, Interleukin-2 KW - Recombinant Proteins KW - Interleukin-4 KW - 207137-56-2 KW - Interferon-gamma KW - 82115-62-6 KW - picolinic acid KW - QZV2W997JQ KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Blotting, Northern KW - In Vitro Techniques KW - Gene Expression KW - Mice KW - Drug Synergism KW - Receptors, Interleukin-2 -- genetics KW - Cell Line KW - Macrophage Activation -- drug effects KW - Interleukin-2 -- antagonists & inhibitors KW - Lipopolysaccharides -- administration & dosage KW - Interleukin-2 -- administration & dosage KW - Picolinic Acids -- antagonists & inhibitors KW - Interleukin-4 -- pharmacology KW - Macrophages -- physiology KW - Interferon-gamma -- pharmacology KW - Picolinic Acids -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72451370?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=IL-4+inhibits+the+costimulatory+activity+of+IL-2+or+picolinic+acid+but+not+of+lipopolysaccharide+on+IFN-gamma-treated+macrophages.&rft.au=Cox%2C+G+W%3BChattopadhyay%2C+U%3BOppenheim%2C+J+J%3BVaresio%2C+L&rft.aulast=Cox&rft.aufirst=G&rft.date=1991-12-01&rft.volume=147&rft.issue=11&rft.spage=3809&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-18 N1 - Date created - 1991-12-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Bovine papillomavirus with a mutation in the E2 serine 301 phosphorylation site replicates at a high copy number. AN - 72448382; 1658358 AB - The E2 open reading frame of bovine papillomavirus type 1 (BPV-1) encodes at least three proteins with transcriptional regulatory properties. The full-length E2 open reading frame encodes a transcriptional transactivator, and the 3' region encodes two smaller polypeptides that repress E2-mediated transactivation. The full-length gene product is also required for viral DNA replication. We have demonstrated that the BPV-1 E2 polypeptides are phosphorylated primarily on two serine residues at a site adjacent to the carboxy-terminal DNA binding domain, which is common to all three E2 proteins (A. A. McBride, J. B. Bolen, and P. M. Howley, J. Virol. 63:5076-5085, 1989). These serine residues, at amino acid positions 298 and 301, were substituted with alanine residues in the context of the entire BPV-1 genome. The mutated BPV-1 genomes were introduced into rodent cell lines and assayed for focus formation, viral gene expression, and extrachromosomal viral DNA replication. Viral DNAs containing the E2 serine-to-alanine substitution mutants transformed C127 cells with efficiencies comparable to that of wild-type BPV-1. However, the viral genome containing the serine-to-alanine substitution at position 301 of the E2 polypeptide replicated to a copy number 20-fold higher than that of wild-type DNA. JF - Journal of virology AU - McBride, A A AU - Howley, P M AD - Laboratory of Tumor Virus Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 6528 EP - 6534 VL - 65 IS - 12 SN - 0022-538X, 0022-538X KW - DNA, Viral KW - 0 KW - Viral Proteins KW - Serine KW - 452VLY9402 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Transcription, Genetic KW - Amino Acid Sequence KW - Plasmids KW - Transcriptional Activation KW - Phenotype KW - DNA -- isolation & purification KW - Phosphorylation KW - Transfection KW - DNA -- genetics KW - Molecular Sequence Data KW - DNA, Viral -- isolation & purification KW - Cell Line, Transformed KW - DNA, Viral -- genetics KW - Cell Line KW - Virus Replication KW - Viral Proteins -- genetics KW - Mutagenesis, Site-Directed KW - Gene Expression Regulation, Viral KW - Open Reading Frames KW - Bovine papillomavirus 1 -- physiology KW - Bovine papillomavirus 1 -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72448382?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Bovine+papillomavirus+with+a+mutation+in+the+E2+serine+301+phosphorylation+site+replicates+at+a+high+copy+number.&rft.au=McBride%2C+A+A%3BHowley%2C+P+M&rft.aulast=McBride&rft.aufirst=A&rft.date=1991-12-01&rft.volume=65&rft.issue=12&rft.spage=6528&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-26 N1 - Date created - 1991-12-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Virology. 1986 Apr 15;150(1):221-30 [3006336] Virology. 1980 Jun;103(2):369-75 [6247821] Cell. 1987 Jul 3;50(1):69-78 [3036366] Cell. 1989 Nov 17;59(4):675-80 [2573431] J Virol. 1989 Dec;63(12):5076-85 [2555544] Mol Cell Biol. 1989 Jun;9(6):2424-30 [2548081] J Virol. 1989 Apr;63(4):1743-55 [2538655] J Virol. 1989 Jul;63(7):3151-4 [2542621] J Virol. 1989 Jan;63(1):259-66 [2535732] Proc Natl Acad Sci U S A. 1989 Jan;86(2):510-4 [2536165] EMBO J. 1989 Apr;8(4):1111-9 [2663470] J Biol Chem. 1989 May 5;264(13):7345-8 [2708368] Biochim Biophys Acta. 1988 Sep 16;971(2):227-31 [2901861] J Virol. 1984 Nov;52(2):377-88 [6092667] Cell. 1991 Feb 8;64(3):573-84 [1846781] Proc Natl Acad Sci U S A. 1991 Jul 15;88(14):6363-7 [1648739] EMBO J. 1991 Feb;10(2):449-57 [1846806] J Virol. 1991 Feb;65(2):649-56 [1846189] Science. 1990 Dec 21;250(4988):1694-9 [2176744] FEBS Lett. 1988 Sep 12;237(1-2):225-8 [3169237] J Biol Chem. 1988 Nov 5;263(31):15872-5 [3053682] Proc Natl Acad Sci U S A. 1987 Dec;84(24):8834-8 [3321056] EMBO J. 1988 Sep;7(9):2823-9 [2846285] Nature. 1988 Aug 11;334(6182):494-8 [2900470] Cell. 1985 Aug;42(1):183-91 [2990724] Science. 1986 Oct 17;234(4774):364-8 [2876518] EMBO J. 1988 Dec 20;7(13):4245-53 [2854060] EMBO J. 1988 Feb;7(2):533-9 [2835232] EMBO J. 1988 Apr;7(4):1197-204 [2841117] J Virol. 1987 Dec;61(12):3889-95 [2824822] EMBO J. 1988 Dec 1;7(12):3807-16 [2850174] Mol Cell Biol. 1985 Nov;5(11):3310-5 [3018516] Mol Cell Biol. 1986 Mar;6(3):859-69 [3022134] Proc Natl Acad Sci U S A. 1987 Mar;84(5):1215-8 [3029771] J Virol. 1986 Nov;60(2):626-34 [3021996] Nature. 1987 Jan 1-7;325(6099):70-3 [3025749] J Virol. 1987 Apr;61(4):1248-52 [3029420] Nature. 1987 Sep 3-9;329(6134):81-4 [3306402] Nature. 1990 Apr 5;344(6266):517-22 [2157164] Nature. 1990 Apr 12;344(6267):678-82 [2157987] Cell. 1990 Jun 1;61(5):735-8 [2160857] J Virol. 1990 Feb;64(2):950-6 [2153256] J Virol. 1990 Feb;64(2):944-9 [2153255] Genes Dev. 1990 Jun;4(6):955-67 [2200737] Virology. 1982 May;119(1):22-34 [6280384] Proc Natl Acad Sci U S A. 1981 May;78(5):2727-31 [6265905] Proc Natl Acad Sci U S A. 1982 Dec;79(23):7147-51 [6296820] J Virol. 1987 Jul;61(7):2128-37 [3035214] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Site-directed mutagenesis of the m3 muscarinic receptor: identification of a series of threonine and tyrosine residues involved in agonist but not antagonist binding. AN - 72445578; 1657592 AB - The hydrophobic core of all muscarinic receptors contains several conserved serine, threonine and tyrosine residues, most of which do not occur in any other G-protein coupled receptor. Since these amino acids can serve as potential hydrogen bond donors or acceptors, we have tested the hypothesis that they may be involved in the selective binding of muscarinic ligands. To eliminate the OH groups present in these residues, we have created nine single point mutations in the rat m3 muscarinic receptor by converting serine and threonine residues to alanine, and tyrosine residues to phenylalanine. The ligand binding and functional properties of these receptors were studied after transient expression in COS-7 cells. Six out of the nine mutant receptors (threonine and tyrosine mutations) showed strong reductions (approximately 10- to 40-fold lower than the wild-type receptor) in agonist binding affinities and reduced potencies in agonist-induced activation of phosphoinositide hydrolysis. Their antagonist binding properties, however, were similar to those of the wild-type m3 receptor. Despite their location on different transmembrane domains (III, V, VI and VII), all six mutations are positioned at a similar level (one to two helical turns away from the membrane surface) within the outer leaflet of the plasma membrane and may thus define the plain in which muscarinic agonists (but not antagonists) bind to their target receptor. JF - The EMBO journal AU - Wess, J AU - Gdula, D AU - Brann, M R AD - National Institute of Neurological Disorders and Stroke, Laboratory of Molecular Biology, Bethesda, MD 20892. Y1 - 1991/12// PY - 1991 DA - December 1991 SP - 3729 EP - 3734 VL - 10 IS - 12 SN - 0261-4189, 0261-4189 KW - Ligands KW - 0 KW - Muscarinic Antagonists KW - Phosphatidylinositols KW - Receptors, Muscarinic KW - Threonine KW - 2ZD004190S KW - Tyrosine KW - 42HK56048U KW - Carbachol KW - 8Y164V895Y KW - Acetylcholine KW - N9YNS0M02X KW - Index Medicus KW - Animals KW - Phosphatidylinositols -- metabolism KW - Amino Acid Sequence KW - Plasmids KW - Hydrolysis KW - Binding Sites KW - Carbachol -- metabolism KW - Rats KW - Mutagenesis, Site-Directed KW - Acetylcholine -- metabolism KW - Molecular Sequence Data KW - Cell Line KW - Receptors, Muscarinic -- genetics KW - Threonine -- metabolism KW - Tyrosine -- metabolism KW - Receptors, Muscarinic -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72445578?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+EMBO+journal&rft.atitle=Site-directed+mutagenesis+of+the+m3+muscarinic+receptor%3A+identification+of+a+series+of+threonine+and+tyrosine+residues+involved+in+agonist+but+not+antagonist+binding.&rft.au=Wess%2C+J%3BGdula%2C+D%3BBrann%2C+M+R&rft.aulast=Wess&rft.aufirst=J&rft.date=1991-12-01&rft.volume=10&rft.issue=12&rft.spage=3729&rft.isbn=&rft.btitle=&rft.title=The+EMBO+journal&rft.issn=02614189&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-19 N1 - Date created - 1991-12-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Anal Biochem. 1976 May 7;72:248-54 [942051] Biochem Pharmacol. 1973 Dec 1;22(23):3099-108 [4202581] Mol Pharmacol. 1990 Oct;38(4):517-23 [2172767] EMBO J. 1990 Dec;9(13):4381-90 [2124972] Eur J Biochem. 1991 Feb 26;196(1):1-10 [1848179] J Pharmacol Exp Ther. 1991 Feb;256(2):727-33 [1994002] J Biol Chem. 1991 Jan 5;266(1):5-8 [1670767] Mol Pharmacol. 1990 Dec;38(6):872-7 [2174507] J Biol Chem. 1989 Aug 15;264(23):13572-8 [2547766] FEBS Lett. 1989 Nov 20;258(1):133-6 [2556294] Nature. 1987 Mar 5-11;326(6108):73-7 [2881211] EMBO J. 1987 Nov;6(11):3269-75 [2828022] J Biol Chem. 1988 Jul 25;263(21):10267-71 [2899076] Annu Rev Neurosci. 1987;10:195-236 [2436543] Mol Cell Biol. 1987 Aug;7(8):2745-52 [3670292] Science. 1987 Jul 31;237(4814):527-32 [3037705] Biochem J. 1986 Sep 15;238(3):625-42 [2948499] Mol Pharmacol. 1989 Dec;36(6):840-7 [2557534] Annu Rev Neurosci. 1989;12:67-83 [2648960] J Biol Chem. 1989 Jan 5;264(1):489-95 [2909533] Neuron. 1988 Jul;1(5):403-10 [3272174] FEBS Lett. 1988 Dec 5;241(1-2):119-25 [3197827] EMBO J. 1987 Dec 20;6(13):3923-9 [3443095] Nature. 1986 Oct 2-8;323(6087):411-6 [3762692] Annu Rev Pharmacol Toxicol. 1990;30:633-73 [2188581] J Biol Chem. 1990 Aug 15;265(23):13702-8 [2380182] J Mol Biol. 1990 Jun 20;213(4):899-929 [2359127] Mol Cell Biol. 1983 Feb;3(2):280-9 [6300662] Biochem J. 1983 May 15;212(2):473-82 [6309146] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Biochem Soc Trans. 1991 Feb;19(1):133-8 [1903735] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenesis and cancer: different perspectives on the same disease. AN - 72442337; 1933881 JF - Cancer research AU - Sporn, M B AD - Laboratory of Chemoprevention, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/12/01/ PY - 1991 DA - 1991 Dec 01 SP - 6215 EP - 6218 VL - 51 IS - 23 Pt 1 SN - 0008-5472, 0008-5472 KW - Vitamin A KW - 11103-57-4 KW - Index Medicus KW - Vitamin A -- therapeutic use KW - Neoplasm Staging KW - Syphilis -- therapy KW - Humans KW - Cell Differentiation KW - Terminology as Topic KW - Time Factors KW - Neoplasms -- pathology KW - Neoplasms -- prevention & control KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72442337?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Carcinogenesis+and+cancer%3A+different+perspectives+on+the+same+disease.&rft.au=Sporn%2C+M+B&rft.aulast=Sporn&rft.aufirst=M&rft.date=1991-12-01&rft.volume=51&rft.issue=23+Pt+1&rft.spage=6215&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-16 N1 - Date created - 1991-12-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of 8-chloroadenosine 3',5'-monophosphate and N6-benzyl-cyclic adenosine 5'-monophosphate on cell cycle kinetics of HL-60 leukemia cells. AN - 72441446; 1657383 AB - Site-selective cyclic AMP (cAMP) analogues have been shown to inhibit growth and induce differentiation in several human leukemia cell lines. However, detailed studies of the effects exerted by cAMP analogues on cell cycle kinetics have been lacking. We have examined the effects of 8-Cl-cAMP and N6-benzyl-cAMP on the cell cycle kinetics of the HL-60 human promyelocytic leukemia cell line. A cell cycle study was performed by univariate DNA analysis after 24-72 h of treatment with noncytotoxic concentrations of 8-Cl-cAMP and N6-benzyl-cAMP capable of inducing 50-60% growth inhibition in these cells. HL-60 cells treated with 5 microM 8-Cl-cAMP showed no significant change in the cell distribution in the cycle as compared to the untreated control cells, whereas the treatment with 10 microM N6-benzyl-cAMP transiently increased the percentage of cells in the G0/G1 phase after 48 h, followed by a partial recovery at 72 h. Combined treatment with low doses of 8-Cl-cAMP and N6-benzyl-cAMP, each of which alone produced 20% growth inhibition, exerted a growth inhibitory effect of 65% and delayed increase of the G0/G1 phase by 72 h. To better understand the cell cycle effects induced by 8-Cl-cAMP, flow cytometric analysis of bromodeoxyuridine incorporation was also performed. 8-Cl-cAMP treatment exhibited a slowing down of the cell cycle; thus, the delayed appearance of the G0/G1 cell accumulation after combined treatment could be due to this effect of 8-Cl-cAMP on the HL-60 cell cycle. At a toxic dose, 8-Cl-cAMP brought about a G2M block, whereas N6-benzyl-cAMP brought about an increase of the G0/G1 compartment. G2M block produced by toxic doses of 8-Cl-cAMP was not related to its adenosine metabolite since 8-Cl-adenosine did not produce any specific block in the cell cycle. Our results show, for the first time, that these site-selective cAMP analogues could affect cell cycle kinetics at different points. These data may provide the basis for combination treatments involving cAMP analogues and other agents in the treatment of human leukemia. JF - Cancer research AU - Pepe, S AU - Tortora, G AU - Noguchi, P D AU - Marti, G E AU - Washington, G C AU - Cho-Chung, Y S AD - Cellular Biochemistry Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/12/01/ PY - 1991 DA - 1991 Dec 01 SP - 6263 EP - 6267 VL - 51 IS - 23 Pt 1 SN - 0008-5472, 0008-5472 KW - Antineoplastic Agents KW - 0 KW - 8-Bromo Cyclic Adenosine Monophosphate KW - 23583-48-4 KW - N(6)-benzyl-cyclic adenosine 5'-monophosphate KW - 32115-08-5 KW - 8-chloro-cyclic adenosine monophosphate KW - 41941-56-4 KW - Cyclic AMP KW - E0399OZS9N KW - Index Medicus KW - Humans KW - Tumor Cells, Cultured -- pathology KW - Flow Cytometry KW - Drug Synergism KW - Time Factors KW - Resting Phase, Cell Cycle -- drug effects KW - Cell Cycle -- drug effects KW - 8-Bromo Cyclic Adenosine Monophosphate -- analogs & derivatives KW - Cyclic AMP -- pharmacology KW - Cyclic AMP -- analogs & derivatives KW - Leukemia, Promyelocytic, Acute -- pathology KW - Antineoplastic Agents -- pharmacology KW - 8-Bromo Cyclic Adenosine Monophosphate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72441446?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Effects+of+8-chloroadenosine+3%27%2C5%27-monophosphate+and+N6-benzyl-cyclic+adenosine+5%27-monophosphate+on+cell+cycle+kinetics+of+HL-60+leukemia+cells.&rft.au=Pepe%2C+S%3BTortora%2C+G%3BNoguchi%2C+P+D%3BMarti%2C+G+E%3BWashington%2C+G+C%3BCho-Chung%2C+Y+S&rft.aulast=Pepe&rft.aufirst=S&rft.date=1991-12-01&rft.volume=51&rft.issue=23+Pt+1&rft.spage=6263&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-16 N1 - Date created - 1991-12-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The role of infection by Opisthorchis viverrini, hepatitis B virus, and aflatoxin exposure in the etiology of liver cancer in Thailand. A correlation study. AN - 72172591; 1657355 AB - The incidence of the two principle types of liver cancer (hepatocellular carcinoma and cholangiocarcinoma) in five different areas of Thailand was compared with the prevalence of exposure to the main risk factors in samples of the population. Cholangiocarcinoma showed striking variations in incidence, which correlated closely with markers of exposure to the liver fluke, Opisthorchis viverrini. However, there was little geographic variation in incidence of hepatocellular carcinoma or in prevalence of the major risk factors (chronic carriage of hepatitis B virus and exposure to aflatoxin), and apparently there was little relationship between them. JF - Cancer AU - Srivatanakul, P AU - Parkin, D M AU - Jiang, Y Z AU - Khlat, M AU - Kao-Ian, U T AU - Sontipong, S AU - Wild, C AD - National Cancer Institute, Bangkok, Thailand. Y1 - 1991/12/01/ PY - 1991 DA - 1991 Dec 01 SP - 2411 EP - 2417 VL - 68 IS - 11 SN - 0008-543X, 0008-543X KW - Aflatoxins KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Bile Duct Neoplasms -- epidemiology KW - Humans KW - Carcinoma, Hepatocellular -- epidemiology KW - Adenoma, Bile Duct -- epidemiology KW - Carcinoma, Hepatocellular -- etiology KW - Risk Factors KW - Adult KW - Environmental Exposure KW - Adenoma, Bile Duct -- etiology KW - Bile Duct Neoplasms -- etiology KW - Incidence KW - Thailand -- epidemiology KW - Statistics as Topic KW - Female KW - Male KW - Liver Neoplasms -- pathology KW - Hepatitis B -- complications KW - Opisthorchiasis -- complications KW - Opisthorchiasis -- epidemiology KW - Liver Neoplasms -- epidemiology KW - Liver Neoplasms -- etiology KW - Aflatoxins -- adverse effects KW - Hepatitis B -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72172591?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+molecular+biology&rft.atitle=Nucleosome+core+binding+region+of+chromosomal+protein+HMG-17+acts+as+an+independent+functional+domain.&rft.au=Crippa%2C+M+P%3BAlfonso%2C+P+J%3BBustin%2C+M&rft.aulast=Crippa&rft.aufirst=M&rft.date=1992-11-20&rft.volume=228&rft.issue=2&rft.spage=442&rft.isbn=&rft.btitle=&rft.title=Journal+of+molecular+biology&rft.issn=00222836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-13 N1 - Date created - 1991-12-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A preliminary evaluation of 566C80 for the treatment of Pneumocystis pneumonia in patients with the acquired immunodeficiency syndrome. AN - 72464261; 1944437 AB - The drug 566C80 is an investigational hydroxynaphthoquinone that is active against Pneumocystis carinii in vitro and in animal models. Initial studies in humans indicate that 566C80 is safe and has adequate bioavailability after oral administration. We conducted an open-label trial of 566C80 in 34 adults with the acquired immunodeficiency syndrome (AIDS) and untreated pneumocystis pneumonia. All the patients had a partial pressure of arterial oxygen of at least 60 mm Hg while breathing room air. They were enrolled sequentially in three cohorts taking 566C80 at different dosages, all administered orally: 750 mg three times daily for 5 days, then twice daily for 16 days; 750 mg three times daily for 21 days; and 750 mg four times daily for 21 days. All 34 patients survived, and 27 (79 percent) were successfully treated with 566C80 alone. The mean partial pressure of oxygen in 33 patients was 78 mm Hg at entry and 93 mm Hg after the course of 566C80 (P less than 0.001). In five patients (15 percent) the drug was discontinued because of lack of response. In four patients (12 percent), the drug was discontinued because of toxicity (fever and rash in two patients each). In two of these, treatment was considered to have succeeded because 566C80 was not discontinued because of toxicity until after day 14. Five of the successfully treated patients had rashes that resolved despite continued therapy. In nine patients, serum alanine aminotransferase levels rose above 100 U per liter. During the first three months after the completion of therapy, pneumocystis pneumonia recurred in 4 of the 27 successfully treated patients, and another 3 patients had recurrences between month 3 and month 6 of follow-up. The mean (+/- SEM) steady-state plasma levels of 566C80 were similar in the three cohorts: 16.3 +/- 2.10, 20.4 +/- 2.48, and 18.9 +/- 3.08 micrograms per milliliter in the patients taking the drug twice daily, three times daily, and four times daily, respectively. From these preliminary data, the investigational compound 566C80 appears to be a safe, effective, and well-tolerated therapy for P. carinii pneumonia of mild-to-moderate severity in patients with AIDS. JF - The New England journal of medicine AU - Falloon, J AU - Kovacs, J AU - Hughes, W AU - O'Neill, D AU - Polis, M AU - Davey, R T AU - Rogers, M AU - LaFon, S AU - Feuerstein, I AU - Lancaster, D AD - Department of Critical Care Medicine, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/11/28/ PY - 1991 DA - 1991 Nov 28 SP - 1534 EP - 1538 VL - 325 IS - 22 SN - 0028-4793, 0028-4793 KW - Naphthoquinones KW - 0 KW - Atovaquone KW - Y883P1Z2LT KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Administration, Oral KW - Drug Evaluation KW - Drug Administration Schedule KW - Humans KW - Adult KW - Treatment Outcome KW - Follow-Up Studies KW - Recurrence KW - Partial Pressure KW - Male KW - Female KW - Naphthoquinones -- therapeutic use KW - Acquired Immunodeficiency Syndrome -- complications KW - Pneumonia, Pneumocystis -- drug therapy KW - Naphthoquinones -- administration & dosage KW - Naphthoquinones -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72464261?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+New+England+journal+of+medicine&rft.atitle=A+preliminary+evaluation+of+566C80+for+the+treatment+of+Pneumocystis+pneumonia+in+patients+with+the+acquired+immunodeficiency+syndrome.&rft.au=Falloon%2C+J%3BKovacs%2C+J%3BHughes%2C+W%3BO%27Neill%2C+D%3BPolis%2C+M%3BDavey%2C+R+T%3BRogers%2C+M%3BLaFon%2C+S%3BFeuerstein%2C+I%3BLancaster%2C+D&rft.aulast=Falloon&rft.aufirst=J&rft.date=1991-11-28&rft.volume=325&rft.issue=22&rft.spage=1534&rft.isbn=&rft.btitle=&rft.title=The+New+England+journal+of+medicine&rft.issn=00284793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-04 N1 - Date created - 1991-12-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Creation of "super" glucocorticoid receptors by point mutations in the steroid binding domain. AN - 72448555; 1939229 AB - Almost all modifications of the steroid binding domain of glucocorticoid receptors are known to cause a reduction or loss of steroid binding activity. Nonetheless, we now report that mutations of cysteine 656 of the rat receptor, which was previously suspected to be a crucial amino acid for the binding process, have produced "super" receptors. These receptors displayed an increased affinity for glucocorticoid steroids and a decreased relative affinity for cross-reacting steroids such as progesterone and aldosterone. The increased in vitro affinity of the super receptors was maintained in a whole cell bioassay. These results indicate that additional modifications of the glucocorticoid receptor, and probably the other steroid receptors, may further increase the binding affinity and/or specificity. JF - The Journal of biological chemistry AU - Chakraborti, P K AU - Garabedian, M J AU - Yamamoto, K R AU - Simons, S S AD - Steroid Hormones Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/11/25/ PY - 1991 DA - 1991 Nov 25 SP - 22075 EP - 22078 VL - 266 IS - 33 SN - 0021-9258, 0021-9258 KW - Antibodies, Monoclonal KW - 0 KW - Receptors, Glucocorticoid KW - Recombinant Fusion Proteins KW - Steroids KW - Dexamethasone KW - 7S5I7G3JQL KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - Recombinant Fusion Proteins -- metabolism KW - Cytosol -- metabolism KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Animals KW - Blotting, Western KW - Transfection KW - Kinetics KW - Dexamethasone -- pharmacology KW - Chloramphenicol O-Acetyltransferase -- metabolism KW - Cell Line KW - Binding Sites KW - Mutagenesis, Site-Directed KW - Steroids -- pharmacology KW - Receptors, Glucocorticoid -- metabolism KW - Receptors, Glucocorticoid -- genetics KW - Steroids -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72448555?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Creation+of+%22super%22+glucocorticoid+receptors+by+point+mutations+in+the+steroid+binding+domain.&rft.au=Chakraborti%2C+P+K%3BGarabedian%2C+M+J%3BYamamoto%2C+K+R%3BSimons%2C+S+S&rft.aulast=Chakraborti&rft.aufirst=P&rft.date=1991-11-25&rft.volume=266&rft.issue=33&rft.spage=22075&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-26 N1 - Date created - 1991-12-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Structure-function relationships in the mast cell high affinity receptor for IgE. Role of the cytoplasmic domains and of the beta subunit. AN - 72448064; 1658002 AB - To define functionally critical regions of the high affinity receptor for IgE (Fc epsilon RI), we stably transfected P815 cells with mutated cDNAs coding for subunits with truncated cytoplasmic domains (CD). In addition, to examine further the role of the beta subunit, stable transfectants expressing chimeric Fc epsilon RI without beta subunits were generated. Transfectants were tested for receptor-mediated changes in intracellular Ca2+, for stimulated hydrolysis of phosphoinositides, and for protein tyrosine phosphorylation. In all cases these biochemical signals were affected coordinately, suggesting that they are coupled, possibly in a single pathway. Truncation of the alpha subunit or of the NH2-terminal CD of the beta subunit had no effect, but Fc epsilon RIs with beta subunits missing the COOH-terminal CD were inactive. Interestingly, receptors in cells transfected only with human Fc epsilon RI(alpha) (which utilize the gamma chains endogenously synthesized by the P815 cells but which contain no beta subunits) responded normally. Therefore, the beta subunit influences the functions studied but is not essential. Although structural analysis excluded a straightforward mechanism, truncation of the CD of the gamma chain led to loss of signaling. JF - The Journal of biological chemistry AU - Alber, G AU - Miller, L AU - Jelsema, C L AU - Varin-Blank, N AU - Metzger, H AD - National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institute of Health, Bethesda, Maryland 20892. Y1 - 1991/11/25/ PY - 1991 DA - 1991 Nov 25 SP - 22613 EP - 22620 VL - 266 IS - 33 SN - 0021-9258, 0021-9258 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Differentiation, B-Lymphocyte KW - Macromolecular Substances KW - Phosphatidylinositols KW - Receptors, Fc KW - Receptors, IgE KW - Immunoglobulin E KW - 37341-29-0 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Phosphatidylinositols -- metabolism KW - Mice KW - Molecular Weight KW - Calcium -- metabolism KW - Mutagenesis, Site-Directed KW - Phosphorylation KW - Transfection KW - Plasmacytoma KW - Cytoplasm -- immunology KW - Genetic Vectors KW - Kinetics KW - Cell Line KW - Antigens, Differentiation, B-Lymphocyte -- metabolism KW - Mast Cells -- immunology KW - Antigens, Differentiation, B-Lymphocyte -- genetics KW - Receptors, Fc -- metabolism KW - Receptors, Fc -- genetics KW - Immunoglobulin E -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72448064?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Structure-function+relationships+in+the+mast+cell+high+affinity+receptor+for+IgE.+Role+of+the+cytoplasmic+domains+and+of+the+beta+subunit.&rft.au=Alber%2C+G%3BMiller%2C+L%3BJelsema%2C+C+L%3BVarin-Blank%2C+N%3BMetzger%2C+H&rft.aulast=Alber&rft.aufirst=G&rft.date=1991-11-25&rft.volume=266&rft.issue=33&rft.spage=22613&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-26 N1 - Date created - 1991-12-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of a cis-acting element required for efficient transcriptional activation of the collagen IV enhancer. AN - 72447732; 1939251 AB - Two regulatory regions in the murine collagen IV enhancer were identified. Transient transfection assays delimited a 210-base pair fragment within the first intron of the alpha 1(IV) collagen gene that had significant transcriptional enhancer activity. DNase I protection and gel mobility shift confirmed that two regions, designated footprints A and B, within this fragment bound nuclear factors. Gel shift studies suggested that the CCTTATCTCTGATGG motif (A-34) in the footprint A region was important for specific nuclear factor binding. Mutations in the A-34 motif abolished factor binding as detected by gel shift and resulted in a significant decrease in enhancer activity in transient transfection assays of F9 teratocarcinoma cells. Two putative transcription factors of Mr = 37,000 and Mr = 94,000, which interact with the A-34 motif, were purified from Engelbreth-Holm-Swarm tumor tissue using DEAE-Sephacel, heparin-Sepharose, salmon sperm DNA-Sepharose, and specific A-34 oligonucleotide affinity chromatography. Southwestern analysis revealed that both of these factors were capable of binding the A-34 oligonucleotide directly and did not require additional subunits for binding. These data suggest that positively acting transcription factor(s) interact with the A-34 site in the enhancer and are required for efficient transcription of the alpha 1 and alpha 2(IV) collagen chain genes. JF - The Journal of biological chemistry AU - Burbelo, P D AU - Bruggeman, L A AU - Gabriel, G C AU - Klotman, P E AU - Yamada, Y AD - Laboratory of Developmental Biology, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/11/25/ PY - 1991 DA - 1991 Nov 25 SP - 22297 EP - 22302 VL - 266 IS - 33 SN - 0021-9258, 0021-9258 KW - DNA-Binding Proteins KW - 0 KW - Collagen KW - 9007-34-5 KW - Deoxyribonuclease I KW - EC 3.1.21.1 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Immunoblotting KW - Animals KW - Chromosome Deletion KW - Base Sequence KW - Transfection KW - Humans KW - Restriction Mapping KW - Molecular Sequence Data KW - Introns KW - Mice KW - Plasmids KW - Teratoma KW - Cell Line KW - Binding Sites KW - Collagen -- genetics KW - Enhancer Elements, Genetic KW - Transcription, Genetic KW - Gene Expression Regulation KW - DNA-Binding Proteins -- isolation & purification KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72447732?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft.atitle=Post-transcriptional+regulation+of+early+T+cell+development+by+T+cell+receptor+signals.&rft.au=Takahama%2C+Y%3BSinger%2C+A&rft.aulast=Takahama&rft.aufirst=Y&rft.date=1992-11-27&rft.volume=258&rft.issue=5087&rft.spage=1456&rft.isbn=&rft.btitle=&rft.title=Science+%28New+York%2C+N.Y.%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-26 N1 - Date created - 1991-12-26 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M55199; GENBANK; S66785; S66549; M55195; M55196; M55197; M55198; M55194; M55201; M55200 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Recombinant toxins for cancer treatment. AN - 72500118; 1683495 AB - Recombinant toxins target cell surface receptors and antigens on tumor cells. They kill by mechanisms different from conventional chemotherapy, so that cross resistance to conventional chemotherapeutic agents should not be a problem. Furthermore, they are not mutagens and should not induce secondary malignancies or accelerate progression of benign malignancies. They can be mass-produced cheaply in bacteria as homogeneous proteins. Either growth factor-toxin fusions or antibody-toxin fusions can be chosen, depending on the cellular target. JF - Science (New York, N.Y.) AU - Pastan, I AU - FitzGerald, D AD - Division of Cancer Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/11/22/ PY - 1991 DA - 1991 Nov 22 SP - 1173 EP - 1177 VL - 254 IS - 5035 SN - 0036-8075, 0036-8075 KW - erbB-2 KW - Antigens, Neoplasm KW - 0 KW - Bacterial Toxins KW - Exotoxins KW - Immunotoxins KW - Proto-Oncogene Proteins KW - Receptors, Immunologic KW - Receptors, Interleukin-2 KW - Receptors, Interleukin-6 KW - Recombinant Fusion Proteins KW - Toxins, Biological KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Receptor, ErbB-2 KW - Index Medicus KW - Receptors, Interleukin-2 -- metabolism KW - Exotoxins -- administration & dosage KW - Receptor, Epidermal Growth Factor -- metabolism KW - Receptors, Immunologic -- metabolism KW - Humans KW - Proto-Oncogene Proteins -- metabolism KW - Immunotoxins -- therapeutic use KW - Antigens, Neoplasm -- metabolism KW - Toxins, Biological -- administration & dosage KW - Neoplasms -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72500118?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft.atitle=Recombinant+toxins+for+cancer+treatment.&rft.au=Pastan%2C+I%3BFitzGerald%2C+D&rft.aulast=Pastan&rft.aufirst=I&rft.date=1991-11-22&rft.volume=254&rft.issue=5035&rft.spage=1173&rft.isbn=&rft.btitle=&rft.title=Science+%28New+York%2C+N.Y.%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-27 N1 - Date created - 1991-12-27 N1 - Date revised - 2017-01-13 N1 - Gene symbol - erbB-2 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA deaminating ability and genotoxicity of nitric oxide and its progenitors. AN - 72479471; 1948068 AB - Nitric oxide (NO), a multifaceted bioregulatory agent and an environmental pollutant, can also cause genomic alterations. In vitro, NO deaminated deoxynucleosides, deoxynucleotides, and intact DNA at physiological pH. That similar DNA damage can also occur in vivo was tested by treating Salmonella typhimurium strain TA1535 with three NO-releasing compounds, including nitroglycerin. All proved mutagenic. Observed DNA sequence changes were greater than 99% C----T transitions in the hisG46 (CCC) target codon, consistent with a cytosine-deamination mechanism. Because exposure to endogenously and exogenously produced NO is extensive, this mechanism may contribute to the incidence of deamination-related genetic disease and cancer. JF - Science (New York, N.Y.) AU - Wink, D A AU - Kasprzak, K S AU - Maragos, C M AU - Elespuru, R K AU - Misra, M AU - Dunams, T M AU - Cebula, T A AU - Koch, W H AU - Andrews, A W AU - Allen, J S AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, MD 21702. Y1 - 1991/11/15/ PY - 1991 DA - 1991 Nov 15 SP - 1001 EP - 1003 VL - 254 IS - 5034 SN - 0036-8075, 0036-8075 KW - Codon KW - 0 KW - DNA, Bacterial KW - Nitric Oxide KW - 31C4KY9ESH KW - Index Medicus KW - Deamination KW - Salmonella typhimurium KW - Mutagenesis KW - DNA, Bacterial -- chemistry KW - DNA Damage KW - Nitric Oxide -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72479471?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft.atitle=DNA+deaminating+ability+and+genotoxicity+of+nitric+oxide+and+its+progenitors.&rft.au=Wink%2C+D+A%3BKasprzak%2C+K+S%3BMaragos%2C+C+M%3BElespuru%2C+R+K%3BMisra%2C+M%3BDunams%2C+T+M%3BCebula%2C+T+A%3BKoch%2C+W+H%3BAndrews%2C+A+W%3BAllen%2C+J+S&rft.aulast=Wink&rft.aufirst=D&rft.date=1991-11-15&rft.volume=16&rft.issue=6&rft.spage=1035&rft.isbn=&rft.btitle=&rft.title=Alcoholism%2C+clinical+and+experimental+research&rft.issn=01456008&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-18 N1 - Date created - 1991-12-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A detailed functional and structural analysis of a major thyroid hormone inhibitory element in the human thyrotropin beta-subunit gene. AN - 72452021; 1657975 AB - The first exon of the human thyrotropin-beta (hTSH beta) gene has been demonstrated in our laboratory to contain a major thyroid hormone inhibitory element. In order to characterize fully this element, we have performed a detailed functional and structural scanning mutational analysis of this element. Various -1192 to +37 (base pairs) bp fragments of the hTSH beta gene containing consecutive five deoxythymidine substitution mutations of the first exon were inserted into a luciferase reporter plasmid and transiently transfected into human embryonal cells (293) and stably transfected into rat pituitary cells (GH3). Two domains (domain 1 and 2) were identified by scanning mutations that were essential for function of the thyroid hormone inhibitory element: +3 to +13 bp and +28 to +37 bp. Biotinylated DNA fragments containing -12 to +43 bp of the hTSH beta gene and the identical scanning mutations demonstrate that in vitro synthesized c-erbA-beta binding is disrupted as much as 95% by mutations from -3 to +17 bp and to a lesser extent (20-30%) by mutations from +23 to +27 bp and from +33 to +43 bp. Domain 1 displayed a higher affinity for c-erbA-beta than domain 2 in avidin-biotin complex DNA-binding and gel-mobility assays. Using increasing amounts of in vitro synthesized c-erbA-beta, we were unable to demonstrate more than one protein-DNA complex in gel-mobility assays. However, using the avidin-biotin complex DNA-binding assay and the cross-linking reagent, 1,6-bismaleimidohexane, we were able to demonstrate thyroid hormone receptor dimer formation on domain 1 but not to any significant extent on domain 2. In conclusion, functional and DNA-binding studies suggest that the thyroid hormone receptor binds to two distinct regions in the first exon of the hTSH beta gene. The upstream site (domain 1) binds c-erbA-beta with higher affinity and is capable of binding c-erbA-beta as a dimer under some conditions, while the downstream site (domain 2) appears to bind a single molecule of c-erbA-beta with lower affinity. These results suggest that thyroid hormone receptor, binding to at least two sites in the first exon, act in conjunction to mediate T3 inhibition of hTSH beta expression. JF - The Journal of biological chemistry AU - Bodenner, D L AU - Mroczynski, M A AU - Weintraub, B D AU - Radovick, S AU - Wondisford, F E AD - Molecular, Cellular, and Nutritional Endocrinology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1991/11/15/ PY - 1991 DA - 1991 Nov 15 SP - 21666 EP - 21673 VL - 266 IS - 32 SN - 0021-9258, 0021-9258 KW - Oligodeoxyribonucleotides KW - 0 KW - Proto-Oncogene Proteins KW - Receptors, Thyroid Hormone KW - Thyrotropin KW - 9002-71-5 KW - Luciferases KW - EC 1.13.12.- KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Index Medicus KW - Animals KW - Exons KW - Humans KW - Proto-Oncogene Proteins -- metabolism KW - Luciferases -- metabolism KW - Protein-Tyrosine Kinases -- metabolism KW - Plasmids KW - Binding Sites KW - Base Sequence KW - Transfection KW - Molecular Sequence Data KW - Luciferases -- genetics KW - Methylation KW - Cell Line KW - Mutagenesis, Site-Directed KW - Thyrotropin -- genetics KW - Genes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72452021?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=A+detailed+functional+and+structural+analysis+of+a+major+thyroid+hormone+inhibitory+element+in+the+human+thyrotropin+beta-subunit+gene.&rft.au=Bodenner%2C+D+L%3BMroczynski%2C+M+A%3BWeintraub%2C+B+D%3BRadovick%2C+S%3BWondisford%2C+F+E&rft.aulast=Bodenner&rft.aufirst=D&rft.date=1991-11-15&rft.volume=266&rft.issue=32&rft.spage=21666&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-23 N1 - Date created - 1991-12-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Specific pathogen-free BALB/cAn mice are refractory to plasmacytoma induction by pristane. AN - 72451292; 1682379 AB - Forty to sixty percent of conventionally (CON) raised BALB/cAnPt (BALB/c) mice develop plasmacytomas (PCT) when injected with three 0.5 ml i.p. injections of pristane. When CON-BALB/c mice were converted to specific pathogen free (SPF) status by foster nursing caesarean delivered term mice on C3H/HeN SPF mothers and maintained under strict SPF conditions, less than 5% of the mice developed pristane-induced PCT. FACS analysis of the cellular composition of oil granulomatous tissue revealed a dramatic influx of CD4+ cells in CON mice that was significantly reduced in SPF mice. Moreover, while both CON and SPF mice had similar patterns of gut flora colonization, only CON-BALB/c mice had occasional circulating antibodies to mouse hepatitis virus and Sendai viruses. Maintenance in strict SPF conditions, therefore, results in a prolonged state of relative Ag deprivation and a failure to continuously activate new T and B cell populations. The results suggest that PCT formation depends on exogenous antigenic stimulation and that the presence of minimal gut flora is insufficient to render these mice susceptible to PCT induction. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Byrd, L G AU - McDonald, A H AU - Gold, L G AU - Potter, M AD - Laboratory of Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/11/15/ PY - 1991 DA - 1991 Nov 15 SP - 3632 EP - 3637 VL - 147 IS - 10 SN - 0022-1767, 0022-1767 KW - Terpenes KW - 0 KW - pristane KW - 26HZV48DT1 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Ascitic Fluid -- immunology KW - Granuloma -- immunology KW - CD4-Positive T-Lymphocytes -- immunology KW - Mice KW - Mice, Inbred BALB C -- immunology KW - Germ-Free Life KW - Plasmacytoma -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72451292?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Specific+pathogen-free+BALB%2FcAn+mice+are+refractory+to+plasmacytoma+induction+by+pristane.&rft.au=Byrd%2C+L+G%3BMcDonald%2C+A+H%3BGold%2C+L+G%3BPotter%2C+M&rft.aulast=Byrd&rft.aufirst=L&rft.date=1991-11-15&rft.volume=147&rft.issue=10&rft.spage=3632&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-16 N1 - Date created - 1991-12-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanism of mutual activation of the tryptophan synthase alpha and beta subunits. Analysis of the reaction specificity and substrate-induced inactivation of active site and tunnel mutants of the beta subunit. AN - 72450918; 1939184 AB - The origin of reaction and substrate specificity and the control of activity by protein-protein interaction are investigated using the tryptophan synthase alpha 2 beta 2 complex from Salmonella typhimurium. We have compared some spectroscopic and kinetic properties of the wild type beta subunit and five mutant forms of the beta subunit that have altered catalytic properties. These mutant enzymes, which were engineered by site-directed mutagenesis, have single amino acid replacements in either the active site or in the wall of a tunnel that extends from the active site of the alpha subunit to the active site of the beta subunit in the alpha 2 beta 2 complex. We find that the mutant alpha 2 beta 2 complexes have altered reaction and substrate specificity in beta-elimination and beta-replacement reactions with L-serine and with beta-chloro-L-alanine. Moreover, the mutant enzymes, unlike the wild type alpha 2 beta 2 complex, undergo irreversible substrate-induced inactivation. The mechanism of inactivation appears to be analogous to that first demonstrated by Metzler's group for inhibition of two other pyridoxal phosphate enzymes. Alkaline treatment of the inactivated enzyme yields apoenzyme and a previously described pyridoxal phosphate derivative. We demonstrate for the first time that enzymatic activity can be recovered by addition of pyridoxal phosphate following alkaline treatment. We conclude that the wild type and mutant alpha 2 beta 2 complexes differ in the way they process the amino acrylate intermediate. We suggest that the wild type beta subunit undergoes a conformational change upon association with the alpha subunit that alters the reaction specificity and that the mutant beta subunits do not undergo the same conformational change upon subunit association. JF - The Journal of biological chemistry AU - Ahmed, S A AU - Ruvinov, S B AU - Kayastha, A M AU - Miles, E W AD - Laboratory of Biochemical Pharmacology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/11/15/ PY - 1991 DA - 1991 Nov 15 SP - 21548 EP - 21557 VL - 266 IS - 32 SN - 0021-9258, 0021-9258 KW - Macromolecular Substances KW - 0 KW - Oligodeoxyribonucleotides KW - Recombinant Proteins KW - beta-Alanine KW - 11P2JDE17B KW - 3-chloroalanine KW - 3981-36-0 KW - Tryptophan Synthase KW - EC 4.2.1.20 KW - Index Medicus KW - beta-Alanine -- analogs & derivatives KW - Enzyme Activation KW - Escherichia coli -- genetics KW - beta-Alanine -- pharmacology KW - Binding Sites KW - Cloning, Molecular KW - Recombinant Proteins -- isolation & purification KW - Base Sequence KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Molecular Sequence Data KW - Spectrophotometry KW - Recombinant Proteins -- antagonists & inhibitors KW - Models, Theoretical KW - Mutagenesis, Site-Directed KW - Tryptophan Synthase -- metabolism KW - Tryptophan Synthase -- antagonists & inhibitors KW - Tryptophan Synthase -- genetics KW - Salmonella typhimurium -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72450918?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Mechanism+of+mutual+activation+of+the+tryptophan+synthase+alpha+and+beta+subunits.+Analysis+of+the+reaction+specificity+and+substrate-induced+inactivation+of+active+site+and+tunnel+mutants+of+the+beta+subunit.&rft.au=Ahmed%2C+S+A%3BRuvinov%2C+S+B%3BKayastha%2C+A+M%3BMiles%2C+E+W&rft.aulast=Ahmed&rft.aufirst=S&rft.date=1991-11-15&rft.volume=266&rft.issue=32&rft.spage=21548&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-23 N1 - Date created - 1991-12-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intrathecal 6-mercaptopurine: preclinical pharmacology, phase I/II trial, and pharmacokinetic study. AN - 72440514; 1933871 AB - For over 30 years, oral 6-mercaptopurine (6-MP) has been a mainstay of systemic maintenance therapy for acute lymphoblastic leukemia. Despite its efficacy as an antileukemic agent, 6-MP has not been previously administered by the intrathecal (IT) route. In anticipation of a clinical trial of IT 6-MP, preclinical cytotoxicity and pharmacology studies were performed to define a safe, effective dose. The optimal concentration (greater than 1 microM) and duration of exposure (greater than 12 h) to 6-MP required for cytotoxicity were determined in vitro using human leukemia cell lines. The dose required to achieve the desired cerebrospinal fluid concentrations in humans was derived from pharmacokinetic parameters determined in rhesus monkeys. A phase I/II study was then performed in pediatric patients with refractory meningeal leukemia. Nine patients (aged 3.5 to 16 years) with chronic meningeal leukemia (2 to 6 central nervous system relapses) were entered onto the study. All had previously failed, at a minimum, IT methotrexate, IT cytarabine, and cranial (+/- spinal) radiation. A 10-mg IT dose of 6-MP (calculated to produce cytotoxic cerebrospinal fluid levels for 12 h) was administered twice weekly for 4 weeks. There were four complete responses and three partial responses. The duration of complete responses ranged from 7 to 22 weeks. Observed toxicities were not dose limiting and included mild headache (three patients) and minimal nausea (two patients). Pharmacokinetic studies performed in patients confirmed that cerebrospinal fluid concentrations of 6-MP were greater than 1 microM for 12 h. These results indicate that the IT administration of 6-MP is feasible, is not associated with significant toxicity, and has definite activity in patients with refractory meningeal leukemia. JF - Cancer research AU - Adamson, P C AU - Balis, F M AU - Arndt, C A AU - Holcenberg, J S AU - Narang, P K AU - Murphy, R F AU - Gillespie, A J AU - Poplack, D G AD - Pediatric Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/11/15/ PY - 1991 DA - 1991 Nov 15 SP - 6079 EP - 6083 VL - 51 IS - 22 SN - 0008-5472, 0008-5472 KW - 6-Mercaptopurine KW - E7WED276I5 KW - Index Medicus KW - Lymphoma, Non-Hodgkin -- drug therapy KW - Drug Evaluation KW - Animals KW - Tumor Cells, Cultured KW - Injections, Spinal KW - Humans KW - Macaca mulatta KW - Child KW - Adolescent KW - Male KW - Female KW - Child, Preschool KW - Leukemia -- drug therapy KW - Meningeal Neoplasms -- drug therapy KW - 6-Mercaptopurine -- therapeutic use KW - 6-Mercaptopurine -- pharmacokinetics KW - 6-Mercaptopurine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72440514?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Intrathecal+6-mercaptopurine%3A+preclinical+pharmacology%2C+phase+I%2FII+trial%2C+and+pharmacokinetic+study.&rft.au=Adamson%2C+P+C%3BBalis%2C+F+M%3BArndt%2C+C+A%3BHolcenberg%2C+J+S%3BNarang%2C+P+K%3BMurphy%2C+R+F%3BGillespie%2C+A+J%3BPoplack%2C+D+G&rft.aulast=Adamson&rft.aufirst=P&rft.date=1991-11-15&rft.volume=51&rft.issue=22&rft.spage=6079&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-16 N1 - Date created - 1991-12-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - An ultrastructural study of in vivo interactions between lymphocytes and endothelial cells in the pathogenesis of the vascular leak syndrome induced by interleukin-2. AN - 72118674; 1913455 AB - Lymphokine-activated killer (LAK) cells play a major role in the induction of the vascular leak syndrome (VLS). To understand the mechanism of this syndrome, the authors examined light and electron microscopic alterations in the lung, liver, spleen, kidney, and heart of mice in which VLS was produced by the administration of interleukin-2 (IL-2) (seven injections of 600,000 IU each for a period of 4 days). The results of these studies disclosed that considerable damage had been done to the endothelial cells that consisted of cytoplasmic edema, vacuoles, and myelin figures; in addition, there were frequent sites of transendothelial passage of lymphoid cells, probably IL-2-activated cells, that penetrated through their cytoplasm by means of "temporary migration pores" and accumulated in the perivascular spaces. The results of this study indicate that a direct in vivo interaction between IL-2-activated cells (probably LAK cells) and endothelium results in cytotoxicity to endothelial cells. JF - Cancer AU - Fujita, S AU - Puri, R K AU - Yu, Z X AU - Travis, W D AU - Ferrans, V J AD - Pathology Branch National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/11/15/ PY - 1991 DA - 1991 Nov 15 SP - 2169 EP - 2174 VL - 68 IS - 10 SN - 0008-543X, 0008-543X KW - Interleukin-2 KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Lung -- blood supply KW - Cell Movement KW - Animals KW - Vascular Diseases -- chemically induced KW - Liver -- blood supply KW - Syndrome KW - Mice, Inbred C57BL KW - Vascular Diseases -- physiopathology KW - Microscopy, Electron KW - Mice KW - Female KW - Interleukin-2 -- pharmacology KW - Endothelium, Vascular -- drug effects KW - Capillary Permeability -- drug effects KW - Lymphocytes -- ultrastructure KW - Endothelium, Vascular -- ultrastructure KW - Lymphocytes -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72118674?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=An+ultrastructural+study+of+in+vivo+interactions+between+lymphocytes+and+endothelial+cells+in+the+pathogenesis+of+the+vascular+leak+syndrome+induced+by+interleukin-2.&rft.au=Fujita%2C+S%3BPuri%2C+R+K%3BYu%2C+Z+X%3BTravis%2C+W+D%3BFerrans%2C+V+J&rft.aulast=Fujita&rft.aufirst=S&rft.date=1991-11-15&rft.volume=68&rft.issue=10&rft.spage=2169&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-19 N1 - Date created - 1991-11-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of c-fos mRNA in rat brain after intracerebroventricular administration of corticotropin-releasing hormone. AN - 72642894; 1784425 AB - Expression of the proto-oncogene c-fos is known to increase in rat brain following various types of seizures. Measuring c-fos mRNA or protein levels was shown to be a good cellular marker for neurons activated during central nervous system (CNS) excitation. In this study, we used in situ hybridization analysis of c-fos mRNA to determine brain regions activated by a peptide that has been closely linked to stress responsivity and kindling-like seizure activity. Corticotropin-releasing hormone (CRH) was injected into the left lateral ventricle of rats and produced the late onset of seizures between 1.5-5 h after its administration. Rats were sacrificed at various time points after the administration of CRH or sterile water, and c-fos mRNA levels were determined. In the preseizure state, CRH increased c-fos unilaterally in several cerebral cortical structures (most prominently in the dorsal endopiriform nucleus and in the piriform and insular cortices). CRH-induced seizures increased c-fos bilaterally in the same cortical regions, and in addition, in the hippocampus and olfactory bulb. The data are congruous with the hypothesis that intracerebroventricularly (i.c.v.) administered CRH elicits a rapid kindling-like response. JF - Neuroscience letters AU - Clark, M AU - Weiss, S R AU - Post, R M AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1991/11/11/ PY - 1991 DA - 1991 Nov 11 SP - 235 EP - 238 VL - 132 IS - 2 SN - 0304-3940, 0304-3940 KW - Proto-Oncogene Proteins c-fos KW - 0 KW - RNA, Messenger KW - Corticotropin-Releasing Hormone KW - 9015-71-8 KW - Index Medicus KW - Seizures -- chemically induced KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Seizures -- physiopathology KW - Tissue Distribution KW - Nucleic Acid Hybridization KW - Male KW - Injections, Intraventricular KW - RNA, Messenger -- metabolism KW - Proto-Oncogene Proteins c-fos -- genetics KW - Brain -- metabolism KW - Corticotropin-Releasing Hormone -- pharmacology KW - Brain -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72642894?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+letters&rft.atitle=Expression+of+c-fos+mRNA+in+rat+brain+after+intracerebroventricular+administration+of+corticotropin-releasing+hormone.&rft.au=Clark%2C+M%3BWeiss%2C+S+R%3BPost%2C+R+M&rft.aulast=Clark&rft.aufirst=M&rft.date=1991-11-11&rft.volume=132&rft.issue=2&rft.spage=235&rft.isbn=&rft.btitle=&rft.title=Neuroscience+letters&rft.issn=03043940&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-18 N1 - Date created - 1992-03-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of a small GTP-binding protein by nucleoside diphosphate kinase. AN - 72473576; 1658935 AB - Genes that encode nucleoside diphosphate kinases (NDKs) have been implicated as regulators of mammalian tumor metastasis and development in Drosophila melanogaster. However, the cellular pathways through which NDKs function are not known. One potential mechanism of regulation is phosphorylation of guanosine diphosphate (GDP) bound to regulatory guanosine triphosphate (GTP) binding proteins. NDK-catalyzed phosphorylation of bound GDP was investigated for the adenosine diphosphate ribosylation factor (ARF), a 21-kilodalton GTP-binding protein that functions in the protein secretion pathway. Bovine liver NDK, recombinant human NDK, and the protein product of the mouse gene nm23-1, which suppresses the metastatic potential of certain tumor cells, used ARF-GDP as a substrate, thereby allowing rapid and efficient production of activated ARF (ARF-GTP) in the absence of nucleotide exchange. These data are consistent with the proposed function of NDK as an activator of a small GTP-binding protein and provide a mechanism of activation for a regulatory GTP-binding protein that is independent of nucleotide exchange. JF - Science (New York, N.Y.) AU - Randazzo, P A AU - Northup, J K AU - Kahn, R A AD - Laboratory of Biological Chemistry, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/11/08/ PY - 1991 DA - 1991 Nov 08 SP - 850 EP - 853 VL - 254 IS - 5033 SN - 0036-8075, 0036-8075 KW - Recombinant Proteins KW - 0 KW - Guanosine Diphosphate KW - 146-91-8 KW - Guanosine Triphosphate KW - 86-01-1 KW - Cholera Toxin KW - 9012-63-9 KW - Nucleoside-Diphosphate Kinase KW - EC 2.7.4.6 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Index Medicus KW - Animals KW - Liver -- enzymology KW - Cattle KW - Phosphorylation KW - Recombinant Proteins -- metabolism KW - Guanosine Diphosphate -- metabolism KW - Kinetics KW - Humans KW - Drosophila melanogaster -- metabolism KW - Cholera Toxin -- pharmacology KW - Guanosine Triphosphate -- metabolism KW - GTP-Binding Proteins -- metabolism KW - Nucleoside-Diphosphate Kinase -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72473576?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft.atitle=Activation+of+a+small+GTP-binding+protein+by+nucleoside+diphosphate+kinase.&rft.au=Randazzo%2C+P+A%3BNorthup%2C+J+K%3BKahn%2C+R+A&rft.aulast=Randazzo&rft.aufirst=P&rft.date=1991-11-08&rft.volume=254&rft.issue=5033&rft.spage=850&rft.isbn=&rft.btitle=&rft.title=Science+%28New+York%2C+N.Y.%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-06 N1 - Date created - 1991-12-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Science. 1992 Aug 14;257(5072):862 [1323875] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytotoxic potential of ribonuclease and ribonuclease hybrid proteins. AN - 72451897; 1939162 AB - Pancreatic RNase injected into Xenopus oocytes abolishes protein synthesis at concentrations comparable to the toxin ricin yet has no effect on oocyte protein synthesis when added to the extracellular medium. Therefore RNase behaves like a potent toxin when directed into a cell. To explore the cytotoxic potential of RNase toward mammalian cells, bovine pancreatic ribonuclease A was coupled via a disulfide bond to human transferrin or antibodies to the transferrin receptor. The RNase hybrid proteins were cytotoxic to K562 human erythroleukemia cells in vitro with an IC50 around 10(-7) M whereas greater than 10(-5) M native RNase was required to inhibit protein synthesis. Cytotoxicity requires both components of the conjugate since excess transferrin or ribonuclease inhibitors added to the medium protected the cells from the transferrin-RNase toxicity. Compounds that interfere with transferrin receptor cycling and compartmentalization such as ammonium chloride decreased the cytotoxicity of transferrin-RNase. After a dose-dependent lag period inactivation of protein synthesis by transferrin-RNase followed a first-order decay constant. In a clonogenic assay that measures the extent of cell death 1 x 10(-6) M transferrin-RNase killed at least 4 logs or 99.99% of the cells whereas 70 x 10(-6) M RNase was nontoxic. These results show that RNase coupled to a ligand can be cytotoxic. Human ribonucleases coupled to antibodies also may exhibit receptor-mediated toxicities providing a new approach to selective cell killing possibly with less systemic toxicity and importantly less immunogenicity than the currently employed ligand-toxin conjugates. JF - The Journal of biological chemistry AU - Rybak, S M AU - Saxena, S K AU - Ackerman, E J AU - Youle, R J AD - Biochemistry Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20896. Y1 - 1991/11/05/ PY - 1991 DA - 1991 Nov 05 SP - 21202 EP - 21207 VL - 266 IS - 31 SN - 0021-9258, 0021-9258 KW - Immunotoxins KW - 0 KW - Protein Synthesis Inhibitors KW - Transferrin KW - Ammonium Chloride KW - 01Q9PC255D KW - Monensin KW - 906O0YJ6ZP KW - Ribonucleases KW - EC 3.1.- KW - Index Medicus KW - Clone Cells KW - Animals KW - Protein Biosynthesis KW - Immunotoxins -- toxicity KW - Humans KW - Monensin -- pharmacology KW - Transferrin -- chemistry KW - Microinjections KW - Ammonium Chloride -- pharmacology KW - Cell Death -- drug effects KW - Xenopus laevis KW - In Vitro Techniques KW - Oocytes KW - Time Factors KW - Cell Line KW - Protein Synthesis Inhibitors -- toxicity KW - Ribonucleases -- toxicity KW - Ribonucleases -- antagonists & inhibitors KW - Ribonucleases -- administration & dosage KW - Ribonucleases -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72451897?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Cytotoxic+potential+of+ribonuclease+and+ribonuclease+hybrid+proteins.&rft.au=Rybak%2C+S+M%3BSaxena%2C+S+K%3BAckerman%2C+E+J%3BYoule%2C+R+J&rft.aulast=Rybak&rft.aufirst=S&rft.date=1991-11-05&rft.volume=266&rft.issue=31&rft.spage=21202&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-13 N1 - Date created - 1991-12-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutation of a single amino acid converts germ cell alkaline phosphatase to placental alkaline phosphatase. AN - 72451866; 1939159 AB - Human placental and germ cell alkaline phosphatases (PLAP and GCAP, respectively), are characterized by their differential sensitivities to inhibition by L-leucine, EDTA, and heat. Yet, they differ by only 7 amino acids at positions 15, 67, 68, 84, 241, 254, and 429 within their respective 484 residues. To determine the structural basis and the amino acid(s) involved in these physicochemical differences, we constructed three GCAP mutants by site-directed mutagenesis and six GCAP/PLAP chimeras and then expressed these alkaline phosphatase mutants in COS-1 cells. We report that the differential reactivity of PLAP and GCAP depends critically on a single amino acid at position 429. GCAP with Gly-429 is strongly inhibited by L-leucine, EDTA, and heat, whereas PLAP with Glu-429 is resistant. By substituting Gly-429 of GCAP with a series of amino acids, we demonstrate that the relative sensitivities of these mutants to L-leucine, EDTA, and heat inhibition are, in general, parallel. Mutants in the order of resistance to these treatments are: Glu (most resistant), Asp/Ile/Leu, Gln/Val/Lys, Ser/His, and Arg/Thr/Met/Cys/Phe/Trp/Tyr/Pro/Asn/Ala/Gly (least resistant). However, the Ser-429 and His-429 mutants were more resistant to EDTA and heat inhibition than the wild-type GCAP, but were equally sensitive to L-leucine inhibition. Structural analysis of mammalian alkaline phosphatase modeled on the refined crystal structure of Escherichia coli alkaline phosphatase indicates that the negative charge of Glu-429 of PLAP, which simultaneously stabilizes the protein as a whole and the metal binding specifically, probably acts through interactions with the metal ligand His-320 (His-331 in E. coli alkaline phosphatase). Replacement of codon 429 with Gly in GCAP leads to destabilization and loosening of the metal binding. The data suggest that the natural binding site for L-leucine may be near position 429, with the amino and carboxyl groups of L-leucine interacting with bound phosphate and His-432 (His-412 in E. coli alkaline phosphatase), respectively. JF - The Journal of biological chemistry AU - Watanabe, T AU - Wada, N AU - Kim, E E AU - Wyckoff, H W AU - Chou, J Y AD - Human Genetics Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/11/05/ PY - 1991 DA - 1991 Nov 05 SP - 21174 EP - 21178 VL - 266 IS - 31 SN - 0021-9258, 0021-9258 KW - GCAP KW - PLAP KW - Oligonucleotides KW - 0 KW - Recombinant Fusion Proteins KW - Edetic Acid KW - 9G34HU7RV0 KW - Alkaline Phosphatase KW - EC 3.1.3.1 KW - Leucine KW - GMW67QNF9C KW - Index Medicus KW - Recombinant Fusion Proteins -- antagonists & inhibitors KW - Animals KW - DNA Mutational Analysis KW - Structure-Activity Relationship KW - Binding Sites KW - Hot Temperature KW - Base Sequence KW - Transfection KW - Oligonucleotides -- chemistry KW - Cercopithecus aethiops KW - Leucine -- metabolism KW - Molecular Sequence Data KW - Cell Line KW - Edetic Acid -- pharmacology KW - Alkaline Phosphatase -- chemistry KW - Alkaline Phosphatase -- antagonists & inhibitors KW - Placenta -- enzymology KW - Alkaline Phosphatase -- genetics KW - Germ Cells -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72451866?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Mutation+of+a+single+amino+acid+converts+germ+cell+alkaline+phosphatase+to+placental+alkaline+phosphatase.&rft.au=Watanabe%2C+T%3BWada%2C+N%3BKim%2C+E+E%3BWyckoff%2C+H+W%3BChou%2C+J+Y&rft.aulast=Watanabe&rft.aufirst=T&rft.date=1991-11-05&rft.volume=266&rft.issue=31&rft.spage=21174&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-13 N1 - Date created - 1991-12-13 N1 - Date revised - 2017-01-13 N1 - Gene symbol - GCAP; PLAP N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of RNases and toxins upon injection into Xenopus oocytes. AN - 72450838; 1939163 AB - Several toxins abolish cellular protein synthesis by attacking specific sites in 28 S RNA. One of these toxins, alpha-sarcin, is an RNase that also cleaves nonspecifically on the 3' side of purines in deproteinized RNA. Several other RNases were injected into Xenopus oocytes, examined for their ability to abolish protein synthesis, and compared with alpha-sarcin and ricin. Surprisingly, pancreatic RNase A or B abolished oocyte protein synthesis at concentrations (approximately 0.03 nM) comparable to, or lower than, the amount of alpha-sarcin (approximately 2 nM) or ricin (approximately 0.07 nM) required to abolish protein synthesis. RNases S and T1 only inhibited oocyte protein synthesis when used at concentrations approximately 10 x higher than RNase A whereas RNases C, T2, U2, and nuclease P1 required concentrations approximately 100 times higher than RNase A to abolish protein synthesis. There was a direct correlation between the degradation of oocyte RNA and the inhibition of protein synthesis. The RNase inhibitors RNasin and Inhibit-Ace injected into the oocyte both prevented RNase A from hydrolyzing oocyte rRNA and abolishing protein synthesis. Enzymatically inactive oxidized RNase A did not inhibit protein synthesis when injected into the oocyte. None of the RNases or alpha-sarcin abolished protein synthesis when added to oocyte extracellular medium. Angiogenin is a human plasma protein that induces blood vessel formation in chick embryos, has 35% amino acid identity with RNase A, and cleaves 18 S and 28 S RNA in rabbit reticulocyte lysates (St. Clair, D. K., Rybak, S. M., Riordan, J. F. & Vallee, B. L. (1988) Biochemistry 27, 7263-7268, and references therein). Recombinant angiogenin injected into oocytes abolished protein synthesis, and this toxic effect was inhibited by RNasin but was not inhibited by Inhibit-Ace. Unlike RNase A and the other nucleases that hydrolyzed cellular rRNA, no cleavage of 18 or 28 S RNA by recombinant angiogenin was seen at concentrations 100 x greater than necessary to abolish protein synthesis. Recombinant angiogenin must selectively attack specific RNA(s) or another target in the cell. JF - The Journal of biological chemistry AU - Saxena, S K AU - Rybak, S M AU - Winkler, G AU - Meade, H M AU - McGray, P AU - Youle, R J AU - Ackerman, E J AD - Biochemistry Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/11/05/ PY - 1991 DA - 1991 Nov 05 SP - 21208 EP - 21214 VL - 266 IS - 31 SN - 0021-9258, 0021-9258 KW - Diphtheria Toxin KW - 0 KW - Fungal Proteins KW - Protein Synthesis Inhibitors KW - Proteins KW - RNA, Ribosomal, 28S KW - Toxins, Biological KW - alpha-sarcin KW - 1407-48-3 KW - Ricin KW - 9009-86-3 KW - Endoribonucleases KW - EC 3.1.- KW - Ribonucleases KW - angiogenin KW - EC 3.1.27.- KW - Ribonuclease, Pancreatic KW - EC 3.1.27.5 KW - Index Medicus KW - Proteins -- pharmacology KW - Xenopus laevis KW - Fungal Proteins -- toxicity KW - Animals KW - Ricin -- toxicity KW - Diphtheria Toxin -- toxicity KW - Oocytes KW - RNA, Ribosomal, 28S -- metabolism KW - Microinjections KW - Protein Synthesis Inhibitors -- toxicity KW - Ribonucleases -- toxicity KW - Ribonucleases -- antagonists & inhibitors KW - Toxins, Biological -- administration & dosage KW - Ribonucleases -- administration & dosage KW - Ribonucleases -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72450838?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Comparison+of+RNases+and+toxins+upon+injection+into+Xenopus+oocytes.&rft.au=Saxena%2C+S+K%3BRybak%2C+S+M%3BWinkler%2C+G%3BMeade%2C+H+M%3BMcGray%2C+P%3BYoule%2C+R+J%3BAckerman%2C+E+J&rft.aulast=Saxena&rft.aufirst=S&rft.date=1991-11-05&rft.volume=266&rft.issue=31&rft.spage=21208&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-13 N1 - Date created - 1991-12-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transient IGF-I gene expression during the maturation of functionally related central projection neurons. AN - 85241064; pmid-1658250 AB - Insulin-like growth factor I (IGF-I) is a monomeric peptide with significant homology to proinsulin. IGF-I has a number of potent effects on cultured neural tissue, including the stimulation of mitosis in sympathetic neuroblasts; the promotion of neurite outgrowth in cortical, sensory, and sympathetic neurons; and the induction of oligodendrocyte differentiation. In order to determine the sites in which IGF-I may play a role in neural development in vivo, the pattern of IGF-I gene expression in the developing rat brain has been analyzed by means of in situ hybridization histochemistry. Transient IGF-I gene expression is seen during the maturation of specific groups of functionally related sensory and cerebellar projection neurons. IGF-I mRNA is abundant within developing cerebellar Purkinje cells and in the major cerebellar relay centers, including the inferior olive, medial vestibular and lateral reticular nuclei of the brainstem, and the deep cerebellar and red nuclei. Similarly, IGF-I mRNA is localized in the synaptic stations of the developing olfactory, auditory, visual, and somatosensory systems. For example, in the auditory system, IGF-I mRNA is abundant in the cochlear nucleus, superior olive, lateral lemniscus, medial geniculate body, and inferior colliculus. In each system, IGF-I gene expression is found predominantly in long-axon projection neurons, appearing during a relatively late stage in their development, at a time of maturation of dendrites and synapse formation. The specific timing and selective localization of neuronal IGF-I gene expression described in this study suggest that IGF-I may have a role in the shaping of system-specific synaptic connections or myelinization. JF - The Journal of Neuroscience AU - Bondy, C A AD - Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. PY - 1991 SP - 3442 EP - 3455 VL - 11 IS - 11 SN - 0270-6474, 0270-6474 KW - Rats, Inbred Strains KW - Rats KW - RNA, Messenger KW - Animals, Newborn KW - Cell Aging KW - Neurons KW - Embryo and Fetal Development KW - Brain KW - Animal KW - Nucleic Acid Hybridization KW - Insulin-Like Growth Factor I KW - Histocytochemistry KW - Tissue Distribution KW - Gene Expression KW - Synaptic Transmission UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85241064?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+Neuroscience&rft.atitle=Transient+IGF-I+gene+expression+during+the+maturation+of+functionally+related+central+projection+neurons.&rft.au=Bondy%2C+C+A&rft.aulast=Bondy&rft.aufirst=C&rft.date=1991-11-01&rft.volume=11&rft.issue=11&rft.spage=3442&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Neuroscience&rft.issn=02706474&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Effect of chronic ethanol ingestion on phosphate content of neurofilament proteins and neurofilament associated protein phosphatase in rat spinal cord. AN - 72722432; 1667674 AB - Rats were trained to drink alcohol solution by gradually increasing the ethanol content [2.5-15% (v/v)] in drinking water. After 11 months of alcohol (15% v/v) ingestion, animals were guillotined and the spinal cords were used for the preparation of neurofilaments (NF). NF triplet proteins were separated by SDS-PAGE and the phosphate contents of individual components were estimated. Results indicated a significant increase in phosphate content of 200 KD protein in alcohol fed rats (30.19 +/- 4.12 mol of phosphate/mole of protein: p less than 0.001) compared to control group (18.42 +/- 3.91 mol of phosphate/mole of protein). No significant change in the phosphate content of 150KD and 68KD components of NF were seen in experimental group. Further, the studies on NF associated protein phosphatase activity indicated a significant decrease in phosphatase activity among the alcohol fed rats (14.10 +/- 2.5 mU; p less than 0.001) against NF rich fraction as a substrate, as compared to control (20.15 +/- 2.15 mU). While the observed decrease in NF associated protein phosphatase would possibly explain the increase in phosphate content of NF proteins in alcohol fed rats, the precise mechanism of decrease in enzyme activity remains to be elucidated. Nevertheless, the change seen in phosphate content and NF associated protein phosphatase activity as a result of ethanol ingestion would possibly form the biochemical basis of some of the neuropathological changes seen in alcoholics. JF - Neurochemical research AU - Guru, S C AU - Shetty, K T AU - Shankar, S K AD - Department of Neurochemistry, National Institute of Mental Health and Neuro Sciences, Bangalore, India. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 1193 EP - 1197 VL - 16 IS - 11 SN - 0364-3190, 0364-3190 KW - Neurofilament Proteins KW - 0 KW - Phosphates KW - Phosphoprotein Phosphatases KW - EC 3.1.3.16 KW - Index Medicus KW - Rats KW - Animals KW - Male KW - Phosphates -- metabolism KW - Spinal Cord -- metabolism KW - Alcoholism -- metabolism KW - Phosphoprotein Phosphatases -- chemistry KW - Neurofilament Proteins -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72722432?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurochemical+research&rft.atitle=Effect+of+chronic+ethanol+ingestion+on+phosphate+content+of+neurofilament+proteins+and+neurofilament+associated+protein+phosphatase+in+rat+spinal+cord.&rft.au=Guru%2C+S+C%3BShetty%2C+K+T%3BShankar%2C+S+K&rft.aulast=Guru&rft.aufirst=S&rft.date=1991-11-01&rft.volume=16&rft.issue=11&rft.spage=1193&rft.isbn=&rft.btitle=&rft.title=Neurochemical+research&rft.issn=03643190&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-22 N1 - Date created - 1992-06-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Radiation-induced salivary dysfunction: clinical course and significance. AN - 72709000; 1813995 AB - Salivary gland dysfunction commonly occurs as a result of radiation therapy for cancers of the head and neck region. The effect of radiation on salivary glands is immediate and predictable. Histologic and sialochemical studies indicate both the acini and ducts are affected. The extent of salivary dysfunction is primarily determined by the radiation field and dose. Radiation-induced salivary dysfunction is permanent and leads to a host of clinical sequelae, both oral and systemic. JF - Special care in dentistry : official publication of the American Association of Hospital Dentists, the Academy of Dentistry for the Handicapped, and the American Society for Geriatric Dentistry AU - Valdez, I H AD - National Institute of Dental Research, National Institutes of Health, Bethesda 20892. PY - 1991 SP - 252 EP - 255 VL - 11 IS - 6 SN - 0275-1879, 0275-1879 KW - Dentistry KW - Humans KW - Radiotherapy -- adverse effects KW - Xerostomia -- etiology KW - Salivary Glands -- radiation effects KW - Salivation -- radiation effects KW - Head and Neck Neoplasms -- radiotherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72709000?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=A+new+functional+role+for+P-glycoprotein%3A+efflux+pump+for+benzo%28alpha%29pyrene+in+human+breast+cancer+MCF-7+cells.&rft.au=Yeh%2C+G+C%3BLopaczynska%2C+J%3BPoore%2C+C+M%3BPhang%2C+J+M&rft.aulast=Yeh&rft.aufirst=G&rft.date=1992-12-01&rft.volume=52&rft.issue=23&rft.spage=6692&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-15 N1 - Date created - 1992-06-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of nerve blockade on pulsatile insulin and glucagon secretion in vitro. AN - 72631583; 1780325 AB - We recently reported that the secretion of insulin and glucagon by isolated murine islets is pulsatile and suggested that the pacemaker controlling these hormone oscillations is present in the islet. In the present study, we tested the hypothesis of an intrinsic islet neural controlling mechanism for the observed hormone pulsatility. Nerve blockade was attempted by infusion of tetrodotoxin (TTX) on a background of combined adrenergic and cholinergic blockade with atropine, propranolol, and phentolamine, (ATX). Because TTX acts by blocking Na+ channels, we also studied the effects of other cationic channel manipulations on the amplitude and frequency of the oscillations. The normal frequency and amplitude of glucagon and insulin oscillations were not affected by ATX. In contrast, TTX infusion increased the amplitude of insulin (198.6 +/- 20.9 vs. 507.2 +/- 62.8 pg/min, p less than 0.05, n = 4) and shortened the period from 5.03 +/- 0.26 to 3.33 +/- 0.0 min without affecting glucagon cycles. Whereas the Ca2+ ionophore A23187 had no effect on either hormone oscillation, the ATP-sensitive K+ channel blocker glyburide only increased the amplitude of insulin and decreased the amplitude of glucagon, without altering the frequencies. These data suggest that an intrinsic autonomously functioning islet nervous system is the pacemaker for the insulin oscillations and that the control of glucagon cycles differs from that of insulin. JF - Pancreas AU - Opara, E C AU - Go, V L AD - Division of Digestive Diseases and Nutrition, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 653 EP - 658 VL - 6 IS - 6 SN - 0885-3177, 0885-3177 KW - Insulin KW - 0 KW - Tetrodotoxin KW - 4368-28-9 KW - Atropine KW - 7C0697DR9I KW - Glucagon KW - 9007-92-5 KW - Propranolol KW - 9Y8NXQ24VQ KW - Glyburide KW - SX6K58TVWC KW - Phentolamine KW - Z468598HBV KW - Index Medicus KW - Animals KW - Biological Clocks KW - Phentolamine -- pharmacology KW - Propranolol -- pharmacology KW - Nervous System -- drug effects KW - In Vitro Techniques KW - Mice KW - Tetrodotoxin -- pharmacology KW - Nervous System Physiological Phenomena KW - Atropine -- pharmacology KW - Glyburide -- pharmacology KW - Female KW - Islets of Langerhans -- innervation KW - Glucagon -- secretion KW - Islets of Langerhans -- drug effects KW - Insulin -- secretion KW - Islets of Langerhans -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72631583?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pancreas&rft.atitle=Effect+of+nerve+blockade+on+pulsatile+insulin+and+glucagon+secretion+in+vitro.&rft.au=Opara%2C+E+C%3BGo%2C+V+L&rft.aulast=Opara&rft.aufirst=E&rft.date=1991-11-01&rft.volume=6&rft.issue=6&rft.spage=653&rft.isbn=&rft.btitle=&rft.title=Pancreas&rft.issn=08853177&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-12 N1 - Date created - 1992-03-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - History of clinical trials. AN - 72617327; 1775772 AB - Advances in medical treatments have occurred because of the application of new knowledge gained from clinical experiments conducted over the last 250 years. New sources of compounds with anti-tumor activity in human cancer are constantly under investigation. The development of a new drug is a complex process: screening, formulation, production, toxicology studies, FDA approval, and evaluation in phase I, II, and III clinical trials. JF - Seminars in oncology nursing AU - Jenkins, J AU - Hubbard, S AD - Cancer Nursing Service, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 228 EP - 234 VL - 7 IS - 4 SN - 0749-2081, 0749-2081 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Nursing KW - History of medicine KW - United States KW - Clinical Protocols -- standards KW - History, 20th Century KW - Antineoplastic Agents -- standards KW - Humans KW - History, 18th Century KW - History, 19th Century KW - Research Design -- standards KW - Antineoplastic Agents -- therapeutic use KW - Research -- organization & administration KW - Research -- history KW - Clinical Trials as Topic -- history KW - Research -- standards UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72617327?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+oncology+nursing&rft.atitle=History+of+clinical+trials.&rft.au=Jenkins%2C+J%3BHubbard%2C+S&rft.aulast=Jenkins&rft.aufirst=J&rft.date=1991-11-01&rft.volume=7&rft.issue=4&rft.spage=228&rft.isbn=&rft.btitle=&rft.title=Seminars+in+oncology+nursing&rft.issn=07492081&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-02 N1 - Date created - 1992-03-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prevalence of prescription drug abuse: data from the National Institute on Drug Abuse. AN - 72609296; 1663221 JF - New York state journal of medicine AU - Adams, E H AD - National Institute on Drug Abuse. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 32S EP - 36S VL - 91 IS - 11 Suppl SN - 0028-7628, 0028-7628 KW - Benzodiazepines KW - 12794-10-4 KW - Index Medicus KW - United States KW - New York City -- epidemiology KW - Humans KW - Health Surveys KW - Legislation, Drug KW - Drug Prescriptions KW - United States Substance Abuse and Mental Health Services Administration KW - Prevalence KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72609296?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=New+York+state+journal+of+medicine&rft.atitle=Prevalence+of+prescription+drug+abuse%3A+data+from+the+National+Institute+on+Drug+Abuse.&rft.au=Adams%2C+E+H&rft.aulast=Adams&rft.aufirst=E&rft.date=1991-11-01&rft.volume=91&rft.issue=11+Suppl&rft.spage=32S&rft.isbn=&rft.btitle=&rft.title=New+York+state+journal+of+medicine&rft.issn=00287628&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-27 N1 - Date created - 1992-02-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Bacterial infections in human immunodeficiency virus type 1-infected children: the impact of central venous catheters and antiretroviral agents. AN - 72570269; 1661003 AB - We conducted a retrospective study to analyze the impact of central venous catheters (CVCs) and antiretroviral therapy on the frequency and the patterns of bacterial infections in children infected with human immunodeficiency virus during a 3-year period. Among 204 bacterial infections other than otitis media reviewed, soft tissue infection (n = 69), bacteremia (n = 57), pneumonia (n = 27) and sinusitis (n = 27) were encountered most frequently. Catheter-related staphylococcal infection was the most common infection in children with CVCs, particularly in those who were less than 6 years old. In children without CVCs, Streptococcus pneumoniae was the most frequent organism. Younger children had more CVC-related infections whereas children with lower CD4 counts had more CVC-related and CVC-unrelated infections. A lower frequency of CVC-unrelated infections was detected in patients who received antiretroviral therapy, especially those receiving a continuous infusion of zidovudine. These data suggest that increased frequency and altered patterns of bacterial infections are associated with the use of CVCs in these patients, but antiretroviral therapy may reduce the frequency of CVC-unrelated infections. JF - The Pediatric infectious disease journal AU - Roilides, E AU - Marshall, D AU - Venzon, D AU - Butler, K AU - Husson, R AU - Pizzo, P A AD - Infectious Diseases Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 813 EP - 819 VL - 10 IS - 11 SN - 0891-3668, 0891-3668 KW - Antiviral Agents KW - 0 KW - Zidovudine KW - 4B9XT59T7S KW - Zalcitabine KW - 6L3XT8CB3I KW - Didanosine KW - K3GDH6OH08 KW - Index Medicus KW - AIDS/HIV KW - Zidovudine -- therapeutic use KW - Didanosine -- therapeutic use KW - Humans KW - Retrospective Studies KW - Zalcitabine -- therapeutic use KW - Child KW - Adolescent KW - Male KW - Female KW - Child, Preschool KW - Catheterization, Central Venous -- adverse effects KW - Antiviral Agents -- therapeutic use KW - Bacterial Infections -- etiology KW - HIV Infections -- complications KW - Bacterial Infections -- microbiology KW - HIV Infections -- drug therapy KW - Antiviral Agents -- adverse effects KW - HIV-1 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72570269?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=DNA+polymerase+action+on+benzo%5Ba%5Dpyrene-DNA+adducts.&rft.au=Hruszkewycz%2C+A+M%3BCanella%2C+K+A%3BPeltonen%2C+K%3BKotrappa%2C+L%3BDipple%2C+A&rft.aulast=Hruszkewycz&rft.aufirst=A&rft.date=1992-12-01&rft.volume=13&rft.issue=12&rft.spage=2347&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-22 N1 - Date created - 1992-01-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inverse relationship between CSF TRH concentrations and the TSH response to TRH in abstinent alcohol-dependent patients. AN - 72165582; 1656797 AB - The authors performed the thyrotropin-releasing hormone (TRH) stimulation test and measured CSF concentrations of TRH in 13 abstinent alcohol-dependent subjects. They found an inverse correlation between the thyrotropin (TSH) response to TRH and endogenous CSF TRH concentrations. This finding supports the hypothesis that as the concentration of CSF TRH increases, anterior pituitary TRH receptor density decreases, resulting in a blunted TSH response to TRH stimulation. JF - The American journal of psychiatry AU - Adinoff, B AU - Nemeroff, C B AU - Bissette, G AU - Martin, P R AU - Linnoila, M AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Md. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 1586 EP - 1588 VL - 148 IS - 11 SN - 0002-953X, 0002-953X KW - Receptors, Neurotransmitter KW - 0 KW - Receptors, Thyrotropin-Releasing Hormone KW - Triiodothyronine KW - 06LU7C9H1V KW - Thyrotropin-Releasing Hormone KW - 5Y5F15120W KW - Thyrotropin KW - 9002-71-5 KW - Thyroxine KW - Q51BO43MG4 KW - Abridged Index Medicus KW - Index Medicus KW - Pituitary Gland, Anterior -- metabolism KW - Down-Regulation KW - Triiodothyronine -- blood KW - Receptors, Neurotransmitter -- metabolism KW - Humans KW - Adult KW - Middle Aged KW - Thyroxine -- blood KW - Temperance KW - Male KW - Thyrotropin -- blood KW - Alcoholism -- diagnosis KW - Thyrotropin-Releasing Hormone -- cerebrospinal fluid KW - Alcoholism -- cerebrospinal fluid KW - Alcoholism -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72165582?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+psychiatry&rft.atitle=Inverse+relationship+between+CSF+TRH+concentrations+and+the+TSH+response+to+TRH+in+abstinent+alcohol-dependent+patients.&rft.au=Adinoff%2C+B%3BNemeroff%2C+C+B%3BBissette%2C+G%3BMartin%2C+P+R%3BLinnoila%2C+M&rft.aulast=Adinoff&rft.aufirst=B&rft.date=1991-11-01&rft.volume=148&rft.issue=11&rft.spage=1586&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+psychiatry&rft.issn=0002953X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-20 N1 - Date created - 1991-11-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Upstream sequences within the terminal hairpin positively regulate the P6 promoter of B19 parvovirus. AN - 72161110; 1926783 AB - For the B19 parvovirus P6 promoter, a 96-nt minimal truncation mutant retained activity in transient reporter gene assays. Deletion of sequences further upstream from this minimal promoter markedly diminished reporter activity in certain cell lines. This upstream region lies within the terminal hairpin from -249 to -157 and contains a 14-nt sequence that is protected by DNase I footprinting. The exact sequence is directly repeated further within the hairpin, suggesting a regulatory role. The hairpin termini of parvoviruses were known to serve as origins of replication and to catalyze virion packaging. We now suggest that, in addition to these functions, they exert cis-acting effects on B19 P6-promoted gene expression. JF - Virology AU - Liu, J M AU - Green, S W AU - Hao, Y S AU - McDonagh, K T AU - Young, N S AU - Shimada, T AD - Clinical Hematology Branch, National Heart, Lung and Blood Institute, Bethesda, Maryland 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 39 EP - 47 VL - 185 IS - 1 SN - 0042-6822, 0042-6822 KW - DNA, Viral KW - 0 KW - Recombinant Fusion Proteins KW - Luciferases KW - EC 1.13.12.- KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Deoxyribonuclease I KW - EC 3.1.21.1 KW - Index Medicus KW - Chromosome Deletion KW - HeLa Cells KW - Humans KW - Luciferases -- metabolism KW - Gene Expression KW - Plasmids KW - Chloramphenicol O-Acetyltransferase -- metabolism KW - Nucleic Acid Conformation KW - Recombinant Fusion Proteins -- metabolism KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Base Sequence KW - Leukemia, Erythroblastic, Acute KW - Transfection KW - Recombinant Fusion Proteins -- genetics KW - Molecular Sequence Data KW - Luciferases -- genetics KW - DNA, Viral -- genetics KW - Mutagenesis, Insertional KW - Cell Line KW - DNA Replication KW - Parvoviridae -- genetics KW - Regulatory Sequences, Nucleic Acid KW - Promoter Regions, Genetic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72161110?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Virology&rft.atitle=Upstream+sequences+within+the+terminal+hairpin+positively+regulate+the+P6+promoter+of+B19+parvovirus.&rft.au=Liu%2C+J+M%3BGreen%2C+S+W%3BHao%2C+Y+S%3BMcDonagh%2C+K+T%3BYoung%2C+N+S%3BShimada%2C+T&rft.aulast=Liu&rft.aufirst=J&rft.date=1991-11-01&rft.volume=185&rft.issue=1&rft.spage=39&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=00426822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-21 N1 - Date created - 1991-11-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER -