TY - JOUR T1 - c-myc gene expression in human cells is controlled by glucose. AN - 79423209; 2558650 AB - The c-myc oncogene is implicated in normal growth and differentiation processes. Human cell lines IM9 and HepG2 stably cultured at "low" glucose concentrations (5.5 mM) show c-myc mRNA levels 3-4 times higher than cells cultured at "high" glucose concentrations (25 nM). D-fructose (a metabolizable exose) substitutes for D-glucose in reducing c-myc expression while 3-ortho-methylglucose (a non metabolizable exose) is uneffective. c-myc expression is up-regulated (by PMA) or down-regulated (by dexamethasone and long-term exposure to FCS) in human cells cultured at "low" glucose but not in cells cultured at "high" glucose. We previously demonstrated that insulin receptor gene expression in human cell lines in enhanced by glucose. Therefore, glucose controls in an opposite way the expression of two genes important in the regulation of eukaryotic cell growth and differentiation. JF - Biochemical and biophysical research communications AU - Briata, P AU - Laurino, C AU - Gherzi, R AD - Laboratory of Immunobiology, National Cancer Institute I.S.T. Genova, Italy. Y1 - 1989/12/29/ PY - 1989 DA - 1989 Dec 29 SP - 1123 EP - 1129 VL - 165 IS - 3 SN - 0006-291X, 0006-291X KW - Methylglucosides KW - 0 KW - Proto-Oncogene Proteins KW - Proto-Oncogene Proteins c-myc KW - RNA, Messenger KW - 3-O-Methylglucose KW - 146-72-5 KW - Fructose KW - 30237-26-4 KW - Dexamethasone KW - 7S5I7G3JQL KW - Glucose KW - IY9XDZ35W2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Methylglucosides -- pharmacology KW - Carcinoma, Hepatocellular KW - Dexamethasone -- pharmacology KW - Humans KW - Lymphocytes KW - RNA, Messenger -- biosynthesis KW - Fructose -- pharmacology KW - Liver Neoplasms KW - Cattle KW - Tumor Cells, Cultured KW - Fetal Blood KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Glucose -- pharmacology KW - Gene Expression Regulation -- drug effects KW - Proto-Oncogenes KW - Proto-Oncogene Proteins -- genetics KW - Glucose -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79423209?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-13 N1 - Date created - 1990-02-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A randomized trial comparing combination electron-beam radiation and chemotherapy with topical therapy in the initial treatment of mycosis fungoides. AN - 79368868; 2594037 AB - Mycosis fungoides is a T-cell lymphoma that arises in the skin and progresses at highly variable rates. Nonradomized studies have suggested that early aggressive therapy may improve the prognosis in this usually fatal disease. We studied 103 patients with mycosis fungoides, who, after complete staging, were randomly assigned to receive either combination therapy, consisting of 3000 cGy of electron-beam radiation to the skin combined with parenteral chemotherapy with cyclophosphamide, doxorubicin, etoposide, and vincristine (n = 52) or sequential topical treatment (n = 51). The prognostic factors were well balanced in the two groups. Combined therapy produced considerable toxicity: 12 patients required hospitalization for fever and transient neutropenia, 5 had congestive heart failure, and 2 were later found to have acute nonlymphocytic leukemia. Patients receiving combined therapy had a significantly higher rate of complete response, documented by biopsy, than patients receiving conservative therapy (38 percent vs. 18 percent; P = 0.032). After a median follow-up of 75 months, however, there was no significant difference between the treatment groups in disease-free or overall survival. We conclude that early aggressive therapy with radiation and chemotherapy does not improve the prognosis for patients with mycosis fungoides as compared with conservative treatment beginning with sequential topical therapies. JF - The New England journal of medicine AU - Kaye, F J AU - Bunn, P A AU - Steinberg, S M AU - Stocker, J L AU - Ihde, D C AU - Fischmann, A B AU - Glatstein, E J AU - Schechter, G P AU - Phelps, R M AU - Foss, F M AD - National Cancer Institute-Navy Medical Oncology Branch, Bethesda, Md 20814. Y1 - 1989/12/28/ PY - 1989 DA - 1989 Dec 28 SP - 1784 EP - 1790 VL - 321 IS - 26 SN - 0028-4793, 0028-4793 KW - Vincristine KW - 5J49Q6B70F KW - Etoposide KW - 6PLQ3CP4P3 KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Abridged Index Medicus KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Electrons KW - Neoplasm Staging KW - Random Allocation KW - Humans KW - Vincristine -- administration & dosage KW - Combined Modality Therapy -- adverse effects KW - Doxorubicin -- administration & dosage KW - Etoposide -- administration & dosage KW - Radiotherapy Dosage KW - Middle Aged KW - Female KW - Male KW - Mycosis Fungoides -- therapy KW - Skin Neoplasms -- therapy KW - Skin Neoplasms -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Mycosis Fungoides -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79368868?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-17 N1 - Date created - 1990-01-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: N Engl J Med. 1990 May 17;322(20):1470-1 [2330018] N Engl J Med. 1989 Dec 28;321(26):1822-4 [2594040] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hyperexpression and purification of Escherichia coli adenylate cyclase using a vector designed for expression of lethal gene products. AN - 19624978; 8730733 AB - We describe the construction of a new generation of vectors (pRE) for the hyperexpression of lethal gene products such as adenylate cyclase in Escherichia coli. The pRE vectors are based on the lambda PL promoter and lambda cII ribosome binding site described by Shimatake and Rosenberg (Nature, 292, 128-132, 1981). They have a unique NdeI restriction endonuclease site 3' of the lambda cII ribosome binding site that includes the ATG initiation codon, multilinker cloning sites 3' to the NdeI site, and two lambda transcription terminators 5' and 3' of the lambda PL promoter to eliminate nonspecific transcription and reduce leaky PL transcription, respectively. For hyperexpression of adenylate cyclase, tight control of transcription was necessary since elevation of cAMP levels above the physiological range is lethal to E. coli. Lethality associated with the overproduction of adenylate cyclase was shown to be mediated through the cAMP receptor protein. We used this expression system to overproduce adenylate cyclase 7500 fold, corresponding to 30% of the total cellular protein. Under these conditions the enzyme precipitated with significant loss of activity. Reducing the rate and amount of adenylate cyclase expression to 16% of the total cell protein produced one fourth of the enzyme in a soluble form with high specific activity. The soluble adenylate cyclase was purified to near homogeneity. Images JF - Nucleic Acids Research AU - Reddy, P AU - Peterkofsky, A AU - McKenney, K AD - Laboratory of Biochemical Genetics, National Heart, Lung and Blood Institute, Bethesda, MD 20892. Y1 - 1989/12/25/ PY - 1989 DA - 1989 Dec 25 SP - 10473 EP - 10488 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 17 IS - 24 SN - 0305-1048, 0305-1048 KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - Cyclic AMP KW - Transcription KW - Enzymes KW - Ribosomes KW - Expression vectors KW - Promoters KW - Lethality KW - Protein folding KW - Escherichia coli KW - Codons KW - Endonuclease KW - Adenylate cyclase KW - J 02310:Genetics & Taxonomy KW - N 14810:Methods KW - G 07770:Bacteria UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19624978?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2008-12-01 N1 - Last updated - 2015-03-27 N1 - SubjectsTermNotLitGenreText - Expression vectors; Promoters; Lethality; Protein folding; Cyclic AMP; Codons; Enzymes; Transcription; Ribosomes; Endonuclease; Adenylate cyclase; Escherichia coli ER - TY - JOUR T1 - jun-B inhibits and c-fos stimulates the transforming and trans-activating activities of c-jun. AN - 79382552; 2513129 AB - We have cloned the human jun-B gene and determined its sequence and transforming and trans-activating activities. jun-B is less potent that c-jun in transforming and immortalizing primary rat embryo cells in cooperation with activated ras (effects enhanced by c-fos and TPA); unlike c-jun, jun-B does not transform Rat-1A cells alone. However, cotransfection of c-jun and jun-B into primary rat embryo cells with c-Ha-ras results in a significant decrease in transformation compared with c-jun alone, an event reversed by TPA. Cotransfection of c-jun and jun-B with or without c-fos into F9 teratocarcinoma cells results in decreased trans-activation of AP-1 compared with either gene alone. Introduction of jun-B into primary rat c-jun/ras transformants or c-jun into jun-B/ras transformants also results in a decrease in trans-activation. These findings demonstrate that, whereas jun-B and c-jun each participate in AP-1 trans-activation and malignant transformation, interactions between them involve negative regulation. JF - Cell AU - Schütte, J AU - Viallet, J AU - Nau, M AU - Segal, S AU - Fedorko, J AU - Minna, J AD - NCI-Navy Medical Oncology Branch, Bethesda, Maryland. Y1 - 1989/12/22/ PY - 1989 DA - 1989 Dec 22 SP - 987 EP - 997 VL - 59 IS - 6 SN - 0092-8674, 0092-8674 KW - DNA Probes KW - 0 KW - DNA-Binding Proteins KW - Proto-Oncogene Proteins KW - Proto-Oncogene Proteins c-fos KW - Proto-Oncogene Proteins c-jun KW - RNA Probes KW - Transcription Factors KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Index Medicus KW - Rats KW - Animals KW - Protein-Tyrosine Kinases -- genetics KW - Base Sequence KW - Transfection KW - Humans KW - Restriction Mapping KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Genes, Regulator KW - Oncogenes KW - DNA-Binding Proteins -- genetics KW - Proto-Oncogenes KW - Proto-Oncogene Proteins -- genetics KW - Transcription Factors -- genetics KW - Transcriptional Activation KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79382552?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-07 N1 - Date created - 1990-02-07 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M29039; GENBANK N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Structure of vaccinia virus late promoters. AN - 79441610; 2515287 AB - Functional elements of vaccinia virus late promoters were characterized by mutagenesis. Synthetic oligonucleotides were inserted into a plasmid vector containing the lacZ gene of Escherichia coli flanked by sequences from the thymidine kinase (TK) gene of vaccinia virus. The lacZ gene, under control of the synthetic promoter, was introduced into the vaccinia virus genome at the TK locus by homologous recombination, and each of the 122 recombinants thus obtained was assayed for beta-galactosidase expression. The relative amounts and 5' ends of lacZ mRNAs specified by a subset of the recombinants were determined by primer extension. The analysis indicated that late promoters may be considered in terms of three regions; an upstream sequence of about 20 base-pairs, rich in T and A residues, separated by a spacer region of about six base-pairs from a highly conserved (-1)TAAAT(+4) element within which transcription initiates. All single nucleotide substitutions within the three A residues of the TAAAT, as well as the addition of a fourth A residue, caused drastic reductions in promoter strength. All substitutions of the T residues at -1 and +4 were also detrimental to promoter activity, to an extent that depended on the strength of the promoter as determined by the upstream sequence. mRNA synthesis appeared to initiate within the three A residues regardless of promoter strength. The 5'-poly(A) leader, which is a unique feature of poxvirus late mRNAs, was diminished in length when either of the T residues at -1 and +4 was mutated, was absent or limited to a few nucleotides when any of the three A residues was substituted, but was unaffected by changes outside the TAAAT sequence. The data are consistent with a model for the generation of the normal 5'-poly(A) leader by an RNA polymerase slippage mechanism requiring three consecutive A residues. Single nucleotide substitutions within the six base-pairs upstream and three base-pairs downstream from the TAAAT sequence had modest effects on promoter strength. The most and least favourable changes led to a fourfold increase and an eightfold decrease in activity, respectively. Sequences further upstream were essential for late promoter function; tracts of T or A residues enhanced expression up to 20-fold, the former conferring much greater activity. Highest expression was obtained with a tract of 18 or 20 T residues.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Journal of molecular biology AU - Davison, A J AU - Moss, B AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1989/12/20/ PY - 1989 DA - 1989 Dec 20 SP - 771 EP - 784 VL - 210 IS - 4 SN - 0022-2836, 0022-2836 KW - DNA, Viral KW - 0 KW - beta-Galactosidase KW - EC 3.2.1.23 KW - Index Medicus KW - Base Sequence KW - Gene Expression Regulation, Viral KW - DNA Mutational Analysis KW - Molecular Sequence Data KW - beta-Galactosidase -- genetics KW - Transcription, Genetic KW - DNA, Viral -- genetics KW - Structure-Activity Relationship KW - Vaccinia virus -- genetics KW - Regulatory Sequences, Nucleic Acid KW - Promoter Regions, Genetic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79441610?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-14 N1 - Date created - 1990-03-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synergistic antitumor activity of etoposide and human interleukin-1 alpha against human melanoma cells. AN - 79371873; 2593167 AB - To investigate the possibility of increased activity of cytotoxic anticancer drugs combined with cytokines, we treated human melanoma cells with combinations of etoposide (VP-16) and human recombinant interleukin-1 alpha (rIL-1 alpha). We evaluated the combined cytotoxic effects of VP-16 and rIL-1 alpha using A375-C6 cells, which are sensitive to rIL-1 alpha, and A375-C5 cells, a clonal variant line resistant to rIL-1 alpha. We used the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium-bromid e) assay and the inhibition of [3H]thymidine incorporation into DNA. We analyzed data using the median effects principle of Chou and Talalay (Chou's analysis). The calculated combination index values, at a dose ratio of VP-16 to rIL-1 alpha of 12:1 in simultaneous exposure, indicated synergistic cytotoxicity toward both A375-C6 cells and A375-C5 cells. We observed more pronounced synergism with VP-16 and rIL-1 alpha toward the A375-C5 IL-1 alpha-resistant melanoma cells. These results suggest that rIL-1 alpha combined with cytotoxic antitumor drugs may provide increased benefit in the treatment of malignant melanoma. JF - Journal of the National Cancer Institute AU - Usui, N AU - Mimnaugh, E G AU - Sinha, B K AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/12/20/ PY - 1989 DA - 1989 Dec 20 SP - 1904 EP - 1909 VL - 81 IS - 24 SN - 0027-8874, 0027-8874 KW - Interleukin-1 KW - 0 KW - Recombinant Proteins KW - Etoposide KW - 6PLQ3CP4P3 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Recombinant Proteins -- pharmacology KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - DNA Damage KW - Humans KW - Drug Synergism KW - DNA -- biosynthesis KW - Etoposide -- pharmacology KW - Interleukin-1 -- pharmacology KW - Melanoma -- pathology KW - Interleukin-1 -- administration & dosage KW - Etoposide -- administration & dosage KW - Antineoplastic Combined Chemotherapy Protocols -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79371873?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-22 N1 - Date created - 1990-01-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Thirteen-week toxicity studies of 3,3'-dimethoxybenzidene and C.I. Direct Blue 15 in the Fischer 344 rat. AN - 79504206; 2631298 AB - The benzidine congener 3,3'-dimethoxybenzidine (DMOB), and C.I. Direct Blue 15 (Blue 15), a prototypical compound of the DMOB-derived class of dyes, were evaluated in 13-week studies to characterize the toxicity and establish dose levels for subsequent chronic studies. Groups of 10 Fischer 344 rats of each sex were administered either DMOB, or Blue 15, at 1 of 5 concentrations in drinking water for 13 weeks. DMBO concentrations were 0, 0.017, 0.033, 0.063, 0.125, and 0.25% for males and females. For Blue 15, the concentrations were 0.063, 0.125, 0.25, 0.50, and 1.0% for females and 0, 0.125, 0.25, 0.50, 1.0, and 3.0% for male rats. Rats showed dose-related decreases in water consumption and weight gains. All DMOB-treated rats and their controls survived the 13-week treatment. There were 7 deaths in the 3% level of male rats treated with Blue 15. Liver and kidney weights were increased in rats treated with both compounds. Target organs for DMOB-treated rats were the kidney and thyroid. These lesions were characterized by chronic nephropathy, and increased pigment in the follicular cells of the thyroid. The kidney and liver were identified as target organs for Blue 15-treated rats. In the high-dose rats that died before termination of the study, renal effects were characterized by degeneration and focal necrosis of proximal tubular epithelial cells. Liver lesions in this group consisted of degeneration and necrosis of hepatocytes, fatty metamorphosis, and minimal megalocytosis. Mild chronic nephropathy was the principal histological effect in Blue 15-treated rats surviving to study termination. JF - Toxicology AU - Morgan, D L AU - Jameson, C W AU - Mennear, J H AU - Ulland, B M AU - Lemen, J K AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/12/15/ PY - 1989 DA - 1989 Dec 15 SP - 297 EP - 309 VL - 59 IS - 3 SN - 0300-483X, 0300-483X KW - Azo Compounds KW - 0 KW - Benzidines KW - Coloring Agents KW - direct blue 15 KW - 5C44C6888V KW - Dianisidine KW - MJY508JZXV KW - Index Medicus KW - Weight Gain -- drug effects KW - Animals KW - Chemistry KW - Dose-Response Relationship, Drug KW - Kidney -- drug effects KW - Rats KW - Rats, Inbred F344 KW - Thyroid Gland -- drug effects KW - Drinking -- drug effects KW - Liver -- drug effects KW - Chemical Phenomena KW - Female KW - Male KW - Organ Size -- drug effects KW - Coloring Agents -- toxicity KW - Azo Compounds -- toxicity KW - Dianisidine -- toxicity KW - Benzidines -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79504206?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-05-08 N1 - Date created - 1990-05-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transforming activity of nasopharyngeal carcinoma DNA detectable in mouse JB6 cells. AN - 79416747; 2558076 AB - A JB6 mouse epidermal recipient cell line has been used to detect nasopharyngeal carcinoma (NPC) DNA-associated transforming activity that is not detectable in the NIH 3T3 focus assay. NPC DNA showed both transforming activity and activity for transferring sensitivity to tumor-promoter-induced neoplastic transformation, assayed in 2 different variants of mouse JB6 cells. Comparison of DNAs from various NPC sources that did or did not harbor EBV DNA and that varied in degree of differentiation showed similar transforming activities and similar activities for transferring promotion sensitivity. Thus both a NPC DNA-associated promotion sensitivity and an oncogenic activity function independently of concurrent EBV gene expression. JF - International journal of cancer AU - Colburn, N H AU - Raab-Traub, N AU - Becker, D AU - Cao, Y AU - Winterstein, D AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, MD 21701. Y1 - 1989/12/15/ PY - 1989 DA - 1989 Dec 15 SP - 1012 EP - 1016 VL - 44 IS - 6 SN - 0020-7136, 0020-7136 KW - Carcinogens KW - 0 KW - DNA, Neoplasm KW - Index Medicus KW - Neoplasm Transplantation KW - Carcinogens -- pharmacology KW - Animals KW - Humans KW - Mice, Nude KW - Mice KW - Herpesvirus 4, Human KW - Cell Line KW - Carcinoma -- pathology KW - DNA, Neoplasm -- genetics KW - Cell Transformation, Neoplastic -- drug effects KW - Nasopharyngeal Neoplasms -- genetics KW - Nasopharyngeal Neoplasms -- pathology KW - Cell Transformation, Neoplastic -- genetics KW - Carcinoma -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79416747?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-16 N1 - Date created - 1990-02-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Unique pathway of IL-3-driven hemopoietic differentiation. AN - 79368675; 2480385 AB - The results of this study support a proposed sequence of IL-3-induced hemopoietic cell proliferation and differentiation. Specifically, IL-3 uniquely induces the transient expression of Thy-1 Ag on Thy-1- bone marrow cells during a 2-wk culture period. Thy-1 Ag is expressed on immature myeloid cells that are undergoing lineage restrictions to granulocytes, macrophages, and mast cells. Flow microfluorimetry-separated Thy-1+ cells require the addition of IL-3 or granulocyte/macrophage-CSF to the culture medium for continued growth and, as these cells divide and undergo terminal differentiation they gradually lose Thy-1 Ag expression. The loss of Thy-1 expression is not strictly correlated with cellular proliferation since the expression of Thy-1 decreases on proliferating cells. Last, IL-3 does not maintain the Thy-1- stem cell population that can give rise to Thy-1+ cells in vitro. The relevance of this scheme of differentiation to normal hemopoiesis and to differentiation-arrested IL-3-dependent leukemic cell populations is discussed. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Keller, J R AU - Ihle, J N AD - Biological Carcinogenesis Development Program, NCI-Frederick Cancer Research Facility, MD 21701. Y1 - 1989/12/15/ PY - 1989 DA - 1989 Dec 15 SP - 4025 EP - 4033 VL - 143 IS - 12 SN - 0022-1767, 0022-1767 KW - Antigens, Surface KW - 0 KW - Antigens, Thy-1 KW - Epitopes KW - Interleukin-3 KW - Glucosephosphate Dehydrogenase KW - EC 1.1.1.49 KW - Abridged Index Medicus KW - Index Medicus KW - Phenotype KW - Animals KW - Kinetics KW - Mice KW - Flow Cytometry KW - Cell Separation KW - Antigens, Surface -- metabolism KW - Mice, Inbred BALB C KW - Epitopes -- immunology KW - Glucosephosphate Dehydrogenase -- metabolism KW - Epitopes -- metabolism KW - Hematopoietic Stem Cells -- immunology KW - Interleukin-3 -- physiology KW - Hematopoietic Stem Cells -- enzymology KW - Hematopoietic Stem Cells -- physiology KW - Cell Differentiation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79368675?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-19 N1 - Date created - 1990-01-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sequence requirements for cytochrome P-450IIB1 catalytic activity. Alteration of the stereospecificity and regioselectivity of steroid hydroxylation by a simultaneous change of two hydrophobic amino acid residues to phenylalanine. AN - 79366292; 2574176 AB - The phenobarbital-inducible P-450 forms IIB1 and IIB2 are identical in sequence except for 14 amino acid differences within the carboxyl-terminal half of the molecule. IIB1 has about a 5-10-fold higher turnover number for most monooxygenase substrates examined although the substrate specificities of both enzymes are virtually identical. Both P-450s oxygenate testosterone to yield the 16 alpha-hydroxy, 16 beta-hydroxy, 17-keto, and 16 beta-hydroxy, 17-keto metabolites as major products. A variant IIB2 cDNA, isolated from an uninduced rat liver lambda gt11 library, and when expressed in Hep G2 cells using a vaccinia virus vector, was found to code for a protein that produced the 16 alpha-hydroxy and 17-keto metabolites of testosterone but no 16 beta-hydroxylated products. Although the published sequences of IIB1 and IIB2 are identical within the N-terminal halves of the proteins, sequence analysis of the variant cDNA revealed two amino acid substitutions in this region; Leu58----Phe and I1e114----Phe. When these two amino acid changes were incorporated into IIB1, via construction of a chimeric cDNA, the resultant expressed enzyme did not catalyze the 16 beta-hydroxylation of testosterone or androstenedione. Formation of the 16 alpha-hydroxy and 17-keto metabolites, however, was only slightly reduced compared with the parent IIB1. A IIB1 protein that possessed only the I1e114----Phe replacement catalyzed the production of all four testosterone metabolites with only slightly different product ratios compared with the parent enzyme. The substrate specificity of a IIB1 variant containing only the Leu58----Phe replacement could not be determined, since that protein did not accumulate in cells infected with the corresponding recombinant vaccinia virus. These data suggest that two distinct amino acid residues located within the amino-terminal fourth of IIB1 and IIB2 can affect substrate orientation at the active site. JF - The Journal of biological chemistry AU - Aoyama, T AU - Korzekwa, K AU - Nagata, K AU - Adesnik, M AU - Reiss, A AU - Lapenson, D P AU - Gillette, J AU - Gelboin, H V AU - Waxman, D J AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/12/15/ PY - 1989 DA - 1989 Dec 15 SP - 21327 EP - 21333 VL - 264 IS - 35 SN - 0021-9258, 0021-9258 KW - RNA, Messenger KW - 0 KW - Isoleucine KW - 04Y7590D77 KW - Poly A KW - 24937-83-5 KW - Testosterone KW - 3XMK78S47O KW - Phenylalanine KW - 47E5O17Y3R KW - Steroid Hydroxylases KW - EC 1.14.- KW - Steroid 11-beta-Hydroxylase KW - EC 1.14.15.4 KW - Leucine KW - GMW67QNF9C KW - Index Medicus KW - Vaccinia virus -- genetics KW - Animals KW - Liver -- enzymology KW - Testosterone -- isolation & purification KW - Testosterone -- metabolism KW - Cloning, Molecular -- methods KW - Amino Acid Sequence KW - RNA, Messenger -- genetics KW - Binding Sites KW - Rats, Inbred Strains KW - Rats KW - Base Sequence KW - Chimera KW - Genetic Vectors KW - Molecular Sequence Data KW - Poly A -- genetics KW - Steroid 11-beta-Hydroxylase -- metabolism KW - Steroid Hydroxylases -- genetics KW - Steroid 11-beta-Hydroxylase -- genetics KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79366292?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-19 N1 - Date created - 1990-01-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A phase II study of mitoguazone and vinblastine in advanced transitional cell carcinoma of the urinary tract. AN - 79334619; 2684384 AB - This is a comparative study to evaluate response rate to mitoguazone (MGBG) and vinblastine (VLB) in 52 evaluable patients with advanced transitional cell carcinoma of the urinary tract. Of 38 patients with measurable disease, two of 18 (11%) on MGBG had partial remission (95% confidence interval: 0.01, 0.35), whereas four of 20 (20%) responded on the VLB arm (95% confidence level: 0.06-0.44). Both responses on the MGBG arm were seen in patients given prior chemotherapy. Side effects of both drugs were significant, with 46% of patients given VLB developing severe or life-threatening hematologic toxicity. Data indicate that both drugs, as single agents, are probably inferior to cisplatin for control of advanced transitional cell carcinoma of the urinary tract. JF - Cancer AU - Barrett, J T AU - Orofiamma, B AU - Khandekar, J D AU - Carbone, P P AU - Comis, R L AU - Davis, T E AD - National Cancer Institute, Bethesda, Maryland. Y1 - 1989/12/15/ PY - 1989 DA - 1989 Dec 15 SP - 2445 EP - 2447 VL - 64 IS - 12 SN - 0008-543X, 0008-543X KW - Vinblastine KW - 5V9KLZ54CY KW - Mitoguazone KW - OD5Q0L447W KW - Abridged Index Medicus KW - Index Medicus KW - Drug Evaluation KW - Randomized Controlled Trials as Topic KW - Drug Administration Schedule KW - Neoplasm Staging KW - Infusions, Intravenous KW - Humans KW - Male KW - Female KW - Vinblastine -- therapeutic use KW - Urologic Neoplasms -- pathology KW - Carcinoma, Transitional Cell -- pathology KW - Mitoguazone -- administration & dosage KW - Urologic Neoplasms -- drug therapy KW - Vinblastine -- administration & dosage KW - Mitoguazone -- therapeutic use KW - Mitoguazone -- adverse effects KW - Urologic Neoplasms -- mortality KW - Carcinoma, Transitional Cell -- mortality KW - Vinblastine -- adverse effects KW - Carcinoma, Transitional Cell -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79334619?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-03 N1 - Date created - 1990-01-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immunohistochemical correlates of response to recombinant interleukin-2-based immunotherapy in humans. AN - 79334309; 2582450 AB - We have evaluated immunohistochemical characteristics of tumors and the infiltrating cells in patients treated with various immunotherapy regimens. Forty-eight patients with advanced malignancies were treated with high dose i.v. recombinant interleukin-2 alone or in combination with cyclophosphamide, recombinant tumor necrosis factor, recombinant interferon-alpha, antimelanoma antibody 9.2.27, adoptively transferred tumor infiltrating lymphocytes, or lymphokine-activated killer cells. Thirty-four patients with metastatic melanoma and two patients with breast carcinoma underwent excision of one or more s.c. metastases either before, during, or after treatment. Twelve patients with metastatic renal cell carcinoma underwent pretreatment nephrectomy and these tumors were also studied. Tumor cells were evaluated for class I (HLA-A,B,C) and II (HLA-DR) antigen expression and the mononuclear infiltrate was characterized using an avidin-biotin immunoperoxidase technique. All melanomas were class I antigen positive. Fifty-three % of biopsied metastatic melanoma lesions, 58% of primary renal cell carcinomas, and neither of the two breast carcinomas expressed class II antigen prior to therapy. The pretreatment expression of class II antigens by a tumor was not predictive of a clinical response to recombinant interleukin 2-based therapy. After treatment, however, seven of seven biopsied regressing individual metastases intensely expressed DR antigen on over fifty percent of the cells while only three of ten nonresponding lesions did so. Regressing lesions were permeated with macrophages and both CD4 and CD8 T-cell subsets. There were no CD1 or NKH-1 positive infiltrating cells detected in any lesion. The response to recombinant interleukin 2-based immunotherapy is associated with T-cell as well as macrophage infiltration. DR antigen expression by tumor cells and T-cell infiltrate appear in individual lesions to be associated with this response. JF - Cancer research AU - Rubin, J T AU - Elwood, L J AU - Rosenberg, S A AU - Lotze, M T AD - Surgery Branch, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1989/12/15/ PY - 1989 DA - 1989 Dec 15 SP - 7086 EP - 7092 VL - 49 IS - 24 Pt 1 SN - 0008-5472, 0008-5472 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Neoplasm KW - HLA-D Antigens KW - Interleukin-2 KW - Recombinant Proteins KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - Carcinoma, Renal Cell -- pathology KW - Kidney Neoplasms -- pathology KW - Kidney Neoplasms -- therapy KW - Macrophages -- immunology KW - Carcinoma, Renal Cell -- therapy KW - Humans KW - Breast Neoplasms -- therapy KW - Melanoma -- immunology KW - Breast Neoplasms -- immunology KW - Carcinoma -- therapy KW - Cyclophosphamide -- therapeutic use KW - Breast Neoplasms -- pathology KW - Neoplasm Metastasis KW - Carcinoma, Renal Cell -- immunology KW - T-Lymphocytes -- immunology KW - Recombinant Proteins -- therapeutic use KW - Combined Modality Therapy KW - Antigens, Neoplasm -- analysis KW - Carcinoma -- immunology KW - HLA-D Antigens -- analysis KW - Melanoma -- pathology KW - Carcinoma -- pathology KW - Melanoma -- therapy KW - Immunohistochemistry KW - Kidney Neoplasms -- immunology KW - Neoplasms -- pathology KW - Interleukin-2 -- therapeutic use KW - Neoplasms -- therapy KW - Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79334309?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-11 N1 - Date created - 1990-01-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A transfected m1 muscarinic acetylcholine receptor stimulates adenylate cyclase via phosphatidylinositol hydrolysis. AN - 79334768; 2555356 AB - The m1 muscarinic acetylcholine receptor gene was transfected into and stably expressed in A9 L cells. The muscarinic receptor agonist, carbachol, stimulated inositol phosphate generation, arachidonic acid release, and cAMP accumulation in these cells. Carbachol stimulated arachidonic acid and inositol phosphate release with similar potencies, while cAMP generation required a higher concentration. Studies were performed to determine if the carbachol-stimulated cAMP accumulation was due to direct coupling of the m1 muscarinic receptor to adenylate cyclase via a GTP binding protein or mediated by other second messengers. Carbachol failed to stimulate adenylate cyclase activity in A9 L cell membranes, whereas prostaglandin E2 did, suggesting indirect stimulation. The phorbol ester, phorbol 12-myristate 13-acetate (PMA), stimulated arachidonic acid release yet inhibited cAMP accumulation in response to carbachol. PMA also inhibited inositol phosphate release in response to carbachol, suggesting that activation of phospholipase C might be involved in cAMP accumulation. PMA did not inhibit prostaglandin E2-, cholera toxin-, or forskolin-stimulated cAMP accumulation. The phospholipase A2 inhibitor eicosatetraenoic acid and the cyclooxygenase inhibitors indomethacin and naproxen had no effect on carbachol-stimulated cAMP accumulation. Carbachol-stimulated cAMP accumulation was inhibited with TMB-8, an inhibitor of intracellular calcium release, and W7, a calmodulin antagonist. These observations suggest that carbachol-stimulated cAMP accumulation does not occur through direct m1 muscarinic receptor coupling or through the release of arachidonic acid and its metabolites, but is mediated through the activation of phospholipase C. The generation of cytosolic calcium via inositol 1,4,5-trisphosphate and subsequent activation of calmodulin by m1 muscarinic receptor stimulation of phospholipase C appears to generate the accumulation of cAMP. JF - The Journal of biological chemistry AU - Felder, C C AU - Kanterman, R Y AU - Ma, A L AU - Axelrod, J AD - Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1989/12/05/ PY - 1989 DA - 1989 Dec 05 SP - 20356 EP - 20362 VL - 264 IS - 34 SN - 0021-9258, 0021-9258 KW - Arachidonic Acids KW - 0 KW - Calcium Channel Blockers KW - Calmodulin KW - Inositol Phosphates KW - Phosphatidylinositols KW - Receptors, Muscarinic KW - Sulfonamides KW - Arachidonic Acid KW - 27YG812J1I KW - 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate KW - 57818-92-5 KW - Gallic Acid KW - 632XD903SP KW - W 7 KW - 65595-90-6 KW - Carbachol KW - 8Y164V895Y KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinase C KW - EC 2.7.11.13 KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Calmodulin -- metabolism KW - Animals KW - Gallic Acid -- pharmacology KW - Cell Membrane -- enzymology KW - Inositol Phosphates -- metabolism KW - Cytosol -- enzymology KW - Calmodulin -- antagonists & inhibitors KW - Gene Expression KW - Mice KW - L Cells (Cell Line) -- enzymology KW - Models, Biological KW - Protein Kinase C -- metabolism KW - Genes KW - Calcium Channel Blockers -- pharmacology KW - Sulfonamides -- pharmacology KW - Kinetics KW - Cyclic AMP -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Carbachol -- pharmacology KW - Receptors, Muscarinic -- genetics KW - Phosphatidylinositols -- metabolism KW - Transfection KW - Adenylyl Cyclases -- metabolism KW - Arachidonic Acids -- metabolism KW - Receptors, Muscarinic -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79334768?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-08 N1 - Date created - 1990-01-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phosphorylation of phospholipase C-gamma by cAMP-dependent protein kinase. AN - 79334624; 2479646 AB - The mechanism by which cAMP modulates the activity of phosphoinositide-specific phospholipase C (PLC) was studied. Elevation of cAMP inhibited both basal and norepinephrine-stimulated phosphoinositide breakdown in C6Bu1 cells which contain at least three PLC isozymes, PLC-beta, PLC-gamma, and PLC-delta. Treatment of C6Bu1 cells with cAMP-elevating agents (cholera toxin, isobutylmethylxanthine, forskolin, and 8-bromo-cAMP) increased serine phosphate in PLC-gamma, but the phosphate contents in PLC-beta and PLC-delta were not changed. In addition, cAMP-dependent protein kinase selectively phosphorylated purified PLC-gamma among the three isozymes and added a single phosphate at serine. The serine phosphorylation, nevertheless, did not affect the activity of PLC-gamma in vitro. We propose, therefore, that the phosphorylation of PLC-gamma by cAMP-dependent protein kinase alters its interaction with putative modulatory proteins and leads to its inhibition. JF - The Journal of biological chemistry AU - Kim, U H AU - Kim, J W AU - Rhee, S G AD - Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989/12/05/ PY - 1989 DA - 1989 Dec 05 SP - 20167 EP - 20170 VL - 264 IS - 34 SN - 0021-9258, 0021-9258 KW - Amino Acids KW - 0 KW - Isoenzymes KW - Colforsin KW - 1F7A44V6OU KW - 8-Bromo Cyclic Adenosine Monophosphate KW - 23583-48-4 KW - Cholera Toxin KW - 9012-63-9 KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinases KW - EC 2.7.- KW - Type C Phospholipases KW - EC 3.1.4.- KW - 1-Methyl-3-isobutylxanthine KW - TBT296U68M KW - Index Medicus KW - Animals KW - Amino Acids -- analysis KW - Cholera Toxin -- pharmacology KW - 8-Bromo Cyclic Adenosine Monophosphate -- pharmacology KW - Tumor Cells, Cultured -- enzymology KW - Isoenzymes -- metabolism KW - Rats KW - Colforsin -- pharmacology KW - Phosphorylation KW - Kinetics KW - Cyclic AMP -- metabolism KW - Glioma KW - 1-Methyl-3-isobutylxanthine -- pharmacology KW - Cell Line KW - Protein Kinases -- metabolism KW - Type C Phospholipases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79334624?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-08 N1 - Date created - 1990-01-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Primary biliary cirrhosis: management of an unusual case with severe xanthomata by hepatic transplantation. AN - 85212143; pmid-2584673 AB - We report a patient with advanced primary biliary cirrhosis associated with Sjögren's syndrome, xanthelasma, and extensive, painful xanthomata involving cutaneous lipid deposits on her face, abdomen, hands, and buttocks and extensor surfaces over many joints. Despite conventional dietary and drug therapy, these lesions progressed rapidly over 3 years. There was symptomatic improvement of the xanthomata, but no objective amelioration of the xanthomatosis with the use of plasmapheresis over an 18-month period. Liver transplantation was undertaken for decompensated chronic liver disease and poor quality of life due to complications of xanthomatosis. Twelve months after transplantation, all xanthomata and xanthelasma and symptoms attributable to xanthomata had disappeared. Liver transplantation is a drastic but successful remedy for complications of abnormal lipid metabolism associated with primary biliary cirrhosis. JF - Journal of Clinical Gastroenterology AU - Peters, M G AU - Hoffnagle, J H AU - McGarvey, C AU - Fox, I AU - Gregg, R E AU - Jones, E A AD - Liver Diseases Section, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland. PY - 1989 SP - 694 EP - 697 VL - 11 IS - 6 SN - 0192-0790, 0192-0790 KW - Xanthomatosis KW - Skin Diseases KW - Human KW - Adult KW - Hyperlipidemia KW - Sjogren's Syndrome KW - Case Report KW - Liver Cirrhosis, Biliary KW - Female KW - Liver Transplantation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85212143?accountid=14244 LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Treatment of polymyositis and dermatomyositis. AN - 79554043; 2702045 JF - Current opinion in rheumatology AU - Dalakas, M AD - National Institutes of Health, Bethesda, Maryland. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 443 EP - 449 VL - 1 IS - 4 SN - 1040-8711, 1040-8711 KW - Adrenal Cortex Hormones KW - 0 KW - Immunosuppressive Agents KW - Prednisone KW - VB0R961HZT KW - Index Medicus KW - Adrenal Cortex Hormones -- therapeutic use KW - Muscular Diseases -- chemically induced KW - Prednisone -- therapeutic use KW - Humans KW - Immunosuppressive Agents -- therapeutic use KW - Adrenal Cortex Hormones -- adverse effects KW - Myositis -- drug therapy KW - Dermatomyositis -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79554043?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-11-08 N1 - Date created - 1990-11-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The Callimico goeldii (Primates, Platyrrhini) genome: karyology and middle repetitive (LINE-1) DNA sequences. AN - 79493393; 2560695 AB - Callimico goeldii (Goeldi's marmoset) is a neotropical primate with 2n = 47,X1X2Y in the male, and 2n = 48,X1X1X2X2 in the female, due to a Y-autosome translocation. Karyological comparisons of Callimico, Callithrix jacchus and Cebus apella suggest that Callimico is a member of the Callitrichidae. Isozyme data and restriction mapping of LINE-1 repetitive elements in these species and in a variety of other neotropical primates confirm these findings and supply strong evidence for including Callimico in the Callitrichidae. JF - Chromosoma AU - Seuánez, H N AU - Forman, L AU - Matayoshi, T AU - Fanning, T G AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, MD 21701. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 389 EP - 395 VL - 98 IS - 6 SN - 0009-5915, 0009-5915 KW - DNA Transposable Elements KW - 0 KW - Isoenzymes KW - Index Medicus KW - Karyotyping KW - Isoenzymes -- analysis KW - Animals KW - X Chromosome KW - Chromosome Banding KW - DNA Transposable Elements -- genetics KW - Translocation, Genetic KW - Callitrichinae -- classification KW - Callitrichinae -- genetics KW - Genomic Library UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79493393?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-04-23 N1 - Date created - 1990-04-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Protein kinase C mediates the effect of vasopressin in pituitary corticotrophs. AN - 79489950; 2560804 AB - The role of protein kinase C (PKC) on vasopressin (VP) action was investigated by inhibition of endogenous PKC using prolonged incubation of the cells with phorbol ester, and by direct measurement of PKC activity in pituitary cells. Preincubation of the cells for 6 h with 100 nM TPA at 37 C resulted in a 90% decrease in total PKC activity. In the PKC-depleted cells, cAMP responses to stimulation with 100 nM CRF for 30 min were normal, but the potentiating effects of VP and PMA on CRF-stimulated cAMP production were abolished. The stimulation of ACTH secretion by VP and PMA alone was also abolished in PKC- depleted cells. PKC activity in cytosolic and detergent-solubilized membrane fractions from enriched pituitary corticotrophs obtained by centrifugal elutriation, was directly measured by enzymatic assays and by immunoblotting techniques. Basal PKC activity was higher in the cytosol than in the membranes (8.43 +/- 0.47 and 1.93 +/- 0.11 pmol 32P incorporated/10 min, respectively). After incubation of the cells with VP for 15 min or [3H] phorbol-12-myristate-13-acetate (PMA) for 30 min, PKC activity in cytosol was decreased by 40% and 89%, respectively, while the activity in the membrane was increased by 138% and 405%, respectively. Such VP- and PMA-induced translocation of PKC was also observed when the enzyme content in the cytosol and the membranes was measured by immunoblotting using a specific anti-PKC antibody and [125I]protein A. Autoradiographic analysis of immunoblots revealed an 80 kilodalton band characteristic of PKC, with OD higher in the cytosolic than in the membrane fractions.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Molecular endocrinology (Baltimore, Md.) AU - Carvallo, P AU - Aguilera, G AD - Section of Endocrine Physiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 1935 EP - 1943 VL - 3 IS - 12 SN - 0888-8809, 0888-8809 KW - Phorbol Esters KW - 0 KW - Vasopressins KW - 11000-17-2 KW - Corticotropin-Releasing Hormone KW - 9015-71-8 KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinase C KW - EC 2.7.11.13 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Phorbol Esters -- pharmacology KW - Animals KW - Enzyme Activation KW - Cells, Cultured KW - Cyclic AMP -- metabolism KW - Female KW - Protein Kinase C -- antagonists & inhibitors KW - Pituitary Gland -- enzymology KW - Vasopressins -- pharmacology KW - Protein Kinase C -- physiology KW - Corticotropin-Releasing Hormone -- metabolism KW - Pituitary Gland -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79489950?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-04-25 N1 - Date created - 1990-04-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Similar carcinogenic actions of nitrosoalkylureas of varying structure given to rats by gavage. AN - 79482145; 2626762 AB - To relate the tumorigenic effects of directly acting alkylating nitrosoalkylureas to their chemical structure, a series of these compounds was given to F344 rats by gavage at approximately equimolar doses. In some cases, more than one dose rate was used. Potency, as measured by time to death with tumors, was similar for nitrosomethylurea and nitrosoethylurea, although the tumor pattern was different between the two. Nitrosoallylurea was of similar potency, and induced a spectrum of tumors similar to nitroethylurea. Nitroso-n-butyl-, n-amyl- and n-hexyl-ureas were less potent than nitrosoethylurea, but induced a similar pattern of tumors. All of the nitrosoureas induced tumors of the forestomach, usually in high incidence, except nitroso-2-hydroxypropylurea, which caused death of the rats with thymic lymphoma within 6 months. Nitroso-3-hydroxypropylurea was much less potent than its 2-isomer, but induced no tumors of the thymus and was the only one of this group to induce tumors of the glandular stomach. Only nitrosomethylurea induced a high incidence of tumors of the nervous system, but no mammary carcinomas, which most of the other nitrosoureas induced in high incidence in females. Tumors of the lung, duodenum, colon and intestines were induced by several of the compounds, more commonly in males than in females, but a high incidence of liver tumors was found only in rats of both sexes given nitroso-2-phenylethylurea. JF - Toxicology and industrial health AU - Lijinsky, W AU - Kovatch, R M AD - NCI-Frederick Cancer Research Facility, BRI-Basic Research Program, MD 21701. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 925 EP - 935 VL - 5 IS - 6 SN - 0748-2337, 0748-2337 KW - Nitrosourea Compounds KW - 0 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Duodenal Neoplasms -- chemically induced KW - Chemistry KW - Chemical Phenomena KW - Thymus Neoplasms -- chemically induced KW - Lymphoma -- chemically induced KW - Lung Neoplasms -- chemically induced KW - Colonic Neoplasms -- chemically induced KW - Male KW - Female KW - Neoplasms, Experimental -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79482145?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-04-12 N1 - Date created - 1990-04-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Etiology of retinoic acid-induced cleft palate varies with the embryonic stage. AN - 79476931; 2623642 AB - Retinoic acid (RA) has been shown to be teratogenic in many species, and 13-cis-RA is teratogenic in humans. Exposure to RA during embryonic morphogenesis produced a variety of malformations including limb defects and cleft palate. The type and severity of malformation depended on the stage of development exposed. The purpose of this study was to compare the effects of RA exposure in vivo on different stages of palate development. These results were compared to effects observed after exposure in organ culture. The vehicle used in RA dosing was also shown to be a major factor in the incidence of RA-induced cleft palate. For the in vivo studies, RA (100 mg/kg) in 10 ml corn oil/kg was given p.o. on gestation day (GD) 10 or 12, and the embryos were examined on GD 14 and 16. Exposure to RA in an oil:DMSO vehicle resulted in much higher incidences of cleft palate than were observed after dosing with RA in oil only. After exposure on GD 10, to RA, small palatal shelves formed which did not make contact and fuse on GD 14. The medial cells did not undergo programmed cell death. Instead, the medial cells differentiated into a stratified, squamous, oral-like epithelium. The RA-exposed medial cells did not incorporate 3H-TdR on GD 14 or 16, but the cells expressed EGF receptors and bound 125I-EGF. In contrast, RA-induced clefting after exposure on GD 12 did not involve growth inhibition. Shelves of normal size formed and made contact, but because of altered medial cell differentiation did not fuse. Medial cells differentiated into a pseudostratified, ciliated, nasal-like epithelium. This response was produced in vivo at exposure levels which produced cleft palate, and after exposure of palatal shelves to RA in vitro from GD 12-15. The medial cells exposed on GD 12 incorporated 3H-TdR on GD 14, expressed EGF receptors, and bound 125I-EGF. The responses to RA which lead to cleft palate differed after exposure on GD 10 or 12, and the pathways of differentiation which the medial cells followed depended on the developmental stage exposed. JF - Teratology AU - Abbott, B D AU - Harris, M W AU - Birnbaum, L S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 533 EP - 553 VL - 40 IS - 6 SN - 0040-3709, 0040-3709 KW - Pharmaceutical Vehicles KW - 0 KW - Tretinoin KW - 5688UTC01R KW - Epidermal Growth Factor KW - 62229-50-9 KW - Corn Oil KW - 8001-30-7 KW - Dimethyl Sulfoxide KW - YOW8V9698H KW - Index Medicus KW - Animals KW - Gestational Age KW - Mice, Inbred C57BL KW - Microscopy, Electron KW - Mice KW - Organ Culture Techniques KW - Epidermal Growth Factor -- metabolism KW - Cleft Palate -- chemically induced KW - Palate -- drug effects KW - Tretinoin -- toxicity KW - Palate -- embryology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79476931?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-29 N1 - Date created - 1990-03-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Studies on covalent binding of (-)trans-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene metabolites to cytochromes P-450 LM2 and LM4 and NADPH-cytochrome P-450 reductase. AN - 79460693; 2515665 AB - 1. Metabolism of 14C-labelled benzo[a]pyrene (-)trans-7,8-dihydrodiol to protein- and DNA-binding products in a reconstituted enzyme system proceeds 5 to 10 times faster with rabbit cytochrome P-450 LM4 than with LM2. 2. Either cytochrome converts the substrate to ethyl acetate- and water-soluble metabolites, identified by h.p.l.c. Water-soluble metabolites comprise 78% of the total products with cytochrome P-450 LM2, but only 50% of those formed by LM4. The relative proportion of the two types of metabolites is differentially affected by certain modifiers such as 7,8-benzoflavone. 3. Half of the radioactivity in the aqueous phase of reaction mixtures containing cytochrome P-450 LM4 represents (-)trans-7,8-diol metabolites in complex primarily with NADPH and phosphate. The remaining water-soluble products are bound covalently to proteins in the reconstituted system. 4. Polyacrylamide gel electrophoresis, autoradiography, and measurement of the radioactivity in individual bands indicate that a larger fraction of metabolites is bound to cytochrome P-450 LM4 than to NADPH-cytochrome P-450 reductase, and only marginal binding to cytochrome P-450 LM2 is seen. Metabolite binding to added DNA is likewise substantially greater in magnitude when cytochrome P-450 LM4, as opposed to LM2, catalyses (-)trans-7,8-diol oxygenation. Thus, the degree of metabolite binding to monoxygenase proteins and to DNA correlates well with the catalytic activity of cytochrome P-450 LM4 and LM2 towards (-)trans-7,8-diol. 5. DNA causes a dramatic enhancement in the activity of cytochrome P-450 LM4 with (-)trans-7,8-diol, indicating that the cytochrome and/or the reductase may be functionally impaired by metabolites of this substrate. Such an effect may alter the balance between detoxication and activation of the carcinogenic benzo[a]pyrene. JF - Xenobiotica; the fate of foreign compounds in biological systems AU - Deutsch, J AU - Vatsis, K P AU - Leutz, J C AU - Coon, M J AU - Gelboin, H V AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 1421 EP - 1435 VL - 19 IS - 12 SN - 0049-8254, 0049-8254 KW - Benzoflavones KW - 0 KW - Dihydroxydihydrobenzopyrenes KW - Deoxycholic Acid KW - 005990WHZZ KW - alpha-naphthoflavone KW - 604-59-1 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - NADPH-Ferrihemoprotein Reductase KW - EC 1.6.2.4 KW - Index Medicus KW - Animals KW - Stereoisomerism KW - Deoxycholic Acid -- pharmacology KW - Biotransformation KW - DNA -- metabolism KW - In Vitro Techniques KW - Rabbits KW - Protein Binding KW - Chromatography, High Pressure Liquid KW - Catalysis KW - Benzoflavones -- pharmacology KW - Microsomes, Liver -- enzymology KW - Microsomes, Liver -- drug effects KW - NADPH-Ferrihemoprotein Reductase -- metabolism KW - Cytochrome P-450 Enzyme System -- metabolism KW - Dihydroxydihydrobenzopyrenes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79460693?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-08 N1 - Date created - 1990-03-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A study of the interaction of the alkylating agent, NIH10236, with opioid receptors in vitro and in vivo. AN - 79452662; 2559348 AB - The series of experiments reported in this paper examined the spectrum of subtypes of opioid receptors alkylated in vitro by N-cyclopropylmethyl-7 alpha-methylfumaramido-6,14- endoethenotetrahydronororipavine (NIH10236) and four optical isomers of the methylfumaramidophenethyl derivatives of 3-methylfentanyl. Pretreatment of membranes with NIH10236 resulted in a wash-resistant inhibition of the binding of [3H]6 beta-fluoro-6-desoxyoxymorphone (mu binding sites), the binding of [3H][D-ala2,D-leu5]-enkephalin (both the higher and lower affinity delta binding sites) and was without effect on kappa binding sites labelled with [3H]bremazocine. All four potential alkylating derivatives of 3-methylfentanyl were inactive. Pretreatment of membranes with 1 microM of the reversible ligands, (+)-cis-3-methylfentanyl, but not its enantiomer, inhibited the binding of [3H]6 beta-fluoro-6-desoxyoxymorphone and the binding of [3H][D-ala2,D-leu5]enkephalin to the lower affinity binding sites by over 90%. This phenomenon is termed "pseudo-irreversible inhibition." Incubation of pretreated membranes for 60 min at 37 degrees C, in the presence of 200 mM NaCl and 50 microM GppNHp, only partially reversed the masking of opioid receptors by (+)-cis-3-methylfentanyl. For in vivo experiments, membranes were prepared 18-24 hr after the intracerebroventricular administration of 80 and 50 micrograms of NIH10236. This resulted in decreased labelling of mu binding sites, lower affinity [3H][D-ala2,D-leu5]enkephalin binding sites, as well as kappa binding sites, labelled by [3H]U69,593 and [3H]bremazocine. There was no apparent alteration in the higher affinity [3H][D-ala2,D-leu5]enkephalin binding site.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Neuropharmacology AU - Rothman, R B AU - Long, J B AU - Holaday, J W AU - Bykov, V AU - de Costa, B R AU - Kim, C H AU - Jacobson, A E AU - Rice, K C AD - Unit on Receptor Studies, LCS, NIMH, Bethesda, Maryland 20892. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 1349 EP - 1356 VL - 28 IS - 12 SN - 0028-3908, 0028-3908 KW - Alkylating Agents KW - 0 KW - Ligands KW - Receptors, Opioid KW - Thebaine KW - 2P9MKG8GX7 KW - NIH 10236 KW - 88167-37-7 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - In Vitro Techniques KW - Membranes -- metabolism KW - Male KW - Receptors, Opioid -- metabolism KW - Alkylating Agents -- metabolism KW - Thebaine -- metabolism KW - Receptors, Opioid -- classification KW - Thebaine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79452662?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-06 N1 - Date created - 1990-03-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A note on approximating the cumulative distribution function of the time to tumor onset in multistage models. AN - 79432090; 2611323 AB - The general multistage theory of carcinogenesis is a very special type of interconnected birth and death process in which the final state is absorbing and all states except the first one are empty at time zero. An approximation proposed by Whittemore and Keller (1978, SIAM Review 20, 1-30) is assessed. It is shown that the adequacy of this approximation depends on the number of malignant cells resulting from a single normal cell. If more than one malignant cell is likely to occur, the approximation will fail. JF - Biometrics AU - Kopp, A AU - Portier, C J AD - Biomathematics Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 1259 EP - 1263 VL - 45 IS - 4 SN - 0006-341X, 0006-341X KW - Index Medicus KW - Animals KW - Biometry KW - Cocarcinogenesis KW - Time Factors KW - Neoplasms, Experimental -- etiology KW - Models, Statistical KW - Models, Biological UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79432090?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-12 N1 - Date created - 1990-03-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Relation of arsenic exposure to lung cancer among tin miners in Yunnan Province, China. AN - 79427393; 2611163 AB - The relation of mining and smelting exposure to arsenic and lung cancer was studied among tin miners in Yunnan Province in the People's Republic of China. Interviews were conducted in 1985 with 107 living tin miners who had lung cancer and an equal number of age matched controls from among tin miners without lung cancer to obtain information on risk factors for lung cancer including detailed history of employment and tobacco use. Occupational history was combined with industrial hygiene data to estimate cumulative arsenic exposure. Similar methods were also used to estimate radon exposure for simultaneous evaluation in this analysis. The results indicate that subjects in the highest quarter of cumulative arsenic exposure have a relative risk of 22.6 compared with subjects without exposure after adjusting for tobacco and radon exposure, and a positive dose response relation was observed. Simultaneous evaluation of arsenic and tobacco exposure indicates a greater risk for arsenic, whereas simultaneous assessment of arsenic and radon exposure suggests radon to be the greater risk. There is no evidence of synergism between arsenic and tobacco exposure. Among arsenic exposed individuals, cases of lung cancer have longer duration but lower average intensity of arsenic exposure than controls, indicating that duration of exposure to arsenic may be more important than intensity in the aetiology of lung cancer. Finally, risk of lung cancer among workers exposed to arsenic only in mining is only slightly less than for miners whose exposure to arsenic was limited to smelting, although risks are highest when workers were exposed to both mining and smelting. JF - British journal of industrial medicine AU - Taylor, P R AU - Qiao, Y L AU - Schatzkin, A AU - Yao, S X AU - Lubin, J AU - Mao, B L AU - Rao, J Y AU - McAdams, M AU - Xuan, X Z AU - Li, J Y AD - Division of Cancer Prevention and Control, National Cancer Institute, Bethesda, MD. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 881 EP - 886 VL - 46 IS - 12 SN - 0007-1072, 0007-1072 KW - Tin KW - 7440-31-5 KW - Arsenic KW - N712M78A8G KW - Index Medicus KW - Aged, 80 and over KW - Humans KW - China -- epidemiology KW - Adult KW - Aged KW - Middle Aged KW - Male KW - Arsenic -- adverse effects KW - Lung Neoplasms -- epidemiology KW - Occupational Diseases -- epidemiology KW - Mining KW - Lung Neoplasms -- chemically induced KW - Occupational Diseases -- chemically induced KW - Metallurgy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79427393?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-26 N1 - Date created - 1990-02-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Environ Health Perspect. 1977 Aug;19:127-30 [908288] S Afr Med J. 1969 Oct 25;43(43):1307-12 [4310754] J Natl Cancer Inst. 1969 Jun;42(6):1045-52 [5797547] J Occup Med. 1977 Nov;19(11):754-8 [915570] Yale J Biol Med. 1988 May-Jun;61(3):183-93 [3051699] Arch Environ Health. 1978 Nov-Dec;33(6):325-31 [736617] Scand J Work Environ Health. 1981 Dec;7(4):302-9 [7347915] Am J Epidemiol. 1987 Jun;125(6):929-38 [3578251] Br J Ind Med. 1978 Feb;35(1):8-15 [629894] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 14-day and 90-day toxicity studies of C.I. Pigment Red 3 in Fischer 344 rats and B6C3F1 mice. AN - 79416934; 2606409 AB - Treatment of F344 rats and B6C3F1 mice with C.I. Pigment Red 3 in the diet (10, 5.0, 2.5, 1.25, 0.6 or 0.3%) for 14 and 90 days resulted in haematological alterations consistent with haemolytic anaemia. Rats appeared to be more sensitive than mice to the haematological effects. Histological lesions were observed in rats and mice after exposure for 90 days. Target organs in the rat were the spleen, bone marrow, liver and kidney. Lesions in the spleen consisted of a haematopoietic cell proliferation, iron-positive pigment and congestion of the red pulp, and inflammation of the splenic capsule. Changes in the livers of rats consisted of haematopoietic cell proliferation and iron-positive pigment in Kupffer cells. Haematopoietic cell proliferation also occurred in the bone marrow of treated rats. The presence of iron-positive pigment and a slightly increased incidence of protein casts were seen in the kidney. Target organs in mice were the spleen, liver and kidney. Histological lesions in mice after exposure for 90 days included increased haematopoietic cell proliferation in the liver and spleen, and iron-positive pigment in the spleen. Mild cytomegaly of the renal tubular epithelia was also observed in exposed mice. JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association AU - Morgan, D L AU - Jameson, C W AU - Mennear, J H AU - Prejean, J D AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 793 EP - 800 VL - 27 IS - 12 SN - 0278-6915, 0278-6915 KW - Azo Compounds KW - 0 KW - Coloring Agents KW - toluidine red KW - 2425-85-6 KW - Index Medicus KW - Animals KW - Sex Factors KW - Anemia -- chemically induced KW - Kidney -- drug effects KW - Mice KW - Rats KW - Rats, Inbred F344 KW - Liver -- drug effects KW - Body Weight -- drug effects KW - Spleen -- drug effects KW - Time Factors KW - Species Specificity KW - Bone Marrow -- drug effects KW - Female KW - Male KW - Organ Size -- drug effects KW - Coloring Agents -- toxicity KW - Azo Compounds -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79416934?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-14 N1 - Date created - 1990-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Morphologic characterization of alveolar macrophages from subjects with occupational exposure to inorganic particles. AN - 79411944; 2557785 AB - Alveolar macrophages recovered by bronchoalveolar lavage from 43 nonsmoking or greater than 5-yr ex-smoking subjects with occupational exposure to inorganic particles (asbestos, n 1/2 19; silica, n 1/2 10; coal, n 1/2 14) were evaluated by light microscopy and transmission and scanning electron microscopy to determine the morphologic changes resulting in these cells from chronic inorganic particulate inhalation. Alveolar macrophages from dust-exposed subjects, including those who had been free of exposure to particles for more than 1 yr, contained particles of higher proportion than did those of normal unexposed subjects. Most of these particles were located within phagolysosomes. The frequency of multinucleated alveolar macrophages was significantly higher in the dust-exposed groups. Ultrastructural studies showed alterations of the morphologic aspects of the surfaces of alveolar macrophages from the dust-exposed subjects, including increased numbers of rufflings, filopodia, pinocytotic vesicles, subplasmalemmal linear densities, and increased frequency of macrophage-macrophage and macrophage-lymphocyte interactions. Furthermore, the numbers of lysosomes were significantly increased in alveolar macrophages from the dust-exposed subjects. Together, these morphologic changes are consistent with the sequelae of phagocytosis, and they emphasize both the role of alveolar macrophages in eliminating inorganic particles from the alveolar spaces and the consequences this role has in alveolar macrophage activation. JF - The American review of respiratory disease AU - Takemura, T AU - Rom, W N AU - Ferrans, V J AU - Crystal, R G AD - Pathology Branch, National Heart, Lung and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 1674 EP - 1685 VL - 140 IS - 6 SN - 0003-0805, 0003-0805 KW - Air Pollutants, Occupational KW - 0 KW - Coal KW - Dust KW - Asbestos KW - 1332-21-4 KW - Silicon Dioxide KW - 7631-86-9 KW - Abridged Index Medicus KW - Index Medicus KW - Cell Nucleus -- ultrastructure KW - Humans KW - Adult KW - Middle Aged KW - Bronchoalveolar Lavage Fluid -- cytology KW - Organelles -- ultrastructure KW - Dust -- analysis KW - Air Pollutants, Occupational -- adverse effects KW - Pulmonary Alveoli -- cytology KW - Macrophages -- ultrastructure KW - Dust -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79411944?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-29 N1 - Date created - 1990-01-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The use of chemotherapy in metastatic breast cancer. AN - 79410960; 2481671 AB - Recurrent breast cancer is incurable. Chemotherapeutic agents will be used in most patients with metastatic disease at some time during their course. There is little evidence that such agents prolong survival, and their toxicities are not inconsiderable. The focus of treatment should be on the palliation of symptoms. Single-agent regimens should not be assumed to be less effective than combinations, particularly as salvage therapies. Some new approaches to the management of metastatic disease are explored. JF - Hematology/oncology clinics of North America AU - Garber, J E AU - Henderson, I C AD - Clinical Epidemiology Branch, National Cancer Institute, Boston, Massachusetts. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 807 EP - 821 VL - 3 IS - 4 SN - 0889-8588, 0889-8588 KW - Antineoplastic Agents KW - 0 KW - Hormone Antagonists KW - Immunologic Factors KW - Index Medicus KW - Drug Evaluation KW - Randomized Controlled Trials as Topic KW - Combined Modality Therapy KW - Immunologic Factors -- therapeutic use KW - Humans KW - Hormone Antagonists -- therapeutic use KW - Neoplasm Metastasis KW - Quality of Life KW - Drug Resistance KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Female KW - Remission Induction KW - Breast Neoplasms -- drug therapy KW - Breast Neoplasms -- pathology KW - Palliative Care KW - Breast Neoplasms -- therapy KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79410960?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-13 N1 - Date created - 1990-02-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The acute administration of vasodilators in primary pulmonary hypertension. Experience from the National Institutes of Health Registry on Primary Pulmonary Hypertension. AN - 79410637; 2690706 AB - The hemodynamic responses to acute vasodilator administration were evaluated in 163 patients who were entered into the National Institutes of Health Registry on Primary Pulmonary Hypertension (PPH) between 1981 and 1985. Of a total of 491 drug administrations in these patients, 135 administrations in 104 patients were performed in a manner acceptable to the Registry. A single vasodilator was tried in 79 patients and more than one vasodilator in 25 patients. Two-thirds of the patients were in New York Heart Association Functional Classes III or IV. When the effects of all vasodilators were grouped together, there were significant decreases from baseline in mean pulmonary artery pressure (60 +/- 2 to 57 +/- 2 mm Hg, p less than 0.05) and total pulmonary resistance index (32.5 +/- 1.7 to 25.1 +/- 1.4 mm Hg/L/min/m2, p less than 0.0001), and increases in cardiac index (2.1 +/- 0.1 to 2.7 +/- 0.1 L/min/m2, p less than 0.0001). Mean systemic blood pressure fell (88 +/- 1 to 79 +/- 1 mm Hg, p less than 0.0001), whereas PaO2 was unchanged (70 +/- 3 to 71 +/- 3 mm Hg, p = NS). A fall in total pulmonary resistance greater than 20% was observed in 55% of the adequate drug trials. Adverse effects occurred in 32 of the total 491 patient-drug trials and were generally minor. Hypotension requiring treatment developed in six patients. There were two deaths attributable to vasodilator administration. Patients who died or had hypotension requiring treatment had higher right atrial pressures than did other treated patients (15 +/- 2 versus 9 +/- 1 mm Hg, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS) JF - The American review of respiratory disease AU - Weir, E K AU - Rubin, L J AU - Ayres, S M AU - Bergofsky, E H AU - Brundage, B H AU - Detre, K M AU - Elliott, C G AU - Fishman, A P AU - Goldring, R M AU - Groves, B M AD - Division of Lung Diseases, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 1623 EP - 1630 VL - 140 IS - 6 SN - 0003-0805, 0003-0805 KW - Vasodilator Agents KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Multicenter Studies as Topic KW - Humans KW - Pulmonary Circulation -- drug effects KW - Vascular Resistance -- drug effects KW - Child KW - Blood Pressure -- drug effects KW - Cardiac Output -- drug effects KW - Adolescent KW - Hypertension, Pulmonary -- drug therapy KW - Hypertension, Pulmonary -- physiopathology KW - Vasodilator Agents -- adverse effects KW - Vasodilator Agents -- administration & dosage KW - Vasodilator Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79410637?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-29 N1 - Date created - 1990-01-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Toxicology of chemical mixtures: experimental approaches, underlying concepts, and some results. AN - 79404642; 2690403 AB - The toxicology of chemical mixtures will be the toxicology of the 1990s and beyond. While this branch of toxicology most closely reflects the actual human exposure situation, there is yet no standard protocol or consensus methodology for investigating the toxicology of mixtures. Thus, in this emerging science, experimentation is required just to develop a broadly applicable evaluation system. Several examples are discussed to illustrate the different experimental designs and the concepts behind each. These include the health effects studies of Love Canal soil samples, the Lake Ontario Coho salmon, the water samples repurified from secondary sewage in the city of Denver Potable Water Reuse Demonstration Plant, and the National Toxicology Program (NTP) effort on a mixture of 25 frequently detected groundwater contaminants derived from hazardous waste disposal sites. In the last instance, an extensive research program has been ongoing for the last 2 years at the NTP, encompassing general toxicology, immunotoxicology, developmental and reproductive toxicology, biochemical toxicology, myelotoxicology, genetic toxicology, neurobehavioral toxicology, and hepato- and renal toxicology. JF - Toxicology letters AU - Yang, R S AU - Hong, H L AU - Boorman, G A AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 183 EP - 197 VL - 49 IS - 2-3 SN - 0378-4274, 0378-4274 KW - Environmental Pollutants KW - 0 KW - Water Pollutants KW - Water Pollutants, Chemical KW - Index Medicus KW - Salmon KW - Rats KW - Animals KW - Public Health KW - Mice KW - Research Design KW - Water Pollutants -- toxicity KW - Environmental Pollutants -- toxicity KW - Water Pollutants, Chemical -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79404642?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-01 N1 - Date created - 1990-02-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Site-directed mutagenesis of m1 muscarinic acetylcholine receptors: conserved aspartic acids play important roles in receptor function. AN - 79404152; 2557534 AB - Muscarinic acetylcholine receptors contain a region encompassing the second and third transmembrane domains that is rich in conserved aspartic acid residues. To investigate the role of four conserved aspartic acids at positions 71, 99, 105, and 122 in muscarinic receptor function, point mutations in the rat m1 muscarinic receptor gene were made that converted each Asp to Asn, and wild type or mutant genes were stably expressed in Chinese hamster ovary cells that normally lack muscarinic receptors. Substitution of Asp71 or Asp122 with Asn produced mutant receptors that displayed high affinity for carbachol but decreased efficacy and potency, respectively, in agonist-induced activation of phosphoinositide hydrolysis, suggesting that these residues may mediate receptor-GTP binding protein interactions. Substitution of Asp99 or Asp105 with Asn produced marked decreases in ligand binding affinities and/or covalent incorporation of [3H] propylbenzilylcholine mustard, suggesting that these residues may be involved in receptor-ligand interactions. JF - Molecular pharmacology AU - Fraser, C M AU - Wang, C D AU - Robinson, D A AU - Gocayne, J D AU - Venter, J C AD - Section of Receptor Biochemistry and Molecular Biology, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 840 EP - 847 VL - 36 IS - 6 SN - 0026-895X, 0026-895X KW - Phosphatidylinositols KW - 0 KW - Receptors, Muscarinic KW - Aspartic Acid KW - 30KYC7MIAI KW - Propylbenzilylcholine Mustard KW - 36167-80-3 KW - Pirenzepine KW - 3G0285N20N KW - Quinuclidinyl Benzilate KW - 6581-06-2 KW - otenzepad KW - OM7J0XAL0S KW - Index Medicus KW - Rats KW - Phosphatidylinositols -- metabolism KW - Animals KW - Pirenzepine -- metabolism KW - Quinuclidinyl Benzilate -- metabolism KW - Pirenzepine -- analogs & derivatives KW - Propylbenzilylcholine Mustard -- metabolism KW - Mutation KW - Structure-Activity Relationship KW - Cricetinae KW - Aspartic Acid -- physiology KW - Receptors, Muscarinic -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79404152?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-31 N1 - Date created - 1990-01-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selective inhibition of polymorphonuclear neutrophil activity by 2,3,7,8-tetrachlorodibenzo-p-dioxin. AN - 79403986; 2557688 AB - Although the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), via its interaction with the Ah receptor, is an extremely potent carcinogen and immunosuppressive agent in experimental animals, its possible actions on polymorphonuclear (PMN) function have not been determined. In addition to their importance against infectious organisms, PMNs have been implicated in antitumor resistance. The present studies examined the effects of in vivo exposure to TCDD on PMN function in B6C3F1 (TCDD sensitive, presence of high affinity Ah receptor) and DBA/2N (TCDD resistant at low doses, defective Ah receptor) mice. Animals received a single oral exposure of 5 or 10 micrograms/kg of TCDD and PMNs were obtained 5 days later from the peritoneal cavity following elicitation with sodium caseinate. TCDD reduced the cytolytic and cytostatic activity of PMA-activated PMNs in B6C3F1, but not in DBA/2N mice, suggesting that this response segregates with the Ah locus. Furthermore, TCDD was found to bind specifically to PMNs from Ah-responsive mice. Neither the production of superoxide and hydrogen peroxide nor degranulation, the latter measured by beta-glucuronidase release, was impaired. Supernatants recovered from PMN cell cultures of TCDD-sensitive mice, but not from resistant DBA/2N mice, showed reduced killing capacity for actinomycin D-treated L929 tumor cells, while their ability to bind to tumor cells was not altered. These data suggest that TCDD interferes with PMN-mediated tumor cell killing by altering the production or secretion of a cytolytic factor. Examination of bone marrow stem cells revealed that granulocytic but not monocytic colonies were reduced after TCDD exposure in vivo and in vitro. Although mature PMNs had detectable levels of Ah receptor, exposure in vitro of these cells to TCDD had no effect on antitumor activity. Thus, it is possible that TCDD may affect PMNs at the level of hematopoiesis, via a direct interaction with granulocyte precursor cells, or modulate PMNs at different stages of maturation. JF - Toxicology and applied pharmacology AU - Ackermann, M F AU - Gasiewicz, T A AU - Lamm, K R AU - Germolec, D R AU - Luster, M I AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences/NIH Research, Triangle Park, North Carolina 27709. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 470 EP - 480 VL - 101 IS - 3 SN - 0041-008X, 0041-008X KW - Dioxins KW - 0 KW - Polychlorinated Dibenzodioxins KW - Receptors, Aryl Hydrocarbon KW - Receptors, Drug KW - Superoxides KW - 11062-77-4 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Glucuronidase KW - EC 3.2.1.31 KW - Index Medicus KW - Animals KW - Tumor Cells, Cultured -- drug effects KW - Glucuronidase -- metabolism KW - Hydrogen Peroxide -- metabolism KW - Hematopoietic Stem Cells -- cytology KW - Mice KW - Receptors, Drug -- physiology KW - Killer Cells, Natural -- drug effects KW - Mice, Inbred DBA KW - Binding Sites KW - Hematopoietic Stem Cells -- drug effects KW - Superoxides -- metabolism KW - Cell Survival -- drug effects KW - Receptors, Drug -- drug effects KW - Mice, Inbred C3H KW - Mice, Inbred C57BL KW - Colony-Forming Units Assay KW - Neutrophils -- drug effects KW - Neutrophils -- immunology KW - Polychlorinated Dibenzodioxins -- toxicity KW - Neutrophils -- physiology KW - Dioxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79403986?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-08 N1 - Date created - 1990-02-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Spontaneous EEG changes during tobacco abstinence and nicotine substitution in human volunteers. AN - 79401160; 2600826 AB - Electroencephalographic correlates of tobacco abstinence and nicotine substitution were measured in adult male cigarette smokers in residence on a research ward in two experiments. After ad libitum smoking, seven subjects were deprived of nicotine for 10 days and then resumed smoking. During tobacco abstinence, there were significant decreases in alpha frequency and beta frequency and increases in theta power. These effects were observed as early as 29 hr and in some instances persisted for 7 days. In the second experiment, a group of eight heavy smokers chewed 12 pieces of either placebo or nicotine-containing polacrilex gum (2 or 4 mg) per day while deprived of cigarettes. In the placebo condition, electroencephalographic signs were similar to those accompanying tobacco deprivation in the first experiment. Administration of nicotine polacrilex prevented the appearance of these tobacco withdrawal signs. This study provides new information on the time course of certain electrophysiologic components of the tobacco withdrawal syndrome and confirms that the effects are specific to the deprivation of nicotine. The data also suggest that the 4-mg polacrilex was more effective than the 2-mg dose when the results across all measures were considered. JF - The Journal of pharmacology and experimental therapeutics AU - Pickworth, W B AU - Herning, R I AU - Henningfield, J E AD - National Institute on Drug Abuse Addiction Research Center, Baltimore, Maryland. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 976 EP - 982 VL - 251 IS - 3 SN - 0022-3565, 0022-3565 KW - Nicotine KW - 6M3C89ZY6R KW - Index Medicus KW - Humans KW - Adult KW - Male KW - Smoking -- physiopathology KW - Substance Withdrawal Syndrome -- physiopathology KW - Nicotine -- pharmacology KW - Electroencephalography UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79401160?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-30 N1 - Date created - 1990-01-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The sequential development of cancer: a morphological perspective. AN - 79400647; 2690406 AB - Cancer development proceeds through sequential or contemporaneous morphological changes from normal, preneoplastic, and premalignant lesions to highly malignant neoplasms. The morphological continuum that comprises cancer development is usually divided into diagnostic categories of hyperplasia (or dysplasia), benign neoplasia, and malignant neoplasia based on perceived biological behavior. Although a morphological continuum may be evident from the histological evaluation of preneoplastic and neoplastic lesions, it is not axiomatic that all preneoplastic or benign lesions progress. The probability of regression or progression from one category to another, or the rates at which these might occur, are seldom known for spontaneous or induced neoplasms. Host factors as well as exogenous stimuli may influence these events. The concept of neoplastic progression and the limitations of our knowledge of the biological behavior of preneoplastic lesions and benign neoplasms are important considerations in the interpretation of pathology data from carcinogenicity studies. JF - Toxicology letters AU - Eustis, S L AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 267 EP - 281 VL - 49 IS - 2-3 SN - 0378-4274, 0378-4274 KW - Index Medicus KW - Rats KW - Animals KW - Carcinogenicity Tests KW - Hyperplasia -- pathology KW - Neoplasms, Experimental -- pathology KW - Precancerous Conditions -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79400647?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-01 N1 - Date created - 1990-02-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Triggers for higher-order toxicity testing. AN - 79400593; 2690402 AB - Strategies for selecting chemicals for definitive, higher-order toxicology tests are important because physical and personnel resources are limited and chemicals vary widely in the need for testing. The National Toxicology Program has developed strategies for selection of chemicals for definitive tests in several areas of toxicology. In addition to the number of people, the extent of human exposure, structure-activity considerations, and reports of observations in humans, specific triggers are sought from animal studies and short-term tests or in vitro screens which impact the chemical selection process and the design of definitive studies. Specific triggers in reproductive toxicology, for example, include observations in prechronic toxicology studies in rats and mice--weights and histopathologic examinations of reproductive organs, measurements of sperm production and function in males, and estrus cyclicity in females. Comparable tissue-specific triggers do not exist for developmental toxicity studies, and screening tests are not widely used for setting priorities for the conduct of definitive developmental toxicology studies. JF - Toxicology letters AU - Schwetz, B A AU - Morrissey, R E AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 171 EP - 179 VL - 49 IS - 2-3 SN - 0378-4274, 0378-4274 KW - Index Medicus KW - Rats KW - Animals KW - Mutagenicity Tests KW - Carcinogenicity Tests KW - Mice KW - Male KW - Female KW - Drug Evaluation, Preclinical KW - Toxicology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79400593?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-01 N1 - Date created - 1990-02-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cooperation of c-raf-1 and c-myc protooncogenes in the neoplastic transformation of simian virus 40 large tumor antigen-immortalized human bronchial epithelial cells. AN - 79398712; 2557616 AB - Overexpression of c-raf-1 and the myc family of protooncogenes is primarily associated with small cell carcinoma, which accounts for approximately 25% of human lung cancer. To determine the functional significance of the c-raf-1 and/or c-myc gene expression in lung carcinogenesis and to delineate the relationship between protooncogene expression and tumor phenotype, we introduced both protooncogenes, alone or in combination, into human bronchial epithelial cells. Two retroviral recombinants, pZip-raf and pZip-myc, containing the complete coding sequences of the human c-raf-1 and murine c-myc genes, respectively, were constructed and transfected into simian virus 40 large tumor antigen-immortalized bronchial epithelial cells (BEAS-2B); this was followed by selection for G418 resistance. BEAS-2B cells expressing both the transfected c-raf-1 and c-myc sequences formed large cell carcinomas in athymic nude mice with a latency of 4-21 weeks, whereas either pZip-raf- or pZip-myc-transfected cells were nontumorigenic after 12 months. Cell lines established from tumors (designated RMT) revealed the presence of the cotransfected c-raf-1 and c-myc sequences and expressed morphological, chromosomal, and isoenzyme markers, which identified BEAS-2B cells as the progenitor line of the tumors. A significant increase in the mRNA levels of neuron-specific enolase was detected in BEAS-2B cells containing both the c-raf-1 and c-myc genes and derived tumor cell lines. The data demonstrate that the concomitant expression of the c-raf and c-myc protooncogenes causes neoplastic transformation of human bronchial epithelial cells resulting in large cell carcinomas with certain neuroendocrine markers. The presented model system should be useful in studies of molecular events involved in multistage lung carcinogenesis. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Pfeifer, A M AU - Mark, G E AU - Malan-Shibley, L AU - Graziano, S AU - Amstad, P AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 10075 EP - 10079 VL - 86 IS - 24 SN - 0027-8424, 0027-8424 KW - Antigens, Polyomavirus Transforming KW - 0 KW - Proto-Oncogene Proteins KW - Proto-Oncogene Proteins c-myc 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 - Animals KW - Humans KW - Gene Expression KW - Mice KW - Mice, Nude KW - Molecular Weight KW - Neoplasm Transplantation KW - Chimera KW - Bronchi KW - Transfection KW - Blotting, Southern KW - Transplantation, Heterologous KW - Epithelium KW - Cell Line KW - Immunoassay KW - Protein-Tyrosine Kinases -- genetics KW - Simian virus 40 -- genetics KW - Proto-Oncogene Proteins -- isolation & purification KW - Proto-Oncogenes KW - Proto-Oncogene Proteins -- genetics KW - Antigens, Polyomavirus Transforming -- genetics KW - Simian virus 40 -- immunology KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79398712?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-01 N1 - Date created - 1990-02-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Virol. 1980 Oct;36(1):62-78 [6160263] Mol Carcinog. 1988;1(3):151-60 [2855021] Mol Cell Biol. 1983 Feb;3(2):280-9 [6300662] Cancer Res. 1983 Jun;43(6):2806-11 [6303568] Nature. 1983 Jun 2-8;303(5916):401-6 [6304522] Nature. 1983 Aug 18-24;304(5927):596-602 [6308472] Science. 1983 Nov 18;222(4625):765-71 [6356357] Nature. 1983 Nov 10-16;306(5939):194-6 [6646201] Proc Natl Acad Sci U S A. 1984 Jan;81(1):71-5 [6320174] Cell. 1984 May;37(1):151-8 [6609772] Cell. 1984 Jun;37(2):521-8 [6327072] Biochem Biophys Res Commun. 1984 Jul 18;122(1):340-4 [6743336] Cell. 1984 Jul;37(3):1053-62 [6331674] J Natl Cancer Inst. 1984 Oct;73(4):801-7 [6148444] Cell. 1984 Oct;38(3):627-37 [6488314] Cancer Res. 1985 Jan;45(1):272-5 [2578097] Science. 1985 Mar 8;227(4691):1250-2 [2579430] Cancer Res. 1985 Jun;45(6):2913-23 [2985257] Cancer Res. 1985 Jun;45(6):2924-30 [2985258] Nucleic Acids Res. 1985 Mar 11;13(5):1431-42 [2987824] Virology. 1985 Oct 15;146(1):78-89 [2994296] Nature. 1985 Nov 7-13;318(6041):69-73 [2997622] Nature. 1985 Dec 19-1986 Jan 1;318(6047):667-70 [4079980] Cancer Res. 1986 Mar;46(3):1530-4 [3002619] Nucleic Acids Res. 1986 Jan 24;14(2):1009-15 [3003687] J Cell Biochem. 1986;30(3):195-218 [3084503] J Clin Invest. 1986 Aug;78(2):525-32 [3016030] Cancer Res. 1987 Apr 15;47(8):2148-55 [3030544] Mol Cell Biol. 1987 May;7(5):2031-4 [3037341] Science. 1987 Aug 28;237(4818):1036-9 [3616624] Science. 1987 Aug 28;237(4818):1039-41 [3616625] N Engl J Med. 1987 Oct 8;317(15):929-35 [3041218] Nature. 1987 Oct 1-7;329(6138):451-4 [2821400] Cancer. 1987 Dec 1;60(11):2669-74 [3677003] Cancer Res. 1987 Dec 1;47(23):6236-42 [2824028] Eur J Immunol. 1987 Oct;17(10):1491-8 [3119352] Cancer Res. 1988 Apr 1;48(7):1904-9 [2450641] Oncogene. 1988 Feb;2(2):187-93 [3285297] Am J Pathol. 1988 Jun;131(3):444-51 [3381877] Cell. 1988 Jun 17;53(6):857-67 [2454746] Science. 1988 Jul 15;241(4863):353-7 [2838909] Cell. 1988 Jul 15;54(2):275-83 [2839300] Am J Pathol. 1988 Jul;132(1):13-7 [2456019] Cancer Res. 1988 Aug 15;48(16):4689-94 [3293776] Adv Biochem Psychopharmacol. 1988;44:45-55 [3041752] Cancer Res. 1988 Sep 15;48(18):5163-6 [2842046] Proc Natl Acad Sci U S A. 1988 Sep;85(17):6523-7 [2842776] Cancer Res. 1988 Oct 15;48(20):5738-41 [3048648] Proc Natl Acad Sci U S A. 1988 Nov;85(22):8506-10 [2847163] Proc Natl Acad Sci U S A. 1988 Dec;85(23):8855-9 [3057494] Oncogene Res. 1988;3(1):99-103 [2905034] Mol Cell Biol. 1988 Aug;8(8):3373-81 [2850489] Oncogene Res. 1988;3(4):401-8 [3067190] Science. 1989 Mar 10;243(4896):1354-6 [2466340] Mol Cell Biol. 1989 Jan;9(1):67-73 [2784537] Cell. 1989 May 5;57(3):379-92 [2541911] Science. 1982 Jan 8;215(4529):181-2 [6274023] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sensitization, kindling, and anticonvulsants in mania. AN - 79394790; 2689434 AB - Cocaine can induce manic syndromes ranging from mild hypomania to severe dysphoric and psychotic mania, in part depending on the number and duration of drug administrations. Repeated cocaine administration in animals results in increased motor (behavioral sensitization) and convulsive (pharmacologic kindling) responses. Study of these progressive syndromes in animals may provide insights into principles underlying the longitudinal evolution of manic syndromes in man, including the increased vulnerability to recurrence following successive episodes. Different phases in the evolution of behavioral sensitization are differentially responsive to neuroleptics while the same principle is evident for different anticonvulsants in kindling. The authors examine whether pharmaco-responsivity may also differ as a function of stage of progression of mania. Antimanic effects of lithium, neuroleptics, and the newer anticonvulsants, such as carbamazepine, valproic acid, and clonazepam, are discussed in this context. JF - The Journal of clinical psychiatry AU - Post, R M AU - Weiss, S R AD - Biological Psychiatric Branch, National Institute of Mental Health, Bethesda, Md. 20892. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 23 EP - 30; discussion 45-7 VL - 50 Suppl SN - 0160-6689, 0160-6689 KW - Anticonvulsants KW - 0 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Rats KW - Animals KW - Humans KW - Disease Models, Animal KW - Stereotyped Behavior -- drug effects KW - Motor Activity -- drug effects KW - Mice KW - Cocaine -- pharmacology KW - Behavior, Animal -- drug effects KW - Anticonvulsants -- pharmacology KW - Kindling, Neurologic KW - Bipolar Disorder -- etiology KW - Bipolar Disorder -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79394790?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-01 N1 - Date created - 1990-02-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chromatographic analysis of the aminoacyl-tRNAs which are required for translation of codons at and around the ribosomal frameshift sites of HIV, HTLV-1, and BLV. AN - 79388802; 2556852 AB - An examination of the frameshift signals or proposed signals within published sequences of retroviruses and other genetic elements from higher animals shows that each site utilizes a tRNA which normally contains Wybutoxine (Wye) base or Queuine (Q) base in the anticodon loop. We find experimentally that most of the Phe-tRNA present in HIV-1 infected cells lacks the highly modified Wye base in its anticodon loop and most of the Asn-tRNA in HTLV-1 and BLV infected cells lacks the highly modified Q base in its anticodon loop. Interestingly, Phe-tRNA translates a UUU codon within the ribosomal frameshift signal in HIV and Asn-tRNA translates a AAC codon within the proposed frameshift signals in HTLV-1 and BLV. Thus, the lack of a highly modified base in the anticodon loop of tRNAs in retroviral infected cells is correlated with the participation of these undermodified tRNAs in the corresponding frameshift event. This suggests that the "shifty" tRNAs proposed by Jacks et al. (Cell 55, 447-458, 1988) to carry out frameshifting may be hypomodified isoacceptors. JF - Virology AU - Hatfield, D AU - Feng, Y X AU - Lee, B J AU - Rein, A AU - Levin, J G AU - Oroszlan, S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 736 EP - 742 VL - 173 IS - 2 SN - 0042-6822, 0042-6822 KW - Codon KW - 0 KW - RNA, Messenger KW - RNA, Transfer, Amino Acyl KW - Index Medicus KW - AIDS/HIV KW - Protein Biosynthesis KW - Animals KW - Tumor Cells, Cultured KW - Chromatography KW - Ribosomes KW - Cell Line KW - Human T-lymphotropic virus 1 -- genetics KW - Codon -- genetics KW - Leukemia Virus, Bovine -- genetics KW - RNA, Transfer, Amino Acyl -- genetics KW - Retroviridae -- genetics KW - RNA, Transfer, Amino Acyl -- analysis KW - RNA, Messenger -- genetics KW - HIV -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79388802?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-24 N1 - Date created - 1990-01-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - CD4-Pseudomonas exotoxin hybrid protein blocks the spread of human immunodeficiency virus infection in vitro and is active against cells expressing the envelope glycoproteins from diverse primate immunodeficiency retroviruses. AN - 79371865; 2480605 AB - We previously described an unusual recombinant protein, designated CD4(178)-PE40, containing the gp120 binding region of human CD4 linked to active regions of Pseudomonas exotoxin A. The ability of this molecule to selectively inhibit protein synthesis in cells expressing the surface envelope glycoprotein of human immunodeficiency virus (HIV) suggested this molecule may be useful in treating infected individuals. To further evaluate its therapeutic potential, several in vitro properties of this hybrid toxin were examined. CD4(178)-PE40 was found to be an extremely potent cytotoxic agent, selectively killing HIV-infected cells with IC50 values around 100 pM. In a coculture system employing mixtures of HIV-infected and -uninfected cells, the hybrid toxin inhibited spread of the infection, as judged by a delay in HIV-induced cell killing and a dramatic suppression of free virus production. Experiments with control recombinant proteins indicated that this protective effect was primarily due to selective killing of the HIV-infected cells, rather than to a simple blocking effect of the CD4 moiety of the hybrid toxin. Using recombinant vaccinia viruses as expression vectors, we found the hybrid toxin to be active against cells expressing the envelope glycoproteins of divergent isolates of HIV-1, as well as HIV-2 and simian immunodeficiency virus. These results provide further support for the therapeutic potential of CD4(178)-PE40 in the treatment of HIV-infected individuals. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Berger, E A AU - Clouse, K A AU - Chaudhary, V K AU - Chakrabarti, S AU - FitzGerald, D J AU - Pastan, I AU - Moss, B AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20852. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 9539 EP - 9543 VL - 86 IS - 23 SN - 0027-8424, 0027-8424 KW - Antigens, CD4 KW - 0 KW - Antiviral Agents KW - Bacterial Proteins KW - CD4-Pseudomonas toxin KW - Exotoxins KW - Immunotoxins KW - Recombinant Proteins KW - Viral Envelope Proteins KW - RNA-Directed DNA Polymerase KW - EC 2.7.7.49 KW - Index Medicus KW - AIDS/HIV KW - Cell Survival -- drug effects KW - Bacterial Proteins -- pharmacology KW - Humans KW - RNA-Directed DNA Polymerase -- metabolism KW - Cell Line KW - HIV -- drug effects KW - Exotoxins -- pharmacology KW - Recombinant Proteins -- pharmacology KW - Antiviral Agents -- pharmacology KW - Viral Envelope Proteins -- biosynthesis KW - Immunotoxins -- pharmacology KW - HIV -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79371865?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-19 N1 - Date created - 1990-01-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1984 May 4;224(4648):497-500 [6200935] Proc Natl Acad Sci U S A. 1989 Apr;86(7):2433-7 [2648404] Science. 1986 Feb 7;231(4738):600-2 [3003906] Cell. 1986 Jul 4;46(1):1-4 [3013415] J Exp Med. 1986 Jul 1;164(1):280-90 [3014036] J Immunol Methods. 1986 Nov 6;93(2):157-65 [3490518] Proc Natl Acad Sci U S A. 1986 Nov;83(21):8122-6 [3095828] Mol Cell Biol. 1987 Jul;7(7):2538-44 [3112559] Nature. 1987 Aug 6-12;328(6130):539-43 [3497350] Cell. 1987 Sep 11;50(6):975-85 [2441877] Virology. 1987 Oct;160(2):323-9 [2444031] J Bacteriol. 1987 Nov;169(11):4967-71 [2889718] Science. 1987 Dec 18;238(4834):1704-7 [3500514] Nature. 1988 Jan 7;331(6151):76-8 [2829022] Nature. 1988 Jan 7;331(6151):78-81 [2829023] Nature. 1988 Jan 7;331(6151):82-4 [3257544] Nature. 1988 Jan 7;331(6151):84-6 [2829024] Cell. 1988 Mar 11;52(5):631-3 [2830988] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2357-61 [2451247] J Biol Chem. 1988 Jul 5;263(19):9470-5 [3132465] AIDS. 1988 Apr;2(2):101-5 [2454642] Nature. 1988 Sep 22;335(6188):369-72 [2843774] J Immunol. 1989 Jan 15;142(2):431-8 [2463307] Proc Natl Acad Sci U S A. 1985 Jul;82(13):4539-43 [2989831] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prostaglandin hydroperoxidase-dependent activation of heterocyclic aromatic amines. AN - 79362298; 2512013 AB - Heterocyclic aromatic amines, derived from the pyrolysis of amino acids and proteins, are potent mutagens in the Ames Salmonella assay with rodent liver activation. Additionally, heterocyclic aromatic amines are multipotent carcinogens. We report evidence that these compounds are substrates for the hydroperoxidase activity of prostaglandin H synthase, as measured by alterations in UV/visible spectra, and are bioactivated to macromolecule-reactive species by this enzyme. Indirect electron paramagnetic resonance studies indicate that this activation may occur via a one-electron mechanism. 2-Amino-3-methylimidazo[4,5f]quinoline (IQ), 2-amino-3,4-dimethylimidazo[4,5-f]quinoline (MeIQ), and 3-amino-1-methyl-5H-pyrido[4,3-b]indole (Trp-P-2) are direct-acting mutagens in TA98. The mutagenicity of IQ and MeIQ, but not Trp-P-2, were enhanced by activation with ram seminal vesicle microsomes (a rich source of prostaglandin H synthase). Subsequent experiments utilized the newly constructed tester strain TA1538/1,8-DNP6 (pYG 121), which has enhanced arylamine N-acetyltransferase activity. In this strain IQ, MeIQ and 2-amino-6-methyldipyrido-[1,2-a:3',2'-d]imidazole (Glu-P-1) were mutagenic with ram seminal vesicle microsome activation. 3-Amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) was a weak direct-acting mutagen, and was not activated by the ram seminal vesicles (RSV) system. The responses of IQ and MeIQ were markedly enhanced in TA1538/1.8-DNP6 (pYG 121), relative to TA98. These data are consistent with the involvement of prostaglandin H synthase-catalyzed activation in heterocyclic aromatic amine-induced extrahepatic neoplasia. JF - Carcinogenesis AU - Petry, T W AU - Josephy, P D AU - Pagano, D A AU - Zeiger, E 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 - 1989/12// PY - 1989 DA - December 1989 SP - 2201 EP - 2207 VL - 10 IS - 12 SN - 0143-3334, 0143-3334 KW - Amines KW - 0 KW - Heterocyclic Compounds KW - Proteins KW - prostaglandin hydroperoxidase KW - EC 1.11.- KW - Peroxidases KW - EC 1.11.1.- KW - Prostaglandin-Endoperoxide Synthases KW - EC 1.14.99.1 KW - Index Medicus KW - Animals KW - Mutagenicity Tests KW - Biotransformation KW - Sheep KW - Prostaglandin-Endoperoxide Synthases -- metabolism KW - Salmonella typhimurium -- drug effects KW - Microsomes -- enzymology KW - Proteins -- metabolism KW - Protein Binding KW - Seminal Vesicles -- enzymology KW - Male KW - Heterocyclic Compounds -- metabolism KW - Heterocyclic Compounds -- pharmacology KW - Amines -- pharmacology KW - Amines -- metabolism KW - Peroxidases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79362298?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-22 N1 - Date created - 1990-01-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cell specificity for the pulmonary metabolism of tobacco-specific nitrosamines in the Fischer rat. AN - 79358686; 2591016 AB - The activity and distribution of the metabolic pathways of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), its major metabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and the structurally related nitrosamine, N'-nitrosonornicotine (NNN) were examined in pulmonary cells from F344 rats in order to investigate the mechanisms by which NNK and NNAL, but not NNN, cause lung tumors. The tritium labeled nitrosamines were incubated with Clara cells, alveolar macrophages, alveolar type II cells, or small cells and metabolites were analyzed by HPLC. O6-Methyl-guanine (O6MG) formation was also quantified in the cells incubated with NNK. Clara cells metabolized all compounds more extensively than the other cell types. Total alpha-hydroxylation, carbonyl reduction to NNAL, and pyridine N-oxidation in cells incubated with NNK, as well as concentrations of O6MG in DNA were higher in Clara cells than in other cell types. Carbonyl reduction of NNK predominated over the other metabolic pathways in all cell types. The high activity for alpha-hydroxylation of NNK in Clara cells is consistent with previous studies which proposed that the cell specificity for O6MG formation and the accumulation of this adduct during low-dose exposure to NNK may stem from the presence of a high affinity pathway in Clara cells for NNK activation. Metabolism of NNAL by alpha-hydroxylation, and by reconversion to NNK followed by alpha-hydroxylation were observed. Total alpha-hydroxylation of NNAL was less extensive than alpha-hydroxylation of NNK. NNN was metabolized by both the 2'- and 5'-alpha-hydroxylation pathways. 2'-Hydroxylation of NNN produces the same DNA pyridyloxobutylating agent as does methyl hydroxylation of NNK. However, NNN is not a methylating agent and does not induce lung tumors in rats. Metabolism of NNN by 2'-hydroxylation was, depending on cell type, 41-85% as extensive as total alpha-hydroxylation of NNK, indicating that the rates of formation of the DNA pyridyloxobutylating agent were similar from NNN and NNK. The results of this study demonstrate that Clara cells have a high capacity to metabolically activate NNK, NNAL and NNN and provide further support for the hypothesis that DNA methylation of pulmonary cells is important in NNK carcinogenesis. JF - Carcinogenesis AU - Belinsky, S A AU - White, C M AU - Trushin, N AU - Hecht, S S AD - Laboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 2269 EP - 2274 VL - 10 IS - 12 SN - 0143-3334, 0143-3334 KW - Carcinogens KW - 0 KW - Mutagens KW - Nitrosamines KW - Tritium KW - 10028-17-8 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Biotransformation KW - Kinetics KW - DNA -- metabolism KW - Chromatography, High Pressure Liquid KW - Structure-Activity Relationship KW - Alkylation KW - Plants, Toxic KW - Nitrosamines -- metabolism KW - Tobacco KW - Lung -- metabolism KW - Macrophages -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79358686?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-22 N1 - Date created - 1990-01-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Substance abuse education in residency training programs in emergency medicine. NIAAA Task Force of the American College of Emergency Physicians. AN - 79358660; 2589703 AB - The emergency department is the focal point for many social ills, not the least of which is substance abuse. We conducted a study to determine to what degree substance abuse education is taught in emergency medicine residency training programs. A set of educational objectives was developed by a task force composed of representatives of the American College of Emergency Physicians, the Society of Teachers of Emergency Medicine, and the University Association for Emergency Medicine. A questionnaire then was sent to the directors of all emergency medicine residency programs accredited by the Accreditation Council for Graduate Medical Education to determine the degree to which those objectives are covered in residency training. A 62% response rate was achieved. The data revealed that such topics as narcotic prescription law, patterns of risk, and issues pertaining to substance abuse by physicians were covered by fewer than half of the programs responding. Respondents were generally satisfied with the adequacy of training of residents and faculty in the area of substance abuse; however, they were dissatisfied with the adequacy of available training materials. Recommendations for changes in graduate curriculum as well as avenues for further research are provided. JF - Annals of emergency medicine AU - Taliaferro, E H AU - Rund, D A AU - Brown, C G AU - Goldfrank, L R AU - Jorden, R C AU - Ling, L J AU - Gallery, M E AD - NIAAA Task Force of the American College of Emergency Physicians, Dallas, Texas 75261-9911. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 1344 EP - 1347 VL - 18 IS - 12 SN - 0196-0644, 0196-0644 KW - Abridged Index Medicus KW - Index Medicus KW - Attitude of Health Personnel KW - Humans KW - Curriculum KW - Surveys and Questionnaires KW - Emergency Medicine -- education KW - Substance-Related Disorders KW - Internship and Residency UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79358660?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-11 N1 - Date created - 1990-01-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment of obsessive-compulsive disorder with clomipramine and desipramine in children and adolescents. A double-blind crossover comparison. AN - 79358323; 2686576 AB - Forty-eight children and adolescents with severe primary obsessive-compulsive disorder completed a 10-week double-blind crossover trial of clomipramine hydrochloride (mean dose [+/- SD], 150 +/- 53 mg/d) and desipramine hydrochloride (mean dose [+/- SD], 153 +/- 55 mg/d). Clomipramine was clearly superior to desipramine in significantly reducing obsessive-compulsive symptoms. Age at onset, duration and severity of illness, type of symptom, and plasma drug concentrations did not predict clinical response to clomipramine. Sixty-four percent of patients who received clomipramine as their first active treatment showed at least some sign of relapse during desipramine treatment. We further document the specificity of the antiobsessional effect of clomipramine and the need for maintenance treatment. JF - Archives of general psychiatry AU - Leonard, H L AU - Swedo, S E AU - Rapoport, J L AU - Koby, E V AU - Lenane, M C AU - Cheslow, D L AU - Hamburger, S D AD - Child Psychiatry Branch, National Institute of Mental Health, Bethesda, Md 20892. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 1088 EP - 1092 VL - 46 IS - 12 SN - 0003-990X, 0003-990X KW - Placebos KW - 0 KW - Clomipramine KW - NUV44L116D KW - Desipramine KW - TG537D343B KW - Abridged Index Medicus KW - Index Medicus KW - Age Factors KW - Psychiatric Status Rating Scales KW - Double-Blind Method KW - Humans KW - Adult KW - Clinical Trials as Topic KW - Child KW - Adolescent KW - Recurrence KW - Male KW - Female KW - Obsessive-Compulsive Disorder -- diagnosis KW - Desipramine -- blood KW - Desipramine -- therapeutic use KW - Desipramine -- adverse effects KW - Obsessive-Compulsive Disorder -- psychology KW - Obsessive-Compulsive Disorder -- drug therapy KW - Clomipramine -- blood KW - Clomipramine -- adverse effects KW - Clomipramine -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79358323?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-03 N1 - Date created - 1990-01-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The human debrisoquine 4-hydroxylase (CYP2D) locus: sequence and identification of the polymorphic CYP2D6 gene, a related gene, and a pseudogene. AN - 79356983; 2574001 AB - The debrisoquine-4-hydroxylase polymorphism is a genetic variation in oxidative drug metabolism characterized by two phenotypes, the extensive metabolizer (EM) and poor metabolizer (PM). Of the Caucasian populations of Europe and North America, 5%-10% are of the PM phenotype and are unable to metabolize debrisoquine and numerous other drugs. The defect is caused by several mutant alleles of the CYP2D6 gene, two of which are detected in about 70% of PMs. We have constructed a genomic library from lymphocyte DNA of an EM positively identified by pedigree analysis to be homozygous for the normal CYP2D6 allele. The normal CYP2D6 gene was isolated; was completely sequenced, including 1,531 and 3,522 bp of 5' and 3' flanking DNA, respectively; and was found to contain nine exons within 4,378 bp. Two other genes, designated CYP2D7 and CYP2D8P, were also cloned and sequenced. CYP2D8P contains several gene-disrupting insertions, deletions, and termination codons within its exons, indicating that this is a pseudogene. CYP2D7, which is just downstream of CYP2D8P, is apparently normal, except for the presence, in the first exon, of an insertion that disrupts the reading frame. A hypothesis is presented that the presence of a pseudogene within the CYP2D subfamily transfers detrimental mutations via gene conversions into the CYP2D6 gene, thus accounting for the high frequency of mutations observed in the CYP2D6 gene in humans. JF - American journal of human genetics AU - Kimura, S AU - Umeno, M AU - Skoda, R C AU - Meyer, U A AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 889 EP - 904 VL - 45 IS - 6 SN - 0002-9297, 0002-9297 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Mixed Function Oxygenases KW - EC 1.- KW - Cytochrome P-450 CYP2D6 KW - EC 1.14.14.1 KW - Index Medicus KW - Phenotype KW - Base Sequence KW - Humans KW - Restriction Mapping KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Genomic Library KW - Male KW - Female KW - Pseudogenes KW - Polymorphism, Restriction Fragment Length KW - Cytochrome P-450 Enzyme System -- genetics KW - Multigene Family KW - Mixed Function Oxygenases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79356983?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-11 N1 - Date created - 1990-01-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Genomics. 1988 Feb;2(2):174-9 [3410476] Proc Natl Acad Sci U S A. 1988 Jul;85(14):5240-3 [2899325] Pharmacol Rev. 1988 Dec;40(4):243-88 [3072575] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Drug Metab Rev. 1979;9(2):301-17 [158499] Anal Biochem. 1983 Feb 15;129(1):216-23 [6305233] Biochemistry. 1984 Jun 5;23(12):2787-95 [6432035] J Biol Chem. 1985 Jul 25;260(15):9057-67 [4019462] Proc Natl Acad Sci U S A. 1986 Jan;83(1):130-4 [3001719] Prog Clin Biol Res. 1986;214:157-67 [3523506] J Biol Chem. 1986 Sep 5;261(25):11734-43 [3745165] DNA. 1987 Apr;6(2):149-61 [3582092] Am J Hum Genet. 1988 Jan;42(1):4-7 [3276177] Nature. 1988 Feb 4;331(6155):442-6 [3123997] Mol Biol Evol. 1987 Nov;4(6):572-93 [3484338] Mol Cell Biol. 1988 Feb;8(2):802-13 [2832737] DNA. 1989 Jan-Feb;8(1):1-13 [2651058] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tyrosine kinase oncogenes abrogate interleukin-3 dependence of murine myeloid cells through signaling pathways involving c-myc: conditional regulation of c-myc transcription by temperature-sensitive v-abl. AN - 79342912; 2555703 AB - Retroviral expression vectors carrying the tyrosine kinase oncogenes abl, fms, src, and trk abrogate the requirements of murine myeloid FDC-P1 cells for interleukin-3 (IL-3). Factor-independent clones constitutively express c-myc in the absence of IL-3, whereas in parental cultures c-myc transcription requires the presence of the ligand. To directly test the effect of a tyrosine kinase oncogene on c-myc expression, retroviral constructs containing three different temperature-sensitive mutants of v-abl were introduced into myeloid IL-3-dependent FDC-P1 and 32D cells. At the permissive temperature, clones expressing temperature-sensitive abl behaved like wild-type abl-containing cells in their growth properties and expressed c-myc constitutively. Temperature shift experiments demonstrated that both IL-3 abrogation and the regulation of c-myc expression correlated with the presence of functional v-abl. Induction of c-myc expression by reactivation of temperature-sensitive v-abl mimicked c-myc induction by IL-3 in that it did not require protein synthesis and occurred at the level of transcription, with effects on both initiation and a transcription elongation block. However, v-abl-regulated FDC-P1 cell growth differed from IL-3-regulated growth in that c-fos and junB, which are normally induced by IL-3, were not induced by activation of v-abl. JF - Molecular and cellular biology AU - Cleveland, J L AU - Dean, M AU - Rosenberg, N AU - Wang, J Y AU - Rapp, U R AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, Maryland 21701. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 5685 EP - 5695 VL - 9 IS - 12 SN - 0270-7306, 0270-7306 KW - Interleukin-3 KW - 0 KW - Proto-Oncogene Proteins KW - Proto-Oncogene Proteins c-myc KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Index Medicus KW - Clone Cells KW - Animals KW - Promoter Regions, Genetic KW - Temperature KW - Moloney murine leukemia virus -- genetics KW - Cell Line KW - Gene Expression Regulation, Neoplastic KW - Protein-Tyrosine Kinases -- genetics KW - Leukemia Virus, Murine -- genetics KW - Oncogenes -- drug effects KW - Interleukin-3 -- pharmacology KW - Signal Transduction -- drug effects KW - Transcription, Genetic KW - Protein-Tyrosine Kinases -- metabolism KW - Proto-Oncogene Proteins -- genetics KW - Proto-Oncogenes -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79342912?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-11 N1 - Date created - 1990-01-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Virology. 1983 May;127(1):134-48 [6305011] J Immunol. 1983 Jul;131(1):282-7 [6190911] Nature. 1983 Aug 18-24;304(5927):596-602 [6308472] Cell. 1983 Dec;35(3 Pt 2):603-10 [6606489] Cell. 1984 Feb;36(2):241-7 [6692471] Biochem J. 1984 Aug 15;222(1):195-201 [6089758] Nature. 1984 Oct 4-10;311(5985):433-8 [6090941] Cell. 1985 Jul;41(3):677-83 [2988782] Cell. 1985 Jul;41(3):685-93 [2988783] Virology. 1985 Oct 15;146(1):78-89 [2994296] Recent Results Cancer Res. 1985;99:221-36 [4070776] J Cell Sci Suppl. 1985;3:187-98 [3011822] Proc Natl Acad Sci U S A. 1987 Mar;84(5):1345-9 [2434953] Mol Cell Biol. 1986 Nov;6(11):4133-5 [3025637] Mol Cell Biol. 1986 Oct;6(10):3545-9 [3540594] Nucleic Acids Res. 1986 Nov 11;14(21):8331-46 [3537956] EMBO J. 1986 Nov;5(11):2859-65 [3024965] J Virol. 1983 Mar;45(3):1195-9 [6300457] J Exp Med. 1980 Oct 1;152(4):1036-47 [6968334] Oncogene. 1989 Sep;4(9):1129-35 [2674855] Proc Natl Acad Sci U S A. 1978 May;75(5):2488-92 [209468] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] Oncogene. 1989 Apr;4(4):451-5 [2566144] J Immunol. 1987 May 15;138(10):3495-504 [3106484] J Immunol. 1987 Jun 1;138(11):3829-35 [2438328] J Immunol. 1987 Jul 1;139(1):123-9 [3495596] Mol Cell Biol. 1987 May;7(5):1673-80 [3037331] Cell. 1987 Sep 25;50(7):1021-9 [2441878] Proc Natl Acad Sci U S A. 1987 Nov;84(22):8021-5 [2825174] Oncogene. 1987 Mar;1(1):29-35 [2449644] Proc Natl Acad Sci U S A. 1988 Mar;85(5):1487-91 [3422745] Oncogene Res. 1987 Aug;1(3):279-96 [2453016] Oncogene Res. 1988 Feb;2(3):277-84 [3259302] Proc Natl Acad Sci U S A. 1988 May;85(10):3522-6 [3368463] Nature. 1988 Aug 11;334(6182):494-8 [2900470] Proc Natl Acad Sci U S A. 1988 Nov;85(21):7982-6 [2460860] Proc Natl Acad Sci U S A. 1988 Dec;85(23):8855-9 [3057494] J Biol Chem. 1988 Dec 15;263(35):19203-9 [2461935] Proc Natl Acad Sci U S A. 1989 Jan;86(2):505-9 [2463629] Oncogene Res. 1988;3(4):357-75 [2976141] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Attenuation and cell culture adaptation of hepatitis A virus (HAV): a genetic analysis with HAV cDNA. AN - 79340308; 2555561 AB - RNA transcripts of hepatitis A virus (HAV) HM-175 cDNA from attenuated, cell culture-adapted HAV were infectious in cell culture. A full-length HAV cDNA from wild-type HAV (propagated in marmosets in vivo) was constructed. Chimeric cDNAs that contained portions of both wild-type and attenuated genomes were produced. Oligonucleotide-directed mutagenesis was used to engineer a point mutation into the VP1 gene of attenuated HAV cDNA, so that the sequence of this capsid protein would be identical to that of the wild-type virus. Transfection of monkey kidney cells with RNA transcripts from several of the chimeric cDNAs and from the mutagenized cDNA induced production of HAV. Comparison of the growth of attenuated, wild-type, chimeric, and mutant viruses in vitro indicated that the P2-P3 (nonstructural protein) region is important for cell culture adaptation of the virus; the 5' noncoding region may also contribute to adaptation, but to a lesser extent. Inoculation of marmosets with transfection-derived virus also suggested that the P2-P3 region plays an important role in attenuation of HAV HM-175. JF - Journal of virology AU - Cohen, J I AU - Rosenblum, B AU - Feinstone, S M AU - Ticehurst, J AU - Purcell, R H AD - Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 5364 EP - 5370 VL - 63 IS - 12 SN - 0022-538X, 0022-538X KW - DNA, Viral KW - 0 KW - Viral Structural Proteins KW - Index Medicus KW - Animals KW - Chimera KW - Callitrichinae KW - Transfection KW - Capsid -- genetics KW - Restriction Mapping KW - Plasmids KW - Viral Structural Proteins -- genetics KW - Mutation KW - Cell Line KW - Cloning, Molecular KW - Hepatovirus -- physiology KW - Genes, Viral KW - DNA, Viral -- genetics KW - Hepatovirus -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79340308?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-27 N1 - Date created - 1989-12-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Infect Immun. 1977 Nov;18(2):524-30 [200565] Virology. 1988 Apr;163(2):299-307 [2833008] Science. 1981 Nov 20;214(4523):916-9 [6272391] Proc Natl Acad Sci U S A. 1982 Oct;79(19):5793-7 [6310545] Proc Natl Acad Sci U S A. 1983 Oct;80(19):5885-9 [6310601] Dev Biol Stand. 1983;54:429-32 [6317493] Proc Natl Acad Sci U S A. 1984 Mar;81(5):1539-43 [6324200] J Med Virol. 1984;14(4):373-86 [6096505] Nature. 1985 Apr 11-17;314(6011):548-50 [2986004] J Virol. 1986 May;58(2):348-58 [3009852] J Gen Virol. 1986 Aug;67 ( Pt 8):1741-4 [3016162] J Virol. 1986 Oct;60(1):124-30 [3018280] J Med Virol. 1986 Oct;20(2):165-75 [3021899] J Virol. 1987 Jan;61(1):50-9 [3023706] Proc Natl Acad Sci U S A. 1987 Apr;84(8):2497-501 [3031686] J Virol. 1987 Oct;61(10):3035-9 [3041024] J Virol Methods. 1987 Aug;17(1-2):183-9 [2822753] J Clin Microbiol. 1987 Oct;25(10):1822-9 [2822759] J Infect Dis. 1988 Feb;157(2):338-45 [2826614] Infect Immun. 1981 Apr;32(1):388-93 [6260685] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - trans activation of human immunodeficiency virus type 1 is sequence specific for both the single-stranded bulge and loop of the trans-acting-responsive hairpin: a quantitative analysis. AN - 79339173; 2479775 AB - We have used site-directed mutagenesis to delineate sequence specific domains within the human immunodeficiency virus type 1 (HIV-1) trans-acting-responsive (TAR) RNA element that are required for trans activation by the viral Tat protein. Our data in part corroborate a recent report [S. Feng and E. C. Holland, Nature (London) 334:165-167, 1988] that five nucleotides within the loop (+29 to +33) of the TAR hairpin are important for trans activation. We, however, found no absolute requirement for the CUGGG loop sequence. Mutants with substitutions within the loop retained between 9 and 50% activity compared with the wild type. A second sequence, important for trans activation, was found in the 3-base bulge loop (+22 to +24) of the TAR hairpin. Cross-trans-activation studies of mutant HIV-1 TAR elements with the HIV-2 Tat protein suggest that a similar recognition event(s) forms the basis for trans activation of HIV-1 and HIV-2. JF - Journal of virology AU - Berkhout, B AU - Jeang, K T AD - Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 5501 EP - 5504 VL - 63 IS - 12 SN - 0022-538X, 0022-538X KW - RNA KW - 63231-63-0 KW - Index Medicus KW - AIDS/HIV KW - Base Sequence KW - Molecular Sequence Data KW - Nucleic Acid Conformation KW - Mutation KW - HIV-1 -- genetics KW - Enhancer Elements, Genetic -- genetics KW - HIV-1 -- growth & development KW - Virus Activation KW - Transcriptional Activation KW - RNA -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79339173?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-27 N1 - Date created - 1989-12-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell. 1987 Feb 27;48(4):691-701 [3643816] Nature. 1987 Apr 16-22;326(6114):662-9 [3031510] Cell. 1986 Mar 28;44(6):941-7 [2420471] Nature. 1986 Mar 27-Apr 2;320(6060):367-71 [3007995] Biochemistry. 1987 Mar 24;26(6):1563-8 [3297131] Nature. 1987 Aug 6-12;328(6130):548-50 [3039372] Genes Dev. 1989 Apr;3(4):547-58 [2470647] Nature. 1988 Jul 14;334(6178):165-7 [3386755] Mol Cell Biol. 1988 Jun;8(6):2555-61 [2841583] J Virol. 1988 Dec;62(12):4523-32 [2846868] Proc Natl Acad Sci U S A. 1988 Dec;85(24):9753-7 [2849115] J Virol. 1989 Mar;63(3):1181-7 [2536828] EMBO J. 1989 Mar;8(3):765-78 [2721501] EMBO J. 1987 Dec 1;6(12):3755-60 [2828036] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phosphorylation sites of the E2 transcriptional regulatory proteins of bovine papillomavirus type 1. AN - 79338026; 2555544 AB - The E2 open reading frame of bovine papillomavirus type 1 (BPV-1) encodes three transcriptional regulatory proteins. The full-length open reading frame encodes a protein of 410 amino acids which functions as a transcriptional transactivator. Two transcriptional repressor proteins, E2-TR and E8/E2, contain the C-terminal 249 and 204 amino acids, respectively. We have expressed both the full-length E2 protein and the E2-TR repressor protein in insect cells, by using recombinant baculoviruses, and in mammalian COS-1 cells, by using a chimeric simian virus 40/BPV-1 virus. Analysis of the E2 proteins revealed that both the transactivator and repressor forms are phosphorylated predominately on serine residues at similar sites in both expression systems. By a combination of peptide mapping and site-directed mutagenesis techniques, the serine residues at positions 298 and 301 were determined to be the major phosphorylation sites of the BPV-1 E2 proteins. JF - Journal of virology AU - McBride, A A AU - Bolen, J B AU - Howley, P M AD - Laboratory of Tumor Virus Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 5076 EP - 5085 VL - 63 IS - 12 SN - 0022-538X, 0022-538X KW - Amino Acids KW - 0 KW - DNA, Viral KW - Repressor Proteins KW - Trans-Activators KW - Transcription Factors KW - Viral Structural Proteins KW - Index Medicus KW - Animals KW - Peptide Mapping KW - Insect Viruses -- genetics KW - Amino Acids -- analysis KW - Gene Expression KW - Amino Acid Sequence KW - Plasmids KW - Base Sequence KW - Phosphorylation KW - Genetic Vectors KW - Molecular Sequence Data KW - Genes, Viral KW - Viral Structural Proteins -- genetics KW - DNA, Viral -- genetics KW - Mutation KW - Cell Line KW - Bovine papillomavirus 1 -- metabolism KW - Trans-Activators -- metabolism KW - Transcription Factors -- metabolism KW - Trans-Activators -- genetics KW - Repressor Proteins -- metabolism KW - Papillomaviridae -- genetics KW - Transcription Factors -- genetics KW - Repressor Proteins -- genetics KW - Bovine papillomavirus 1 -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79338026?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-27 N1 - Date created - 1989-12-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1975 May 25;250(10):4007-21 [236308] EMBO J. 1988 Dec 1;7(12):3807-16 [2850174] Virology. 1982 May;119(1):22-34 [6280384] Mol Cell Biol. 1983 Dec;3(12):2156-65 [6318086] J Biol Chem. 1984 Oct 10;259(19):11686-94 [6434530] Cell. 1985 Aug;42(1):183-91 [2990724] Cell. 1985 Dec;43(2 Pt 1):393-404 [2416464] Proc Natl Acad Sci U S A. 1985 Dec;82(24):8404-8 [3878519] Mol Cell Biol. 1985 Oct;5(10):2860-5 [3915537] Science. 1986 Oct 17;234(4774):364-8 [2876518] Nature. 1987 Jan 1-7;325(6099):70-3 [3025749] Proc Natl Acad Sci U S A. 1987 Mar;84(5):1215-8 [3029771] EMBO J. 1987 Jan;6(1):145-52 [3034572] J Virol. 1987 Jul;61(7):2128-37 [3035214] Cell. 1987 Jul 3;50(1):69-78 [3036366] J Biol Chem. 1987 Jul 5;262(19):9136-40 [3474230] J Biol Chem. 1987 Oct 15;262(29):14042-8 [2820993] EMBO J. 1988 Feb;7(2):533-9 [2835232] J Virol. 1988 Jun;62(6):1925-31 [2835497] Oncogene Res. 1987 Sep-Oct;1(4):357-74 [2835736] Oncogene Res. 1988 May;2(4):385-401 [3041347] J Virol. 1988 Sep;62(9):3242-9 [2841476] Nature. 1988 Aug 11;334(6182):494-8 [2900470] Cell. 1988 Sep 9;54(6):855-64 [3044613] Proc Natl Acad Sci U S A. 1988 Aug;85(16):5864-8 [2842752] Biochim Biophys Acta. 1988 Sep 16;971(2):227-31 [2901861] FEBS Lett. 1988 Sep 12;237(1-2):225-8 [3169237] Proc Natl Acad Sci U S A. 1988 Oct;85(19):7206-10 [2845402] EMBO J. 1988 Sep;7(9):2815-22 [2846284] EMBO J. 1988 Sep;7(9):2823-9 [2846285] Proc Natl Acad Sci U S A. 1989 Jan;86(2):510-4 [2536165] Cell. 1989 Feb 10;56(3):409-19 [2644045] Virology. 1989 Mar;169(1):236-8 [2538035] EMBO J. 1988 Dec 20;7(13):4245-53 [2854060] EMBO J. 1989 Jan;8(1):127-32 [2540954] J Virol. 1989 Jul;63(7):3151-4 [2542621] Proc Natl Acad Sci U S A. 1989 Jun;86(12):4352-6 [2525256] Cell. 1989 Jun 16;57(6):891-3 [2544293] Nature. 1989 Jun 29;339(6227):679-84 [2662013] EMBO J. 1989 Apr;8(4):1111-9 [2663470] Genes Dev. 1989 May;3(5):620-7 [2545525] J Virol. 1989 Apr;63(4):1743-55 [2538655] Proc Natl Acad Sci U S A. 1988 Dec;85(23):9007-11 [2848252] Proc Natl Acad Sci U S A. 1981 May;78(5):2727-31 [6265905] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Combination therapy with interleukin-2 and alpha-interferon for the treatment of patients with advanced cancer. AN - 79337982; 2685181 AB - We performed an escalating dose study of the combined administration of interleukin-2 (IL-2) and alpha-interferon (alpha-IFN) in 94 patients with metastatic cancer. Patients received alpha-IFN at a dose of 3 x 10(6) U/m2 in conjunction with IL-2 at doses of either 1 x 10(6) U/m2 (six patients), 3 x 10(6) U/m2 (32 patients), or 4.5 x 10(6) U/m2 (26 patients). Thirty patients received alpha-IFN at 6 x 10(6) U/m2 plus IL-2 at 4.5 x 10(6) U/m2. Patients each received cytokine as an intravenous bolus infusion every 8 hours for up to 5 consecutive days and after a 10-day rest received a second cycle of combination cytokines. Of the 91 patients evaluable for response, seven patients had a complete regression of cancer, and 18 had a partial regression. At the four increasing dose levels used in patients with renal cell cancer (35 patients) or melanoma (39 patients), objective responses were seen in 17% (of six patients), 24% (of 25 patients), 38% (of 16 patients), and 41% (of 27 patients), respectively. Of the 25 total responding patients, 16 are still responding 5 to 14 months after treatment. The toxicities associated with the combined administration of IL-2 and alpha-IFN were similar to those expected from each agent alone. There was one treatment-related death in the 94 patients treated in this study. Thus, using increasing doses of the combination of IL-2 and alpha-IFN, it appears that response rates may be related to the doses of the cytokines used, and that at the highest doses of these combination cytokines, response rates may be higher than those for either cytokine alone. A prospective randomized trial comparing the cytokine combinations with each cytokine administered alone is necessary as is the extension of this combination cytokine treatment to patients with other types of solid cancer. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Rosenberg, S A AU - Lotze, M T AU - Yang, J C AU - Linehan, W M AU - Seipp, C AU - Calabro, S AU - Karp, S E AU - Sherry, R M AU - Steinberg, S AU - White, D E AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 1863 EP - 1874 VL - 7 IS - 12 SN - 0732-183X, 0732-183X KW - Interferon Type I KW - 0 KW - Interleukin-2 KW - Recombinant Proteins KW - Index Medicus KW - Humans KW - Adult KW - Neoplasm Metastasis KW - Clinical Trials as Topic KW - Middle Aged KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Immunotherapy -- methods KW - Neoplasms -- drug therapy KW - Interferon Type I -- adverse effects KW - Interleukin-2 -- adverse effects KW - Interleukin-2 -- administration & dosage KW - Interferon Type I -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79337982?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-10 N1 - Date created - 1990-01-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interleukin-2 induces profound reversible cholestasis: a detailed analysis in treated cancer patients. AN - 79337951; 2585024 AB - Interleukin-2 (IL-2)-based immunotherapy is associated with profound reversible cholestasis and hyperbilirubinemia. We performed a nonrandomized retrospective and prospective analysis to determine the incidence, characteristics, clinical course, and nature of the IL-2-induced liver dysfunction in patients with cancer. Patients received IL-2 at a dose of 20,000 to 100,000 units (U)/kg thrice daily for up to 5 days. Fifty-one patients on adjuvant treatment protocols received a mean of 10.18 +/- 2.38 IL-2 doses and 11.67 +/- 4.16 doses were delivered to 210 patients with advanced disease during this period. Retrospective analysis of all patients receiving this therapy revealed increases in the following liver function tests expressed as median, 25th percentile, and 75th percentile (range): bilirubin (mg/dL) 4.5, 2.6, 6.5 (.4 to 38.5); alkaline phosphatase (U/L) 256, 179, 378 (56-1680); SGOT (U/L) 80, 52, 117 (18 to 483); SGPT (U/L) 91, 64, 132 (20-540); prothrombin time 13.4, 12.8, 14.5 (10.8 to 35.4); and albumin (g/dL) values decreased (trough) slightly 3.0, 2.8, 3.2 (2.3 to 3.8). Multiple regression analysis revealed several factors that were significantly associated with the increase in bilirubin when jointly considered (model P2 less than or equal to .001) including total IL-2 dosage, increase in creatinine, alkaline phosphatase, weight, and SGOT. Similar increases were noted in a prospectively evaluated group of 10 patients. A return to normal levels of bilirubin was noted within 5.6 days of stopping IL-2. Fasting serum cholylglycine increased from a mean of 32.3 +/- 1.6 to a peak of 1556.0 +/- 625.0 mg/mL. Although conventional ultrasound examinations were unrevealing, tissue ultrasound examinations revealed a mean scatterer spacing (MSS) increase compared to baseline of .10 +/- .04 (P less than .02) suggesting hepatic edema or an infiltrative process. Further, computerized hepatobiliary nuclear medicine scans revealed a delay in uptake (2.2 +/- 0.5 fold greater) and excretion (8.0 +/- 5.9 fold greater) of technetium-99m labeled disofenin. These findings support the development of profound reversible cholestasis as the primary basis for the elevated bilirubin in patients undergoing IL-2 treatment and may have implications for understanding the jaundice observed in some patients postoperatively as well as that associated with sepsis and other inflammatory disorders. Specifically, the release of IL-2 or the induction of other factors similarly induced by IL-2 may be responsible for these findings. Tissue ultrasound and computerized hepatobiliary scans provide additional noninvasive assessments of liver function and physiology. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Fisher, B AU - Keenan, A M AU - Garra, B S AU - Steinberg, S M AU - White, D E AU - DiBisceglie, A M AU - Hoofnagle, J H AU - Yolles, P AU - Rosenberg, S A AU - Lotze, M T AD - Surgery Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 1852 EP - 1862 VL - 7 IS - 12 SN - 0732-183X, 0732-183X KW - Interleukin-2 KW - 0 KW - Glycocholic Acid KW - G59NX3I3RT KW - Bilirubin KW - RFM9X3LJ49 KW - Index Medicus KW - Regression Analysis KW - Neoplasms -- drug therapy KW - Glycocholic Acid -- blood KW - Prospective Studies KW - Humans KW - Retrospective Studies KW - Liver Diseases -- diagnostic imaging KW - Bilirubin -- blood KW - Liver Function Tests KW - Radionuclide Imaging KW - Cholestasis -- chemically induced KW - Interleukin-2 -- adverse effects KW - Chemical and Drug Induced Liver Injury UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79337951?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-10 N1 - Date created - 1990-01-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dermatologic complications associated with administration of 2',3'-dideoxycytidine in patients with human immunodeficiency virus infection. AN - 79336836; 2555402 AB - We describe a distinctive mucocutaneous eruption that occurred in 14 of 20 (70%) patients with human immunodeficiency virus infection while they were being treated with a new therapeutic agent, 2'3'-dideoxycytidine. A maculopapular eruption developed in these patients on day 10 or 11 of treatment. Seven of 14 patients, especially those receiving higher-dose therapy, also had systemic symptoms. In addition, oral ulcers developed in 9 of 14 patients on days 4 to 6 of therapy. The occurrence of the cutaneous and oral lesions correlated with dose, route, and schedule of administration of 2'3'-dideoxycytidine. In most instances the mucocutaneous lesions resolved even with continuation of therapy. JF - Journal of the American Academy of Dermatology AU - McNeely, M C AU - Yarchoan, R AU - Broder, S AU - Lawley, T J AD - Dermatology Branch, National Institutes of Health, Bethesda, MD 20892. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 1213 EP - 1217 VL - 21 IS - 6 SN - 0190-9622, 0190-9622 KW - HIV Antigens KW - 0 KW - Zalcitabine KW - 6L3XT8CB3I KW - 2',3'-dideoxycytidinene KW - CI9X00489L KW - Index Medicus KW - AIDS/HIV KW - Drug Evaluation KW - HIV Antigens -- analysis KW - Drug Administration Schedule KW - Humans KW - Adult KW - Middle Aged KW - Ulcer -- etiology KW - T-Lymphocytes, Helper-Inducer -- metabolism KW - Male KW - Drug Eruptions -- etiology KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Drug Eruptions -- pathology KW - Zalcitabine -- analogs & derivatives KW - Zalcitabine -- adverse effects KW - Mouth Diseases -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79336836?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-11 N1 - Date created - 1990-01-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selective immunosuppression of activated T cells with the chimeric toxin IL-2-PE40. Inhibition of experimental autoimmune uveoretinitis. AN - 79336615; 2511243 AB - A characteristic of activated T lymphocytes is the expression of high affinity IL-2R. We studied a new method of selective immunosuppression directed against activated T cells by using a chimeric recombinant protein (IL-2-PE40) composed of IL-2 fused to a modified Pseudomonas exotoxin lacking its cell recognition domain. As a model of T cell-mediated disease, we used experimental autoimmune uveoretinitis (EAU) produced in Lewis rats by active immunization with the retinal S-Ag. The treatment protocol consisted of i.p. injection of IL-2-PE40 at 0.25 micrograms/g every 12 h. Controls were PBS, PE40, or IL-2-PE40asp553 a mutant form of the molecule with reduced activity. Treatment with IL-2-PE40 resulted in a significant reduction of the incidence and severity of EAU over controls. The analysis of the effect of i.p. injection of IL-2-PE40 on the popliteal draining lymph nodes of immunized animals showed a marked reduction in the lymphocytes content. Transfer experiments demonstrated that IL-2-PE40 prevented the development of EAU effector T cells. Interestingly, although activated B cells were reported to express IL-2R, there was no significant reduction of antibody production against the immunizing Ag under IL-2-PE40 treatment, suggesting sparing of the B cells. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Roberge, F G AU - Lorberboum-Galski, H AU - Le Hoang, P AU - de Smet, M AU - Chan, C C AU - Fitzgerald, D AU - Pastan, I AD - Laboratory of Immunology, National Eye Institute, Bethesda, MD 20892. Y1 - 1989/12/01/ PY - 1989 DA - 1989 Dec 01 SP - 3498 EP - 3502 VL - 143 IS - 11 SN - 0022-1767, 0022-1767 KW - Autoantibodies KW - 0 KW - Bacterial Toxins KW - Exotoxins KW - Immunosuppressive Agents KW - Immunotoxins KW - 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 - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred Lew KW - Pseudomonas aeruginosa -- immunology KW - Chimera KW - Humans KW - Lymphocyte Depletion KW - Recombinant Fusion Proteins -- pharmacology KW - Autoantibodies -- biosynthesis KW - Male KW - Cell Line KW - Lymphocyte Activation -- drug effects KW - Interleukin-2 -- pharmacology KW - Exotoxins -- pharmacology KW - Retinitis -- etiology KW - Retinitis -- immunology KW - Autoimmune Diseases -- etiology KW - Immunotoxins -- pharmacology KW - Immunosuppressive Agents -- pharmacology KW - Autoimmune Diseases -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79336615?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-05 N1 - Date created - 1990-01-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Changes in estrogen receptor, DNA ploidy, and estrogen metabolism in rat hepatocytes during a two-stage model for hepatocarcinogenesis using 17 alpha-ethinylestradiol as the promoting agent. AN - 79332761; 2573415 AB - 17 alpha-Ethylestradiol (EE2) was administered chronically to diethylnitrosamine (DEN)-initiated (200/mg/kg, i.p.) adult ovariectomized Sprague-Dawley rats, by means of Silastic implants at an estimated dose of 90 micrograms/kg/day. Isolated hepatocytes from DEN/EE2-treated animals exhibited a 2- to 3-fold increase in nuclear estrogen receptor (ER) levels throughout the promotion period. Furthermore, approximately 30-40% of the receptor was occupied when quantified by an exchange assay. For all groups the ER had a sedimentation coefficient of approximately 8S for unoccupied ER and a binding affinity for 17 beta-estradiol of 0.25 nM. An ER of lower affinity for estradiol was present in animals initiated with DEN and/or promoted with EE2. The increase in hepatocyte ER was associated with a 5.2-fold increase in gamma-glutamyl transpeptidase and 2.5-fold decrease in glucose-6-phosphatase activity at 20 weeks. EE2 treatment caused a 50% increase in the maximal binding capacity (Bmax) of hepatic epidermal growth factor receptors, but the equilibrium binding constant (Kd) did not change. Modulation of mitotic activity of hepatocyte subpopulations by EE2 treatment was indicated by an increase in the proportion of diploid hepatocytes and an increase in the number of hepatocytes undergoing DNA synthesis. In general, effects on ER, epidermal growth factor receptor, gamma-glutamyl transpeptidase and glucose-6-phosphatase were greater in DEN/EE2-treated animals than in rats receiving only EE2. Modification of receptor pathways associated with hepatocyte growth control, ER and epidermal growth factor receptor, may be contributing factors in the clonal expansion of preneoplastic cells during EE2 promotion of hepatocarcinogenesis. JF - Cancer research AU - Vickers, A E AU - Nelson, K AU - McCoy, Z AU - Lucier, G W AD - Laboratory of Biochemical Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/12/01/ PY - 1989 DA - 1989 Dec 01 SP - 6512 EP - 6520 VL - 49 IS - 23 SN - 0008-5472, 0008-5472 KW - Biomarkers, Tumor KW - 0 KW - Carcinogens KW - DNA, Neoplasm KW - Estrogens KW - Receptors, Estrogen KW - Ethinyl Estradiol KW - 423D2T571U KW - Epidermal Growth Factor KW - 62229-50-9 KW - gamma-Glutamyltransferase KW - EC 2.3.2.2 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Rats KW - Biomarkers, Tumor -- metabolism KW - Animals KW - Receptor, Epidermal Growth Factor -- metabolism KW - gamma-Glutamyltransferase -- metabolism KW - Ovariectomy KW - Epidermal Growth Factor -- metabolism KW - DNA, Neoplasm -- metabolism KW - Female KW - Ethinyl Estradiol -- pharmacology KW - Cell Division KW - Liver Neoplasms, Experimental -- genetics KW - Liver Neoplasms -- metabolism KW - Estrogens -- metabolism KW - Liver Neoplasms, Experimental -- metabolism KW - Liver Neoplasms -- chemically induced KW - Liver Neoplasms, Experimental -- chemically induced KW - Receptors, Estrogen -- metabolism KW - Liver Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79332761?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-27 N1 - Date created - 1989-12-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Environmental cancer risks--real and unreal. AN - 79331431; 2583068 JF - Environmental research AU - Lijinsky, W AD - BRI Basic Research Program, National Cancer Institute-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1989/12// PY - 1989 DA - December 1989 SP - 207 EP - 209 VL - 50 IS - 2 SN - 0013-9351, 0013-9351 KW - Carcinogens, Environmental KW - 0 KW - Pesticides KW - Index Medicus KW - Risk Factors KW - Humans KW - Pesticides -- adverse effects KW - Carcinogens, Environmental -- adverse effects KW - Neoplasms -- chemically induced KW - Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79331431?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-10 N1 - Date created - 1990-01-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Relationships among benzo(a)pyrene metabolism, benzo(a)pyrene-diol-epoxide:DNA adduct formation, and sister chromatid exchanges in human lymphocytes from smokers and nonsmokers. AN - 79330428; 2510927 AB - In the present study, benzo(a)pyrene (BP) metabolism, DNA adduct formation, ethoxyresorufin-O-deethylase activity, and sister chromatid exchange induction by BP were compared in human lymphocytes prepared from whole blood of smokers and nonsmokers following an in vitro incubation with BP. There was an approximate 7- to 10-fold variation in all parameters measured. To determine the source of this variation, participants were resampled, the assays were repeated, and all the data were analyzed to assess (a) smoking-related effects, (b) differences in multiple samples from the same individual, and (c) intraindividual, experimental, and interindividual variation. No smoking-related effects were observed except for baseline sister chromatid exchange frequency. The variation observed for BP-related DNA adducts and ethoxyresorufin-O-deethylase activity was primarily due to interindividual variation. For example, in vitro formation of DNA adducts did not change when samples were obtained at different times from the same individual and were not influenced significantly by culture conditions. No significant correlation existed between DNA adduct formation and BP metabolism [correlation coefficient (r) = 0.27] for either the total population or when segregated based on smoking status. Furthermore, no correlation was seen between DNA adducts and sister chromatid exchange induction by BP. Our studies have compared a number of commonly used lymphocyte markers and conclude that it is difficult to predict changes in one marker based on changes in another. However, in vitro formation, of PB-derived DNA adducts is consistent over time for individuals. JF - Cancer research AU - Thompson, C L AU - McCoy, Z AU - Lambert, J M AU - Andries, M J AU - Lucier, G W AD - National Institute of Environmental Health Sciences, Laboratory of Biochemical Risk Analysis, Research Triangle Park, North Carolina 27709. Y1 - 1989/12/01/ PY - 1989 DA - 1989 Dec 01 SP - 6503 EP - 6511 VL - 49 IS - 23 SN - 0008-5472, 0008-5472 KW - Dihydroxydihydrobenzopyrenes KW - 0 KW - Benzo(a)pyrene KW - 3417WMA06D KW - 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide KW - 55097-80-8 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Oxidoreductases KW - EC 1.- KW - Cytochrome P-450 CYP1A1 KW - EC 1.14.14.1 KW - Index Medicus KW - Oxidoreductases -- metabolism KW - Cells, Cultured KW - Humans KW - Adult KW - Cytochrome P-450 Enzyme System -- metabolism KW - Male KW - Female KW - 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide -- metabolism KW - Sister Chromatid Exchange KW - DNA Damage KW - Smoking -- metabolism KW - Lymphocytes -- metabolism KW - Dihydroxydihydrobenzopyrenes -- metabolism KW - Benzo(a)pyrene -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79330428?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-27 N1 - Date created - 1989-12-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Developmental pattern of estrogen receptor expression in female mouse genital tracts. AN - 79330313; 2583044 AB - The distribution of the estrogen receptor (ER) was investigated in neonatal female genital tracts (uterus, oviduct, cervix, and vagina) from days 1-22 after birth, using immunohistochemistry employing an anti-ER monoclonal antibody. In uteri, the ER in epithelial cells began to be observed by day 4. The number of positive epithelial cells and the staining intensity gradually increased until day 22 of age. On the other hand, uterine stroma cells gave a strong ER immunostaining even on day 1. The staining intensity reached a maximum by days 4-7 and then slightly decreased with age. In the oviduct, cervix, and vagina, epithelial cells showed positive ER immunostaining on day 1, and the intensity increased gradually until day 22. ER immunostaining in stroma cells was almost constant during the development period. The ER in both epithelial and stroma cells from these younger animals showed similar biochemical properties, i.e. an increased affinity for nuclei and resistance to extraction with PBS. Thus, during neonatal development of the female reproductive tract, ER is present not only in stroma cells but also in epithelial cells. This ER protein exhibits properties and characteristics similar to those of adult mice. The presence of ER suggests that some of the estrogen actions of cell proliferation, differentiation, and tissue abnormalities resulting from prenatal and postnatal estrogen administration may be mediated by receptor interactions. JF - Endocrinology AU - Yamashita, S AU - Newbold, R R 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 - 1989/12// PY - 1989 DA - December 1989 SP - 2888 EP - 2896 VL - 125 IS - 6 SN - 0013-7227, 0013-7227 KW - Receptors, Estrogen KW - 0 KW - Diethylstilbestrol KW - 731DCA35BT KW - Abridged Index Medicus KW - Index Medicus KW - Uterus -- growth & development KW - Aging -- metabolism KW - Animals KW - Cell Nucleus -- metabolism KW - Cervix Uteri -- metabolism KW - Vagina -- growth & development KW - Mice KW - Tissue Distribution KW - Cervix Uteri -- growth & development KW - Endometrium -- metabolism KW - Uterus -- metabolism KW - Fallopian Tubes -- metabolism KW - Diethylstilbestrol -- pharmacology KW - Endometrium -- growth & development KW - Fallopian Tubes -- growth & development KW - Immunohistochemistry KW - Vagina -- metabolism KW - Female KW - Genitalia, Female -- drug effects KW - Genitalia, Female -- metabolism KW - Receptors, Estrogen -- analysis KW - Receptors, Estrogen -- metabolism KW - Animals, Newborn -- metabolism KW - Genitalia, Female -- growth & development UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79330313?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-09 N1 - Date created - 1990-01-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Duration of desensitization and ultrastructural changes in dorsal root ganglia in rats treated with resiniferatoxin, an ultrapotent capsaicin analog. AN - 79432629; 2611660 AB - We have previously demonstrated resiniferatoxin (RTX) to be an ultrapotent analog of capsaicin. Like capsaicin, RTX initially induces neurogenic inflammation, pain, and hypothermia and then causes desensitization of these responses. We examine here the duration of desensitization following acute treatment with the maximal tolerated dose of RTX. Desensitization to neurogenic inflammation began to diminish by 7 days, whereas desensitization to pain and to induction of hypothermia persisted for several weeks. Interestingly, a partial hypothermic response returned within 24 h if challenge was with RTX at 500-fold its ED50 for control animals; the animals, moreover, maintained their ability to thermoregulate in a hot environment. The time course of the morphological changes--ultrastructure and calcium staining--of dorsal root ganglion neurons was examined in parallel. The ultrastructural changes were evident by 4 h and persisted for the duration of the experiments. Limited calcium staining was visible at 12 and 24 h after treatment but then diminished. In comparison with capsaicin treatment, RTX caused more long-lasting desensitization as well as a distinct spectrum of response. JF - Brain research AU - Szallasi, A AU - Joo, F AU - Blumberg, P M AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute Bethesda, MD 20892. Y1 - 1989/11/27/ PY - 1989 DA - 1989 Nov 27 SP - 68 EP - 72 VL - 503 IS - 1 SN - 0006-8993, 0006-8993 KW - Diterpenes KW - 0 KW - resiniferatoxin KW - A5O6P1UL4I KW - Capsaicin KW - S07O44R1ZM KW - Index Medicus KW - Rats KW - Drug Tolerance KW - Animals KW - Mitochondria -- ultrastructure KW - Dose-Response Relationship, Drug KW - Mitochondria -- drug effects KW - Hypothermia -- chemically induced KW - Diterpenes -- pharmacology KW - Body Temperature Regulation -- drug effects KW - Diterpenes -- toxicity KW - Ganglia, Spinal -- ultrastructure KW - Ganglia, Spinal -- physiology KW - Neurons, Afferent -- ultrastructure KW - Capsaicin -- analogs & derivatives KW - Neurons, Afferent -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79432629?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-14 N1 - Date created - 1990-03-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Suppression of carrageenan-induced hyperalgesia, hyperthermia and edema by a bradykinin antagonist. AN - 79464764; 2482813 AB - Although bradykinin (BK) antagonists have antinociceptive effects, they have not been evaluated for anti-inflammatory activity. When administered with carrageenan into the rat hindpaw, NPC567 significantly blocked carrageenan-induced hyperalgesia, hyperthermia and edema. In addition, NPC567 did not alter the in vitro release of immunoreactive BK by plasma kallikrein. These results indicate that the antinociceptive activity of NPC567, a BK antagonist, may be related to its overall anti-inflammatory activity and that is mechanism of action does not include inhibition of plasma kallikrein. JF - European journal of pharmacology AU - Costello, A H AU - Hargreaves, K M AD - Neurobiology and Anesthesiology Branch, National Institutes of Health, Bethesda, MD 20892. Y1 - 1989/11/21/ PY - 1989 DA - 1989 Nov 21 SP - 259 EP - 263 VL - 171 IS - 2-3 SN - 0014-2999, 0014-2999 KW - Analgesics KW - 0 KW - Anti-Inflammatory Agents, Non-Steroidal KW - Carrageenan KW - 9000-07-1 KW - Aprotinin KW - 9087-70-1 KW - NPC 567 KW - DV64B0PLEH KW - Kallikreins KW - EC 3.4.21.- KW - Bradykinin KW - S8TIM42R2W KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Kallikreins -- antagonists & inhibitors KW - Aprotinin -- pharmacology KW - Male KW - Fever -- chemically induced KW - Edema -- chemically induced KW - Pain -- prevention & control KW - Edema -- prevention & control KW - Bradykinin -- antagonists & inhibitors KW - Bradykinin -- analogs & derivatives KW - Pain -- chemically induced KW - Fever -- prevention & control KW - Analgesics -- pharmacology KW - Bradykinin -- pharmacology KW - Bradykinin -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79464764?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-19 N1 - Date created - 1990-03-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of the second promoter of the transforming growth factor-beta 1 gene by transforming growth factor-beta 1 and phorbol ester occurs through the same target sequences. AN - 79297070; 2808430 AB - Two distinct regions of the transforming growth factor-beta 1 (TGF-beta 1) promoter are responsive to autoregulation and activation by phorbol ester (12-O-tetradecanoylphorbol-13-acetate): sequences located between nucleotides -454 to -323 (first promoter) and between the two transcriptional start sites. We have now characterized in detail the induction of the second promoter (sequences between nucleotides + 1 to +271) of the TGF-beta 1 gene by both TGF-beta 1 and phorbol ester. By assaying progressively deleted mutations in the second promoter, we have found two regions responsible for the induction; each contains a phorbol ester-responsive element. In vitro transcription of the second promoter-chloramphenicol acetyltransferase chimeric genes using nuclear extracts of A-549 cells showed that deletion of the putative phorbol ester-responsive elements results in a 70-80% decrease in activity. DNase I footprinting and gel mobility shift assays showed that binding to an Sp1 site and the putative TRE elements are required for maximal expression of the second promoter region of the TGF-beta 1 gene. These results suggest that AP-1, which is capable of conferring phorbol ester or TGF-beta 1 responsiveness, is the major transcription factor involved in the second promoter-derived transcription of the TGF-beta 1 gene. JF - The Journal of biological chemistry AU - Kim, S J AU - Denhez, F AU - Kim, K Y AU - Holt, J T AU - Sporn, M B AU - Roberts, A B AD - Laboratory of Chemoprevention, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/11/15/ PY - 1989 DA - 1989 Nov 15 SP - 19373 EP - 19378 VL - 264 IS - 32 SN - 0021-9258, 0021-9258 KW - Transforming Growth Factors KW - 76057-06-2 KW - Deoxyribonuclease I KW - EC 3.1.21.1 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Fibrosarcoma KW - Humans KW - Transcription, Genetic KW - Mice KW - Homeostasis KW - Plasmids KW - Base Sequence KW - Transfection KW - Cells, Cultured KW - Lung Neoplasms KW - Molecular Sequence Data KW - Mutation KW - Cell Line KW - Promoter Regions, Genetic -- drug effects KW - Genes -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Gene Expression Regulation -- drug effects KW - Transforming Growth Factors -- pharmacology KW - Transforming Growth Factors -- biosynthesis KW - Transforming Growth Factors -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79297070?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-15 N1 - Date created - 1989-12-15 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - J05114; GENBANK; X02812 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hepatic lesions in Danish epileptics after long-term exposure to anticonvulsant drugs including phenobarbitone. AN - 79291225; 2509719 JF - Journal of the National Cancer Institute AU - Ward, J M AU - Konishi, N AU - Ostergaard, K AD - Tumor Pathology and Pathogenesis Section, National Cancer Institute, Frederick, MD 21701. Y1 - 1989/11/15/ PY - 1989 DA - 1989 Nov 15 SP - 1753 EP - 1754 VL - 81 IS - 22 SN - 0027-8874, 0027-8874 KW - Anticonvulsants KW - 0 KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Rats KW - Animals KW - Phenobarbital -- adverse effects KW - Humans KW - Adult KW - Retrospective Studies KW - Aged KW - Middle Aged KW - Mice KW - Long-Term Care KW - Denmark KW - Male KW - Chemical and Drug Induced Liver Injury -- etiology KW - Anticonvulsants -- adverse effects KW - Epilepsy -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79291225?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-27 N1 - Date created - 1989-11-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment On: J Natl Cancer Inst. 1989 May 10;81(10):803-8 [2716074] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vivo distribution of adoptively transferred indium-111-labeled tumor infiltrating lymphocytes and peripheral blood lymphocytes in patients with metastatic melanoma. AN - 79291176; 2810387 AB - Patients with metastatic melanoma undergoing therapy with cyclophosphamide (CPM), tumor-infiltrating lymphocytes (TIL), and interleukin-2 (IL-2) were studied for the ability of their 111In-labeled TIL or peripheral blood lymphocytes (PBL) to localize in sites of tumor using gamma camera imaging and biopsies. Nineteen infusions of radiolabeled TIL were given to 18 patients, while five patients received radiolabeled autologous PBL during TIL therapy. Clear tumor localization was seen on 13 of 18 nuclear scan series performed on 111In-TIL recipients, while tumor was imaged in only one of four scan sequences on patients given 111In-PBL. Nineteen paired biopsies of tumor and normal skin were completed on 10 patients receiving 111In-TIL, while eight biopsies were done on three PBL patients receiving 111In-PBL. The mean percentage of total injectate activity localizing per gram of tumor tissue was 0.0049% in the TIL group and 0.0010% in the PBL group (P2 = .0004). The mean of the tumor to normal skin ratios of the 111In-TIL group was three times that for 111In-PBL (P2 = .0072). One patient was studied by nuclear scanning on three consecutive treatment courses of CPM, TIL, and IL-2. He initially demonstrated clear tumor localization by 111In-TIL at several sites, then faint localization with 111In-PBL at a single site, and subsequently positive tumor imaging on repeat 111In-TIL infusion at multiple sites. These results confirm and expand our initial data demonstrating that human TIL transferred with CPM pretreatment and followed by IL-2 preferentially localize to tumor sites and indicate that this localization is greater for TIL than PBL. JF - Journal of the National Cancer Institute AU - Griffith, K D AU - Read, E J AU - Carrasquillo, J A AU - Carter, C S AU - Yang, J C AU - Fisher, B AU - Aebersold, P AU - Packard, B S AU - Yu, M Y AU - Rosenberg, S A AD - Department of Transfusion Medicine, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/11/15/ PY - 1989 DA - 1989 Nov 15 SP - 1709 EP - 1717 VL - 81 IS - 22 SN - 0027-8874, 0027-8874 KW - Indium Radioisotopes KW - 0 KW - Interleukin-2 KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - Evaluation Studies as Topic KW - Drug Therapy, Combination KW - Infusions, Intravenous KW - Cells, Cultured KW - Immunotherapy KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Biopsy KW - Male KW - Female KW - Radionuclide Imaging KW - Cyclophosphamide -- administration & dosage KW - Interleukin-2 -- administration & dosage KW - Melanoma -- pathology KW - Melanoma -- diagnostic imaging KW - Lymphocytes -- diagnostic imaging KW - Indium Radioisotopes -- pharmacokinetics KW - Skin Neoplasms -- therapy KW - Skin Neoplasms -- pathology KW - Skin Neoplasms -- diagnostic imaging KW - Melanoma -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79291176?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-27 N1 - Date created - 1989-11-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modified Box-Cox transform for modulating the dynamic range of flow cytometry data. AN - 85266052; pmid-2582974 AB - We describe an algorithm, Vout = Integer ([2(12)-1/2(12 lambda)-1] V lambda in-1) + 1; lambda greater than 0 based upon Box-Cox transformations as an alternative to nonlinear electronic amplifiers to expand or compress high- or low-amplitude flow cytometer-derived signals. If the indexing parameter lambda less than 1, input channels in the high-amplitude input range are compressed in the output range as occurs when an electronic logarithmic amplifier is used. However, if lambda greater than 1, input channels in the low-amplitude input range are compressed in the output range as occurs when an electronic power amplifier is used. Our modified Box-Cox transform can be implemented either during data collection or off-line for the transformation of previously collected raw data. The transform is the equivalent of an infinite class of nonlinear amplifiers. As the transform is implemented in software, it does not suffer from many of the disadvantages of nonlinear electronic amplifiers. JF - Cytometry AU - Dvorak, J A AU - Banks, S M AD - Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. PY - 1989 SP - 811 EP - 813 VL - 10 IS - 6 SN - 0196-4763, 0196-4763 KW - Software KW - Amplifiers KW - Automatic Data Processing KW - Flow Cytometry KW - Algorithms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85266052?accountid=14244 LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Primary lymphoma of the liver in a patient with acquired immune deficiency syndrome and chronic hepatitis B. AN - 85219545; pmid-2683745 AB - We describe the case of a homosexual man with asymptomatic infection with human immunodeficiency virus and hepatitis B virus who developed primary hepatic lymphoma. The lymphoma presented with rapid enlargement of the liver, and ultrasound examination revealed multiple hypoechoic lesions within the liver. Histological examination of the liver showed massive replacement by lymphomatous tissue, as well as changes of chronic active hepatitis B. Immunohistochemical stains for hepatitis B surface and core antigens were strongly positive in almost all hepatocytes, but not in tumor tissue. Whereas the occurrence of lymphoma probably is related to HIV infection, possible interactions between hepatitis B virus and HIV infection are discussed. Thus, the presence of mass lesions within the liver in a patient with HIV infection should raise the possibility of hepatic lymphoma even if there is no evidence of generalized lymphadenopathy. JF - The American Journal of Gastroenterology AU - Lisker-Melman, M AU - Pittaluga, S AU - Pluda, J M AU - Kleiner, D E AU - Thompson, P AU - Martin, P AU - Yarchoan, R AU - Di Bisceglie A M AD - Liver Diseases Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Cancer Institute, Bethesda, Maryland. PY - 1989 SP - 1445 EP - 1448 VL - 84 IS - 11 SN - 0002-9270, 0002-9270 KW - Human KW - Acquired Immunodeficiency Syndrome KW - Antigens, Viral KW - Hepatitis B Virus KW - Ultrasonography KW - HIV-1 KW - Liver Neoplasms KW - Antibodies, Viral KW - Adult KW - Hepatitis B KW - Case Report KW - Chronic Disease KW - Lymphoma KW - Male UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85219545?accountid=14244 LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Immunocytochemical localization of neurofilament subunits in the spiral ganglion of normal and neomycin-treated guinea pigs. AN - 85144375; pmid-2606806 AB - Neurofilaments are a major component of the neuronal cytoskeleton and present in all neurons. The expression of subunits of neurofilaments has been shown to be altered by conditions such as development, aging, degeneration and regeneration of the neuron. In the present study, we determined 1) the distribution of neurofilament subunits in spiral ganglion cells of normal guinea pigs and 2) if this distribution is altered by hair cell degeneration. Immunocytochemical analyses were done with monoclonal antibodies to the 200,000 (NF 200), 160,000 (NF 160), and 68,000 (NF 68) daltons neurofilament subunits. In the normal guinea pig, type II spiral ganglion cells were intensely labeled with NF 200, NF 160, NF 68 antibodies, whereas type I cells were significantly labeled only with NF 200 antibody. Neurofilament subunit immunoreactivity was also localized in the auditory nerve and afferent and efferent fibers to the hair cells. To determine the effects of hair cell loss on neurofilament expression in spiral ganglion cells, guinea pigs were treated with neomycin at doses known to cause extensive hair cell damage. Type I and type II spiral ganglion cells responded differently to this treatment. Type II cells remained strongly immunoreactive after treatment although the number of such cells was reduced, especially in the longer surviving animals. NF 160 and NF 68 immunoreactivities increased gradually from base to apex in type I cells after neomycin treatment, while NF 200 immunoreactivity decreased in all turns. JF - Hearing Research AU - Dau, J AU - Wenthold, R J AD - Neurochemistry Section, National Institute on Deafness and Other Communication Disorders, Bethesda, MD 20892. PY - 1989 SP - 253 EP - 263 VL - 42 IS - 2-3 SN - 0378-5955, 0378-5955 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85144375?accountid=14244 LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Differentiation and oncogenesis: phenotypically distinct lens tumors in transgenic mice. AN - 79577938; 2562221 AB - We report on two lines of transgenic mice that express a murine alpha A-crystallin/SV40 tumor antigen fusion gene in the eye lens. The alpha T1 line develops fast growing, poorly differentiated lens tumors, whereas the alpha T2 line produces lens tumors that are slow growing and well differentiated. There is a striking difference between these two lines in the temporal and spatial patterns of tumor antigen expression during initial lens development. In the alpha T1 line, the transgene is expressed very early in development in most lens cells, and no primary fiber differentiation takes place. In the alpha T2 line, transgene expression occurs after primary fiber formation has been initiated, and is restricted to differentiating fiber cells. The anterior epithelium from both alpha T lines undergoes normal development and remains morphologically normal until after birth, although in alpha T1 mice, these anterior cells produce considerable amounts of SV40 tumor antigens. This suggests that the state of differentiation of the lens cell plays an important role in its response to oncogene products. JF - The New biologist AU - Nakamura, T AU - Mahon, K A AU - Miskin, R AU - Dey, A AU - Kuwabara, T AU - Westphal, H AD - Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 193 EP - 204 VL - 1 IS - 2 SN - 1043-4674, 1043-4674 KW - Antigens, Polyomavirus Transforming KW - 0 KW - Crystallins KW - RNA, Messenger KW - RNA, Neoplasm KW - Recombinant Fusion Proteins KW - Index Medicus KW - Phenotype KW - Neoplasm Invasiveness KW - Animals KW - Mice, Transgenic -- embryology KW - Simian virus 40 -- genetics KW - RNA, Messenger -- analysis KW - Cell Differentiation KW - Mice KW - RNA, Neoplasm -- analysis KW - Epithelium -- pathology KW - Cell Transformation, Neoplastic -- genetics KW - Gene Expression Regulation, Neoplastic KW - Recombinant Fusion Proteins -- biosynthesis KW - Eye Neoplasms -- genetics KW - Lens, Crystalline -- pathology KW - Recombinant Fusion Proteins -- genetics KW - Lens, Crystalline -- embryology KW - Recombinant Fusion Proteins -- toxicity KW - Eye Neoplasms -- pathology KW - Crystallins -- genetics KW - Antigens, Polyomavirus Transforming -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79577938?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-16 N1 - Date created - 1991-05-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Context-dependent cocaine sensitization: differential effect of haloperidol on development versus expression. AN - 79479283; 2623021 AB - Repeated, intermittent administration of psychomotor stimulants has been shown to produce increasing effects (behavioral sensitization) in many species of animals. In a novel two-day sensitization paradigm, rats that received a single high dose of cocaine (40 mg/kg) compared with saline on day 1 showed an increased locomotor response to a challenge dose (10 mg/kg) on day 2. This effect is conditioned or context-dependent; i.e., it is only observed if the rats received cocaine in an environment similar to the test environment. If the cocaine-induced hyperactivity on day 1 is prevented with pharmacological agents such as haloperidol and diazepam, sensitization on day 2 does not occur. Furthermore, although moderate (0.2 mg/kg) and high doses (0.5 mg/kg) of haloperidol (day 1) prevented the development of sensitization to cocaine, they were ineffective when given prior to the day 2 challenge dose in preventing the expression of sensitization. Thus, this type of cocaine sensitization appears to involve conditioning, show stimulus generalization, and offer a possible model for clinical neuroleptic nonresponsiveness once stimulant-induced pathological behavior has been induced. JF - Pharmacology, biochemistry, and behavior AU - Weiss, S R AU - Post, R M AU - Pert, A AU - Woodward, R AU - Murman, D AD - Biological Psychiatry Branch, National Institute of Mental Health 20892. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 655 EP - 661 VL - 34 IS - 3 SN - 0091-3057, 0091-3057 KW - Cocaine KW - I5Y540LHVR KW - Haloperidol KW - J6292F8L3D KW - Diazepam KW - Q3JTX2Q7TU KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Drug Interactions KW - Dose-Response Relationship, Drug KW - Motor Activity -- drug effects KW - Male KW - Behavior, Animal -- drug effects KW - Haloperidol -- pharmacology KW - Diazepam -- pharmacology KW - Homing Behavior KW - Cocaine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79479283?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-26 N1 - Date created - 1990-03-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Acute toxicity of perfluorodecanoic acid in C57BL/6 mice differs from 2,3,7,8-tetrachlorodibenzo-p-dioxin. AN - 79468819; 2620793 AB - Perfluorodecanoic acid (PFDA) is a 10-carbon straight-chain fatty acid. Its toxicity in rats has been reported to resemble that produced by exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Mice which are "responsive" to TCDD toxicity carry the Ahb allele, while mice homozygous for the Ahd gene are less sensitive to TCDD toxicity. To characterize the toxicity of PFDA and determine if it is under the control of the Ah locus, female responsive C57BL/6N (Ahb/b) mice and congenic C57BL/6J mice, differing only at the Ah locus (responsive, Ahb/b; heterozygous responsive, Ahb/d and "nonresponsive," Ahd/d), were administered a single oral dose of PFDA, at levels from 0 to 320 mg/kg body weight, observed daily for overt signs of toxicity, and weighed three times weekly. In the wild-type congenic C57BL/6J (Ahb/b) subline, mice were killed at 2, 7, 14, and 30 days following exposure. All other mice were killed on Day 30. Serum was taken from the C57BL/6N mice for analysis of thyroid hormone levels. Selected organs from all mice were weighed and fixed for histopathological examination. Dose-related mortality was observed as early as 5 days postexposure and time-to-death was inversely related to dose. Dramatic decreases in body weight occurred shortly following treatment in all strains. Serum triiodothyronine (T3) and thyroxine (T4) levels increased with increasing dose. There was a marked increase (p less than 0.05) in absolute and relative liver weights and a significant decrease in thymus weights. Hepatocellular hypertrophy was observed in all treated mice other than controls. A marked increase in hepatocyte peroxisomes was observed in all treatment groups. Thus, in contrast to TCDD, the acute toxicity of PFDA in the female C57BL/6 mouse does not vary with the Ah allele and is distinct from that reported for TCDD. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Harris, M W AU - Uraih, L C AU - Birnbaum, L S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 723 EP - 736 VL - 13 IS - 4 SN - 0272-0590, 0272-0590 KW - Decanoic Acids KW - 0 KW - Dioxins KW - Fluorocarbons KW - Polychlorinated Dibenzodioxins KW - Thyroid Hormones KW - perfluorodecanoic acid KW - 335-76-2 KW - Index Medicus KW - Animals KW - Liver -- pathology KW - Chemical and Drug Induced Liver Injury -- pathology KW - Body Weight -- drug effects KW - Mice, Inbred C57BL KW - Mice KW - Thyroid Hormones -- blood KW - Species Specificity KW - Female KW - Organ Size -- drug effects KW - Mice, Inbred DBA KW - Polychlorinated Dibenzodioxins -- toxicity KW - Fluorocarbons -- toxicity KW - Dioxins -- toxicity KW - Decanoic Acids -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79468819?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-19 N1 - Date created - 1990-03-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effect of ethanol on 35S-TBPS binding to mouse brain membranes in the presence of chloride. AN - 79468511; 2622867 AB - The effect of in vitro and in vivo administration of ethanol on the binding of 35S-t-butyl-bicyclophosphorothionate (35S-TBPS) to cortical brain membranes of C57Bl mice was investigated using KCl (100 mM) containing assay media. The in vitro addition of ethanol produced a dose-dependent inhibition of basal 35S-TBPS binding. In the presence of chloride ions, GABA and pentobarbital had a biphasic action (stimulation followed by inhibition) on 35S-TBPS binding, whereas diazepam only stimulated the binding. Ethanol reduced the stimulatory effects of GABA and pentobarbital in a dose-dependent manner, but had no effect on the enhancement of 35S-TBPS binding produced by diazepam. 35S-TBPS binding to cortical brain membranes was inhibited by the putative Cl- channel blocking agent DIDS. This inhibitory action of DIDS was significantly, and dose-dependently reduced by ethanol (greater than or equal to 100 mM ethanol). Chronic ethanol ingestion in vivo, which produced tolerance to and physical dependence on ethanol in the animals, did not alter the stimulatory and inhibitory effects of GABA and pentobarbital on 35S-TBPS binding. The enhancement of 35S-TBPS binding produced by diazepam was slightly, but significantly, enhanced in brain membranes from animals which had undergone 24 hours of ethanol withdrawal. Chronic ethanol treatment did not change the potency of picrotoxin and of the peripheral BDZ-receptor ligand RO 5-4864 to competitively inhibit 35S-TBPS binding. Our results suggest that in vitro addition of ethanol alters the activity of the GABA/benzodiazepine (BDZ) receptor complex.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Pharmacology & toxicology AU - Liljequist, S AU - Culp, S AU - Tabakoff, B AD - Laboratory for Studies of Neuroadaptive Processes, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 362 EP - 367 VL - 65 IS - 5 SN - 0901-9928, 0901-9928 KW - Benzodiazepinones KW - 0 KW - Bridged Bicyclo Compounds KW - Bridged Bicyclo Compounds, Heterocyclic KW - Bridged-Ring Compounds KW - Chlorides KW - Sulfur Radioisotopes KW - 4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid KW - 27816-59-7 KW - 4'-chlorodiazepam KW - 2QW0IK1742 KW - Ethanol KW - 3K9958V90M KW - gamma-Aminobutyric Acid KW - 56-12-2 KW - tert-butylbicyclophosphorothionate KW - 70636-86-1 KW - Pentobarbital KW - I4744080IR KW - 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid KW - Q1O6DSW23R KW - Diazepam KW - Q3JTX2Q7TU KW - Index Medicus KW - Animals KW - gamma-Aminobutyric Acid -- pharmacology KW - Diazepam -- pharmacology KW - 4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid -- pharmacology KW - Chlorides -- metabolism KW - Mice KW - 4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid -- analogs & derivatives KW - Pentobarbital -- pharmacology KW - Drug Tolerance KW - Mice, Inbred C57BL KW - Substance-Related Disorders -- metabolism KW - Benzodiazepinones -- pharmacology KW - Male KW - Bridged Bicyclo Compounds -- pharmacology KW - Ethanol -- pharmacology KW - Brain -- drug effects KW - Bridged-Ring Compounds -- pharmacology KW - Brain -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79468511?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-23 N1 - Date created - 1990-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Allosteric binding of nickel(II) to calmodulin. AN - 79466678; 2620798 AB - The binding of Ni(II) to calmodulin (CAM) in the presence and in the absence of Ca(II) was investigated by equilibrium dialysis in order to test the physicochemistry of direct Ni(II)-CAM interactions that might be responsible for the effects of this metal on CAM observed in vivo. Samples containing 5 microM CAM, 5 mM Tris/HCl buffer (pH 7.4), and NaCl to maintain the ionic strength I = 3600 microM, with or without 200 microM CaCl2, were dialyzed at 37 degrees C against 1-300 microM 63NiCl2. In the presence of Ca(II), the CAM molecule has two binding sites for Ni(II) (K1 = 7.25 x 10(5) M-1; K2 = 3.79 x 10(5) M-1) (Hill coefficient = 1.20 +/- 0.03 SE). In the absence of Ca(II), a complicated Ni(II)-binding curve is obtained indicating formation of many mutually interacting complex species. Binding of Ni(II) to CAM in the presence of Ca(II) is inhibited slightly by added MnCl2 (50 microM) and very strongly by CuCl2 and ZnCl2 (10 microM). To elucidate the mechanism of this inhibition, binding of Zn(II) (0.5-50 microM 65ZnCl2) to CAM in the presence of Ca(II) (200 microM) was also studied. The maximum molecular ratio of Zn(II) to CAM in the Zn(II)/Ca(II)/CAM complex approached 0.5. Thus, the observed inhibition by Zn(II) of the Ni(II) binding to Ca(II)/CAM does not involve competition for the same binding sites but is rather caused by a conformational arrangement of CAM in its Ca(II)/Zn(II) complex that is different than the Ca(II) complex.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Raos, N AU - Kasprzak, K S AD - Inorganic Carcinogenesis Section, National Cancer Institute, FCRF, Frederick, Maryland 21701. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 816 EP - 822 VL - 13 IS - 4 SN - 0272-0590, 0272-0590 KW - Calmodulin KW - 0 KW - Copper KW - 789U1901C5 KW - Nickel KW - 7OV03QG267 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Calcium -- metabolism KW - Dialysis KW - Kinetics KW - Copper -- metabolism KW - Protein Binding KW - Calmodulin -- metabolism KW - Nickel -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79466678?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-19 N1 - Date created - 1990-03-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Results and evaluations of 48 continuous breeding reproduction studies conducted in mice. AN - 79463423; 2620795 AB - Results of 48 continuous breeding reproduction (RACB) studies are summarized and control data from these studies are used to determine the statistical sensitivity of each endpoint from different parts of these studies. Results of testing individual chemicals compared well with results of multigeneration studies reported in the literature. Continuous breeding studies were able to discriminate reproductive toxicants from nontoxicants, and provided valuable structure-activity information. When mice in continuous cohabitation produce multiple litters, the statistical sensitivity of fertility endpoints is quite high and is comparable to that associated with other sensitive indicators of reproductive function, such as testis weight and sperm parameter measures. The principal advantages of the RACB protocol in comparison to multigeneration studies are: (1) the increased sensitivity and statistical power, (2) the ability to monitor progression of toxicity and to detect subfertility, (3) use of a battery of endpoints including sperm measures, (4) the ability to determine the affected sex(es), and (5) slightly reduced testing time. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Morrissey, R E AU - Lamb, J C AU - Morris, R W AU - Chapin, R E AU - Gulati, D K AU - Heindel, J J AD - Developmental and Reproductive Toxicology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 747 EP - 777 VL - 13 IS - 4 SN - 0272-0590, 0272-0590 KW - Index Medicus KW - Sexual Behavior, Animal -- drug effects KW - Evaluation Studies as Topic KW - Mice, Inbred Strains KW - Animals KW - Reference Values KW - Sex Factors KW - Mice KW - Birth Weight -- drug effects KW - Statistics as Topic KW - Male KW - Female KW - Pregnancy KW - Fertility -- drug effects KW - Reproduction -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79463423?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-19 N1 - Date created - 1990-03-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Assessment in rats of the gonadotoxic and hepatorenal toxic potential of dibromochloropropane (DBCP) in drinking water. AN - 79460117; 2620797 AB - This investigation was undertaken to assess the potential of ingested 1,2-dibromo-3-chloropropane (DBCP) to cause testicular and hepatorenal injury, in light of the paucity of data applicable to risk assessment of DBCP in drinking water. Adult male Sprague-Dawley rats were supplied ad libitum with water containing 0, 5, 50, 100, and 200 ppm DBCP for 64 days. A dose-related decrease in water consumption occurred during the study. The 200-ppm animals drank less than half as much water as controls, consumed less food, and subsequently exhibited significantly lower body weight gain. DBCP ingestion thus was not directly proportional to the level of chemical in the water, although daily and cumulative intake of DCP were concentration dependent. Average daily intake of DBCP for the 64-day exposure period was as follows: 5 ppm = 0.4 mg/kg/day; 50 ppm = 3.3 mg/kg/day; 100 ppm = 5.4 mg/kg/day; 200 ppm = 9.7 mg/kg/day. Blood samples were taken after 2, 4, and 6 weeks of exposure and at the terminal sacrifice and assayed for serum glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, sorbitol dehydrogenase, and ornithine-carbamyl transferase activities and BUN levels. No evidence of liver damage at any exposure level was indicated by either the clinical chemistry indices or histopathology. Histologic examination revealed an apparent increase in the number of nuclei per renal proximal tubule cross-section in the 200-ppm group, possibly indicative of an increased turnover of proximal tubular cells. A slight, but statistically significant, decrease in absolute testicular weight was manifest in the 200-ppm animals, although the decrease was not significant when testicular weight was calculated as g/100 g body wt. Epididymal sperm counts and serum luteinizing hormone, follicle stimulating hormone, and intratesticular testosterone levels were not altered by any dose of DBCP. A qualitative histopathological examination of the testicular seminiferous epithelium failed to reveal any abnormalities in the spermatogenic process. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Heindel, J J AU - Berkowitz, A S AU - Kyle, G AU - Luthra, R AU - Bruckner, J V AD - National Institute of Environmental Health Sciences, National Toxicology Program, Research Triangle Park, North Carolina 27709. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 804 EP - 815 VL - 13 IS - 4 SN - 0272-0590, 0272-0590 KW - Enzymes KW - 0 KW - Gonadal Steroid Hormones KW - Insecticides KW - 1,2-dibromo-3-chloropropane KW - 96K0FD4803 KW - Propane KW - T75W9911L6 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Enzymes -- blood KW - Drinking -- drug effects KW - Dose-Response Relationship, Drug KW - Body Weight -- drug effects KW - Gonadal Steroid Hormones -- blood KW - Male KW - Organ Size -- drug effects KW - Propane -- toxicity KW - Propane -- administration & dosage KW - Insecticides -- toxicity KW - Kidney Diseases -- physiopathology KW - Chemical and Drug Induced Liver Injury -- etiology KW - Testis -- drug effects KW - Insecticides -- administration & dosage KW - Propane -- analogs & derivatives KW - Endocrine System Diseases -- chemically induced KW - Chemical and Drug Induced Liver Injury -- physiopathology KW - Kidney Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79460117?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-19 N1 - Date created - 1990-03-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Metabolism, disposition, and mutagenicity of 2,6-diaminotoluene, a mutagenic noncarcinogen. AN - 79441275; 2575496 AB - 2,6-Diaminotoluene (2,6-DAT) is a major industrial chemical; approximately 100 million pounds are used annually in the synthesis of 2,6-toluene diisocyanate. 2,6-DAT is mutagenic in Salmonella typhimurium TA98 requiring metabolic activation, but has been previously shown to be a noncarcinogen in male and female F344 rats and male and female 86C3F1 mice dosed orally in 2-year bioassays. 2,6-DAT was rapidly and extensively absorbed following oral administration, indicating that its lack of carcinogenicity is not due to poor absorption from the gastrointestinal tract. 2,6-DAT was also rapidly excreted, with 85% of 2,6-DAT-associated radioactivity being recovered in the urine within 24 hr. Resolution of the urine by reverse phase HPLC demonstrated the presence of four metabolites, but none of the parent 2,6-DAT. Therefore, the lack of carcinogenicity of 2,6-DAT is not due to lack of biotransformation in vivo. Following separation by HPLC, the metabolites were analyzed by electron impact and fast atom bombardment mass spectroscopy and by NMR spectroscopy. The metabolites were identified as a) 3-hydroxy-2,6-DAT, b) 4-hydroxy-2-acetylamino-6-aminotoluene, c) 2-acetylamino-6-aminotoluene, and d) 2,6-di(acetylamino)-toluene. Metabolites b and d were found to be mutagenic in Salmonella typhimurium TA98 and then only in the presence of an activation system. Results of this study indicate that 2,6-DAT, which is a mutagen in in vitro tests, is also metabolized by the rat to compounds which are proximate mutagens.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Drug metabolism and disposition: the biological fate of chemicals AU - Cunningham, M L AU - Burka, L T AU - Matthews, H B AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1989 SP - 612 EP - 617 VL - 17 IS - 6 SN - 0090-9556, 0090-9556 KW - Mutagens KW - 0 KW - Phenylenediamines KW - 2,6-diaminotoluene KW - H838Q10551 KW - Index Medicus KW - Rats KW - Feces -- analysis KW - Animals KW - Rats, Inbred F344 KW - Mutagenicity Tests KW - Biotransformation KW - In Vitro Techniques KW - Salmonella typhimurium -- drug effects KW - Tissue Distribution KW - Salmonella typhimurium -- genetics KW - Male KW - Phenylenediamines -- toxicity KW - Phenylenediamines -- pharmacokinetics KW - Phenylenediamines -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79441275?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-06 N1 - Date created - 1990-03-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Thyroid peroxidase: rat cDNA sequence, chromosomal localization in mouse, and regulation of gene expression by comparison to thyroglobulin in rat FRTL-5 cells. AN - 79420285; 2691880 AB - A rat thyroid peroxidase cDNA has been isolated from a FRTL-5 thyroid cell library and sequenced. The cDNA is 2776 base pairs long with an open reading frame of 770 amino acids. By comparison to full-length human thyroid peroxidase cDNA and based on its identification of a 3.2 kilobase mRNA in rat thyroid FRTL-5 cell Northern blots, the rat peroxidase cDNA appears to lack 400-500 base pairs at the 5'-end of the mRNA. It exhibits only a 74% nucleotide and 77% amino acid sequence similarity to human thyroid peroxidase cDNA within the total aligned sequences, although the predicted active site regions are highly conserved (greater than 90-100%). The cDNA has been used to map the thyroid peroxidase gene in mice to chromosome 12 and to compare thyroid peroxidase and thyroglobulin gene expression in FRTL-5 rat thyroid cells. Despite the fact TSH action in both cases is duplicated, and presumably mediated, by cAMP, TSH-induced increases in thyroid peroxidase and thyroglobulin mRNA levels differ. Differences exist with respect to hormone concentration and time. The ability of TSH to increase thyroglobulin, but not thyroid peroxidase mRNA levels, requires insulin, 5% serum, or insulin-like growth factor-I. Insulin or insulin-like growth factor-I alone can increase thyroglobulin mRNA levels as well as or better than TSH but have only a small effect on thyroid peroxidase mRNA levels by comparison to TSH. The ability of TSH to increase thyroglobulin gene expression is readily detected in nuclear run-on assays but not the ability of TSH to increase thyroid peroxidase gene expression. Cycloheximide inhibits TSH-increased thyroglobulin but not peroxidase mRNA levels. Finally, methimazole and phorbol 12-myristate 13-acetate show different effects on TSH-induced increases in thyroglobulin and thyroid peroxidase mRNA levels. JF - Molecular endocrinology (Baltimore, Md.) AU - Isozaki, O AU - Kohn, L D AU - Kozak, C A AU - Kimura, S AD - Laboratory of Biochemistry and Metabolism, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 1681 EP - 1692 VL - 3 IS - 11 SN - 0888-8809, 0888-8809 KW - Actins KW - 0 KW - Amanitins KW - Insulin KW - Dactinomycin KW - 1CC1JFE158 KW - 8-Bromo Cyclic Adenosine Monophosphate KW - 23583-48-4 KW - Methimazole KW - 554Z48XN5E KW - Insulin-Like Growth Factor I KW - 67763-96-6 KW - Thyrotropin KW - 9002-71-5 KW - DNA KW - 9007-49-2 KW - Thyroglobulin KW - 9010-34-8 KW - Cycloheximide KW - 98600C0908 KW - Iodide Peroxidase KW - EC 1.11.1.8 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Sequence Homology, Nucleic Acid KW - Humans KW - Insulin -- pharmacology KW - Amino Acid Sequence KW - Methimazole -- pharmacology KW - Insulin-Like Growth Factor I -- pharmacology KW - 8-Bromo Cyclic Adenosine Monophosphate -- pharmacology KW - Chromosome Mapping KW - Dactinomycin -- pharmacology KW - Rats, Inbred F344 KW - Base Sequence KW - Thyrotropin -- pharmacology KW - Genes KW - Amanitins -- pharmacology KW - Cycloheximide -- pharmacology KW - DNA -- genetics KW - Molecular Sequence Data KW - Thyroid Gland -- enzymology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Gene Expression Regulation -- drug effects KW - Actins -- biosynthesis KW - Cell Line KW - Iodide Peroxidase -- biosynthesis KW - Thyroglobulin -- biosynthesis KW - Mice -- genetics KW - Iodide Peroxidase -- genetics KW - Rats -- genetics KW - Thyroglobulin -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79420285?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-15 N1 - Date created - 1990-02-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vitro maturation and fertilization of domestic cat follicular oocytes. AN - 79390743; 2599509 AB - The time course and conditions necessary for oocyte maturation and subsequent fertilization in vitro were studied in the domestic cat. Darkly pigmented oocytes surrounded by cumulus cells and a tight corona radiata were collected from ovaries removed at ovariohysterectomy. After culture in Eagle's minimum essential medium, oocytes were evaluated for nuclear maturation by analyzing chromosomal spreads. Oocytes achieved metaphase II after intervals of 40-48 hr of in vitro incubation. The incidence of maturation was enhanced (P less than 0.05) when oocytes were recovered from inactive (54%) or follicular (56%) stage donors compared to those recovered from luteal phase (29%) or pregnant (35%) cats. The proportion of oocytes successfully maturing in vitro in medium containing no hormone supplementation (37%) was less (P less than 0.01) than counterparts cultured in follicle-stimulating hormone (FSH) only (48%) or FSH and luteinizing hormone (LH) (54%). The efficiency of maturation was not influenced (P greater than 0.05) by either maintenance/transport temperature (4 degrees C vs. 22 degrees C) or delaying recovery of oocytes from antral follicles (2-8 hr vs. 24-32 hr). Approximately 36% of the in vitro matured oocytes cocultured with spermatozoa demonstrated evidence of fertilization; however, there appeared to be a critical development period for maximizing the incidence of fertilization. These results demonstrate that domestic cat antral oocytes are capable of maturing in vitro, and maturation is influenced by the reproductive status of the donor and the presence of gonadotropins in the culture medium. These oocytes are capable of forming embryos and developing to at least the 16-cell stage in vitro. JF - Gamete research AU - Johnston, L A AU - O'Brien, S J AU - Wildt, D E AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, Maryland 21701. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 343 EP - 356 VL - 24 IS - 3 SN - 0148-7280, 0148-7280 KW - Gonadotropins KW - 0 KW - Index Medicus KW - Gonadotropins -- pharmacology KW - Animals KW - Embryonic and Fetal Development KW - Kinetics KW - Cats KW - Chromosomes -- ultrastructure KW - Female KW - Ovarian Follicle -- physiology KW - Fertilization in Vitro KW - Oogenesis KW - Ovarian Follicle -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79390743?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-01 N1 - Date created - 1990-02-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Benzene risk assessments: review and update. AN - 79387267; 2688843 JF - Cell biology and toxicology AU - Bailer, A J AU - Hoel, D G AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 287 EP - 295 VL - 5 IS - 3 SN - 0742-2091, 0742-2091 KW - Benzene KW - J64922108F KW - Index Medicus KW - Risk KW - Animals KW - Maximum Allowable Concentration KW - Humans KW - Benzene -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79387267?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-30 N1 - Date created - 1990-01-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cycloleucine blocks NMDA responses in cultured hippocampal neurones under voltage clamp: antagonism at the strychnine-insensitive glycine receptor. AN - 79356683; 2556198 AB - 1. Radioligand binding studies have demonstrated that the neutral amino acid cycloleucine may act as a competitive antagonist at the glycine modulatory site on the N-methyl-D-aspartate (NMDA) receptor complex. In the present study, we examined the effects of cycloleucine on NMDA-evoked inward current responses in dissociated hippocampal neuronal cultures using the whole cell voltage-clamp technique. 2. In the presence of 1 microM glycine, cycloleucine caused a reversible, dose-dependent inhibition of NMDA responses with an IC50 of 24 microM. An increase in glycine to 100 microM resulted in a shift to the right of the cycloleucine concentration-effect curve (IC50, 1.4 mM). However, with cycloleucine concentrations less than or equal to 100 microM, a fraction of the block could not be overcome by glycine even at concentrations as high as 1 mM. 3. The cycloleucine block was unaffected by shifts in the holding potential (-60 to +60 mV), and there was no effect of cycloleucine on the reversal potential of the NMDA-evoked current. 4. Cycloleucine failed to effect kainic acid- and quisqualic acid-evoked currents at concentrations which inhibited NMDA responses. 5. We conclude that cycloleucine is a potent and selective antagonist of NMDA-receptor mediated responses. Although this effect occurs in part via competitive antagonism at the glycine modulatory site, the cycloleucine block cannot be completely reversed by glycine indicating an interaction with an additional site on the receptor-channel complex. JF - British journal of pharmacology AU - Hershkowitz, N AU - Rogawski, M A AD - Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 1005 EP - 1013 VL - 98 IS - 3 SN - 0007-1188, 0007-1188 KW - Amino Acids KW - 0 KW - Receptors, Glycine KW - Receptors, Neurotransmitter KW - Cycloleucine KW - 0TQU7668EI KW - Aspartic Acid KW - 30KYC7MIAI KW - N-Methylaspartate KW - 6384-92-5 KW - Strychnine KW - H9Y79VD43J KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Cells, Cultured KW - Strychnine -- pharmacology KW - Membrane Potentials -- drug effects KW - Electrophysiology KW - Female KW - Pregnancy KW - Aspartic Acid -- analogs & derivatives KW - Hippocampus -- physiology KW - Receptors, Neurotransmitter -- metabolism KW - Cycloleucine -- pharmacology KW - Neurons -- drug effects KW - Hippocampus -- cytology KW - Amino Acids -- pharmacology KW - Aspartic Acid -- antagonists & inhibitors KW - Hippocampus -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79356683?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-25 N1 - Date created - 1990-01-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1987 Nov 20;238(4830):1114-6 [2825347] Proc Natl Acad Sci U S A. 1987 Nov;84(21):7744-8 [2823273] Eur J Pharmacol. 1987 Oct 27;142(3):489-90 [2448149] Proc Natl Acad Sci U S A. 1988 Feb;85(4):1307-11 [2448800] J Physiol. 1987 Dec;394:501-27 [2451020] Neurosci Lett. 1988 Feb 3;84(3):351-5 [2451195] Neurosci Lett. 1988 Jun 7;88(3):325-30 [3386879] J Pharmacol Exp Ther. 1988 Jul;246(1):137-42 [2455788] Science. 1988 Aug 12;241(4867):835-7 [2841759] Proc Natl Acad Sci U S A. 1988 Sep;85(17):6547-50 [2842779] Eur J Pharmacol. 1988 Jun 22;151(1):161-2 [2901361] Eur J Pharmacol. 1988 Jun 22;151(1):165-6 [2843389] J Neurophysiol. 1988 Aug;60(2):645-63 [2902200] Eur J Pharmacol. 1988 Sep 1;154(1):85-7 [2846328] J Neurosci. 1988 Oct;8(10):3733-41 [2848107] J Neurosci. 1988 Oct;8(10):3822-6 [2903914] Eur J Pharmacol. 1988 Jul 26;152(1-2):141-6 [3061829] Eur J Pharmacol. 1988 Oct 26;156(1):149-55 [3061832] Eur J Pharmacol. 1988 Oct 26;156(1):177-80 [2905271] Mol Pharmacol. 1989 Mar;35(3):360-8 [2564633] Nature. 1989 Mar 30;338(6214):425-7 [2538755] Science. 1989 Mar 24;243(4898):1611-3 [2467381] Eur J Pharmacol. 1989 Mar 7;172(1):9-17 [2541002] Neurosci Lett. 1989 Jan 30;96(3):323-8 [2541381] Eur J Pharmacol. 1989 Feb 28;161(2-3):281-2 [2542048] Neurosci Lett. 1989 Apr 10;98(3):333-8 [2657505] Biochim Biophys Acta. 1976 May 21;433(3):482-95 [179590] J Theor Biol. 1976 May 21;58(2):383-400 [181640] Am J Physiol. 1978 Aug;235(2):E97-102 [686171] J Neurophysiol. 1983 Dec;50(6):1249-64 [6663325] Nature. 1984 Feb 2-8;307(5950):462-5 [6320006] Nature. 1984 May 17-23;309(5965):261-3 [6325946] Neurosci Lett. 1985 Oct 24;61(1-2):135-9 [2417168] Nature. 1987 Feb 5-11;325(6104):529-31 [2433595] J Neurophysiol. 1987 Aug;58(2):251-66 [2443623] Eur J Pharmacol. 1987 Oct 27;142(3):487-8 [2828080] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Research on alcohol metabolism among Asians and its implications for understanding causes of alcoholism. AN - 79348648; 2511595 AB - Research into the causes of alcoholism is a relatively recent scientific endeavor. One area of study which could lead to better understanding of the disease is the possibility of a genetic predisposition to alcoholism. Recent work has demonstrated that people have varying complements of enzymes to metabolize alcohol. Current knowledge is examined about the influence of various ethanol metabolizing enzymes on alcohol consumption by Asians and members of other ethnic groups. The two principal enzymes involved in ethanol oxidative metabolism are alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH). ADH is responsible for the metabolism of ethanol to acetaldehyde. ALDH catalyzes the conversion of acetaldehyde to acetate. The different isozymes account for the diversity of alcohol metabolism among individuals. An isozyme of ADH (beta 2 beta 2) is found more frequently in Asians than in whites, and an ALDH isozyme (ALDH2), although present in Asians, often is in an inactive form. The presence of an inactive form of ALDH2 is thought to be responsible for an increase in acetaldehyde levels in the body. Acetaldehyde is considered responsible for the facial flushing reaction often observed among Asians who have consumed alcohol. A dysphoric reaction to alcohol, producing uncomfortable sensations, is believed to be a response to deter further consumption. Although the presence of an inactive ALDH2 isozyme may serve as a deterrent to alcohol consumption, its presence does not fully explain the levels of alcohol consumption by those with the inactive isozyme. Other conditions, such as social pressure, and yet undetermined biological factors, may play a significant role in alcohol consumption. JF - Public health reports (Washington, D.C. : 1974) AU - Suddendorf, R F AD - National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857. PY - 1989 SP - 615 EP - 620 VL - 104 IS - 6 SN - 0033-3549, 0033-3549 KW - Isoenzymes KW - 0 KW - Ethanol KW - 3K9958V90M KW - Alcohol Dehydrogenase KW - EC 1.1.1.1 KW - Aldehyde Dehydrogenase KW - EC 1.2.1.3 KW - Acetaldehyde KW - GO1N1ZPR3B KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Flushing KW - Acetaldehyde -- metabolism KW - Asia KW - Isoenzymes -- analysis KW - Aldehyde Dehydrogenase -- genetics KW - Alcoholism -- enzymology KW - Alcohol Dehydrogenase -- genetics KW - Aldehyde Dehydrogenase -- analysis KW - Alcohol Dehydrogenase -- metabolism KW - Ethanol -- metabolism KW - Aldehyde Dehydrogenase -- metabolism KW - Alcoholism -- genetics KW - Alcohol Dehydrogenase -- analysis KW - Isoenzymes -- genetics KW - Isoenzymes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79348648?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-02 N1 - Date created - 1990-01-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Pharmacol Biochem Behav. 1983;18 Suppl 1:127-33 [6356156] Am J Hum Genet. 1983 Nov;35(6):1107-16 [6650498] Alcohol Clin Exp Res. 1983 Fall;7(4):372-7 [6362460] Biochem Genet. 1984 Feb;22(1-2):169-80 [6370230] Biochemistry. 1984 Aug 28;23(18):4082-7 [6487592] Biochemistry. 1984 Nov 20;23(24):5847-53 [6395883] Alcohol Clin Exp Res. 1985 May-Jun;9(3):263-71 [3893198] Alcohol. 1985 Jan-Feb;2(1):53-6 [3893465] Eur J Biochem. 1985 Nov 15;153(1):13-28 [4065146] Hepatology. 1986 May-Jun;6(3):502-10 [3519419] Ann Emerg Med. 1986 Sep;15(9):997-1004 [3526998] Contemp Issues Clin Biochem. 1984;1:135-48 [6400496] Ann N Y Acad Sci. 1987;492:11-24 [3474921] Ann N Y Acad Sci. 1987;492:25-34 [3474929] Clin Pharmacol Ther. 1967 Nov-Dec;8(6):824-9 [6059287] J Biol Chem. 1970 May 25;245(10):2505-12 [4315645] Ann Hum Genet. 1971 Feb;34(3):251-71 [5548434] Ann Hum Genet. 1973 Apr;36(4):401-14 [4748759] Ann Hum Genet. 1973 Jul;37(1):49-67 [4796765] Biochem Biophys Res Commun. 1975 Mar 3;63(1):202-8 [1125010] N Engl J Med. 1976 Jan 1;294(1):9-13 [1244489] Am J Hum Genet. 1975 Nov;27(6):789-96 [1200030] Biochim Biophys Acta. 1977 Jul 8;483(1):35-45 [18196] Adv Enzymol Relat Areas Mol Biol. 1977;45:427-83 [335822] Hum Genet. 1978 Jan 19;40(2):215-20 [624549] Alcohol Clin Exp Res. 1978 Jan;2(1):89-92 [345859] Hum Genet. 1978 Oct 31;44(2):181-5 [730161] Pharmacol Biochem Behav. 1979 Feb;10(2):303-11 [450943] Life Sci. 1980 May 26;26(21):1773-80 [6985464] Proc Natl Acad Sci U S A. 1980 Oct;77(10):5784-8 [7003596] Biochem Biophys Res Commun. 1981 Jan 15;98(1):122-30 [7011320] J Biol Chem. 1981 Dec 25;256(24):12968-73 [7031053] Semin Liver Dis. 1981 Aug;1(3):179-88 [7051301] Biochemistry. 1983 Apr 12;22(8):1852-7 [6342668] Am J Hum Genet. 1983 Jul;35(4):769-72 [6881146] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Rationale for continuous dopaminomimetic therapy of Parkinson's disease. AN - 79347784; 2685653 AB - Levodopa combined with carbidopa (Sinemet) remains the most effective approach to the symptomatic relief of Parkinson's disease. Over time, however, an increasing number of parkinsonian patients evidence motor response complications, notably abnormal involuntary movements and motor fluctuations. Clinical pharmacologic studies suggest that these phenomena may arise as a consequence of factors reflecting both natural disease progression and levodopa toxicity. Simple wearing-off responses appear primarily related to advancing degenerative changes afflicting the dopamine system. The appearance of peak-dose dyskinesias and complex, random motor fluctuations of the on-off type, on the other hand, may signal secondary postjunctional changes arising as a consequence of chronic intermittent excitation of postsynaptic dopamine receptors that are normally tonically stimulated. Therapeutically, prompt correction of wearing-off fluctuations can ordinarily be achieved by measures that deliver dopaminomimetics continuously to the central nervous system. In contrast, fluctuations of the on-off type initially persist despite stable circulating levodopa levels. With continuous levodopa treatment, however, the threshold for dyskinesias begins to rise and the dose-response relation shifts to the right; clinically, the severity of both dyskinesias and on-off fluctuations tends to diminish. It is thus tempting to speculate that the early and continuing treatment of Parkinson's disease with compounds providing a relatively constant level of central dopamine stimulation will preclude wearing-off phenomena and mitigate on-off fluctuations and severe dyskinesias. JF - Neurology AU - Chase, T N AU - Baronti, F AU - Fabbrini, G AU - Heuser, I J AU - Juncos, J L AU - Mouradian, M M AD - Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 7 EP - 10; discussion 19 VL - 39 IS - 11 Suppl 2 SN - 0028-3878, 0028-3878 KW - Antiparkinson Agents KW - 0 KW - Drug Combinations KW - carbidopa, levodopa drug combination KW - Levodopa KW - 46627O600J KW - Carbidopa KW - MNX7R8C5VO KW - Abridged Index Medicus KW - Index Medicus KW - Drug Combinations -- pharmacokinetics KW - Humans KW - Drug Combinations -- therapeutic use KW - Levodopa -- pharmacokinetics KW - Parkinson Disease -- metabolism KW - Levodopa -- therapeutic use KW - Antiparkinson Agents -- therapeutic use KW - Carbidopa -- therapeutic use KW - Carbidopa -- pharmacokinetics KW - Parkinson Disease -- drug therapy KW - Antiparkinson Agents -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79347784?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-04 N1 - Date created - 1990-01-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanism of inhibition of prostaglandin H synthase by eugenol and other phenolic peroxidase substrates. AN - 79344511; 2511429 AB - The mechanism of inhibition of prostaglandin H synthase (PHS) by eugenol was investigated using purified apoenzyme reconstituted with either manganese protoporphyrin IX (Mn-PHS) or hematin (Fe-PHS). Eugenol stimulated Fe-PHS activity at low concentrations and inhibited at higher concentrations, an activity typical of many phenolic compounds. Eugenol was also an excellent reducing cosubstrate for the peroxidase, being cooxidized to a reactive quinone methide in the process. Higher concentrations of eugenol were required to inhibit Fe-PHS than Mn-PHS (which retains cyclooxygenase activity but not peroxidase activity). Inhibition by eugenol was highly dependent on arachidonic acid concentration. In experiments using Mn-PHS, eugenol increased the time required for the initiation of O2 consumption after addition of arachidonic acid and also inhibited the rate of O2 uptake. Eugenol did not, however, affect the total amount of O2 consumed. The addition of 10 microM hydroperoxide (prostaglandin G2) to these incubations did not prevent the inhibitory effects of eugenol. Other phenolic compounds, including guaiacol, butylated hydroxyanisole, and acetaminophen inhibited Mn-PHS in a manner similar to eugenol. These results demonstrate that eugenol and other phenolic compounds specifically inhibit the cyclooxygenase component of PHS and that this inhibition occurs in addition to, or independent of, the effect of these compounds on peroxide tone or their peroxidative metabolism. We suggest that this inhibition is due to competition with arachidonic acid for the active site of PHS. JF - Molecular pharmacology AU - Thompson, D AU - Eling, T AD - National Institute of Environmental Health Sciences, Laboratory of Molecular Biophysics, Research Triangle Park, North Carolina 27709. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 809 EP - 817 VL - 36 IS - 5 SN - 0026-895X, 0026-895X KW - Apoenzymes KW - 0 KW - Arachidonic Acids KW - Cyclooxygenase Inhibitors KW - Phenols KW - Prostaglandins G KW - Butylated Hydroxyanisole KW - 25013-16-5 KW - Arachidonic Acid KW - 27YG812J1I KW - Eugenol KW - 3T8H1794QW KW - Manganese KW - 42Z2K6ZL8P KW - prostaglandin G2 KW - 51982-36-6 KW - Flufenamic Acid KW - 60GCX7Y6BH KW - Guaiacol KW - 6JKA7MAH9C KW - Iron KW - E1UOL152H7 KW - Peroxidases KW - EC 1.11.1.- KW - Ascorbic Acid KW - PQ6CK8PD0R KW - Index Medicus KW - Animals KW - Manganese -- metabolism KW - Phenols -- pharmacology KW - Sheep KW - Guaiacol -- pharmacology KW - Microsomes -- enzymology KW - Arachidonic Acids -- metabolism KW - Ascorbic Acid -- pharmacology KW - Seminal Vesicles -- enzymology KW - Iron -- metabolism KW - Oxidation-Reduction KW - Kinetics KW - Flufenamic Acid -- pharmacology KW - Prostaglandins G -- metabolism KW - Apoenzymes -- metabolism KW - Butylated Hydroxyanisole -- pharmacology KW - Male KW - Peroxidases -- metabolism KW - Eugenol -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79344511?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-02 N1 - Date created - 1990-01-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The human chromogranin A gene: chromosome assignment and RFLP analysis. AN - 79325070; 2573279 AB - Chromogranin A/secretory protein I (CgA) is a glycoprotein that is stored and released along with peptide hormones and neurotransmitters from several tissues, although its exact function is not known. A cDNA (gene symbol CHGA) clone was used as a probe in Southern blot analyses of human-rodent somatic cell hybrid DNAs. Discordancy analysis allowed confirmation of the assignment of the gene to chromosome 14. These results were extended using in situ chromosome hybridization, and a signal was found at 14q32. BglII digestion of genomic DNA from 28 unrelated Caucasian individuals probed with CHGA detected a two-allele RFLP with allelic frequencies of .34 and .66. JF - American journal of human genetics AU - Modi, W S AU - Levine, M A AU - Seuanez, H N AU - Dean, M AU - O'Brien, S J AD - Biological Carcinogenesis and Development Program, National Cancer Institute-Frederick Research Facility, MD 21701. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 814 EP - 818 VL - 45 IS - 5 SN - 0002-9297, 0002-9297 KW - CHGA protein, human KW - 0 KW - Chromogranin A KW - Chromogranins KW - Nerve Tissue Proteins KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Pedigree KW - Polymorphism, Restriction Fragment Length KW - Blotting, Southern KW - Humans KW - DNA -- genetics KW - Nucleic Acid Hybridization KW - Chromosome Mapping KW - Nerve Tissue Proteins -- genetics KW - Chromosomes, Human, Pair 14 KW - Chromogranins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79325070?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-08 N1 - Date created - 1989-12-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Histochem Cytochem. 1978 Aug;26(8):677-9 [99471] Neuroscience. 1976;1(2):65-80 [794758] J Biol Chem. 1982 Apr 10;257(7):3581-8 [7061498] Cytogenet Cell Genet. 1982;32(1-4):58-67 [6291862] Nature. 1983 Apr 28;302(5911):839-42 [6843651] Proc Natl Acad Sci U S A. 1982 Oct;79(19):6056-9 [6821132] Biochem Biophys Res Commun. 1984 Apr 30;120(2):493-9 [6547335] J Biol Chem. 1984 Sep 25;259(18):11597-600 [6147355] Nature. 1986 Sep 4-10;323(6083):82-6 [3018587] Biochem Biophys Res Commun. 1987 Jan 15;142(1):141-6 [3814131] Proc Natl Acad Sci U S A. 1987 Jul;84(14):5043-7 [3474638] J Pediatr. 1987 Oct;111(4):490-5 [2888841] J Biol Chem. 1988 Aug 15;263(23):11559-63 [3403545] Genomics. 1988 May;2(4):310-4 [3265409] Cytogenet Cell Genet. 1987;46(1-4):213-41 [3507275] Gene Anal Tech. 1987 Jul-Aug;4(4):75-85 [3507390] Mol Pharmacol. 1967 Jan;3(1):81-9 [6030895] Nature. 1967 Jul 1;215(5096):58-9 [6053402] Am J Hum Genet. 1980 May;32(3):314-31 [6247908] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Psychiatric disorders in the first-degree relatives of probands with bulimia nervosa. AN - 79322672; 2817120 AB - Data from a family study of psychiatric disorders showed higher rates of major affective disorders, eating disorders, and alcoholism in first-degree relatives of 40 bulimic probands than in first-degree relatives of 24 control subjects. More importantly, the data showed higher rates of major affective disorders in relatives of bulimic probands who themselves had no history of major affective disorders than in relatives of control subjects. This significant finding indicates a familial relationship between bulimia nervosa and major affective disorders, which suggests the possibility of a common diathesis. JF - The American journal of psychiatry AU - Kassett, J A AU - Gershon, E S AU - Maxwell, M E AU - Guroff, J J AU - Kazuba, D M AU - Smith, A L AU - Brandt, H A AU - Jimerson, D C AD - Laboratory of Clinical Science, NIMH, Bethesda, MD. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 1468 EP - 1471 VL - 146 IS - 11 SN - 0002-953X, 0002-953X KW - Abridged Index Medicus KW - Index Medicus KW - Feeding and Eating Disorders -- genetics KW - Humans KW - Adult KW - Antisocial Personality Disorder -- genetics KW - Alcoholism -- genetics KW - Substance-Related Disorders -- genetics KW - Mood Disorders -- genetics KW - Female KW - Mental Disorders -- genetics KW - Bulimia -- complications KW - Mental Disorders -- complications KW - Bulimia -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79322672?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-29 N1 - Date created - 1989-11-29 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Am J Psychiatry. 1990 Oct;147(10):1381-2 [2271032] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of a tumor-suppressor gene in the negative control of anchorage-independent growth of Syrian hamster cells. AN - 79312026; 2813423 AB - Tumor-suppressor genes control the neoplastic phenotype of tumor cells, but the function of these genes in normal cells is unknown. In this report we show that the loss of a tumor-suppressor gene function releases negative controls on the growth of cells in agar. This conclusion is based on observations of cell hybrids and studies of cell variants that have retained or lost a tumor-suppressor gene function. Nontumorigenic cell hybrids between normal Syrian hamster embryo cells and a benzo[a]pyrene-transformed tumor-cell line (BP6T) continued to secrete autocrine and/or paracrine growth factors produced by the tumor cells but failed to respond to these factors by growing in agar. Normal diploid cells also failed to grow in agar in response to the growth factors produced by the tumor cells. Clonal variants of nontumorigenic, immortal Syrian hamster cell lines were isolated that either retained (termed supB+) or had lost (termed supB-) the ability to suppress tumorigenicity of BP6T tumor cells after cell hybridization. Neither supB+ nor supB- variants grew in agar under conditions that allowed efficient growth of the tumor cells. However, supB- cells were reversibly induced to grow in agar with high colony-forming efficiencies in the presence of tumor cell-conditioned medium or by supplementation of the medium with a combination of growth factors. Under the same conditions, the supB+ cells failed to grow in agar. This enhanced growth-factor responsiveness in agar was used to select for supB- variants existing at a low frequency in the supB+ population. These two phenotypes, loss of tumor-suppressor function and enhanced growth-factor responsiveness in agar, were seen to cosegregate. These results indicate the tumor-suppressor gene function in these cells negatively regulates the growth response of cells in agar to mitogenic stimuli. This growth regulation may depend on cell shape or adhesion because supB+ and supB- cells grown attached to plastic responded similarly to growth factors. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Koi, M AU - Afshari, C A AU - Annab, L A AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 8773 EP - 8777 VL - 86 IS - 22 SN - 0027-8424, 0027-8424 KW - Growth Substances KW - 0 KW - Index Medicus KW - Phenotype KW - Clone Cells KW - Animals KW - Growth Substances -- pharmacology KW - Mesocricetus KW - Hybrid Cells -- cytology KW - Tumor Stem Cell Assay KW - DNA Replication KW - Cell Line KW - Cricetinae KW - Cell Adhesion KW - Oncogenes KW - Cell Division -- drug effects KW - Suppression, Genetic KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79312026?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-21 N1 - Date created - 1989-12-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 1986 Apr;46(4 Pt 1):1573-80 [2418950] Cancer Res. 1986 Mar;46(3):1015-29 [3002607] Proc Natl Acad Sci U S A. 1986 Jul;83(14):5209-13 [3523486] Proc Natl Acad Sci U S A. 1986 Aug;83(16):5992-6 [3461473] Mol Cell Biol. 1985 Dec;5(12):3386-96 [2427928] Science. 1986 Oct 10;234(4773):161-6 [3018928] Mol Cell Biol. 1986 Mar;6(3):870-7 [3022135] Nature. 1986 Oct 16-22;323(6089):643-6 [2877398] Proc Natl Acad Sci U S A. 1986 Nov;83(21):8167-71 [3490663] Science. 1987 Mar 13;235(4794):1394-9 [3823889] Science. 1987 Apr 10;236(4798):175-80 [3031816] Cancer Res. 1987 May 1;47(9):2514-20 [3471327] Science. 1987 Jun 26;236(4809):1657-61 [2885916] Mol Cell Biol. 1987 Jul;7(7):2649-52 [3475570] Nature. 1987 Aug 13-19;328(6131):616-9 [2886919] Science. 1987 Dec 11;238(4833):1539-45 [3317834] Proc Natl Acad Sci U S A. 1988 Mar;85(5):1590-4 [3125552] Cancer Res. 1988 Mar 15;48(6):1623-32 [2449958] Cancer Res. 1988 Jun 15;48(12):3302-6 [3370633] Cancer Res. 1988 Jul 1;48(13):3716-9 [3378214] Oncogene. 1987;1(3):271-6 [3330775] Proc Natl Acad Sci U S A. 1988 Aug;85(15):5576-80 [2456572] Cell. 1989 Jan 13;56(1):77-84 [2642744] Mol Carcinog. 1988;1(3):180-8 [3074813] Proc Natl Acad Sci U S A. 1977 Sep;74(9):3845-9 [269435] Proc Natl Acad Sci U S A. 1977 Oct;74(10):4481-5 [270695] Nature. 1978 Jun 1;273(5661):345-9 [661946] Proc Natl Acad Sci U S A. 1978 Aug;75(8):3761-5 [278986] Science. 1982 Jan 15;215(4530):252-9 [7053574] Cancer Res. 1983 Apr;43(4):1581-6 [6299525] Cell. 1983 Jul;33(3):653-5 [6307524] Cell. 1983 Jul;33(3):931-8 [6307528] Nature. 1983 Oct 27-Nov 2;305(5937):779-84 [6633649] Science. 1984 Mar 9;223(4640):1028-33 [6320372] Proc Natl Acad Sci U S A. 1984 Apr;81(8):2396-400 [6326125] Nature. 1984 Aug 23-29;310(5979):655-60 [6088986] Mol Cell Biol. 1984 Aug;4(8):1572-6 [6092919] Cancer Res. 1985 Feb;45(2):726-32 [2981612] Nature. 1985 Feb 28-Mar 6;313(6005):745-7 [3883191] Cancer Res. 1985 Apr;45(4):1437-43 [2983882] Proc Natl Acad Sci U S A. 1985 Apr;82(7):2062-6 [3856884] J Cell Biochem. 1985;27(2):143-56 [3886675] Nature. 1985 Aug 15-21;316(6029):636-9 [2993900] Mutat Res. 1986 Jul;168(1):3-14 [3012326] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Non-metallothionein-bound cadmium in the pathogenesis of cadmium nephrotoxicity in the rat. AN - 79309856; 2815080 AB - Male rats were injected SC with 0.6 mg Cd/kg/day for 5 days per week for 2, 4, 6, and 8 weeks. Liver and kidney were examined morphologically and analyzed for metallothionein, cadmium, zinc, and copper. Morphologic changes were found in kidney but not in liver. The earliest ultrastructural change consisted of myelin figures in vacuoles in cytoplasm of proximal tubular lining cells reflecting degeneration of membranes. This change occurred after 4 weeks with 801 +/- 25 nmol/g (89.9 micrograms/g) total kidney cadmium or 390 nmol/g (43.7 micrograms/g) of cadmium not bound to metallothionein. Similar changes were observed after 6 weeks but after 8 weeks pathological changes consisted of focal cellular necrosis and interstitial fibrosis. Other ultrastructural changes included altered mitochondria and increased numbers of microbodies. Renal cadmium after 8 weeks exposure was 1827 +/- 48 nmol/g (215.3 +/- 5.8 micrograms/g) or 628 nmol/g (70.2 micrograms/g) of cadmium not bound to metallothionein. Total cadmium was higher in liver than in kidney but partitioning between bound and nonbound cadmium differed in the two organs. The fraction not bound to metallothionein increased with time of exposure in both liver and kidney. However, total cadmium in the liver did not exceed potentially available binding sites of metallothionein, whereas total cadmium did exceed potentially available binding sites of metallothionein in the kidney where pathologic changes occurred. The results indicated that degeneration of cellular membranes is an early cellular effect of cadmium exposure followed later by toxicity to organelles, cellular necrosis, and interstitial fibrosis. Cadmium-induced cellular toxicity is more directly related to the fraction of cadmium in the kidney that is not bound to metallothionein than is total cadmium per se. JF - Toxicology and applied pharmacology AU - Goyer, R A AU - Miller, C R AU - Zhu, S Y AU - Victery, W AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27514. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 232 EP - 244 VL - 101 IS - 2 SN - 0041-008X, 0041-008X KW - Cadmium KW - 00BH33GNGH KW - Copper KW - 789U1901C5 KW - Metallothionein KW - 9038-94-2 KW - Zinc KW - J41CSQ7QDS KW - Index Medicus KW - Animals KW - Dose-Response Relationship, Drug KW - Kidney Tubules, Proximal -- ultrastructure KW - Liver -- analysis KW - Rats, Inbred Strains KW - Liver -- ultrastructure KW - Rats KW - Zinc -- analysis KW - Kidney Cortex -- drug effects KW - Kidney Cortex -- ultrastructure KW - Copper -- analysis KW - Kidney Tubules, Proximal -- drug effects KW - Microscopy, Electron KW - Male KW - Cadmium -- metabolism KW - Metallothionein -- analysis KW - Cadmium -- toxicity KW - Cadmium -- pharmacokinetics KW - Metallothionein -- metabolism KW - Kidney Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79309856?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-21 N1 - Date created - 1989-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A comparison of three nucleoside analogs with anti-retroviral activity on immune and hematopoietic functions in mice: in vitro toxicity to precursor cells and microstromal environment. AN - 79308446; 2554533 AB - A number of 2'3'-dideoxynucleosides have been reported to markedly inhibit the in vitro growth of HIV, the causative agent of acquired immunodeficiency syndrome (AIDS). Clinical trials have shown that the continued therapeutic use of these nucleoside derivatives can be associated with adverse side effects. Since these side effects include myelotoxicity, as occurs in many patients treated with zidovudine (AZT; 3'-azido'3-deoxythymidine), and AIDS patients already represent an immunologically compromised population, we examined the immunological effects of three nucleoside inhibitors, including zidovudine, 2'3'-dideoxycytidine, and 2'3'-dideoxyadenosine (DDA) in a mouse model. Additional studies were conducted to further determine and characterize the potential toxic effects associated with these drugs on the hematopoietic system. Of the three dideoxynucleosides examined, only DDA altered immune functions following a 30-day subchronic exposure in mice. This was evidenced by a marked suppression of the antibody plaque-forming cell response and a slight alteration in macrophage function. None of the nucleoside derivatives affected bone marrow function following in vivo exposure, although AZT produced a mild macrocytic anemia in vivo and was myelotoxic when added in vitro to bone marrow cell cultures. In vitro studies indicated that AZT was capable of affecting both proliferating stem cells as well as the stromal cell microenvironment, both of which play a role in hematopoiesis. These data indicate that, although the mice may not develop the identical toxicities associated with nucleoside therapy in humans, certain adverse immunological and hematological effects were readily discerned which could have relevance to humans. JF - Toxicology and applied pharmacology AU - Luster, M I AU - Germolec, D R AU - White, K L AU - Fuchs, B A AU - Fort, M M AU - Tomaszewski, J E AU - Thompson, M AU - Blair, P C AU - McCay, J A AU - Munson, A E AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 328 EP - 339 VL - 101 IS - 2 SN - 0041-008X, 0041-008X KW - Antiviral Agents KW - 0 KW - Zidovudine KW - 4B9XT59T7S KW - Dideoxyadenosine KW - 4Q86AH641A KW - Zalcitabine KW - 6L3XT8CB3I KW - Index Medicus KW - AIDS/HIV KW - Stem Cells -- drug effects KW - HIV -- growth & development KW - Animals KW - HIV -- drug effects KW - Macrophages -- immunology KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Mice KW - Macrophages -- drug effects KW - Virus Replication -- drug effects KW - Mice, Inbred C57BL KW - Immunity, Cellular -- drug effects KW - Spleen -- immunology KW - T-Lymphocytes -- drug effects KW - Spleen -- drug effects KW - Bone Marrow -- drug effects KW - T-Lymphocytes -- immunology KW - Bone Marrow -- immunology KW - Female KW - Antigen-Antibody Reactions -- drug effects KW - Zidovudine -- therapeutic use KW - Zidovudine -- toxicity KW - Hematopoiesis -- drug effects KW - Dideoxyadenosine -- therapeutic use KW - Zalcitabine -- toxicity KW - Zalcitabine -- therapeutic use KW - Dideoxyadenosine -- toxicity KW - Antiviral Agents -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79308446?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-21 N1 - Date created - 1989-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Combination of interleukins 3 and 6 preserves stem cell function in culture and enhances retrovirus-mediated gene transfer into hematopoietic stem cells. AN - 79307883; 2813429 AB - The effects of several hematopoietic growth factors on primitive murine bone marrow progenitor cells [colony-forming unit(s)-spleen (CFU-S)] have been investigated during culture for 2-6 days. Interleukin 3 (IL-3) was required for CFU-S survival in culture, and the combination of IL-3 and interleukin 6 (IL-6) increased the number of CFU-S in culture 10-fold over the number obtained with IL-3 alone. Stem cell function was measured by competitive repopulation; IL-3 was required, and IL-3 and IL-6 appear to act synergistically to enhance stem cell recovery from these cultures. These data appear to be relevant for retroviral-mediated gene transfer into stem and progenitor cells. Murine bone marrow cells were infected with a retrovirus containing the human beta-globin gene in the presence of various growth factors. Only 2 of 17 mice reconstituted with cells infected in the presence of IL-3 alone showed long-term expression of the human beta-globin gene (12 months), as opposed to 6 of 11 mice reconstituted with cells infected in the presence of IL-3 and IL-6. Medium conditioned by 5637 bladder carcinoma cells, a source of several hematopoietic growth factors, increased the frequency of infection of CFU-S but did not enhance stem cell infection or the repopulating potential of cultured bone marrow cells. Stem cells containing the human beta-globin provirus from these animals were shown to be capable of reconstituting secondary recipients in which the human beta-globin gene was expressed. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Bodine, D M AU - Karlsson, S AU - Nienhuis, A W AD - Clinical Hematology Branch, National Heart, Lung and Blood Institute, Bethesda, MD 20892. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 8897 EP - 8901 VL - 86 IS - 22 SN - 0027-8424, 0027-8424 KW - Interleukin-3 KW - 0 KW - Interleukin-6 KW - RNA, Messenger KW - Recombinant Proteins KW - Globins KW - 9004-22-2 KW - Index Medicus KW - Animals KW - Recombinant Proteins -- pharmacology KW - Humans KW - RNA, Messenger -- analysis KW - Gene Expression KW - Mice KW - Mice, Inbred Strains KW - Cell Survival -- drug effects KW - Cells, Cultured KW - Mice, Inbred C57BL KW - Helper Viruses -- genetics KW - Retroviridae -- genetics KW - Colony-Forming Units Assay KW - Drug Synergism KW - Female KW - Transfection -- drug effects KW - Genes KW - Interleukin-3 -- pharmacology KW - Hematopoietic Stem Cells -- cytology KW - Globins -- genetics KW - Interleukin-6 -- pharmacology KW - Hematopoietic Stem Cells -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79307883?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-21 N1 - Date created - 1989-12-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nucleic Acids Res. 1987 Dec 23;15(24):10159-77 [3480506] Proc Natl Acad Sci U S A. 1989 Nov;86(22):8892-6 [2573068] Nature. 1988 Jan 7;331(6151):35-41 [2893284] J Immunol. 1988 May 1;140(9):3040-4 [3258892] Proc Natl Acad Sci U S A. 1988 Jun;85(12):4360-4 [3288992] J Exp Med. 1988 Jun 1;167(6):1825-40 [3260264] Science. 1988 Jul 1;241(4861):58-62 [2898810] Proc Natl Acad Sci U S A. 1988 Aug;85(16):6062-6 [3413076] Proc Natl Acad Sci U S A. 1988 Oct;85(19):7099-103 [3262872] Blood. 1989 Feb;73(2):425-30 [2563662] Mol Cell Biol. 1988 Dec;8(12):5116-25 [3072474] Mol Cell Biol. 1989 Feb;9(2):798-808 [2565534] Blood. 1989 May 15;73(7):1828-35 [2469502] Nature. 1979 Oct 4;281(5730):381-2 [481601] Blood. 1980 Jan;55(1):77-81 [6985804] Virology. 1981 Apr 15;110(1):202-7 [7210505] Blood. 1983 May;61(5):823-9 [6338973] Proc Natl Acad Sci U S A. 1983 May;80(10):2931-5 [6574462] J Exp Med. 1984 Mar 1;159(3):679-90 [6699542] Mol Cell Biol. 1984 Jan;4(1):151-9 [6538258] Proc Natl Acad Sci U S A. 1984 Feb;81(4):1070-4 [6322187] Nature. 1984 Aug 9-15;310(5977):476-80 [6087158] Science. 1984 Oct 26;226(4673):401-9 [6093246] Cell. 1985 Aug;42(1):71-9 [4016956] J Cell Physiol. 1985 Aug;124(2):182-90 [3930522] Nature. 1985 Nov 14-20;318(6042):149-54 [3903518] Science. 1985 Dec 20;230(4732):1395-8 [2999985] Exp Hematol. 1986 Mar;14(3):222-9 [3512279] Cell. 1986 Jun 20;45(6):917-27 [2871944] Science. 1986 Aug 1;233(4763):566-9 [3726549] Blood. 1989 May 15;73(7):1836-41 [2653465] Nature. 1989 May 4;339(6219):27-30 [2469962] EMBO J. 1989 Feb;8(2):441-8 [2542015] Genes Dev. 1989 Mar;3(3):314-23 [2721958] Mol Cell Biol. 1989 Apr;9(4):1426-34 [2657395] Proc Natl Acad Sci U S A. 1987 Dec;84(24):9035-9 [3501121] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antitumor activity in mice of an immunotoxin made with anti-transferrin receptor and a recombinant form of Pseudomonas exotoxin. AN - 79300261; 2510169 AB - LysPE40 is a modified form of Pseudomonas exotoxin that lacks the cell-binding domain and has a chemically reactive lysine residue near the amino terminus. LysPE40 is made in Escherichia coli and secreted into the medium from which it is readily purified. Two immunotoxins were constructed by coupling LysPE40 to an antibody to the human transferrin receptor (TFR) or to an antibody to the human interleukin-2 receptor. These immunotoxins were selectively cytotoxic to receptor-bearing cells in tissue culture. Anti-TFR-LysPE40 given intraperitoneally to mice appeared rapidly in the blood and caused regression of A431 tumors growing as subcutaneous xenografts. These results show that it is possible to cause regression of a solid carcinoma by an immunotoxin if proper targeting can be achieved. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Batra, J K AU - Jinno, Y AU - Chaudhary, V K AU - Kondo, T AU - Willingham, M C AU - FitzGerald, D J AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 8545 EP - 8549 VL - 86 IS - 21 SN - 0027-8424, 0027-8424 KW - Antibodies, Monoclonal KW - 0 KW - Bacterial Toxins KW - Exotoxins KW - Immunotoxins KW - Neoplasm Proteins KW - Protein Synthesis Inhibitors KW - Receptors, Interleukin-2 KW - Receptors, Transferrin 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 - Neoplasm Proteins -- biosynthesis KW - Recombinant Proteins -- pharmacology KW - Humans KW - Recombinant Proteins -- blood KW - Mice KW - Mice, Nude KW - Mice, Inbred BALB C KW - Antibodies, Monoclonal -- therapeutic use KW - Neoplasm Transplantation KW - Transplantation, Heterologous KW - Pseudomonas aeruginosa KW - Recombinant Proteins -- therapeutic use KW - Cell Line KW - Female KW - Exotoxins -- pharmacology KW - Exotoxins -- blood KW - Immunotoxins -- blood KW - Receptors, Interleukin-2 -- immunology KW - Carcinoma, Squamous Cell -- pathology KW - Immunotoxins -- therapeutic use KW - Receptors, Transferrin -- immunology KW - Exotoxins -- therapeutic use KW - Immunotoxins -- pharmacology KW - Carcinoma, Squamous Cell -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79300261?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-08 N1 - Date created - 1989-12-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1986 Sep;83(17):6627-30 [3018739] Eur J Biochem. 1986 Feb 17;155(1):1-10 [3948873] Cell. 1987 Jan 16;48(1):129-36 [3098436] Cancer Res. 1987 Feb 15;47(4):947-52 [3492271] Proc Natl Acad Sci U S A. 1987 Apr;84(8):2474-8 [3104916] Proc Natl Acad Sci U S A. 1987 Jul;84(13):4538-42 [3299371] J Natl Cancer Inst. 1987 Nov;79(5):1163-72 [3500356] Science. 1987 Nov 20;238(4830):1098-104 [3317828] Cancer. 1988 May 1;61(9):1766-75 [2451555] Proc Natl Acad Sci U S A. 1988 May;85(9):2939-43 [3283735] J Biol Chem. 1988 Jul 5;263(19):9470-5 [3132465] Cancer Res. 1988 Nov 15;48(22):6396-403 [3263186] J Urol. 1989 Feb;141(2):428-31 [2643730] Proc Natl Acad Sci U S A. 1989 May;86(10):3778-81 [2786202] Cancer Res. 1989 Jul 1;49(13):3482-8 [2786451] J Immunol. 1981 Apr;126(4):1393-7 [6970774] J Immunol. 1981 Jul;127(1):347-51 [6787129] Proc Natl Acad Sci U S A. 1983 Jan;80(2):529-33 [6572905] Cancer Res. 1985 Feb;45(2):751-7 [2981613] Cell. 1986 Dec 5;47(5):641-8 [3536124] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular analysis of O6-substituted guanine-induced mutagenesis of ras oncogenes. AN - 79299260; 2682655 AB - We have designed an Ha-ras/thymidine kinase (TK) cassette that permits the incorporation of chemically synthesized adducts within specific domains of the rat Ha-ras protooncogene. This cassette has been used to evaluate the mutagenicity of O6-substituted guanine residues, including O6-methylguanine and O6-benzylguanine, incorporated within the 12th codon of this locus. Mutations were monitored by the ability of these modified Ha-ras DNAs to transform Rat4 TK-cells. Our results indicate that both types of O6-substituted guanines are substantially mutagenic, although the methyl substituent induced a 2-fold higher percentage of transformed Rat4 TK+ colonies than its bulkier benzyl analogue. Interestingly, the mutagenicity of both O6-substituted guanines was found to be independent of their relative position within codon 12, therefore suggesting that the specific activation of Ha-ras oncogenes by GGA----GAA mutations in tumors induced by methylating carcinogens might be due to differences in the accessibility of these guanine residues to the carcinogen rather than to a differential rate of repair. Molecular analysis of the mutations induced by these O6-substituted guanines indicated that O6-methylguanine exclusively induced G----A transitions. In contrast, O6-benzylguanine produced G----C and G----T transversions in addition to G----A transitions. These results suggest that O6-methylguanine and its bulkier analogue O6-benzylguanine may induce mutagenesis by different mechanisms. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Mitra, G AU - Pauly, G T AU - Kumar, R AU - Pei, G K AU - Hughes, S H AU - Moschel, R C AU - Barbacid, M AD - Developmental Oncology, National Cancer Institute-Frederick Cancer Research Facility, MD 21701. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 8650 EP - 8654 VL - 86 IS - 22 SN - 0027-8424, 0027-8424 KW - Oligonucleotide Probes KW - 0 KW - Guanine KW - 5Z93L87A1R KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - Index Medicus KW - Rats KW - Animals KW - Base Sequence KW - Transfection KW - Restriction Mapping KW - Molecular Sequence Data KW - Escherichia coli -- genetics KW - Plasmids KW - Cell Line KW - Gene Amplification KW - Alkylation KW - Genes, ras KW - Guanine -- analysis KW - Guanine -- analogs & derivatives KW - Mutation KW - Guanine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79299260?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-21 N1 - Date created - 1989-12-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Z Krebsforsch. 1967;69(2):103-201 [4230610] Oncogene. 1988 Dec;3(6):647-51 [2578002] J Natl Cancer Inst. 1975 Feb;54(2):401-14 [1113323] Nature. 1980 May 22;285(5762):207-10 [6246445] Virology. 1981 Aug;113(1):408-11 [7269249] Annu Rev Biochem. 1982;51:655-93 [7051963] Nature. 1983 Dec 15-21;306(5944):658-61 [6318112] Cancer Invest. 1984;2(3):223-31 [6733565] Proc Natl Acad Sci U S A. 1984 Jul;81(13):4008-12 [6330729] Nature. 1985 May 30-Jun 5;315(6018):382-5 [3923365] J Biol Chem. 1986 Jul 25;261(21):9879-85 [3525535] Proc Natl Acad Sci U S A. 1986 Aug;83(16):5825-9 [3016723] Mol Cell Biol. 1987 Jan;7(1):379-87 [3031469] Annu Rev Biochem. 1987;56:779-827 [3304147] J Mol Biol. 1987 Apr 5;194(3):385-90 [3305959] Science. 1987 Sep 11;237(4820):1309-16 [3629242] Science. 1988 Jan 29;239(4839):487-91 [2448875] Carcinogenesis. 1988 May;9(5):691-6 [3284662] Carcinogenesis. 1988 Sep;9(9):1607-10 [3044637] Carcinogenesis. 1988 Nov;9(11):2139-43 [3180351] Mol Cell Biol. 1988 Aug;8(8):3565-9 [3062384] Adv Cancer Res. 1988;51:147-82 [3066145] Chem Res Toxicol. 1988 Jan-Feb;1(1):1-18 [2979705] Chem Res Toxicol. 1988 Nov-Dec;1(6):391-7 [2979756] Virology. 1973 Apr;52(2):456-67 [4705382] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dietary restriction, tumors, and aging in rodents. AN - 79294054; 2681366 AB - A chronic 30-50% restriction of dietary energy intake (but without malnutrition) typically and strongly lowers the incidence of most spontaneous and induced tumors, delays their onsets, and extends maximum life span in rodents. When compared to normally fed controls, animals fed these dietary restriction (DR) regimens show decreased rates of change for most (but not all) age-sensitive biologic indexes studied to date. DR's impact on chemically induced tumors appears to depend more on energy than on fat restriction, and result from less promotion (and not less initiation). The molecular and cellular events underlying these various outcomes of DR are unclear. Viable explanations include less cellular oxidative damage, a retardation in the age-related changes in the immune system, hormonal changes, less exposure to dietary carcinogens and promoters, less energy for tumor growth, less carcinogen activation, and better DNA repair. New findings are consistent with the notion that DR reduces cellular damage mediated by active oxygen. A lower production or higher detoxification rate of active oxygen species, which damages molecules and promotes tumor growth, could explain DR's effects on aging and tumors. JF - Journal of gerontology AU - Weindruch, R AD - National Institute on Aging, Biomedical Research and Clinical Medicine Program, Bethesda, MD 20892. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 67 EP - 71 VL - 44 IS - 6 SN - 0022-1422, 0022-1422 KW - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Animals KW - Mice KW - Longevity KW - Aging -- metabolism KW - Energy Intake KW - Neoplasms, Experimental -- metabolism KW - Neoplasms, Experimental -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79294054?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-21 N1 - Date created - 1989-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Anxiety and alcoholism. AN - 79287268; 2681171 AB - Patients with alcohol dependence commonly experience symptoms of anxiety, depression, and insomnia. It is essential that clinicians recognize and treat anxiety disorders in alcoholic patients. Panic attacks with and without agoraphobia are especially prevalent among alcoholics and their families. Treatments of choice for panic disorder are the monoamine oxidase inhibitors, as well as tricyclic antidepressants and the benzodiazepine alprazolam. Benzodiazepines seem to be effective in controlling two pathophysiologic characteristics of alcohol withdrawal--noradrenergic and hypothalamic-pituitary-adrenocortical overactivity. They also can be used to prevent and treat withdrawal seizures and delirium tremens. They are not indicated for the treatment of alcohol dependence per se. JF - The Journal of clinical psychiatry AU - Linnoila, M I AD - Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Md. 20892. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 26 EP - 29 VL - 50 Suppl SN - 0160-6689, 0160-6689 KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Ethanol -- adverse effects KW - Substance Withdrawal Syndrome -- diagnosis KW - Humans KW - Substance Withdrawal Syndrome -- therapy KW - Anxiety Disorders -- etiology KW - Alcoholism -- therapy KW - Alcoholism -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79287268?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-15 N1 - Date created - 1989-12-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comments on the reanalysis of the National Cancer Institute study of workers exposed to formaldehyde. AN - 79286554; 2809794 JF - Journal of occupational medicine. : official publication of the Industrial Medical Association AU - Blair, A AU - Stewart, P A AD - National Cancer Institute, Division of Cancer Etiology, Bethesda, MD 20892. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 881 EP - 884 VL - 31 IS - 11 SN - 0096-1736, 0096-1736 KW - Formaldehyde KW - 1HG84L3525 KW - Index Medicus KW - Risk Factors KW - Humans KW - Cohort Studies KW - Adult KW - Environmental Exposure KW - Middle Aged KW - Male KW - Formaldehyde -- adverse effects KW - Lung Neoplasms -- mortality KW - Occupational Diseases -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79286554?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-08 N1 - Date created - 1989-12-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment On: J Occup Med. 1988 Nov;30(11):895-901 [3230440] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alkyl and aryl carcinogen adducts detected in human peripheral lung. AN - 79284801; 2805234 AB - Human peripheral lung tissue samples were obtained at autopsy from 17 individuals of known occupational and smoking histories. A spectrum of different carcinogen-DNA adducts was detected using a variety of sensitive techniques. High-pressure liquid chromatography-linked synchronous fluorescent spectrophotometry and an ultrasensitive enzyme radioimmunoassay detected adducts derived from benzo[a]pyrene diol epoxide and other apparent polycyclic aromatic hydrocarbons. An amplified enzyme-linked immunosorbent assay demonstrated the presence of 4-aminobiphenyl-DNA adducts in many of these samples. A number of these specimens also contained O6-alkyldeoxyguanosine as measured by 32P-postlabeling techniques. Thus this pilot study indicates not only that human lung contains a spectrum of carcinogen-DNA adducts, but also that a full scale molecular dosimetry study of human exposure to both aryl and alkyl chemical carcinogens is warranted. JF - Carcinogenesis AU - Wilson, V L AU - Weston, A AU - Manchester, D K AU - Trivers, G E AU - Roberts, D W AU - Kadlubar, F F AU - Wild, C P AU - Montesano, R AU - Willey, J C AU - Mann, D L AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 2149 EP - 2153 VL - 10 IS - 11 SN - 0143-3334, 0143-3334 KW - Carcinogens KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Smoking KW - DNA Damage KW - Humans KW - Adult KW - Environmental Exposure KW - Aged KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Chromatography, High Pressure Liquid KW - Alkylation KW - Lung -- analysis KW - DNA -- analysis KW - Carcinogens -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79284801?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-18 N1 - Date created - 1989-12-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Epoxidation of 7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene via a hydroperoxide-dependent mechanism catalyzed by lipoxygenases. AN - 79284360; 2553290 AB - The lipoxygenase catalyzed epoxidation of 7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene (BP-7,8-diol) was examined. Epoxidation of the BP-7,8-diol was catalyzed by 5- and 15-lipoxygenase in the presence of either arachidonic acid, gamma-linolenic acid, or 15-hydroperoxyeicosatetraenoic acid (15-HPETE). The anti-9,10-epoxy-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene isomer was formed in greater quantities than the syn isomer, indicative of peroxyl radical mediated epoxidation. Epoxidation was dependent on time, enzyme and fatty acid concentration. There was no difference in the time course of epoxidation with either arachidonic acid or 15-HPETE, although the initial rate of oxygen consumption was approximately 55-fold greater with arachidonic acid. The lipoxygenase inhibitor and anti-oxidant nordihydroguaiaretic acid inhibited epoxidation in a dose-dependent manner in incubations initiated with either arachidonic acid or 15-HPETE. The anti-oxidant butylated hydroxyanisole also inhibited the epoxidation. Incubations conducted under anaerobic conditions with 15-lipoxygenase and either arachidonic acid or 15-HPETE significantly decreased epoxidation. This suggests that the oxygen inserted into BP-7,8-diol is derived from the atmosphere. The epoxidizing peroxyl radicals could not be detected but their precursors, carbon-centered radicals, were detected by using the ESR spin trapping technique in incubations of 15-lipoxygenase with 15-HPETE. This radical, formed by reduction and rearrangement of the hydroperoxide, may trap oxygen to form a peroxyl radical. We propose that the epoxidizing species is a peroxyl radical derived from 15-HPETE rather than from arachidonic acid. This proposal is based on the similar amounts of epoxidation, but dissimilar amount of oxygen consumed with both fatty acids. Since lipoxygenases are widely distributed in vivo, especially in areas where tumors arise such as the pulmonary epithelium, peroxyl radical formation by these enzymes may have an important role in chemical carcinogenesis. JF - Carcinogenesis AU - Hughes, M F AU - Chamulitrat, W AU - Mason, R P AU - Eling, T E AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 2075 EP - 2080 VL - 10 IS - 11 SN - 0143-3334, 0143-3334 KW - Dihydroxydihydrobenzopyrenes KW - 0 KW - Epoxy Compounds KW - Leukotrienes KW - Lipid Peroxides KW - Peroxides KW - benzo(a)pyrene 7,8-dihydrodiol KW - 13345-25-0 KW - 15-hydroperoxy-5,8,11,13-eicosatetraenoic acid KW - 67675-14-3 KW - Masoprocol KW - 7BO8G1BYQU KW - Lipoxygenase KW - EC 1.13.11.12 KW - Index Medicus KW - Peroxides -- metabolism KW - Oxygen Consumption KW - Electron Spin Resonance Spectroscopy KW - In Vitro Techniques KW - Lipid Peroxides -- metabolism KW - Leukotrienes -- metabolism KW - Masoprocol -- pharmacology KW - Lipoxygenase -- metabolism KW - Dihydroxydihydrobenzopyrenes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79284360?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-18 N1 - Date created - 1989-12-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - N-nitrosocimetidine as an initiator of murine skin tumors with associated H-ras oncogene activation. AN - 79283760; 2680143 AB - N-Nitrosocimetidine (NCM) is a derivative of the drug cimetidine, a methylguanidine derivative used in the treatment of peptic ulcer, and is known to be inactive as a complete mouse skin carcinogen, even when given in repeated high doses for a long period. In the current experiment, NCM was tested for its ability to initiate skin tumors on Sencar mice. It was applied at doses of 1 or 0.3 mg, 5 times/week for 6 weeks, followed by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA), 1 microgram, 2 times/week for 50 weeks. Controls received acetone. The higher NCM dose had significant effects on TPA-promotable tumors, resulting in shortened time to first tumor, increased incidence of all tumors (2-fold) and of malignant tumors (4-fold), and greater tumor growth rate (2-fold), compared with the acetone/TPA-treated mice. The mice given the lower NCM dose did not exhibit increased tumor incidence, but their tumors had a significantly higher growth rate (3-fold) than those of the TPA controls. NCM without TPA treatment caused no tumors. Thus, NCM is a definitive, though weak initiator of TPA-promotable tumors. Nine tumors from the NCM-treatment groups were analyzed for activated oncogenes by the NIH 3T3 cell transfection assay. Five were positive and four of these were found by selective oligonucleotide hybridization analysis to have an A to T transversion in the second position of codon 61 of the H-ras oncogene. One of two tumors from the acetone/TPA group also contained transforming DNA and demonstrated this mutation. None of the tumors had a G----A transition mutation at the second position of codon 12 of this oncogene. Tumor initiation by NCM may then be associated with the same oncogene mutation reported for mouse skin tumors initiated by other types of carcinogens, although occurrence of the mutated oncogene in TPA controls precludes a definitive conclusion. JF - Carcinogenesis AU - Anderson, L M AU - Enomoto, T AU - Perantoni, A O AU - Riggs, C W AU - Kovatch, R M AU - Reed, C D AU - Giner-Sorolla, A AU - Rice, J M AD - Division of Cancer Etiology, NCI-Frederick Cancer Research Facility, MD 21701. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 2009 EP - 2013 VL - 10 IS - 11 SN - 0143-3334, 0143-3334 KW - Carcinogens KW - 0 KW - nitrosocimetidine KW - 73785-40-7 KW - Cimetidine KW - 80061L1WGD KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Gene Expression Regulation, Neoplastic KW - Animals KW - Cocarcinogenesis KW - Dose-Response Relationship, Drug KW - Mice KW - Mutation KW - Survival Analysis KW - Skin Neoplasms -- genetics KW - Genes, ras KW - Skin Neoplasms -- chemically induced KW - Skin Neoplasms -- pathology KW - Cimetidine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79283760?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-18 N1 - Date created - 1989-12-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Similar molecular requirements for antigen receptor-triggered secretion of interferon and granule enzymes by cytolytic T lymphocytes. AN - 79274653; 2478302 AB - At least two biologically significant responses are triggered by the crosslinking of the T-cell receptor (TcR) on the surface of cloned cytotoxic T lymphocytes (CTL): synthesis and secretion of macrophage-activating factor(s) (MAF) that can be attributed to interferon-gamma (IFN) and release of preformed cytolytic granules. We directly compared the molecular requirements for synthesis and secretion of IFN and secretion of granule enzymes triggered in the same cell by the same activating ligand (antigen or monoclonal antibody (mAb) to TcR). An increase in the surface density of activating ligand (immobilized anti-TcR mAb) enhanced both secretion of IFN and secretion of granules. Secretion of IFN occurred immediately after synthesis: only low (but detectable) levels of IFN were detected in cell cytosolic or particulate fractions isolated from Percoll gradients of lysed CTL, while very high levels of IFN were found in the stimulated CTL culture fluids. Inhibitors of RNA synthesis and protein synthesis blocked secretion of IFN, but did not inhibit release of preformed cytolytic granules. The requirement for TcR crosslinking in triggering both secretion of granules and secretion of IFN from CTL was pharmacologically reproduced by the synergistic action of PMA, a protein kinase C activator, and the Ca2+ ionophore A23187. Both secretion of IFN and secretion of granules were absolutely dependent upon extracellular Ca2+: EGTA completely blocked both TcR- and PMA/A23187-induced secretion of IFN and exocytosis of granules. These studies suggest that similar molecular mechanisms are involved in secretion of newly synthesized IFN and secretion of preformed cytolytic granules. One notable difference between the molecular requirements for the two secretory events was a much lower concentration requirement for PMA for IFN synthesis and secretion than for granule secretion in the synergistic interactions with A23187. Implications of these studies for the exocytosis model of cell-mediated cytotoxicity are discussed. JF - Cellular immunology AU - Fortier, A H AU - Nacy, C A AU - Sitkovsky, M V AD - Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 64 EP - 76 VL - 124 IS - 1 SN - 0008-8749, 0008-8749 KW - Receptors, Antigen, T-Cell KW - 0 KW - Interferons KW - 9008-11-1 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Granzymes KW - EC 3.4.21.- KW - Serine Endopeptidases KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Serine Endopeptidases -- secretion KW - Calcium -- physiology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - Protein Kinase C -- physiology KW - Mice, Inbred DBA KW - Cytoplasmic Granules -- enzymology KW - Interferons -- secretion KW - Receptors, Antigen, T-Cell -- physiology KW - T-Lymphocytes, Cytotoxic -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79274653?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-07 N1 - Date created - 1989-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Novel exogenous heme-dependent expression of mammalian cytochrome P450 using baculovirus. AN - 79271344; 2679389 AB - Rat P450 IIA1 is a membrane-bound hemoprotein that catalyzes the 7 alpha- and 6 alpha-hydroxylation of testosterone. A recombinant baculovirus, containing the cDNA encoding IIA1, was constructed and used to infect Spodoptera frugiperda cells. Infected cells contained up to 10% IIA1 protein as quantified by Western blot analysis; however, only a small percentage of this protein contained heme and was catalytically active. Addition of hemin to the culture medium during the course of viral infection resulted in a marked sixfold increase in both testosterone hydroxylase activity and heme-containing IIA1 protein. When the exogenously added protoheme was substituted with modified heme molecules containing hydrogen or ethyl groups at the 2 and 4 positions of the protoporphyrin IX, enzymes with only marginal changes in catalytic properties were produced. These data indicate that baculovirus can be used as a system to produce high levels of mammalian cytochrome P450s containing custom modified heme moieties. JF - Archives of biochemistry and biophysics AU - Asseffa, A AU - Smith, S J AU - Nagata, K AU - Gillette, J AU - Gelboin, H V AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/11/01/ PY - 1989 DA - 1989 Nov 01 SP - 481 EP - 490 VL - 274 IS - 2 SN - 0003-9861, 0003-9861 KW - Apoproteins KW - 0 KW - Heme KW - 42VZT0U6YR KW - Hemin KW - 743LRP9S7N 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 - testosterone 7-alpha-hydroxylase, hamster KW - Index Medicus KW - Rats KW - Hemin -- pharmacology KW - Animals KW - Genetic Vectors KW - Recombination, Genetic KW - Steroid Hydroxylases -- metabolism KW - Spectrophotometry KW - Apoproteins -- metabolism KW - Insect Viruses -- genetics KW - Heme -- pharmacology KW - Cytochrome P-450 Enzyme System -- metabolism KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Heme -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79271344?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-03 N1 - Date created - 1989-11-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interleukin 2, interleukin 2 receptor, and interferon-gamma synthesis and mRNA expression in phorbol myristate acetate and calcium ionophore A23187-stimulated T cells from elderly humans. AN - 79226848; 2507204 AB - The levels of interleukin 2 (IL-2), interleukin 2 receptor (IL-2R), and interferon-gamma (IFN-gamma) specific mRNA and their gene products were examined in phorbol myristate acetate (PMA) and calcium ionophore A23187-costimulated purified T cells from young and elderly humans. In addition, the number of high-affinity IL-2R per activated cell, the high-affinity IL-2R density, and the proliferative response of the cells were measured. Among PMA/A23187-stimulated T cells, there was no statistically significant age-related difference in IL-2 or IL-2R specific mRNA accumulation or in the amount of IL-2 or IL-2R synthesized. IFN-gamma specific mRNA was increased significantly in T cells from elderly individuals and the amount of IFN-gamma synthesized by PMA/A23187-activated T cells was nearly double that produced by cells from young individuals. Quantification of the number of high-affinity IL-2R by [125I]IL-2 binding demonstrated there was no decrease in either the mean number or the dissociation constant of the high-affinity IL-2R on activated T cells of the elderly. Despite producing large amounts of IL-2 and having comparable numbers of both low- and high-affinity IL-2R. PMA/A23187-stimulated T cells from elderly subjects still proliferated less vigorously than did T cells from young persons. The addition of exogenous IL-2 to the cultured cells did not fully correct this age difference. Our findings that the expression of the IL-2, IL-2R, and IFN-gamma genes are not constitutionally defective in the elderly support the hypothesis that the age-related decline in proliferation observed in mitogen-stimulated T cells of the elderly is most likely attributable to alterations in the transmission of signals from the cell membrane to the nucleus. JF - Clinical immunology and immunopathology AU - Chopra, R K AU - Holbrook, N J AU - Powers, D C AU - McCoy, M T AU - Adler, W H AU - Nagel, J E AD - Clinical Immunology Section, National Institute on Aging, Baltimore, Maryland 21224. Y1 - 1989/11// PY - 1989 DA - November 1989 SP - 297 EP - 308 VL - 53 IS - 2 Pt 1 SN - 0090-1229, 0090-1229 KW - Interleukin-2 KW - 0 KW - RNA, Messenger KW - Receptors, Interleukin-2 KW - Calcimycin KW - 37H9VM9WZL KW - Interferon-gamma KW - 82115-62-6 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Humans KW - Adult KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Aged KW - Gene Expression Regulation -- drug effects KW - Calcimycin -- pharmacology KW - RNA, Messenger -- genetics KW - Lymphocyte Activation -- drug effects KW - Receptors, Interleukin-2 -- physiology KW - Aging KW - Interferon-gamma -- biosynthesis KW - T-Lymphocytes -- physiology KW - Interleukin-2 -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79226848?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-21 N1 - Date created - 1989-11-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ultraviolet mutagenesis in a plasmid vector replicated in lymphoid cells from patient with the melanoma-prone disorder dysplastic nevus syndrome. AN - 79225097; 2790806 AB - The hereditary dysplastic nevus syndrome (DNS) is an autosomal dominant disorder in which affected individuals have increased numbers of dysplastic (premalignant) nevi and a greater than 100-fold increased risk of developing cutaneous melanoma. Epstein-Barr virus-transformed lymphoblastoid cell lines from patients with hereditary DNS have been shown to be hypermutable to UV radiation (M.I.R. Perera et al., Cancer Res., 46: 1005-1009, 1986). To examine the mechanism involved in this UV hypermutability, we used a shuttle vector plasmid, pZ189, which carries a 160-base pair marker gene, supF, and can replicate in human cells. pZ189 was treated with UV radiation and transfected into DNS6BE, a lymphoblastoid cell line from a patient with hereditary DNS. Plasmid survival after UV was similar with the DNS6BE line and with a lymphoblastoid cell line from a normal donor. Plasmid mutation frequency was greater with the DNS line in accord with the DNS cellular hypermutability. Base sequence analysis was performed on 69 mutated plasmids recovered from the DNS line. There were significantly more plasmids with single base substitution mutations (P less than 0.01) in comparison to UV-treated plasmids passed through normal fibroblasts. pZ189 hypermutability and an increased frequency of single base substitutions was previously found with a cell line from a melanoma-prone xeroderma pigmentosum patient. These differences may be related to the increased melanoma susceptibility in both DNS and xeroderma pigmentosum. JF - Cancer research AU - Seetharam, S AU - Waters, H L AU - Seidman, M M AU - Kraemer, K H AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/11/01/ PY - 1989 DA - 1989 Nov 01 SP - 5918 EP - 5921 VL - 49 IS - 21 SN - 0008-5472, 0008-5472 KW - DNA, Neoplasm KW - 0 KW - Index Medicus KW - DNA, Neoplasm -- radiation effects KW - Base Sequence KW - Base Composition KW - Disease Susceptibility KW - Humans KW - Adult KW - Molecular Sequence Data KW - DNA, Neoplasm -- genetics KW - Lymphocytes -- cytology KW - Female KW - Cell Line KW - Ultraviolet Rays KW - DNA Replication -- radiation effects KW - Melanoma -- genetics KW - Genetic Vectors KW - Dysplastic Nevus Syndrome -- genetics KW - Plasmids -- radiation effects KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79225097?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-20 N1 - Date created - 1989-11-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Neurogenic component of phorbol ester-induced mouse skin inflammation. AN - 79221543; 2790819 AB - Tumor-promoting phorbol esters are potent inflammatory agents for mouse skin, and the potential mechanistic role of inflammation in tumor promotion is under active investigation. We have shown previously that resiniferatoxin, a uniquely irritant phorbol-related diterpene, acts as a capsaicin analogue to induce and then to block neurogenic inflammation. We report here that pretreatment of CD-1 mice with resiniferatoxin blocked the early (3 h) erythema and edema (6 h) in response to phorbol 12-myristate 13-acetate (PMA), whereas the edema at later times (12-24 h) was only partially blocked. Since the efficiency of resiniferatoxin pretreatment decreased as a function of time if PMA was applied 24, 48, or 96 h after resiniferatoxin administration, the late edema response to PMA may be a combination of increasing edema of nonneurogenic origin and the recovering neurogenic response due to the decreasing desensitization. For other phorbol esters, 12-deoxyphorbol mono- and diesters, and mezerein, differing kinetics of edema and differing degrees of blockade of edema following resiniferatoxin pretreatment were observed, as expected from the discrepancies between their inflammatory and tumor-promoting activities. PMA-induced skin hyperplasia, unlike edema, was not inhibited by resiniferatoxin pretreatment, suggesting that the early component of neurogenic inflammation was not essential for hyperplasia under our conditions. Distinction between inflammatory mechanisms may help to clarify the role of inflammation in tumor promotion. JF - Cancer research AU - Szallasi, A AU - Blumberg, P M AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/11/01/ PY - 1989 DA - 1989 Nov 01 SP - 6052 EP - 6057 VL - 49 IS - 21 SN - 0008-5472, 0008-5472 KW - Diterpenes KW - 0 KW - Phorbol Esters KW - Terpenes KW - mezerein KW - 34807-41-5 KW - resiniferatoxin KW - A5O6P1UL4I KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Terpenes -- toxicity KW - Tetradecanoylphorbol Acetate -- toxicity KW - Mice, Inbred Strains KW - Animals KW - Hyperplasia KW - Dose-Response Relationship, Drug KW - Mice KW - Female KW - Administration, Topical KW - Inflammation KW - Erythema -- chemically induced KW - Diterpenes -- pharmacology KW - Skin -- drug effects KW - Diterpenes -- administration & dosage KW - Skin -- pathology KW - Skin -- innervation KW - Phorbol Esters -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79221543?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-20 N1 - Date created - 1989-11-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Enhancement of hydroxylation and deglycosylation of 2'-deoxyguanosine by carcinogenic nickel compounds. AN - 79220351; 2790811 AB - The effects of nickel subsulfide (Ni3S2) and nickel chloride [Ni(II)] on hydroxylation and deglycosylation of pure 2'-deoxyguanosine (dG) and on hydroxylation of guanine (Gu) residues in calf thymus DNA in the absence or presence of hydrogen peroxide (H2O2) and/or ascorbate (Ascb) were studied with the use of high-performance liquid chromatography. Incubation of 0.75 mM dG with 5 mg Ni3S2/ml (particle size less than 5 microns) at 37 degrees C in aerated 50 mM Tris/HCl buffer, pH 7.4, resulted in slow hydroxylation of dG to 8-hydroxy-2'-deoxyguanosine (8-OH-dG). This effect was greatly enhanced by 20 mM H2O2. Ni(II) alone at concentrations up to 10 mM was inactive but produced 8-OH-dG in the presence of 20 mM H2O2; the latter caused no dG hydroxylation by itself. Both Ni3S2 and Ni(II) increased the formation of 8-OH-dG from dG exposed to H2O2 + Ascb. At pH 7.4 and constant concentration of H2O2 and Ascb (20 and 8 mM, respectively), Ni(II) over the concentration range 1-10 mM raised the hydroxylation yield by up to five times that without Ni(II). Also, addition of 7.5 mM Ni(II) more than doubled the hydroxylation yield of Gu residues by the 20 mM H2O2 + 8 mM Ascb mixture (pH 7.4) in denatured DNA and doubled it in native DNA. Ni3S2 and Ni(II) alone had no effect on deglycosylation of dG and did not significantly influence the slow rate of Gu production from dG reacting with H2O2 or Ascb at pH 7.4. However, Ni(II), unlike Ni3S2, increased the extent of dG deglycosylation when added to the dG + H2O2 + Ascb system; 10 mM Ni(II) increased deglycosylation by a factor of 2.5 in 24 h. Thus, nickel carcinogens were shown for the first time to cause and/or enhance both hydroxylation and deglycosylation reactions of dG which may contribute to the observed genotoxic and carcinogenic effects of this metal. JF - Cancer research AU - Kasprzak, K S AU - Hernandez, L AD - Inorganic Carcinogenesis Section, National Cancer Institute, Frederick, Maryland 21701-1013. Y1 - 1989/11/01/ PY - 1989 DA - 1989 Nov 01 SP - 5964 EP - 5968 VL - 49 IS - 21 SN - 0008-5472, 0008-5472 KW - Carcinogens KW - 0 KW - nickel subsulfide KW - 12035-72-2 KW - nickel chloride KW - 696BNE976J KW - Nickel KW - 7OV03QG267 KW - DNA KW - 9007-49-2 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Deoxyguanosine KW - G9481N71RO KW - Ascorbic Acid KW - PQ6CK8PD0R KW - Index Medicus KW - Chemistry KW - Kinetics KW - Hydrogen-Ion Concentration KW - Chemical Phenomena KW - Hydrolysis KW - Hydroxylation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79220351?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-20 N1 - Date created - 1989-11-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - FAB/MS/MS for the determination of biomolecules: A compendium AN - 21267212; 11793918 AB - First page of article. JF - Mass Spectrometry Reviews AU - Tomer, Kenneth B AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, P.O. Box 12233, Research Triangle Park, North Carolina 27709 Y1 - 1989/11// PY - 1989 DA - Nov 1989 SP - 483 EP - 511 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 USA VL - 8 IS - 6 SN - 0277-7037, 0277-7037 KW - Biotechnology and Bioengineering Abstracts KW - Reviews KW - Mass spectroscopy KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/21267212?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2010-02-01 N1 - Last updated - 2015-03-31 N1 - SubjectsTermNotLitGenreText - Reviews; Mass spectroscopy DO - http://dx.doi.org/10.1002/mas.1280080603 ER - TY - JOUR T1 - MPTP treatment combined with ethanol or acetaldehyde selectively destroys dopaminergic neurons in mouse substantia nigra. AN - 79271336; 2572305 AB - We have previously reported that ethanol and acetaldehyde potentiate 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity in mice, enhancing dopamine (DA) depletion in the striatum. The present study was designed to determine whether such enhancement of neurotoxicity was specific for the nigro-striatal DA pathway. In 5-week-old mice acetaldehyde treatment did not enhance DA depletion seen 7 days after MPTP treatment. In 8-week-old animals, however, acetaldehyde or ethanol given with MPTP decreased striatal DA content to about 10% of controls, whereas the depletion was to 43% of controls when MPTP was given alone. In acetaldehyde or ethanol and MPTP-treated mice, changes in DA levels were observed only in the striatum. DA contents in the hypothalamus, olfactory bulb and frontal cortex were similar to that in controls. Contents of norepinephrine and serotonin in striatum, hypothalamus, olfactory bulb and cerebral cortex were not affected by any of the treatments. Three months after MPTP alone, striatal DA recovered to 74% of controls in 8-week-old mice, whereas no recovery occurred in acetaldehyde and MPTP-treated mice. Moreover, both tyrosine hydroxylase (TH) immunocytochemistry and Cresyl violet staining showed an extensive and selective cell loss in the pars compacta of the substantia nigra (SNc) of the mice treated with acetaldehyde or ethanol and MPTP, whereas MPTP alone caused only a limited cell degeneration. JF - Brain research AU - Zuddas, A AU - Corsini, G U AU - Schinelli, S AU - Johannessen, J N AU - di Porzio, U AU - Kopin, I J AD - Clinical Neuroscience Branch, NINDS, Bethesda, MD 20892. Y1 - 1989/10/30/ PY - 1989 DA - 1989 Oct 30 SP - 1 EP - 10 VL - 501 IS - 1 SN - 0006-8993, 0006-8993 KW - Serotonin KW - 333DO1RDJY KW - Ethanol KW - 3K9958V90M KW - Tyrosine 3-Monooxygenase KW - EC 1.14.16.2 KW - Acetaldehyde KW - GO1N1ZPR3B KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Animals KW - Tyrosine 3-Monooxygenase -- metabolism KW - Drug Interactions KW - Norepinephrine -- metabolism KW - Mice, Inbred C57BL KW - Mice KW - Serotonin -- metabolism KW - Male KW - Substantia Nigra -- metabolism KW - Aging -- metabolism KW - Acetaldehyde -- pharmacology KW - Substantia Nigra -- pathology KW - Ethanol -- pharmacology KW - MPTP Poisoning KW - Substantia Nigra -- drug effects KW - Dopamine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79271336?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-20 N1 - Date created - 1989-12-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Acetaldehyde directly enhances MPP+ neurotoxicity and delays its elimination from the striatum. AN - 79268665; 2804689 AB - We have previously shown that ethanol and acetaldehyde (ACE) potentiate MPTP toxicity in mice, selectively enhancing dopamine (DA) depletion in the striatum and markedly increasing loss of DA neurons in the substantia nigra. Several months after these combined treatments there is no evidence of any recovery. In the present study, we measured the accumulation of the MPTP toxic metabolite 1-methyl-4-phenylpyridinium ion (MPP+) in both striatum and whole brain, after MPTP alone or after combined treatments with ethanol or acetaldehyde, in order to determine whether this enhancement of toxicity is caused by changes in the MPTP metabolism. We also investigated whether acetaldehyde interfered with the conversion of MPTP to MPP+ by glial cells in vitro and studied its effects on the MPP+ uptake and spontaneous release from mesencephalic DA neurons or striatal astrocytes in primary cell cultures from E13 mouse embryos. The results from the in vivo experiments indicated that relatively low doses of ethanol or acetaldehyde potentiate directly MPP+ toxicity, apparently without interfering with its pharmacokinetics. However when higher doses of these drugs were administered, they also decreased MPP+ clearance from the striatum. ACE also increased initial MPTP accumulation in the whole brain but failed to enhance MPP+ levels, thus indicating that ACE effect is not related to MPTP metabolism. In vitro studies confirmed that ACE does not modify MPTP metabolism in striatal or mesencephalic astrocytes in culture. In mesencephalic neuronal cultures ACE does not change the levels of MPP+ uptake (MPP+ is accumulated in putative DA neurons in vitro with a mechanism similar to that of the DA high affinity uptake) nor its spontaneous release. These results indicate that the slower MPP+ clearance from the stratum after ACE is not related to a direct effect of ACE on DA neurons or astrocytes. JF - Brain research AU - Zuddas, A AU - Corsini, G U AU - Schinelli, S AU - Barker, J L AU - Kopin, I J AU - di Porzio, U AD - Clinical Neuroscience Branch, NINDS, Bethesda, MD 20892. Y1 - 1989/10/30/ PY - 1989 DA - 1989 Oct 30 SP - 11 EP - 22 VL - 501 IS - 1 SN - 0006-8993, 0006-8993 KW - Ethanol KW - 3K9958V90M KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Acetaldehyde KW - GO1N1ZPR3B KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Index Medicus KW - Animals KW - Drug Interactions KW - Astrocytes -- cytology KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- metabolism KW - Astrocytes -- drug effects KW - Mice, Inbred C57BL KW - Ethanol -- toxicity KW - Mice KW - Male KW - Astrocytes -- metabolism KW - Corpus Striatum -- cytology KW - 1-Methyl-4-phenylpyridinium -- pharmacokinetics KW - Acetaldehyde -- pharmacology KW - 1-Methyl-4-phenylpyridinium -- toxicity KW - MPTP Poisoning KW - Corpus Striatum -- metabolism KW - Corpus Striatum -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79268665?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-20 N1 - Date created - 1989-12-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phosphoroselenoate oligodeoxynucleotides: synthesis, physico-chemical characterization, anti-sense inhibitory properties and anti-HIV activity. AN - 79306829; 2682524 AB - Oligodeoxynucleotides with a phosphorus atom in which one of the non-bridging oxygen atoms is substituted by selenium were prepared and investigated with respect to their antisense properties. A general synthesis of phosphoroselenoate analogs of oligonucleotides is described using potassium selenocyanate as the selenium donor. The compounds, characterized by 31P NMR, were shown to decompose to phosphate with a half-life of ca. 30 days. Melting temperatures of duplexes between poly(rA) or poly(rI) with oligo(dT) and oligo(dC), respectively, indicate diminished hybridization capability of phosphoroselenoate oligomers relative to both the unmodified phosphodiester oligomers and the phosphorothioate congeners. A phosphoroselenoate 17-mer is a sequence specific inhibitor of rabbit beta-globin synthesis in wheat germ extract and in injected Xenopus oocytes. In contrast phosphoroselenoate analogs are potent non-sequence specific inhibitors in rabbit reticulocyte lysate. In vitro HIV assays were carried out on a phosphoroselenoate sequence and compared with a phosphorothioate analogue that has previously been shown to exhibit anti-HIV activity (Matsukura et al., Proc. Natl. Acad. Sci. (1987) 84, 7706-7710). The phosphoroselenoate was somewhat less active, and was much more toxic to the cells. JF - Nucleic acids research AU - Mori, K AU - Boiziau, C AU - Cazenave, C AU - Matsukura, M AU - Subasinghe, C AU - Cohen, J S AU - Broder, S AU - Toulmé, J J AU - Stein, C A AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/10/25/ PY - 1989 DA - 1989 Oct 25 SP - 8207 EP - 8219 VL - 17 IS - 20 SN - 0305-1048, 0305-1048 KW - Antiviral Agents KW - 0 KW - DNA, Antisense KW - Indicators and Reagents KW - Oligodeoxyribonucleotides KW - Organophosphorus Compounds KW - Polyribonucleotides KW - RNA, Messenger KW - Globins KW - 9004-22-2 KW - DNA KW - 9007-49-2 KW - Selenium KW - H6241UJ22B KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Nucleic Acid Denaturation KW - Plants -- metabolism KW - Globins -- genetics KW - Rabbits KW - Magnetic Resonance Spectroscopy KW - Base Sequence KW - Oocytes -- metabolism KW - Reticulocytes -- metabolism KW - Molecular Sequence Data KW - Xenopus KW - Female KW - RNA, Messenger -- antagonists & inhibitors KW - Protein Biosynthesis -- drug effects KW - HIV -- drug effects KW - Antiviral Agents -- chemical synthesis KW - RNA, Messenger -- drug effects KW - Selenium -- pharmacology KW - Oligodeoxyribonucleotides -- pharmacology KW - Organophosphorus Compounds -- pharmacology KW - Organophosphorus Compounds -- chemical synthesis KW - Oligodeoxyribonucleotides -- chemical synthesis KW - RNA, Messenger -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79306829?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-04 N1 - Date created - 1989-12-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Gene. 1988 Dec 10;72(1-2):343-7 [3243433] Proc Natl Acad Sci U S A. 1988 Oct;85(19):7079-83 [3174622] Biochemistry. 1989 Feb 7;28(3):1340-6 [2469468] Pharm Res. 1988 Sep;5(9):539-49 [3073387] Nucleic Acids Res. 1989 Jun 12;17(11):4255-73 [2472605] Anal Biochem. 1978 Apr;85(2):506-18 [646104] Methods Enzymol. 1983;101:370-86 [6193395] Annu Rev Biochem. 1985;54:367-402 [2411211] J Chromatogr. 1985 Jun 19;326:263-80 [4030945] Biochemistry. 1985 Jul 2;24(14):3630-8 [4041432] Nucleic Acids Res. 1986 Aug 26;14(16):6433-51 [3018671] Nucleic Acids Res. 1987 May 11;15(9):3877-90 [3588311] Nucleic Acids Res. 1987 Jun 25;15(12):4717-36 [3037483] Nucleic Acids Res. 1987 Jul 24;15(14):5749-63 [3475677] Proc Natl Acad Sci U S A. 1987 Nov;84(21):7706-10 [3499613] Cancer Res. 1988 May 15;48(10):2659-68 [3282648] EMBO J. 1988 Feb;7(2):427-34 [2452730] Nucleic Acids Res. 1988 Apr 25;16(8):3209-21 [2836790] Nucleic Acids Res. 1988 Jun 10;16(11):5137-51 [3387220] Proc Natl Acad Sci U S A. 1988 Jul;85(14):5011-5 [2839827] Gene. 1988 Dec 10;72(1-2):51-8 [2468575] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of the expression of a multidrug resistance gene (mdr-1/P-glycoprotein) by differentiating agents. AN - 79288511; 2572588 AB - Acquired resistance to multiple natural products in vitro is mediated by P-glycoprotein (Pgp). Expression of this protein has been demonstrated in some normal tissues and in tumor samples obtained from both untreated and treated patients. In situ hybridizations with RNA probes have demonstrated higher levels of expression of mdr-1/Pgp in well-differentiated tumors and in well-differentiated areas in tumors with mixed histologies. Expression of mdr-1/Pgp in human colon carcinoma cell lines was increased by the differentiating agents sodium butyrate, dimethyl sulfoxide, and dimethylformamide. In the SW-620 cell line addition of sodium butyrate resulted in a rapid induction of mdr-1/Pgp mRNA that was sustained for the duration of the exposure. The levels of P-glycoprotein were measured by immunoblotting and were also increased. Similar results were obtained in three other cell lines including the HCT-15 line. This induction occurred without alterations in nuclease sensitivity. Discontinuation of sodium butyrate was followed by a rapid fall in the levels of mRNA. The levels of P-glycoprotein returned to normal with a half-life of about 24 h. In spite of a 20-25-fold increase in the level of mdr-1/Pgp mRNA and P-glycoprotein, the SW-620 cell line did not demonstrate increased resistance to doxorubicin and vinblastine or decreased accumulation of vinblastine. In contrast, in the HCT-15 cell line, a 5-fold increase of mdr-1/Pgp was accompanied by a comparable fall in vinblastine accumulation which was reversed by verapamil. In the SW-620 cell line, the induced protein could be photolabeled using [3H]azidopine. Expression of mdr-1/Pgp appears to correlate with the degree of differentiation. However, its induction is not always accompanied by expression of the multidrug-resistance phenotype. JF - The Journal of biological chemistry AU - Mickley, L A AU - Bates, S E AU - Richert, N D AU - Currier, S AU - Tanaka, S AU - Foss, F AU - Rosen, N AU - Fojo, A T AD - Medicine Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/10/25/ PY - 1989 DA - 1989 Oct 25 SP - 18031 EP - 18040 VL - 264 IS - 30 SN - 0021-9258, 0021-9258 KW - Blood Proteins KW - 0 KW - Butyrates KW - Membrane Glycoproteins KW - P-Glycoprotein KW - RNA Probes KW - RNA, Messenger KW - Sulfuric Acid Esters KW - Sulfuric Acids KW - Butyric Acid KW - 107-92-6 KW - Dimethylformamide KW - 8696NH0Y2X KW - dimethyl sulfate KW - JW5CW40Z50 KW - Index Medicus KW - Transcription, Genetic -- drug effects KW - Humans KW - Cell Division -- drug effects KW - RNA, Messenger -- genetics KW - Cell Differentiation -- drug effects KW - Colonic Neoplasms KW - Cell Line KW - Blood Proteins -- genetics KW - Drug Resistance -- genetics KW - Dimethylformamide -- pharmacology KW - Genes, Neoplasm -- drug effects KW - Butyrates -- pharmacology KW - Sulfuric Acids -- pharmacology KW - Sulfuric Acid Esters -- pharmacology KW - Gene Expression KW - Membrane Glycoproteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79288511?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-27 N1 - Date created - 1989-11-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synergy between a selective D1 antagonist and a selective D2 antagonist in the induction of catalepsy. AN - 79568903; 2485878 AB - The cataleptogenic effects of the selective D1 dopamine receptor antagonist, SCH 23390, and the selective D2 dopamine receptor antagonist, raclopride, when administered alone or in combination were studied in rats using the vertical grid and horizontal bar methods. In either model both agents, given alone, produced dose-dependent catalepsy. When administered together, there was a marked synergy between the two drugs. Thus, a low dose of SCH 23390 resulted in a 10-fold shift to the left of the raclopride dose-effect curve. When the same low dose of SCH 23390 was administered together with a subcataleptogenic dose of raclopride, marked catalepsy was produced. The finding of synergy between selective D1 and D2 dopamine antagonists in the induction of catalepsy suggests that mixed antagonists may possess greater antipsychotic activity than neuroleptics acting mainly on one receptor subtype. JF - Neuroscience letters AU - Parashos, S A AU - Marin, C AU - Chase, T N AD - Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892. Y1 - 1989/10/23/ PY - 1989 DA - 1989 Oct 23 SP - 169 EP - 173 VL - 105 IS - 1-2 SN - 0304-3940, 0304-3940 KW - Benzazepines KW - 0 KW - Dopamine Antagonists KW - Salicylamides KW - Raclopride KW - 430K3SOZ7G KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Behavior, Animal -- drug effects KW - Animals KW - Benzazepines -- pharmacology KW - Dose-Response Relationship, Drug KW - Salicylamides -- pharmacology KW - Drug Synergism KW - Male KW - Catalepsy -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79568903?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-12-06 N1 - Date created - 1990-12-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alcohols selectively stimulate phospholipase D-mediated hydrolysis of phosphatidylethanolamine in NIH 3T3 cells. AN - 79284746; 2806564 AB - Addition of alcohols to NIH 3T3 fibroblasts, prelabeled with [2-14C]ethanolamine, resulted in increased degradation of [14C]phosphatidylethanolamine (PtdEtn). Long-chain alcohols, like octanol or nonanol, were more potent than methanol or ethanol. The main water-soluble product of alcohol-stimulated [14C]PtdEtn hydrolysis was [14C]ethanolamine. Addition of ethanol to cells, specifically prelabeled with [32P]PtdEtn, enhanced the formation of [32P]phosphatidic acid (PtdOH), suggesting the involvement of a phospholipase D-type enzyme. At lower concentration (10-150 mM), ethanol acted through a protein kinase C (PKC)-independent mechanism. At higher concentrations (150-300 mM), the effect of ethanol was partially inhibited both by the PKC inhibitor H7 and by the down-regulation of PKC achieved by treatment of cells with 200 nM TPA for 24 h, suggesting that activation of PKC contributed to the ethanol effect. JF - FEBS letters AU - Kiss, Z AU - Anderson, W B AD - Laboratory of Cellular Oncology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/10/23/ PY - 1989 DA - 1989 Oct 23 SP - 45 EP - 48 VL - 257 IS - 1 SN - 0014-5793, 0014-5793 KW - Alcohols KW - 0 KW - Phosphatidylethanolamines KW - Ethanol KW - 3K9958V90M KW - Phospholipases KW - EC 3.1.- KW - Phospholipase D KW - EC 3.1.4.4 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Ethanol -- pharmacology KW - Cells, Cultured KW - Kinetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - Hydrolysis KW - Phospholipase D -- metabolism KW - Phosphatidylethanolamines -- metabolism KW - Phospholipases -- metabolism KW - Alcohols -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79284746?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-21 N1 - Date created - 1989-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tat trans-activates the human immunodeficiency virus through a nascent RNA target. AN - 79275812; 2478293 AB - Expression of the human immunodeficiency virus type 1 (HIV-1) genome is greatly dependent on the viral trans-activator protein Tat. Tat functions through the TAR element, which is represented in both viral DNA and RNA. At present, there is no definitive evidence that determines whether Tat acts through a DNA or RNA form of TAR. We have used an intramolecular mutagenesis approach to change selectively the RNA secondary structure of TAR without affecting its primary sequence. We show that a specific RNA secondary structure for TAR is needed for biological activity. Furthermore, transcripts that only transiently form a native TAR RNA hairpin, which is not maintained in the mature mRNA, are completely trans-activated by Tat, suggesting that TAR is recognized as a nascent RNA. JF - Cell AU - Berkhout, B AU - Silverman, R H AU - Jeang, K T AD - Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1989/10/20/ PY - 1989 DA - 1989 Oct 20 SP - 273 EP - 282 VL - 59 IS - 2 SN - 0092-8674, 0092-8674 KW - Gene Products, tat KW - 0 KW - RNA, Antisense KW - RNA, Messenger KW - RNA, Viral KW - Trans-Activators KW - Viral Structural Proteins KW - tat Gene Products, Human Immunodeficiency Virus KW - RNA KW - 63231-63-0 KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Gene Expression Regulation, Viral KW - Gene Expression KW - Transcription, Genetic KW - RNA, Messenger -- genetics KW - Plasmids KW - RNA, Messenger -- antagonists & inhibitors KW - Base Sequence KW - Enhancer Elements, Genetic KW - Molecular Sequence Data KW - Mutation KW - Cell Line KW - RNA -- genetics KW - Trans-Activators -- metabolism KW - HIV-1 -- genetics KW - HIV-1 -- growth & development KW - Genes, Viral KW - RNA, Viral -- genetics KW - Virus Activation KW - Gene Products, tat -- metabolism KW - Viral Structural Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79275812?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-04 N1 - Date created - 1989-12-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evaluation of the effects of erythro-9(2-hydroxy-3-nonyl) adenine (EHNA) on HIV-1 production in vitro. AN - 79272428; 2478129 AB - Effects of erythro-9(2-hydroxy-3-nonyl) adenine (EHNA), an inhibitor of the common Adenosine deaminase (adenosine aminohydrolase, EC 3.5.4.4.), on HIV-1 production was evaluated in vitro. Reverse transcriptase (RT) activity in the supernatant was inhibited by nearly 50% in EHNA-treated HIV-1 infected H9 cells, when compared with untreated but infected H9 cells. There was also a significant decrease in cell viability, but this was reversed following the addition of deoxycytidine (dC) to these cultures. The combined treatment was also effective in suppressing HIV-1 release from HIV-1-infected U937 cells. This combined EHNA plus dC treatment had no effect on RT activity in the cell lysates, suggesting that the inhibition of HIV-1 production may be due to the disturbance of virus release from infected cells. JF - Biochemical and biophysical research communications AU - Sei, Y AU - Inoue, M AU - Tsuboi, I AU - Yokoyama, M M AU - Arora, P K AD - Laboratory of Neuroscience, NIDDK, Bethesda, MD 20892. Y1 - 1989/10/16/ PY - 1989 DA - 1989 Oct 16 SP - 345 EP - 350 VL - 164 IS - 1 SN - 0006-291X, 0006-291X KW - Adenosine Deaminase Inhibitors KW - 0 KW - Antiviral Agents KW - HIV Envelope Protein gp120 KW - Deoxycytidine KW - 0W860991D6 KW - 9-(2-hydroxy-3-nonyl)adenine KW - 59262-86-1 KW - RNA-Directed DNA Polymerase KW - EC 2.7.7.49 KW - Adenine KW - JAC85A2161 KW - Index Medicus KW - AIDS/HIV KW - HIV Envelope Protein gp120 -- metabolism KW - Flow Cytometry KW - RNA-Directed DNA Polymerase -- metabolism KW - Drug Synergism KW - Deoxycytidine -- pharmacology KW - Cell Line KW - Virus Replication -- drug effects KW - Antiviral Agents -- pharmacology KW - HIV-1 -- physiology KW - HIV-1 -- drug effects KW - Adenine -- analogs & derivatives KW - Adenine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79272428?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-20 N1 - Date created - 1989-11-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Excitatory amino acid neurotoxicity at the N-methyl-D-aspartate receptor in cultured neurons: role of the voltage-dependent magnesium block. AN - 79270458; 2572299 AB - Results of the present report show that cerebellar neurons in primary culture are resistant to glutamate concentrations as high as 5 mM in the presence of glucose and Mg2+, but sensitive to glutamate concentrations lower than 35 microM when the neurons are deprived of glucose. Glutamate toxicity is also potentiated when Mg2+ is removed but glucose and EDTA are present; in this case, higher concentrations of glutamate (1 mM) are required for full toxicity. Glucose concentrations as low as 50 microM are fully protective against the toxicity of 100 microM glutamate; pyruvate and, to a lesser extent, lactate are also protective. Significantly, increasing concentrations of extracellular Mg2+ are fully protective against the toxicity of 100 microM glutamate in the absence of glucose and against the toxicity of 1 mM glutamate in the presence of glucose and EDTA. We interpret these results as support for our hypothesis that the pivotal event in glutamate's transition to neurotoxin is relief of the Mg2+ block of the N-methyl-D-aspartate (NMDA) receptor channel, which is known to be voltage-dependent. Partial depolarization in response to depletion of high-energy phosphates relieves the voltage-dependent block enabling glutamate to stimulate an excessive ion influx which results in the death of the neuron by a mechanism which is not yet understood. We propose that this mechanism may be operative in the neuronal damage associated with a variety of neurodegenerative disorders. JF - Brain research AU - Cox, J A AU - Lysko, P G AU - Henneberry, R C AD - Molecular Neurobiology Section, NINDS, Bethesda, MD 20892. Y1 - 1989/10/16/ PY - 1989 DA - 1989 Oct 16 SP - 267 EP - 272 VL - 499 IS - 2 SN - 0006-8993, 0006-8993 KW - Glutamates KW - 0 KW - Neurotoxins KW - Receptors, N-Methyl-D-Aspartate KW - Receptors, Neurotransmitter KW - Glutamic Acid KW - 3KX376GY7L KW - Magnesium KW - I38ZP9992A KW - Index Medicus KW - Receptors, Neurotransmitter -- physiology KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Cells, Cultured KW - Cerebellum -- cytology KW - Cerebellum -- drug effects KW - Magnesium -- pharmacology KW - Neurotoxins -- pharmacology KW - Glutamates -- toxicity KW - Cerebellum -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79270458?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-01 N1 - Date created - 1989-12-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Excitatory amino acid neurotoxicity at the N-methyl-D-aspartate receptor in cultured neurons: pharmacological characterization. AN - 79268503; 2572298 AB - L-Glutamate neurotoxicity at the N-methyl-D-aspartate (NMDA) receptor was characterized in cultured cerebellar granule cells. When deprived of glucose for 40 min, these cells were killed by 20-60 microM L-glutamate. However, the neurons were resistant to glutamate at concentrations as high as 5 mM when glucose and Mg2+ were present throughout. Both competitive and non-competitive NMDA receptor antagonists completely blocked neurotoxicity due to glutamate and other NMDA receptor agonists. CPP [+/-)-3-(2-carboxypiperazin-4-yl)-prophyl-1-phosphonic acid) was the most effective competitive antagonist with full protection at 100 microM while MK-801 [+/-)-10,11-dihydro-5-methyl-5H-dibenzo[a,d]-cyclohepten-5,10-imin e) was the most effective non-competitive antagonist with full protection at 20 nM. Other antagonists with higher selectivity for other subtypes of glutamate receptors were ineffective. We conclude that glutamate toxicity in energy-deprived cerebellar granule cells is mediated by NMDA receptors. Results are discussed in terms of an hypothesis offering an explanation for the transition of glutamate from neurotransmitter to neurotoxin which emphasizes the responsiveness of the receptor to agonists rather than focusing on the presence of high concentrations of agonist. JF - Brain research AU - Lysko, P G AU - Cox, J A AU - Vigano, M A AU - Henneberry, R C AD - Molecular Neurobiology Section, NINDS, Bethesda, MD 20892. Y1 - 1989/10/16/ PY - 1989 DA - 1989 Oct 16 SP - 258 EP - 266 VL - 499 IS - 2 SN - 0006-8993, 0006-8993 KW - Dibenzocycloheptenes KW - 0 KW - Glutamates KW - Neurotoxins KW - Receptors, N-Methyl-D-Aspartate KW - Receptors, Neurotransmitter KW - Glutamic Acid KW - 3KX376GY7L KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - 2-Amino-5-phosphonovalerate KW - 76726-92-6 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Cell Survival -- drug effects KW - 2-Amino-5-phosphonovalerate -- pharmacology KW - Cells, Cultured KW - Receptors, Neurotransmitter -- antagonists & inhibitors KW - Dibenzocycloheptenes -- pharmacology KW - Cerebellum -- cytology KW - Cerebellum -- drug effects KW - Neurotoxins -- pharmacology KW - Glutamates -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79268503?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-01 N1 - Date created - 1989-12-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Digital necrosis and disseminated Pneumocystis carinii infection after aerosolized pentamidine prophylaxis. AN - 79262753; 2802423 JF - Annals of internal medicine AU - Davey, R T AU - Margolis, D AU - Kleiner, D AU - Deyton, L AU - Travis, W AD - National Institute of Allergy and Infectious Diseases, Bethesda, Maryland. Y1 - 1989/10/15/ PY - 1989 DA - 1989 Oct 15 SP - 681 EP - 682 VL - 111 IS - 8 SN - 0003-4819, 0003-4819 KW - Aerosols KW - 0 KW - Pentamidine KW - 673LC5J4LQ KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Pneumonia, Pneumocystis -- prevention & control KW - Acquired Immunodeficiency Syndrome -- complications KW - Necrosis -- chemically induced KW - Humans KW - Adult KW - Pneumonia, Pneumocystis -- etiology KW - Recurrence KW - Male KW - Pentamidine -- administration & dosage KW - Toes -- pathology KW - Pneumocystis KW - Pentamidine -- adverse effects KW - Mycoses -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79262753?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-30 N1 - Date created - 1989-10-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modes of death and types of cardiac diseases in opiate addicts: analysis of 168 necropsy cases. AN - 79259085; 2801561 AB - One hundred sixty-eight opiate addicts, whose hearts were submitted for necropsy study, were examined with prime focus on modes of death and types of cardiac abnormalities. Twenty various modes of death were identified: active infective endocarditis or its consequences in 67 (40%), drug overdose in 39 (24%), coronary artery disease in 14 (8%), pulmonary granulomatosis in 7 (4%) and 15 various diseases (7 cardiac and 8 noncardiac) in the remaining 41 (24%) patients. Of the 168 hearts examined, only 7 (4%) were normal. Although infective endocarditis (active, healed or both) was most common (80 [48%] patients), there was a broad range of other cardiac abnormalities present: cardiomegaly in 114 (68%) (including 22 patients without another cardiac abnormality), coronary artery disease in 35 (21%), acquired valvular heart disease in 16 (10%), myocardial heart disease in 14 (8%) and a congenital cardiac anomaly in 19 (11%). Of the 35 hearts with various coronary artery diseases, 28 had significant (greater than 75%) narrowing of the cross-sectional area of 1 or more of the 4 major (left main, left anterior descending, left circumflex and right) epicardial coronary arteries by atherosclerotic plaque. Of 112 coronary arteries in these 28 hearts, 52 (46%) were significantly narrowed (a mean of 1.9 of the 4 major coronary arteries/patient). In 27 of these 28 cases, each 5-mm segment of the 4 major coronary arteries was examined histologically. Of the 1,435 five-mm segments examined, 189 (13%) were narrowed 76 to 100% in cross-sectional area by plaque; 347 (24%), 51 to 75%; 336 (23%), 26 to 50%; and 563 segments (39%) were narrowed 0 to 25% in cross-sectional area by plaque. The percents of 5-mm segments narrowed 76 to 100% in cross-sectional area were greater in those patients with (128 of 793 [16%]) than without (61 of 642 [9%]) clinical evidence of myocardial ischemia (p = 0.001). In this study a very high frequency of cardiac abnormalities (161 [96%]) was found at necropsy and most deaths (97 [58%]) were related to cardiac disease. Although death was most often due to diseases whose association to opiate addiction is well recognized (such as infective endocarditis, drug overdose and pulmonary granulomatosis from the venous injection of talc), several other modes of death were present. Most prominent among these was coronary artery disease (14 patients [8%]). JF - The American journal of cardiology AU - Dressler, F A AU - Roberts, W C AD - Pathology Branch, National Institutes of Health, Bethesda, Maryland. Y1 - 1989/10/15/ PY - 1989 DA - 1989 Oct 15 SP - 909 EP - 920 VL - 64 IS - 14 SN - 0002-9149, 0002-9149 KW - Narcotics KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Kidney Diseases -- pathology KW - Calcinosis -- pathology KW - Myocardium -- pathology KW - Humans KW - Aged KW - Organ Size KW - Kidney Diseases -- mortality KW - Acquired Immunodeficiency Syndrome -- epidemiology KW - Cardiomyopathies -- pathology KW - Coronary Disease -- pathology KW - Adult KW - Middle Aged KW - Chronic Disease KW - Adolescent KW - Male KW - Female KW - Substance-Related Disorders -- blood KW - Narcotics -- blood KW - Substance-Related Disorders -- mortality KW - Heart Diseases -- mortality KW - Substance-Related Disorders -- complications KW - Heart Diseases -- etiology KW - Heart Diseases -- pathology KW - Cause of Death UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79259085?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-09 N1 - Date created - 1989-11-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The rise in concentration of free Ca2+ and of pH provides sequential, synergistic signals for secretion in antigen-stimulated rat basophilic leukemia (RBL-2H3) cells. AN - 79237327; 2794509 AB - Ag stimulation of rat basophilic leukemia (RBL-2H3) cells results in hydrolysis of inositol phospholipids, a transient increase in concentration of cytosol Ca2+ [( Ca2+]i), a gradual increase in cytosolic pH (pHi) and the activation of protein kinase C. To determine whether all these changes serve as signals for secretion, studies were conducted with cells permeabilized with streptolysin O in which pHi and [Ca2+]i could be varied independently of each other and enzyme activities could be manipulated. At resting pHi (approximately 7.0) and [Ca2+]i (0.1 microM), the permeabilized cells showed little secretory response to Ag. At resting pHi, elevated levels of Ca2+ (0.33 microM) were required for maximal secretory response to Ag. At a pHi of 7.4, however, 0.1 microM [Ca2+]i was sufficient to sustain near maximal responses to Ag. Therefore, a small increase of [Ca2+]i to 0.33 microM was required to initiate secretion, but once the pHi was elevated secretion could be sustained at near basal levels of [Ca2+]i. Since elevating the [Ca2+]i and pHi, by themselves promoted little secretion, another potentiating signal must have been generated by antigen stimulation. This signal was possibly transduced via hydrolysis of inositol phospholipids and protein kinase C. Even with an elevated [Ca2+]i (0.33 microM) the hydrolysis of the phospholipids and secretion stimulated by Ag were inhibited by guanosine 5'(2-O-thio)diphosphate and neomycin. Furthermore, both protein-kinase C and the secretory response to Ag were lost after permeabilized cells were washed but both were retained if cells were exposed to PMA before permeabilization. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Ali, H AU - Collado-Escobar, D M AU - Beaven, M A AD - Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, Bethesda, MD 20892. Y1 - 1989/10/15/ PY - 1989 DA - 1989 Oct 15 SP - 2626 EP - 2633 VL - 143 IS - 8 SN - 0022-1767, 0022-1767 KW - Antigens KW - 0 KW - Dinitrophenols KW - Inositol Phosphates KW - Serum Albumin, Bovine KW - Immunoglobulin E KW - 37341-29-0 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Calcium KW - SY7Q814VUP KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Inositol Phosphates -- metabolism KW - Leukemia -- immunology KW - Hydrogen-Ion Concentration KW - Dinitrophenols -- immunology KW - Hydrolysis KW - Leukemia -- enzymology KW - Rats KW - Immunoglobulin E -- immunology KW - Leukemia -- metabolism KW - Serum Albumin, Bovine -- immunology KW - Cell Membrane Permeability KW - Protein Kinase C -- physiology KW - Drug Synergism KW - Cell Line KW - Cell-Free System KW - Calcium -- metabolism KW - Basophils -- enzymology KW - Basophils -- metabolism KW - Antigens -- immunology KW - Signal Transduction KW - Basophils -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79237327?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-09 N1 - Date created - 1989-11-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Studies of protein kinase C in the rat basophilic leukemia (RBL-2H3) cell reveal that antigen-induced signals are not mimicked by the actions of phorbol myristate acetate and Ca2+ ionophore. AN - 79235936; 2551964 AB - Exogenous activators of protein kinase C such as PMA in combination with a Ca2+ ionophore (A23187), cause secretion in rat basophilic (RBL-2H3) cells,but they do so through stimulatory signals that are not the same as those generated by Ag or oligomers of IgE. On the one hand, the synergy between PMA and A23187 and the suppression of Ag-mediated signals (hydrolysis of inositol phospholipids and rise in concentration of cytosolic Ca2+) by PMA were totally dependent on protein kinase C. The loss of synergistic and inhibitory actions of PMA, for example, correlated with the loss of protein kinase C (as determined by immunoblotting techniques) when cells were continuously exposed to PMA. Furthermore, the permeabilization of RBL-2H3 cells resulted in the loss of both protein kinase C and the inhibitory action of PMA, but both were retained if cells were exposed to PMA before permeabilization Ag-induced secretion, on the other hand, was not as dependent on the presence of protein kinase C. The potent inhibitor of this enzyme, staurosporine, which blocked completely the secretory response to the combination of PMA and A23187, did not inhibit Ag-induced secretion except at concentrations (greater than 10 nM) that inhibited Ag-stimulated hydrolysis of inositol phospholipids as well. Also RBL-2H3 cells still showed some secretory-response (approximately 25% of normal) to Ag when cells were depleted (greater than 98%) of protein kinase C by prolonged treatment with PMA. Previous studies have indicated that the secretory response to PMA and A23187 is much lower than that elicited by Ag when the concentrations of stimulants were matched to give the same increase in concentrations of cytosolic Ca2+. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Cunha-Melo, J R AU - Gonzaga, H M AU - Ali, H AU - Huang, F L AU - Huang, K P AU - Beaven, M A AD - Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, Bethesda, MD 20892. Y1 - 1989/10/15/ PY - 1989 DA - 1989 Oct 15 SP - 2617 EP - 2625 VL - 143 IS - 8 SN - 0022-1767, 0022-1767 KW - Alkaloids KW - 0 KW - Antigens KW - Phosphatidylinositols KW - Calcimycin KW - 37H9VM9WZL KW - Protein Kinase C KW - EC 2.7.11.13 KW - Staurosporine KW - H88EPA0A3N KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Phosphatidylinositols -- metabolism KW - Animals KW - Leukemia -- metabolism KW - Leukemia -- immunology KW - Kinetics KW - Enzyme Activation -- drug effects KW - Alkaloids -- pharmacology KW - Leukemia -- enzymology KW - Cell Line KW - Protein Kinase C -- metabolism KW - Basophils -- physiology KW - Basophils -- enzymology KW - Protein Kinase C -- antagonists & inhibitors KW - Signal Transduction -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Protein Kinase C -- physiology KW - Calcimycin -- pharmacology KW - Basophils -- metabolism KW - Antigens -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79235936?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-09 N1 - Date created - 1989-11-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modeling analysis of the global and microscopic distribution of immunoglobulin G, F(ab')2, and Fab in tumors. AN - 79226846; 2790783 AB - In order to understand the pharmacology of monoclonal antibodies and their conjugates, one must consider both global and microscopic aspects of antibody distribution. Here we present an analysis of antibody distribution in tumors based on the following factors: (a) molecular weight and valence of the antibody; (b) global pharmacokinetic profile following i.v. bolus injection; (c) penetration through the vascular wall; (d) diffusive and convective transport through interstitial space in the tumor; (e) antigen-antibody interaction; (f) antibody metabolism. Partial differential equations were developed to incorporate these factors and then solved numerically using parameter values from animal experiments, from clinical protocols at our institution, from studies of antibody binding characteristics in vitro, and from the literature. Salient findings from this model are that (a) antigen-antibody interaction in the tumor can retard antibody percolation away from blood capillaries, thus constituting a "binding site barrier"; (b) high antibody affinity tends to decrease antibody penetration and result in a more heterogeneous distribution; (c) high molecular weight [IgG greater than F(ab')2 greater than Fab] slows percolation and results in less uniform spatial distribution; (d) the average antibody concentration in the tumor does not increase linearly with antibody dose; (e) raising the rate of antibody metabolism results in low concentration and poor percolation; (f) perhaps most interesting, there is predicted to be a range of antibody dose and affinity within which the specificity ratio and average concentration could be kept high while limiting the heterogeneity of distribution. PERC, the computer program package developed for these analyses, provides a convenient and flexible way to assess the impact of global and microscopic parameters on the distribution of immunoglobulin in tumors. For calculations presented here, the input data were obtained from experimental sources, and qualitative features of the output proved consistent with the few interpretable observations available. However, detailed validation would require much more data than are currently at hand. The mathematical findings should therefore be considered as aids to concept development and as a set of null hypotheses with which to guide experimentation. Experiments and simulations will continue in tandem. It should be noted that the PERC package (and also the general principles delineated here) can be applied as well to biological ligands other than antibodies. JF - Cancer research AU - Fujimori, K AU - Covell, D G AU - Fletcher, J E AU - Weinstein, J N AD - Laboratory of Mathematical Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/10/15/ PY - 1989 DA - 1989 Oct 15 SP - 5656 EP - 5663 VL - 49 IS - 20 SN - 0008-5472, 0008-5472 KW - Immunoglobulin Fab Fragments KW - 0 KW - Immunoglobulin G KW - Immunotoxins KW - Index Medicus KW - Software KW - Neoplasms -- blood supply KW - Antibody Affinity KW - Neoplasms -- therapy KW - Molecular Weight KW - Structure-Activity Relationship KW - Models, Theoretical KW - Immunotoxins -- pharmacokinetics KW - Immunoglobulin G -- pharmacokinetics KW - Immunoglobulin Fab Fragments -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79226846?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-15 N1 - Date created - 1989-11-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sister chromatid exchange and chromosome fragility in the nevoid basal cell carcinoma syndrome. AN - 79223006; 2507127 AB - Previous studies of chromosome stability in the nevoid basal cell carcinoma syndrome have yielded inconsistent results and suffered from small sample sizes and less than optimal controls. We investigated chromosome fragility and sister chromatid exchange in 20 affected individuals from five multiplex pedigrees, and 15 first- or second-degree unaffected relatives. The percentage of case and control cells showing breaks or rearrangements was compared using a test of proportions. A similar procedure was used to compare site-specific sister chromatid exchanges in baseline cultures from affected persons and controls. No significant differences were noted for either chromosome fragility or sister chromatid exchange between the two groups. These results suggest that cancer susceptibility in the nevoid basal cell carcinoma syndrome is not caused by or manifested as chromosome instability. JF - Cancer genetics and cytogenetics AU - Bale, A E AU - Bale, S J AU - Murli, H AU - Ivett, J AU - Mulvihill, J J AU - Parry, D M AD - Clinical Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/10/15/ PY - 1989 DA - 1989 Oct 15 SP - 273 EP - 279 VL - 42 IS - 2 SN - 0165-4608, 0165-4608 KW - Mitomycins KW - 0 KW - Methylnitronitrosoguanidine KW - 12H3O2UGSF KW - Mitomycin KW - 50SG953SK6 KW - 4-Nitroquinoline-1-oxide KW - 56-57-5 KW - Index Medicus KW - Humans KW - 4-Nitroquinoline-1-oxide -- pharmacology KW - Cells, Cultured KW - Adult KW - Chromosome Fragility KW - Methylnitronitrosoguanidine -- pharmacology KW - Lymphocytes -- cytology KW - Middle Aged KW - Mitomycins -- pharmacology KW - Lymphocytes -- drug effects KW - Female KW - Male KW - Carcinoma, Basal Cell -- genetics KW - Sister Chromatid Exchange KW - Basal Cell Nevus Syndrome -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79223006?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-21 N1 - Date created - 1989-11-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Preferential sites for viral integration on mammalian genome. AN - 79221488; 2551486 AB - Chromosomal localization of human papillomavirus (HPV) 16 and 18 on human cervical carcinomas and epithelial cell lines obtained after HPV transfection has uncovered a nonrandom association of viral integration and specific genome sites. Fragile sites appear to be preferential targets for viral integration because of their structural and functional characteristics through which chromosomal anomalies, alterations in protooncogene activity, and gene amplification can occur. Individually or in association, such changes lead to the acquisition of an unlimited cell growth potential but not tumorigenicity. Genetic instability and uncontrolled cell division resulting from HPV integration increase the cell's susceptibility to other exogenous carcinogenic factors that may complete the process of neoplastic development. JF - Cancer genetics and cytogenetics AU - Popescu, N C AU - DiPaolo, J A AD - Laboratory of Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/10/15/ PY - 1989 DA - 1989 Oct 15 SP - 157 EP - 171 VL - 42 IS - 2 SN - 0165-4608, 0165-4608 KW - Index Medicus KW - Karyotyping KW - Chromosome Banding KW - Humans KW - Proto-Oncogenes KW - Chromosome Mapping KW - Female KW - Papillomaviridae -- isolation & purification KW - Uterine Cervical Neoplasms -- microbiology KW - Uterine Cervical Neoplasms -- genetics KW - Papillomaviridae -- genetics KW - Genes, Viral KW - Genomic Library UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79221488?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-21 N1 - Date created - 1989-11-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The bovine papillomavirus E5 transforming protein can stimulate the transforming activity of EGF and CSF-1 receptors. AN - 79222716; 2551505 AB - The bovine papillomavirus E5 transforming gene encodes a 44 amino acid protein product that is localized to cytoplasmic membranes, including the plasma membrane. We now report that E5 can cooperate with human EGF receptors and with human CSF-1 receptors to induce cellular transformation of NIH 3T3 cells. Cooperation occurred in the absence of receptor stimulation by ligand, and it was further augmented by treatment with ligand. Cooperation was not seen between E5 and either c-fes or c-src. The cooperation between E5 and high levels of EGF receptors was associated with inhibition of receptor degradation and persistence of activated receptors on the cell surface. We conclude that E5 may enhance the receptor activity via inhibition of receptor down-modulation. JF - Cell AU - Martin, P AU - Vass, W C AU - Schiller, J T AU - Lowy, D R AU - Velu, T J AD - Laboratory of Cellular Oncology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/10/06/ PY - 1989 DA - 1989 Oct 06 SP - 21 EP - 32 VL - 59 IS - 1 SN - 0092-8674, 0092-8674 KW - Colony-Stimulating Factors KW - 0 KW - Oncogene Proteins, Viral KW - Proto-Oncogene Proteins KW - Receptors, Cell Surface KW - Receptors, Colony-Stimulating Factor KW - oncogene protein E5, Bovine papillomavirus type 1 KW - Transforming Growth Factors KW - 76057-06-2 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Animals KW - Phosphorylation KW - Humans KW - Mice KW - Drug Synergism KW - Transforming Growth Factors -- biosynthesis KW - Proto-Oncogene Proteins -- physiology KW - Cell Line KW - Receptors, Cell Surface -- metabolism KW - Colony-Stimulating Factors -- metabolism KW - Receptor, Epidermal Growth Factor -- metabolism KW - Papillomaviridae -- physiology KW - Receptor, Epidermal Growth Factor -- physiology KW - Oncogene Proteins, Viral -- physiology KW - Bovine papillomavirus 1 -- physiology KW - Receptors, Cell Surface -- physiology KW - Cell Transformation, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79222716?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-08 N1 - Date created - 1989-11-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Targeted toxin therapy for the treatment of cancer. AN - 79203774; 2550658 AB - Protein toxins such as Pseudomonas exotoxin, diphtheria toxin, and ricin may be useful in cancer therapy because they are among the most potent cell-killing agents. One molecule of a toxin delivered to the cytoplasm of a cancer cell will be lethal for that cell. However, to be therapeutically useful, these toxins need to be targeted to specific sites on the surface of cancer cells, then be internalized and ultimately reach the cell cytoplasm. This process is accomplished by eliminating binding to toxin receptors and redirecting the cell-killing activity of the toxin to receptors or antigens present on cancer cells. Typically, toxins are conjugated to cell-binding proteins such as monoclonal antibodies or growth factors. These conjugates bind and kill cancer cells selectively while normal cells, which don't bind the conjugates, are spared. Because the genes for many protein toxins have been cloned, it is possible to make genetic modifications to their structure. By deleting the DNA that codes for the toxin binding region and replacing it with various complementary DNA encoding other cell-binding proteins, it has been possible to make chimeric toxins that kill cells on the basis of the newly acquired binding activity. The ability to make these chimeras may be useful in designing future toxin-based anticancer therapies. JF - Journal of the National Cancer Institute AU - FitzGerald, D AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/10/04/ PY - 1989 DA - 1989 Oct 04 SP - 1455 EP - 1463 VL - 81 IS - 19 SN - 0027-8874, 0027-8874 KW - Antibodies, Monoclonal KW - 0 KW - Diphtheria Toxin KW - Exotoxins KW - Immunotoxins KW - Receptors, Cell Surface KW - Ricin KW - 9009-86-3 KW - Index Medicus KW - Animals KW - Humans KW - Receptors, Cell Surface -- drug effects KW - Neoplasms -- drug therapy KW - Neoplasms -- pathology KW - Ricin -- therapeutic use KW - Immunotoxins -- therapeutic use KW - Diphtheria Toxin -- therapeutic use KW - Pseudomonas KW - Exotoxins -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79203774?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-20 N1 - Date created - 1989-10-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Occupational risks of bladder cancer in the United States: II Nonwhite men. AN - 79199802; 2778835 AB - Occupational risks of bladder cancer among nonwhite men were assessed based on interviews with 126 cases and 383 controls conducted during the National Bladder Cancer Study, a population-based, case-control study conducted in 10 areas of the United States. Our findings indicated that nonwhite men who were ever employed as auto workers have an elevated risk of bladder cancer [relative risk (RR) = 2.3; 95% confidence intervals (CI) = 0.8-6.4] with a significant positive trend in RR with increasing duration of employment (P = .017) and with the RR rising to 4.7 for those employed at least 10 years. Dry cleaners, ironers, and pressers also experienced increased bladder cancer risk (RR = 2.8, CI = 1.1-7.4). Nonsignificant excesses of similar magnitude to those seen among white men were found for nonwhite men employed in several other occupations. Overall, our findings suggest that the risk of occupational bladder cancer among white and nonwhite men is similar. When inconsistencies between whites and nonwhites did occur, they appeared either due to chance or possibly racial differences in exposure among men within the same industry and occupation. In all, we estimate that the population attribute risk for occupation among nonwhite U.S. men is 27% (CI = 9% to 56%), which is slightly higher than the estimate of 21% to 25% previously reported for white U.S. men, although this difference was not statistically significant. JF - Journal of the National Cancer Institute AU - Silverman, D T AU - Levin, L I AU - Hoover, R N AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/10/04/ PY - 1989 DA - 1989 Oct 04 SP - 1480 EP - 1483 VL - 81 IS - 19 SN - 0027-8874, 0027-8874 KW - Index Medicus KW - United States KW - Age Factors KW - Aged, 80 and over KW - Risk Factors KW - Humans KW - Aged KW - Middle Aged KW - Textile Industry KW - Time Factors KW - Male KW - Urinary Bladder Neoplasms -- epidemiology KW - African Americans KW - Occupational Diseases -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79199802?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-20 N1 - Date created - 1989-10-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of a new P450 expressed in human lung: complete cDNA sequence, cDNA-directed expression, and chromosome mapping. AN - 79405439; 2574990 AB - A cDNA coding for a P450 expressed in human lung was isolated from a lambda gt11 library constructed from human lung mRNA using a cDNA probe to rat P450 IVA1. The cDNA-deduced amino acid sequence of this P450, designated IVB1, consisted of 511 amino acids and had a calculated molecular weight of 59,558. The IVB1 amino acid sequence bore 51%, 53%, and 52% similarities to rat IVA1, IVA2, and rabbit P450p-2, respectively. Comparison of the primary amino acid sequence of human IVB1 with rat IVA and rabbit p-2 P450 sequences revealed a region of absolute sequence identity of 17 amino acids between residues 304 and 320. However, the functional significance of this conserved sequence is unknown. Human IVB1 also appears to be related to P450 isozyme 5 that has been extensively characterized in rabbits. The IVB1 cDNA was inserted into a vaccinia virus expression vector and the enzyme expressed in human cell lines. The expressed enzyme had an absorption spectrum with a lambda max at 450 nm when reduced and complexed with carbon monoxide, typical of other cytochrome P450s. Unlike rabbit P450 isozyme 5, however, human IVB1 was unable to activate the promutagen 2-aminofluorene. Human lung microsomal P450s were also unable to metabolize this compound despite the presence of IVB1 mRNA in three out of four human lungs analyzed. In contrast to its expression in lung, IVB1 mRNA was undetectable in livers from 14 individuals, including those from which the lungs were derived. IVB1-related mRNA was also expressed in rat lung and was undetectable in untreated rat liver.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Biochemistry AU - Nhamburo, P T AU - Gonzalez, F J AU - McBride, O W AU - Gelboin, H V AU - Kimura, S AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/10/03/ PY - 1989 DA - 1989 Oct 03 SP - 8060 EP - 8066 VL - 28 IS - 20 SN - 0006-2960, 0006-2960 KW - Mutagens KW - 0 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Vaccinia virus -- genetics KW - Animals KW - Humans KW - Amino Acid Sequence KW - Mutagens -- pharmacokinetics KW - Rabbits KW - Chromosome Mapping KW - Cloning, Molecular KW - Rats KW - Chromosomes, Human, Pair 1 KW - Base Sequence KW - Biotransformation KW - Polymorphism, Restriction Fragment Length KW - Molecular Sequence Data KW - Gene Expression Regulation, Enzymologic KW - Cytochrome P-450 Enzyme System -- genetics KW - DNA -- genetics KW - Cytochrome P-450 Enzyme System -- metabolism KW - Lung -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79405439?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-15 N1 - Date created - 1990-02-15 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - J02871; GENBANK N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Computer-assisted evaluation of polydisperse two-dimensional gel patterns of polysaccharide-protein conjugate preparations with regard to size and net charge. AN - 85269075; pmid-2612463 AB - Native Hemophilus influenzae polysaccharide-protein conjugate particles were analyzed by a two-dimensional agarose electrophoresis procedure. In view of their preparation by random chemical crosslinking, the conjugates necessarily exhibit a polydisperse two-dimensional gel pattern which varies depending on the conditions of the particular preparation. The polydisperse patterns were interpreted with regard to the size and surface net charge density of the conjugate on the basis of the extended Ogston model. Data processing was performed by a new program, designated ZWEIDI.DO, written in the language of M-LAB (modeling laboratory). The program computes particle and gel fiber specific parameters from the positions of standards and unknown(s) on the two-dimensional gel using a simultaneous linear least-square curve fitting routine. Based on these calculations, the program serves to compute a nomogram of iso-size and iso-free-mobility profiles. Superimposing these profiles on the gel patterns, the size and free mobility range of the polydisperse conjugate mixtures is obtained. Potentially, the procedure could serve as a tool for quality control in the production of conjugates as vaccines and for the physical characterization of polydisperse subcellular particles and vesicles. JF - Electrophoresis AU - Tietz, D AU - Chrambach, A AD - Section on Macromolecular Analysis, National Institute of Child Health and Human Development, Bethesda, MD 20892. PY - 1989 SP - 667 EP - 680 VL - 10 IS - 10 SN - 0173-0835, 0173-0835 KW - Software KW - Bacterial Proteins KW - Haemophilus influenzae KW - Electrophoresis, Gel, Two-Dimensional KW - Electrophoresis, Agar Gel KW - Densitometry KW - Models, Theoretical KW - Computer Simulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85269075?accountid=14244 LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - EEG and brainstem auditory evoked response potentials in adult male drug abusers with self-reported histories of aggressive behavior. AN - 85257717; pmid-2790098 AB - Auditory brainstem evoked response (BAER) and spontaneous electroencephalogram (EEG) were measured in 124 adult male drug abusers. We examined the relationships among psychiatric diagnoses, paper and pencil measures of aggression and hostility, and electrophysiological features. Subjects meeting criteria for antisocial personality disorder (ASP), as defined by DSM-III, were not significantly different from non-ASP subjects for either BAER or spontaneous EEG measures. The more overtly aggressive subjects had significant delays in BAER latency. Aggressive subjects also had more delta activity and less alpha activity in the spontaneous EEG, as have been observed in "psychopaths" and "criminals." Although ASP and aggression are related, these data indicate that aggressiveness may be a separate, albeit overlapping, trait. As both early aggression and a diagnosis of ASP are predictors of later drug use, the findings that only aggression was associated with EEG slowing and brainstem delays may indicate that ASP and aggression make independent contributions to vulnerability to the development of drug abuse. JF - Biological Psychiatry AU - Fishbein, D H AU - Herning, R I AU - Pickworth, W B AU - Haertzen, C A AU - Hickey, J E AU - Jaffe, J H AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. PY - 1989 SP - 595 EP - 611 VL - 26 IS - 6 SN - 0006-3223, 0006-3223 KW - Arousal KW - Human KW - MMPI KW - Alcoholism KW - Adult KW - Evoked Potentials, Auditory KW - Brain Stem KW - Substance-Related Disorders KW - Antisocial Personality Disorder KW - Aggression KW - Male KW - Reaction Time KW - Electroencephalography KW - Psychotropic Drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85257717?accountid=14244 LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Induction of a novel damage-specific DNA binding protein correlates with enhanced DNA repair in primate cells. AN - 79579007; 2518795 AB - Pretreatment of mammalian cell with DNA-damaging agents, such as UV light or mitomycin C, but not the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA), results in the enhanced repair of subsequently transfected UV-damaged expression vectors. To determine the cellular factors that are responsible for this enhancement, we have used a modified gel retardation assay to detect the proteins that interact with damaged DNA. We have identified a constitutive DNA binding protein in extracts from primate cells that has a high affinity for UV-irradiated double-stranded DNA. Cells pretreated with UV light, mitomycin C, or aphidicolin, but not TPA or serum starvation, have higher levels of this damage-specific DNA binding (DDB) protein. These results suggest that the signal for induction of DDB protein can either be damage to the DNA or interference with cellular DNA replication. The induction of DDB protein varies among primate cells with different phenotypes: (1) virus-transformed repair-proficient cells have partially or fully lost the ability to induce DDB protein above constitutive levels; (2) primary cells from repair-deficient xeroderma pigmentosum (XP) group C, and transformed XP groups A and D, show constitutive DDB protein, but do not show induced levels of this protein 48 h after UV; and (3) primary and transformed repair-deficient cells from one XP E patient are lacking both the constitutive and the induced DDB activity. The correlation between the induction of the DDB protein and the enhanced repair of UV-damaged expression vectors implies the involvement of the DDB protein in this inducible cellular response. JF - Molecular toxicology AU - Protić, M AU - Hirschfeld, S AU - Tsang, A P AU - Wagner, M AU - Dixon, K AU - Levine, A S AD - Section on Viruses and Cellular Biology, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. PY - 1989 SP - 255 EP - 270 VL - 2 IS - 4 SN - 0883-9492, 0883-9492 KW - Culture Media KW - 0 KW - DNA-Binding Proteins KW - Diterpenes KW - Mitomycins KW - Aphidicolin KW - 38966-21-1 KW - Mitomycin KW - 50SG953SK6 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Diterpenes -- pharmacology KW - Animals KW - Ultraviolet Rays KW - Humans KW - Plasmids -- radiation effects KW - Haplorhini KW - Phenotype KW - Blood KW - Base Sequence KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Plasmids -- drug effects KW - Mitomycins -- pharmacology KW - Cell Line KW - DNA Repair -- radiation effects KW - DNA-Binding Proteins -- drug effects KW - DNA-Binding Proteins -- biosynthesis KW - DNA Damage -- radiation effects KW - DNA-Binding Proteins -- radiation effects KW - DNA Repair -- drug effects KW - DNA Damage -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79579007?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-19 N1 - Date created - 1991-09-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The acidic amino-terminal region of the HIV-1 Tat protein constitutes an essential activating domain. AN - 79572463; 2562188 AB - The Tat protein encoded by the human immunodeficiency virus (HIV) is an efficient activator of HIV gene expression. Many eukaryotic transcriptional activators contain a nucleic acid binding domain and a separate activating domain. These activating regions are acidic and often amphipathic. The amino terminus of the HIV-1 Tat protein is acidic with a periodicity of acidic, polar, and hydrophobic residues consistent with that of an amphipathic alpha helix. This region appears to be important for Tat function. We have analyzed the functional significance of acidic residues within the amino-terminal region of Tat by means of site-directed mutagenesis and by testing the capacity of mutant proteins to trans-activate the viral long terminal repeat (LTR) Conservative changes (acidic to acidic) were well tolerated, whereas acidic to neutral and acidic to basic changes markedly reduced Tat activity. The relative importance of each of the three acidic residues correlated with proximity to the amino terminus. Substitution of the entire domain with heterologous sequences that might form an acidic, amphipathic alpha helix partially restored activity when compared with an amino-terminal truncation mutant. In contrast to the observed importance of acidic residues, hydroxylated residues between amino acids 40 and 47 were dispensable for Tat function. These data suggest that the acidity of the amino terminal region is important for Tat function and that Tat-mediated trans-activation may be similar to that of other known activator proteins. JF - The New biologist AU - Rappaport, J AU - Lee, S J AU - Khalili, K AU - Wong-Staal, F AD - Laboratory of Tumor Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 101 EP - 110 VL - 1 IS - 1 SN - 1043-4674, 1043-4674 KW - Gene Products, tat KW - 0 KW - Recombinant Fusion Proteins KW - tat Gene Products, Human Immunodeficiency Virus KW - DNA KW - 9007-49-2 KW - Index Medicus KW - AIDS/HIV KW - Recombinant Fusion Proteins -- metabolism KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Sequence Homology, Nucleic Acid KW - DNA -- genetics KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Gene Products, tat -- physiology KW - HIV-1 -- genetics KW - Gene Expression Regulation, Viral KW - Gene Products, tat -- genetics KW - Transcriptional Activation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79572463?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-29 N1 - Date created - 1991-04-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Anxiolytic properties of 1-aminocyclopropanecarboxylic acid, a ligand at strychnine-insensitive glycine receptors. AN - 79474881; 2576136 AB - The effects of 1-aminocyclopropanecarboxylic acid were investigated on performance in an elevated plus-maze. This compound is a high-affinity, partial agonist ligand at strychnine-insensitive glycine receptors of the N-methyl-D-aspartate receptor complex. Like chlordiazepoxide, 1-aminocyclopropanecarboxylic acid increased in a dose-dependent manner both the percent entries into and the percent time spent in the open arms of the plus-maze. However, 1-aminocyclopropanecarboxylic acid was significantly less efficacious than chlordiazepoxide in these measures and increased, while chlordiazepoxide decreased, the time spent in the middle platform of the plus-maze. These findings indicate that ligands acting through strychnine-insensitive glycine receptors on the N-methyl-D-aspartate receptor complex may represent a new class of anxiolytic agents with a profile which differs from the benzodiazepines. JF - Pharmacology, biochemistry, and behavior AU - Trullas, R AU - Jackson, B AU - Skolnick, P AD - Laboratory of Neuroscience, NIDDK, Bethesda, MD 20892. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 313 EP - 316 VL - 34 IS - 2 SN - 0091-3057, 0091-3057 KW - Amino Acids KW - 0 KW - Amino Acids, Cyclic KW - Anti-Anxiety Agents KW - Receptors, Glycine KW - Receptors, Neurotransmitter KW - 1-aminocyclopropane-1-carboxylic acid KW - 3K9EJ633GL KW - Strychnine KW - H9Y79VD43J KW - Index Medicus KW - Animals KW - Conflict (Psychology) KW - Task Performance and Analysis KW - Mice KW - Male KW - Anti-Anxiety Agents -- pharmacology KW - Receptors, Neurotransmitter -- metabolism KW - Strychnine -- pharmacology KW - Amino Acids -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79474881?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-27 N1 - Date created - 1990-03-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Toxicology studies of a chemical mixture of 25 groundwater contaminants. I. Chemistry development. AN - 79444509; 2612771 AB - As part of an effort to evaluate the toxicology of a chemically defined mixture of 25 frequently detected groundwater contaminants, we report here the formulation and analytical chemistry of this mixture. Many problems were anticipated, including limitation of solubility, chemical interactions, and extreme volatility in the aqueous solution of 25 chemicals. The final technically achievable stock solution was prepared based on EPA survey concentrations of these chemicals in groundwater around hazardous waste disposal sites, their toxicity information, and solubility of the individual compounds in the matrix of the aqueous solution of these 25 chemicals. Because the anticipated animal studies were to be conducted at various laboratories, for ease of handling and maximum stability, the stock solution was stored or shipped as two substock solutions: an organic substock with 18 neat organic chemicals in a glass vial sealed with minimum headspace and an aqueous substock solution with 6 metals of various salt forms and phenol. The concentrations of the solutions were such that direct mixing of the organic and aqueous substocks produced the desired high dose level for the animal experiments. Analyses of all 25 chemicals in the drinking water mixture required six different chromatographic and spectroscopic methods. Some loss of organic volatiles during mixing of the substocks and during the first 24 hr following preparation did occur. However, the concentrations of acetone, phenol, and all the metals remained constant during preparation. Solutions held under simulated animal cage conditions for 96 hr showed losses of the organic volatiles; the majority of which occurred within the first 24 hr. This study shows that it is possible to conduct animal experiments on an aqueous mixture containing 25 groundwater contaminants. Furthermore, a reasonable estimate of intake of individual chemicals can be achieved provided that dosing solutions are prepared fresh at frequent intervals (e.g., 48 to 72 hr) and that comprehensive analyses are carried out. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Yang, R S AU - Goehl, T J AU - Brown, R D AU - Chatham, A T AU - Arneson, D W AU - Buchanan, R C AU - Harris, R K AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 366 EP - 376 VL - 13 IS - 3 SN - 0272-0590, 0272-0590 KW - Aroclors KW - 0 KW - Hydrocarbons KW - Indicators and Reagents KW - Metals KW - Phenols KW - Water Pollutants KW - Water Pollutants, Chemical KW - aroclor 1260 KW - 11096-82-5 KW - Acetone KW - 1364PS73AF KW - Diethylhexyl Phthalate KW - C42K0PH13C KW - Index Medicus KW - Hydrocarbons -- analysis KW - Drug Stability KW - Chemistry KW - Chromatography, Gas KW - Diethylhexyl Phthalate -- analysis KW - Chemical Phenomena KW - Acetone -- analysis KW - Aroclors -- analysis KW - Phenols -- analysis KW - Metals -- analysis KW - Water Pollutants -- toxicity KW - Water Supply -- analysis KW - Water Pollutants, Chemical -- analysis KW - Water Pollutants, Chemical -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79444509?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-06 N1 - Date created - 1990-03-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Variability of safe dose estimates when using complicated models of the carcinogenic process. A case study: methylene chloride. AN - 79441108; 2612786 AB - Advances in understanding carcinogenesis have led to the development of mathematical models that have biologically interpretable parameters. These models utilize more of the available scientific data than the empirical models routinely employed for quantifying carcinogenic risk. They also require consideration of sources of uncertainty in risk estimates that were previously ignored, such as animal-to-animal variability of physiological and pharmacological constants. A numerical technique is proposed for studying the consequences of incorporating the intrapopulation variability of biologically interpretable parameters into the risk assessment process. To demonstrate the technique, the variability of safe dose estimates for exposure to methylene chloride is considered. The results suggest that intrapopulation variability of the model parameters can increase the variability of safe dose estimates an appreciable amount. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Portier, C J AU - Kaplan, N L AD - Statistics and Biomathematics Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 533 EP - 544 VL - 13 IS - 3 SN - 0272-0590, 0272-0590 KW - Carcinogens KW - 0 KW - Hydrocarbons, Chlorinated KW - Methylene Chloride KW - 588X2YUY0A KW - Index Medicus KW - United States KW - Mice, Inbred Strains KW - Animals KW - United States Environmental Protection Agency KW - Kinetics KW - Humans KW - Body Weight -- drug effects KW - Mice KW - Monte Carlo Method KW - Models, Biological KW - Male KW - Hydrocarbons, Chlorinated -- toxicity KW - Methylene Chloride -- toxicity KW - Carcinogenicity Tests UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79441108?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-06 N1 - Date created - 1990-03-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Toxicology studies of a chemical mixture of 25 groundwater contaminants. III. Male reproduction study in B6C3F1 mice. AN - 79435860; 2612772 AB - A mixture of chemicals has been developed that models contaminated groundwater around hazardous waste sites. We investigated the effects of this mixture on spermatogenesis in B6C3F1 mice. The animals consumed three different concentrations of this mixture for 90 days, after which time they were euthanatized. Although there was a concentration-related decrease in the amount of fluid consumed at the higher two concentrations, there were no differences in body weight among the groups. Similarly, there was no effect of mixture consumption upon the histology of liver, kidney, testis, epididymis, or seminal vesicles or upon the absolute organ weights of these organs. Kidney weight relative to body weight was increased in the high dose group. Epididymal sperm number and testicular spermatid count were not affected by treatment. These studies show that, at exposure levels that decrease fluid intake and increase adjusted kidney weight, there were no effects of this mixture on gametogenesis in male mice. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Chapin, R E AU - Phelps, J L AU - Schwetz, B A AU - Yang, R S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 388 EP - 398 VL - 13 IS - 3 SN - 0272-0590, 0272-0590 KW - Water Pollutants KW - 0 KW - Water Pollutants, Chemical KW - Index Medicus KW - Spermatids -- drug effects KW - Mice, Inbred Strains KW - Animals KW - Spermatids -- cytology KW - Sperm Count KW - Drinking -- drug effects KW - Body Weight -- drug effects KW - Mice KW - Male KW - Organ Size -- drug effects KW - Gametogenesis -- drug effects KW - Water Pollutants -- toxicity KW - Water Supply -- analysis KW - Reproduction -- drug effects KW - Water Pollutants, Chemical -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79435860?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-06 N1 - Date created - 1990-03-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanism of action of GnRH: the participation of calcium mobilization and activation of protein kinase C in gonadotropin secretion. AN - 79402774; 2689778 AB - The role of protein kinase C in luteinizing hormone (LH) release was analyzed in studies on the secretory responses to gonadotropin releasing hormone (GnRH) and phorbol esters in pituitary cell cultures. 12-O-tetradecanoyl-phorbol 13-acetate (TPA), 4 beta-phorbol 12,13-bibenzoate, and 4 beta-phorbol 12,13-diacetate stimulated LH release with ED50s of 5, 10 and 1000 nM, respectively, and with about 70% of the efficacy of GnRH. Phorbol ester-stimulated LH secretion was decreased but not abolished by progressive reduction of [Ca2+] in the incubation medium, and the residual response was identical with that of GnRH in Ca2+-deficient medium. TPA increased [Ca2+]i to a peak after 30 s in normal medium but not in the absence of extracellular Ca2+, indicating that protein kinase C promotes calcium entry but can also mediate secretory responses without changes in calcium influx and [Ca2+]i. The extracellular Ca2+-dependent action of TPA on LH release was blocked by CoCl2 but not by nifedipine. The secretory actions of TPA and GnRH were additive at low doses and converged to a common maximum LH response at high concentrations of the agonists. TPA caused rapid translocation of cytosolic protein kinase C to the particulate fraction, followed by a progressive decrease in total enzyme activity to less than 10% after 6 h. Partial recovery of the cytosolic enzyme (to 20%) occurred after washing and reincubation for 15 h. Such kinase C-depleted cells showed prominent dose-dependent reductions in the actions of both GnRH and TPA on LH release in normal and Ca2+-deficient media. These observations show that the actions of kinase C on LH release include extracellular Ca2+-dependent and independent components, and support the hypothesis that protein kinase C participates in the LH secretory response to GnRH in pituitary gonadotrophs. JF - Journal of steroid biochemistry AU - Stojilković, S S AU - Chang, J P AU - Ngo, D AU - Tasaka, K AU - Izumi, S AU - Catt, K J AD - Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 693 EP - 703 VL - 33 IS - 4B SN - 0022-4731, 0022-4731 KW - Phorbol Esters KW - 0 KW - Pituitary Hormone-Releasing Hormones KW - Luteinizing Hormone KW - 9002-67-9 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Phorbol Esters -- pharmacology KW - Animals KW - Enzyme Activation KW - Cells, Cultured KW - Female KW - Protein Kinase C -- metabolism KW - Luteinizing Hormone -- secretion KW - Calcium -- metabolism KW - Pituitary Gland, Anterior -- drug effects KW - Pituitary Gland, Anterior -- secretion KW - Pituitary Hormone-Releasing Hormones -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79402774?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-06 N1 - Date created - 1990-02-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Current carcinogen perspectives: De minimis, Delaney and decisions. AN - 79401377; 2690341 AB - Advances in analytical chemistry, as applied to foods, as well as further investigations of the role of essential trace elements, constituents of natural products, and metabolic processes, have all shown that the Delaney clause of the 1958 Food Additives Amendment is an anachronism. Although the limitations of this clause are now known, prospects for its deletion are not very promising. JF - The Science of the total environment AU - Weisburger, E K AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/10/01/ PY - 1989 DA - 1989 Oct 01 SP - 5 EP - 13 VL - 86 IS - 1-2 SN - 0048-9697, 0048-9697 KW - Carcinogens KW - 0 KW - Food Additives KW - Index Medicus KW - United States KW - United States Food and Drug Administration KW - Humans KW - Legislation, Food UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79401377?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-02 N1 - Date created - 1990-02-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mammalian genes coordinately regulated by growth arrest signals and DNA-damaging agents. AN - 79344010; 2573827 AB - More than 20 different cDNA clones encoding DNA-damage-inducible transcripts in rodent cells have recently been isolated by hybridization subtraction (A. J. Fornace, Jr., I. Alamo, Jr., and M. C. Hollander, Proc. Natl. Acad. Sci. USA 85:8800-8804, 1988). In most cells, one effect of DNA damage is the transient inhibition of DNA synthesis and cell growth. We now show that five of our clones encode transcripts that are increased by other growth cessation signals: growth arrest by serum reduction, medium depletion, contact inhibition, or a 24-h exposure to hydroxyurea. The genes coding for these transcripts have been designated gadd (growth arrest and DNA damage inducible). Two of the gadd cDNA clones were found to hybridize at high stringency to transcripts from human cells that were induced after growth cessation signals or treatment with DNA-damaging agents, which indicates that these responses have been conserved during mammalian evolution. In contrast to results with growth-arrested cells that still had the capacity to grow after removal of the growth arrest conditions, no induction occurred in HL60 cells when growth arrest was produced by terminal differentiation, indicating that only certain kinds of growth cessation signals induce these genes. All of our experiments suggest that the gadd genes are coordinately regulated: the kinetics of induction for all five transcripts were similar; in addition, overexpression of gadd genes was found in homozygous deletion c14CoS/c14CoS mice that are missing a small portion of chromosome 7, suggesting that a trans-acting factor encoded by a gene in this deleted portion is a negative effector of the gadd genes. The gadd genes may represent part of a novel regulatory pathway involved in the negative control of mammalian cell growth. JF - Molecular and cellular biology AU - Fornace, A J AU - Nebert, D W AU - Hollander, M C AU - Luethy, J D AU - Papathanasiou, M AU - Fargnoli, J AU - Holbrook, N J AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 4196 EP - 4203 VL - 9 IS - 10 SN - 0270-7306, 0270-7306 KW - Culture Media KW - 0 KW - Growth Inhibitors KW - RNA, Messenger KW - Poly A KW - 24937-83-5 KW - Methyl Methanesulfonate KW - AT5C31J09G KW - Hydroxyurea KW - X6Q56QN5QC KW - Index Medicus KW - Animals KW - Ultraviolet Rays KW - Humans KW - Poly A -- biosynthesis KW - Gene Expression KW - Cell Differentiation -- genetics KW - Mice KW - Amino Acid Sequence KW - Hydroxyurea -- pharmacology KW - RNA, Messenger -- biosynthesis KW - Methyl Methanesulfonate -- pharmacology KW - Culture Media -- metabolism KW - Rats KW - Base Sequence KW - Cell Differentiation -- physiology KW - Cells, Cultured KW - Kinetics KW - Molecular Sequence Data KW - Male KW - Female KW - DNA Damage KW - Growth Inhibitors -- pharmacology KW - Cell Division -- genetics KW - Cell Cycle -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79344010?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-29 N1 - Date created - 1989-12-29 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M29238; GENBANK N1 - SuppNotes - Cited By: Nature. 1983 Oct 27-Nov 2;305(5937):779-84 [6633649] Exp Cell Res. 1989 May;182(1):61-74 [2541007] Nucleic Acids Res. 1986 Jul 25;14(14):5793-811 [2426659] Cell. 1979 Feb;16(2):225-37 [36985] Nature. 1981 Apr 30;290(5809):797-9 [7012641] Nature. 1983 Aug 11-17;304(5926):552-4 [6877378] Anal Biochem. 1983 Jul 1;132(1):6-13 [6312838] Mol Cell Biol. 1986 May;6(5):1760-6 [3785178] Mol Cell Biol. 1987 Apr;7(4):1450-8 [3037320] Mol Cell Biol. 1987 May;7(5):1894-9 [3600649] Mol Cell Biol. 1987 Jul;7(7):2644-8 [3039354] J Cell Physiol. 1987 Oct;133(1):151-7 [3312241] Mutat Res. 1988 May;193(3):193-206 [2966294] Nature. 1988 Jun 16;333(6174):676-9 [3287181] Science. 1988 Jul 15;241(4863):317-22 [3291120] Cell. 1988 Sep 9;54(6):787-93 [3409319] Science. 1988 Oct 14;242(4876):229-37 [3051381] Nucleic Acids Res. 1988 Oct 25;16(20):9587-96 [2460824] Proc Natl Acad Sci U S A. 1988 Dec;85(23):8800-4 [3194391] Nucleic Acids Res. 1989 Feb 11;17(3):1215-30 [2537950] Cancer Res. 1989 Apr 1;49(7):1687-92 [2466559] Mol Cell Biol. 1989 Feb;9(2):851-3 [2710127] Nature. 1984 Apr 12-18;308(5960):613-7 [6546784] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of a drug resistance gene in human neuroblastoma cell lines: modulation by retinoic acid-induced differentiation. AN - 79343095; 2573830 AB - Expression of a multidrug resistance gene (mdr1) and its protein product, P-glycoprotein (Pgp), has been correlated with the onset of multidrug resistance in vitro in human cell lines selected for resistance to chemotherapeutic agents derived from natural products. Expression of this gene has also been observed in normal tissues and human tumors, including neuroblastoma. We therefore examined total RNA prepared from human neuroblastoma cell lines before and after differentiation with retinoic acid or sodium butyrate. An increase in the level of mdr1 mRNA was observed after retinoic acid treatment of four neuroblastoma cell lines, including the SK-N-SH cell line. Western blot (immunoblot) analysis demonstrated concomitant increases in Pgp. However, studies of 3H-vinblastine uptake failed to show a concomitant Pgp-mediated decrease in cytotoxic drug accumulation. To provide evidence that Pgp was localized on the cell surface, an immunotoxin conjugate directed against Pgp was added to cells before and after treatment with retinoic acid. Incorporation of [3H]leucine was decreased by the immunotoxin in the retinoic acid-treated cells compared with the undifferentiated cells. These results demonstrate that whereas expression of the mdr1 gene can be modulated by differentiating agents, increased levels of expression are not necessarily associated with increased cytotoxic drug accumulation. JF - Molecular and cellular biology AU - Bates, S E AU - Mickley, L A AU - Chen, Y N AU - Richert, N AU - Rudick, J AU - Biedler, J L AU - Fojo, A T AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 4337 EP - 4344 VL - 9 IS - 10 SN - 0270-7306, 0270-7306 KW - Bacterial Toxins KW - 0 KW - Butyrates KW - Exotoxins KW - Immunotoxins KW - Membrane Glycoproteins KW - P-Glycoprotein KW - RNA, Messenger KW - RNA, Neoplasm KW - Virulence Factors KW - Butyric Acid KW - 107-92-6 KW - Tretinoin KW - 5688UTC01R KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - RNA, Neoplasm -- biosynthesis KW - Clone Cells KW - Butyrates -- pharmacology KW - Humans KW - Gene Expression KW - Pseudomonas KW - Cell Membrane -- analysis KW - RNA, Messenger -- biosynthesis KW - Blotting, Western KW - Tumor Cells, Cultured KW - Cell Differentiation -- drug effects KW - Time Factors KW - Tretinoin -- pharmacology KW - Neuroblastoma -- genetics KW - Drug Resistance -- genetics KW - Membrane Glycoproteins -- biosynthesis KW - Neuroblastoma -- metabolism KW - Membrane Glycoproteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79343095?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-29 N1 - Date created - 1989-12-29 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Cell Physiol. 1974 Feb;83(1):103-16 [4855907] Prog Clin Biol Res. 1988;271:509-24 [3406015] Biochim Biophys Acta. 1976 Nov 11;455(1):152-62 [990323] Cancer Res. 1970 Apr;30(4):1174-84 [5533992] Cancer Res. 1973 Nov;33(11):2643-52 [4748425] Cancer Res. 1977 May;37(5):1364-71 [856461] Natl Cancer Inst Monogr. 1976 Nov;44:49-54 [1030781] Cancer Res. 1978 Nov;38(11 Pt 1):3751-7 [29704] Cancer Res. 1979 Jun;39(6 Pt 1):2070-6 [571759] J Biol Chem. 1979 Dec 25;254(24):12701-5 [500733] World J Surg. 1980 Jan;4(1):29-37 [7385901] J Natl Cancer Inst. 1982 Apr;68(4):589-96 [7040765] Mol Cell Biol. 1982 Aug;2(8):881-9 [6127625] J Pediatr Surg. 1982 Dec;17(6):821-25 [6298396] J Natl Cancer Inst. 1983 Oct;71(4):741-7 [6137586] Exp Cell Res. 1983 Oct;148(1):21-30 [6313408] J Clin Oncol. 1984 Jul;2(7):719-32 [6737018] J Clin Oncol. 1984 Jul;2(7):742-7 [6539811] J Natl Cancer Inst. 1984 Aug;73(2):405-16 [6589432] Cell Differ. 1984 Jun;14(2):135-44 [6467378] J Natl Cancer Inst. 1984 Sep;73(3):649-54 [6590911] Nucleic Acids Res. 1984 Sep 25;12(18):7035-56 [6091052] Nature. 1985 Jan 31-Feb 6;313(6001):404-6 [3855502] Somat Cell Mol Genet. 1985 Mar;11(2):117-26 [3856953] Cancer Res. 1989 Jan 1;49(1):219-25 [2535691] Prog Clin Biol Res. 1985;175:55-68 [2986175] Cancer Res. 1985 Jul;45(7):3002-7 [4005839] Pharmacol Ther. 1985;28(1):51-75 [2865753] J Natl Cancer Inst. 1986 Mar;76(3):375-87 [3456456] J Biol Chem. 1986 Jun 15;261(17):7762-70 [3711108] Proc Natl Acad Sci U S A. 1987 Jan;84(1):265-9 [2432605] Exp Cell Biol. 1986;54(5-6):287-300 [3026862] J Biol Chem. 1987 Jan 15;262(2):505-8 [3027054] J Biol Chem. 1987 Feb 15;262(5):2166-70 [2434476] J Biol Chem. 1987 Jun 5;262(16):7884-8 [3034908] Proc Natl Acad Sci U S A. 1987 Nov;84(21):7735-8 [2444983] J Biol Chem. 1988 Jan 25;263(3):1454-8 [2891711] Oncology. 1988;45(3):148-52 [3368191] Cell. 1988 May 20;53(4):519-29 [2897240] Prog Clin Biol Res. 1988;271:31-9 [3406005] J Natl Cancer Inst. 1976 Sep;57(3):727-9 [185404] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of a human multidrug resistance cDNA (MDR1) in the bone marrow of transgenic mice: resistance to daunomycin-induced leukopenia. AN - 79341462; 2573831 AB - The human multidrug resistance gene (MDR1) encodes a drug efflux pump glycoprotein (P-glycoprotein) responsible for resistance to multiple cytotoxic drugs. A plasmid carrying a human MDR1 cDNA under the control of a chicken beta-actin promoter was used to generate transgenic mice in which the transgene was mainly expressed in bone marrow and spleen. Immunofluorescence localization studies showed that P-glycoprotein was present on bone marrow cells. Furthermore, leukocyte counts of the transgenic mice treated with daunomycin did not fall, indicating that their bone marrow was resistant to the cytotoxic effect of the drug. Since bone marrow suppression is a major limitation to chemotherapy, these transgenic mice should serve as a model to determine whether higher doses of drugs can cure previously unresponsive cancers. JF - Molecular and cellular biology AU - Galski, H AU - Sullivan, M AU - Willingham, M C AU - Chin, K V AU - Gottesman, M M AU - Pastan, I AU - Merlino, G T AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 4357 EP - 4363 VL - 9 IS - 10 SN - 0270-7306, 0270-7306 KW - Actins KW - 0 KW - Membrane Glycoproteins KW - P-Glycoprotein KW - RNA, Messenger KW - Recombinant Fusion Proteins KW - Daunorubicin KW - ZS7284E0ZP KW - Index Medicus KW - Recombinant Fusion Proteins -- biosynthesis KW - Animals KW - Promoter Regions, Genetic -- physiology KW - Daunorubicin -- toxicity KW - Humans KW - Bone Marrow -- metabolism KW - Mice KW - Mice, Transgenic KW - Plasmids KW - RNA, Messenger -- biosynthesis KW - Bone Marrow Cells KW - Actins -- genetics KW - Transfection KW - Fluorescent Antibody Technique KW - Drug Resistance -- genetics KW - Leukopenia -- chemically induced KW - Membrane Glycoproteins -- analysis KW - Leukopenia -- prevention & control KW - Membrane Glycoproteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79341462?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-29 N1 - Date created - 1989-12-29 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 1970 Apr;30(4):1174-84 [5533992] J Biol Chem. 1987 Jan 15;262(2):505-8 [3027054] J Mol Biol. 1975 Nov 5;98(3):503-17 [1195397] Proc Natl Acad Sci U S A. 1976 Aug;73(8):2634-8 [8777] Biochim Biophys Acta. 1976 Nov 11;455(1):152-62 [990323] J Mol Biol. 1977 Jun 15;113(1):237-51 [881736] Cancer Res. 1979 Jun;39(6 Pt 1):2070-6 [571759] Cancer Treat Rep. 1981;65 Suppl 4:9-18 [6809317] Somat Cell Mol Genet. 1985 Mar;11(2):117-26 [3856953] Nature. 1985 Aug 29-Sep 4;316(6031):817-9 [2863759] Annu Rev Genet. 1986;20:465-99 [3545063] Biochem Biophys Res Commun. 1986 Dec 30;141(3):956-62 [2880583] Proc Natl Acad Sci U S A. 1987 May;84(9):3004-8 [3472246] Proc Natl Acad Sci U S A. 1987 Jul;84(14):4831-5 [2440031] Anal Biochem. 1987 Apr;162(1):156-9 [2440339] FASEB J. 1987 Jul;1(1):51-4 [2886389] J Histochem Cytochem. 1987 Dec;35(12):1451-6 [2890686] J Clin Oncol. 1987 Dec;5(12):1922-7 [3681376] Mol Cell Biol. 1988 Jan;8(1):480-5 [3422100] Proc Natl Acad Sci U S A. 1988 Feb;85(3):836-40 [3422466] Proc Natl Acad Sci U S A. 1988 Mar;85(5):1389-93 [3422740] Proc Natl Acad Sci U S A. 1988 Mar;85(5):1595-9 [3422751] Proc Natl Acad Sci U S A. 1988 May;85(10):3580-4 [3368466] Science. 1988 Jun 10;240(4858):1468-74 [3287623] Proc Natl Acad Sci U S A. 1988 Jun;85(12):4486-90 [2898143] J Biol Chem. 1988 Sep 5;263(25):12163-6 [2900833] J Natl Cancer Inst. 1989 Jan 18;81(2):116-24 [2562856] J Biol Chem. 1989 Jun 5;264(16):9539-46 [2722849] Science. 1986 May 2;232(4750):643-5 [3457471] Science. 1986 May 9;232(4751):751-5 [2421411] J Biol Chem. 1986 Jun 15;261(17):7762-70 [3711108] Proc Natl Acad Sci U S A. 1986 Jun;83(11):3847-50 [3459160] J Natl Cancer Inst. 1986 Aug;77(2):459-69 [3461207] Mol Cell Biol. 1985 Oct;5(10):2720-32 [3837182] Annu Rev Biochem. 1986;55:987-1035 [3527055] Cancer Res. 1986 Nov;46(11):5941-6 [3756931] Proc Natl Acad Sci U S A. 1986 Oct;83(20):7785-9 [2429319] Cell. 1986 Nov 7;47(3):371-80 [3768958] Cell. 1986 Nov 7;47(3):381-9 [2876781] Nature. 1986 Oct 23-29;323(6090):728-31 [3022150] Mol Cell Biol. 1986 May;6(5):1671-8 [2431283] Mol Cell Biol. 1986 Nov;6(11):4039-45 [3796599] Proc Natl Acad Sci U S A. 1987 Jan;84(1):265-9 [2432605] Biochim Biophys Acta. 1973 Oct 25;323(3):466-83 [4796512] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytochrome P-450-dependent formation of alkylating metabolites of the 2-chloroethylnitrosoureas MeCCNU and CCNU. AN - 79330507; 2818619 AB - Rat liver microsomes catalyzed the biotransformation of the clinically important nitrosourea anticancer agents 1-(2-chloroethyl)-3-(trans-4-methyl-cyclohexyl)-1-nitrosourea (MeCCNU) and 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU) to alkylating metabolites that bound covalently to microsomal protein and to DNA. The enzyme-mediated microsomal alkylation required NADPH and oxygen and was inhibited by carbon monoxide, indicating the participation of a cytochrome P-450-dependent monooxygenase. Additional studies with inhibitors such as piperonyl butoxide and with the inducers 3-methylcholanthrene and phenobarbital were consistent with this view. In contrast to these observations on the formation of alkylating metabolites, carbamylation reactions were not affected significantly by microsomal metabolism. Reduced glutathione, cysteine or N-acetylcysteine decreased the microsomal alkylation by MeCCNU and produced a corresponding increase in the formation of polar metabolites that was resolved by HPLC as three distinct N-acetylcysteine-MeCCNU adducts. The addition of semicarbazide to the reaction decreased microsomal alkylation by 30%, indicating that the formation of the alkylating species may proceed via an aldehyde intermediate. Renal microsomes were not found to catalyze the alkylation reaction. Moreover, MeCCNU inhibited the renal slice accumulation of p-aminohippuric acid only in the presence of liver microsomes and NADPH, suggesting that a liver metabolite may be responsible for the renal toxicity of the parent nitrosourea. JF - Biochemical pharmacology AU - Kramer, R A AD - Developmental Therapeutics Program, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/10/01/ PY - 1989 DA - 1989 Oct 01 SP - 3185 EP - 3192 VL - 38 IS - 19 SN - 0006-2952, 0006-2952 KW - Alkylating Agents KW - 0 KW - Semustine KW - 13909-09-6 KW - NADP KW - 53-59-8 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Glutathione KW - GAN16C9B8O KW - Acetylcysteine KW - WYQ7N0BPYC KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Phenobarbital -- pharmacology KW - Biotransformation KW - DNA -- metabolism KW - Microsomes, Liver -- enzymology KW - Acetylcysteine -- metabolism KW - NADP -- pharmacology KW - Glutathione -- pharmacology KW - Male KW - Alkylation KW - Alkylating Agents -- metabolism KW - Cytochrome P-450 Enzyme System -- physiology KW - Semustine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79330507?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-28 N1 - Date created - 1989-11-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evolution of the cytochrome P450 genes. AN - 79320542; 2683414 AB - 1. The P450 gene superfamily is presently known to contain more than 78 members, divided into 14 families. 2. The superfamily has undergone divergent evolution, and the ancestral gene is probably more than 2 billion years old. 3. The recent 'burst' in new P450 genes, particularly in the II family during the past 800 million years, appears to be the result of 'animal-plant warfare'. 4. Due to the presence or absence of a particular P450 gene in one species but not the other, it may not be correct to extrapolate toxicity or cancer data from rodent to human. 5. Increases in the P450 gene product (enzyme induction) almost always reflect an elevated rate in gene transcription, although there are several exceptions. 6. The mechanisms of P450 gene regulation (induction) by classes of inducers might become better understood through the comparison of different phyla that differ in response to a particular class of inducers. 7. Amongst several carefully selected phyla, delineation between which electron donor (presence of Fe2S2 protein or NADPH-P450 oxidoreductase, or both) interacts with P450 may provide valuable information about the evolution of eukaryotes from prokaryotes. JF - Xenobiotica; the fate of foreign compounds in biological systems AU - Nebert, D W AU - Nelson, D R AU - Feyereisen, R AD - Laboratory of Developmental Pharmacology, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 1149 EP - 1160 VL - 19 IS - 10 SN - 0049-8254, 0049-8254 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Space life sciences KW - Animals KW - Gene Expression Regulation, Enzymologic KW - Multigene Family KW - Plants -- genetics KW - Genes KW - Cytochrome P-450 Enzyme System -- genetics KW - Biological Evolution KW - Cytochrome P-450 Enzyme System -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79320542?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-21 N1 - Date created - 1989-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Experience with the use of high-dose interleukin-2 in the treatment of 652 cancer patients. AN - 79264434; 2679456 AB - We have administered 1039 courses of high-dose interleukin-2 (IL-2) to 652 cancer patients. Five hundred ninety-six patients had metastatic cancer that either had failed standard effective therapies or had disease for which no standard effective therapy existed, and 56 patients were treated in the absence of evaluable disease in the adjuvant setting. IL-2 was administered either alone (155 patients) or in conjunction with activated immune cells such as lymphokine activated killer (LAK) cells (214 patients) or tumor infiltrating lymphocytes (TIL) (66 patients), with other cytokines such as alpha interferon (a-IFN)(128 patients) or tumor necrosis factor (TNF)(38 patients), with monoclonal antibodies (32 patients), or with the chemotherapeutic agent cyclophosphamide (19 patients). Initial results with the treatment of high-dose IL-2 alone or in conjunction with LAK cells have indicated that objective regressions of cancer can be achieved in 20% to 35% of patients with selected advanced metastatic cancers. Although most responses have been seen in patients with metastatic renal cell cancer, melanoma, colorectal cancer, and non-Hodgkin's lymphoma, many histologic types of cancer have not been treated in significant numbers. These regressions can be durable; of 18 patients achieving a complete response, ten have not experienced recurrence at intervals from 18 to 52 months. Although combinations of IL-2 with TNF do not appear to result in increased responses, there is a suggestion in our initial phase I studies that the combination of a-IFN and IL-2 is more effective than the administration of cytokine alone and this combination deserves further study. Similarly the adoptive transfer of TIL in conjunction with IL-2 also appears to be more effective than the use of IL-2 alone. The toxic side effects in patients treated with high-dose IL-2 are presented and include malaise, nausea and vomiting, hypotension, fluid retention, and organ dysfunction. Treatment-related deaths were seen in 1% of all treatment courses and in 1.5% of patients. These studies demonstrate that a purely immunologic manipulation can mediate the regression of advanced cancers in selected patients and may provide a base for the development of practical, effective biologic treatments for some cancer patients. JF - Annals of surgery AU - Rosenberg, S A AU - Lotze, M T AU - Yang, J C AU - Aebersold, P M AU - Linehan, W M AU - Seipp, C A AU - White, D E AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 474 EP - 84; discussion 484-5 VL - 210 IS - 4 SN - 0003-4932, 0003-4932 KW - Antibodies, Monoclonal KW - 0 KW - Biological Factors KW - Cytokines KW - Interferon Type I KW - Interleukin-2 KW - Tumor Necrosis Factor-alpha KW - Cyclophosphamide KW - 8N3DW7272P KW - Abridged Index Medicus KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Animals KW - Killer Cells, Natural -- transplantation KW - Interferon Type I -- administration & dosage KW - Tumor Necrosis Factor-alpha -- administration & dosage KW - Combined Modality Therapy KW - Humans KW - Aged KW - Mice KW - Biological Factors -- administration & dosage KW - Antibodies, Monoclonal -- administration & dosage KW - Drug Evaluation KW - Adult KW - Neoplasm Metastasis KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Interleukin-2 -- adverse effects KW - Interleukin-2 -- administration & dosage KW - Interleukin-2 -- therapeutic use KW - Immunization, Passive KW - Neoplasms -- therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79264434?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-28 N1 - Date created - 1989-10-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1984 Mar 30;223(4643):1412-4 [6367046] J Clin Oncol. 1989 Mar;7(3):291-4 [2645383] J Immunol. 1985 Oct;135(4):2865-75 [2993418] J Natl Cancer Inst. 1985 Oct;75(4):595-603 [3876465] N Engl J Med. 1985 Dec 5;313(23):1485-92 [3903508] J Immunol. 1985 Dec;135(6):4273-80 [3877766] J Immunol. 1986 Sep 1;137(5):1735-42 [3528289] Science. 1986 Sep 19;233(4770):1318-21 [3489291] Cancer Res. 1986 Oct;46(10):4973-8 [3489517] JAMA. 1986 Dec 12;256(22):3117-24 [3491225] Ann Intern Med. 1987 Feb;106(2):257-74 [2432815] J Immunol. 1987 Feb 1;138(3):989-95 [3100623] N Engl J Med. 1987 Apr 9;316(15):889-97 [3493432] N Engl J Med. 1987 Apr 9;316(15):898-905 [3493433] J Immunol Methods. 1987 Aug 3;101(2):171-81 [3611795] J Immunol Methods. 1987 Aug 24;102(1):127-41 [3305708] Cancer Res. 1988 Jan 1;48(1):122-9 [3257159] Science. 1988 May 27;240(4856):1169-76 [3131876] Important Adv Oncol. 1986;:55-91 [3330541] Cancer Res. 1988 Jul 15;48(14):4011-7 [3260130] Ann Surg. 1988 Aug;208(2):121-35 [3041925] Cancer Res. 1988 Sep 1;48(17):5007-10 [3261630] Cancer Res. 1988 Oct 15;48(20):5810-7 [3262413] Cancer Res. 1988 Oct 15;48(20):5864-7 [3139285] Cancer Res. 1988 Dec 15;48(24 Pt 1):7140-5 [3263900] N Engl J Med. 1988 Dec 22;319(25):1676-80 [3264384] J Clin Oncol. 1989 Feb;7(2):250-61 [2644399] J Immunol. 1985 Aug;135(2):1488-97 [3891854] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Maitotoxin-induced liver cell death involving loss of cell ATP following influx of calcium. AN - 79260978; 2619815 AB - Maitotoxin, one of the most potent marine toxins known, produced cell death in cultures of rat hepatocytes with a TD50 of 80 pM at 24 hr. The cell death, as indicated by a dose- and time-dependent leakage of lactate dehydrogenase (LDH), was also associated with the leakage of [14C]adenine nucleotides from hepatocytes prelabeled with [14C]-adenine. The toxic effect of maitotoxin was completely abolished by the omission of calcium from the culture medium. The cell death induced by maitotoxin increased with increasing concentrations of calcium in the medium. Treatment of hepatocytes with low concentrations of the toxin (less than 0.5 ng/ml) resulted in increases in 45Ca influx into the cells. At higher concentrations of maitotoxin (greater than 1ng/ml), the initial increase in 45Ca influx was followed by the release of the 45Ca from the cells into the medium. Since the 45Ca release paralleled the LDH leakage, the release of calcium was due to cell death. The 45Ca influx, [14C]adenine nucleotide leakage, and LDH leakage were effectively inhibited by verapamil, a calcium channel blocker. Maitotoxin also induced a time- and dose-dependent loss of ATP from hepatocytes, which preceded the [14C]adenine nucleotide and LDH leakage. Thus, it appears that the cell death resulting from maitotoxin treatment is caused by the elevated intracellular calcium, which in turn inhibits mitochondrial oxidative phosphorylation causing depletion of cell ATP. Loss of cell ATP may be the causative event in the maitotoxin-induced cell death. JF - Toxicology and applied pharmacology AU - Kutty, R K AU - Singh, Y AU - Santostasi, G AU - Krishna, G AD - Section on Drug-Tissue Interaction, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 1 EP - 10 VL - 101 IS - 1 SN - 0041-008X, 0041-008X KW - Calcium Radioisotopes KW - 0 KW - Marine Toxins KW - Oxocins KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - maitotoxin KW - 9P59GES78D KW - Verapamil KW - CJ0O37KU29 KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats KW - Animals KW - Cell Survival -- drug effects KW - Cells, Cultured KW - Verapamil -- pharmacology KW - L-Lactate Dehydrogenase -- metabolism KW - Calcium -- metabolism KW - Liver -- cytology KW - Liver -- drug effects KW - Adenosine Triphosphate -- metabolism KW - Calcium -- physiology KW - Liver -- metabolism KW - Marine Toxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79260978?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-14 N1 - Date created - 1989-11-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Toxicol Appl Pharmacol 1990 Jan;102(1):195 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Apparent deficiency of metallothionein in the Wistar rat prostate. AN - 79257043; 2799820 AB - The high affinity metal-binding protein metallothionein (MT) is thought to detoxify cadmium (Cd) but appears to be deficient in several known targets of Cd carcinogenesis. The rat ventral prostate (VP) was recently identified as one of these target tissues. The nature of the Cd-binding proteins in the prostate has not been well defined, and thus this study attempted to define the nature of these proteins in the Wistar rat. A Zn-, Cd-binding protein fraction in the low-molecular-weight range was seen by gel filtration in cytosol from either dorsal prostate (DP) or VP. These prostatic proteins eluted with a relative elution volume similar to that of authentic MT, and were extractable by heat treatment and sequential acetone precipitation, a technique originally developed for purification of MT. Preparations of such partially purified prostatic protein were further purified using a reverse-phase HPLC technique developed for MT isoform isolation. One form was detected from the VP while the DP displayed five separate forms, eluting in a range like that of the two isoforms of rat MT. However, on the basis of amino acid content, none of these prostatic forms were classifiable as MTs, due to the absence of cysteine, a very common amino acid in MT. Unlike MT which is devoid of aromatic amino acids, the prostatic proteins also contained significant amounts of tyrosine and phenylalanine. The prostatic proteins also contained much more glutamate than MT. Cadmium treatment, which is known to cause a marked induction of MT, did not alter levels of this protein in the prostate, while markedly increasing hepatic MT. The present results indicate that these low-molecular-weight Cd-, Zn-binding proteins present in the rat prostate are not MTs and provide a further correlation between MT deficiency and sensitivity to the carcinogenic effects of Cd. JF - Toxicology and applied pharmacology AU - Waalkes, M P AU - Perantoni, A AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research Facility, Frederick, Maryland 21701. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 83 EP - 94 VL - 101 IS - 1 SN - 0041-008X, 0041-008X KW - Amino Acids KW - 0 KW - Carrier Proteins KW - Cadmium KW - 00BH33GNGH KW - Metallothionein KW - 9038-94-2 KW - Zinc KW - J41CSQ7QDS KW - Index Medicus KW - Animals KW - Cytosol -- analysis KW - Amino Acids -- analysis KW - Zinc -- metabolism KW - Tissue Distribution KW - Liver -- analysis KW - Molecular Weight KW - Rats KW - Rats, Inbred Strains KW - Chromatography, Gel KW - Chromatography, High Pressure Liquid -- methods KW - Carrier Proteins -- analysis KW - Male KW - Cadmium -- metabolism KW - Metallothionein -- deficiency KW - Prostate -- analysis KW - Cadmium -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79257043?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-14 N1 - Date created - 1989-11-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Specific inhibition of FSH-stimulated cAMP accumulation by delta 9-tetrahydrocannabinol in cultures of rat Sertoli cells. AN - 79256995; 2552614 AB - delta 9-Tetrahydrocannabinol (THC), the major psychoactive component in marihuana, is a reproductive toxicant in both man and animals. THC acts at both the level of the pituitary-hypothalamic axis and the testis, specifically the Leydig cell; an effect on the Sertoli cell has not been shown. Since THC inhibits cAMP accumulation in several cell types, we have examined the effect of THC on Sertoli cell function using altered cAMP accumulation as a marker of toxicity. THC reduced the FSH-induced accumulation of cAMP at concentrations which were neither cytotoxic nor affected cellular ATP levels. This inhibition was evident after 3 hr and did not affect the dose of FSH which gave half-maximal stimulation, suggesting that THC does not compete with FSH for binding to its receptor. The ability of THC to inhibit cAMP accumulation was not affected by incubation in the presence of phosphodiesterase inhibitors, making it unlikely that it acts via stimulation of phosphodiesterase activity. This THC-induced inhibition of Sertoli cell cAMP is specific for FSH; it does not affect the ability of forskolin, cholera toxin, isoproterenol, or prostaglandin E1 to stimulate Sertoli cell cAMP. Furthermore, inhibition occurs in the presence of pertussis toxin, suggesting that this effect of THC is independent of the inhibitory adenylate cyclase pathway. Inhibition of Sertoli cell cAMP also occurs with other cannabinoids which are present in marihuana, but which are not psychoactive. These data indicate that a part of the testicular toxicity of THC may be due to a specific alteration of the hormonal control of Sertoli cell function via an inhibition of FSH-stimulated cAMP accumulation. JF - Toxicology and applied pharmacology AU - Heindel, J J AU - Keith, W B AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 124 EP - 134 VL - 101 IS - 1 SN - 0041-008X, 0041-008X KW - Adenylyl Cyclase Inhibitors KW - 0 KW - Cannabinoids KW - Dronabinol KW - 7J8897W37S KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Follicle Stimulating Hormone KW - 9002-68-0 KW - Cyclic AMP KW - E0399OZS9N KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Cells, Cultured KW - Adenosine Triphosphate -- metabolism KW - Cannabinoids -- pharmacology KW - Male KW - Microscopy, Electron, Scanning KW - Sertoli Cells -- drug effects KW - Follicle Stimulating Hormone -- antagonists & inhibitors KW - Sertoli Cells -- metabolism KW - Dronabinol -- pharmacology KW - Second Messenger Systems -- drug effects KW - Cyclic AMP -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79256995?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-14 N1 - Date created - 1989-11-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential expression of an 80-kDa protein kinase C substrate in preneoplastic and neoplastic mouse JB6 cells. AN - 79255724; 2798414 AB - An 80-kDa protein (p80), previously reported to be a major protein kinase C substrate in preneoplastic JB6 mouse epidermal cells, has been shown to be transiently phosphorylated by phorbol 12-O-tetradecanoate 13-acetate. Phosphorylation was maximal at 2 hr of phorbol 12-O-tetradecanoate 13-acetate treatment and returned to basal levels by 24 hr. In contrast, using a p80-specific antibody, we found that phorbol 12-O-tetradecanoate 13-acetate treatment produced no increase in p80 concentration. p80 showed a progressive decrease in JB6 cells during progression from a preneoplastic to neoplastic phenotype. The lack of p80 expression in neoplastic cells was not attributable to lack of protein kinase C; the protein kinase activity and protein concentration were similar in cells of all three phenotypes. When p80 mRNA was analyzed by hybridization to a putative p80 cDNA clone, its relative concentration paralleled that of p80 protein, with high levels present in preneoplastic JB6 cells, and little or no evidence for p80-hybridizing RNA in transformed cells. Thus, p80 appears to be regulated pretranslationally at the level of mRNA concentration during preneoplastic progression in mouse epidermal JB6 cells. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Simek, S L AU - Kligman, D AU - Patel, J AU - Colburn, N H AD - Cell Biology Section, National Cancer Institute-Frederick Cancer Research Facility, MD 21701-1013. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 7410 EP - 7414 VL - 86 IS - 19 SN - 0027-8424, 0027-8424 KW - Neoplasm Proteins KW - 0 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Phosphorylation KW - Mice KW - Substrate Specificity KW - Mice, Inbred BALB C KW - Cell Line KW - Protein Kinase C -- metabolism KW - Neoplasm Proteins -- isolation & purification KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Neoplasms, Experimental -- metabolism KW - Precancerous Conditions -- metabolism KW - Neoplasm Proteins -- metabolism KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79255724?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-09 N1 - Date created - 1989-11-09 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1979 Oct 18;281(5732):589-91 [492322] J Biol Chem. 1988 May 5;263(13):6424-31 [3360787] Science. 1965 Oct 8;150(3693):178-85 [5319951] Nature. 1970 Aug 15;227(5259):680-5 [5432063] J Mol Biol. 1977 Jun 15;113(1):237-51 [881736] J Biol Chem. 1977 Nov 25;252(22):8310-9 [914873] Cell. 1980 Jan;19(1):245-54 [6153576] Proc Natl Acad Sci U S A. 1980 Sep;77(9):5201-5 [6159641] Proc Natl Acad Sci U S A. 1981 Nov;78(11):6912-6 [6947266] Teratog Carcinog Mutagen. 1980;1(1):87-96 [6119803] J Cell Biochem. 1982;18(3):261-70 [7068782] Carcinogenesis. 1983;4(4):489-90 [6301704] Proc Natl Acad Sci U S A. 1983 Dec;80(23):7244-8 [6316349] J Cell Physiol. 1984 Feb;118(2):133-42 [6319436] Biochem Biophys Res Commun. 1984 May 16;120(3):1053-9 [6233972] Carcinogenesis. 1984 Sep;5(9):1115-21 [6467502] Mol Cell Biol. 1985 Apr;5(4):890-3 [2985973] J Biol Chem. 1985 Dec 5;260(28):15194-9 [3905792] Int J Cancer. 1986 Feb 15;37(2):293-302 [3002990] EMBO J. 1986 Jan;5(1):77-83 [3956481] Cancer Res. 1986 Jun;46(6):3040-5 [3698022] Proc Natl Acad Sci U S A. 1986 May;83(9):2822-6 [3458242] Mol Cell Biol. 1985 Sep;5(9):2231-7 [3016523] Carcinogenesis. 1986 Dec;7(12):1949-56 [3096584] J Cell Physiol. 1987 Jan;130(1):111-7 [3543027] J Biol Chem. 1987 Dec 5;262(34):16686-91 [3680270] J Cell Physiol. 1987 Nov;133(2):377-82 [3680394] Cancer Res. 1988 Mar 1;48(5):1195-200 [3342399] Oncogene. 1987 Mar;1(1):37-46 [2830575] Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4 [388439] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cell-specific induction of mouse Cyp1a1 mRNA during development. AN - 79254327; 2477842 AB - The dioxin-inducible cytochrome P(1)450 (Cyp1a1 gene) and P(3)450 (Cyp1a2 gene) enzymes have been implicated in the metabolism of numerous polycyclic hydrocarbons and arylamines, respectively. The prototypic inducer 3-methylcholanthrene was given to the pregnant mouse, and the intrauterine response was examined with the use of in situ hybridization. During the early postimplantation stage, inducible Cyp1a1 mRNA is detected in specific cell types in the extraembryonic tissues only. This selective expression along with the lack of detectable constitutive Cyp1a1 and constitutive or inducible Cyp1a2 gene transcripts between 5.3 and 14.5 days of gestation suggest that (i) these two genes appear to play no endogenous role during differentiation and (ii) the metabolic activity of the inducible Cyp1a1 enzyme may be important to the embryo and fetus from the standpoint of protection against toxic foodstuff and other environmental chemicals. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Dey, A AU - Westphal, H AU - Nebert, D W AD - Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 7446 EP - 7450 VL - 86 IS - 19 SN - 0027-8424, 0027-8424 KW - Isoenzymes KW - 0 KW - RNA, Antisense KW - RNA, Messenger KW - Methylcholanthrene KW - 56-49-5 KW - RNA KW - 63231-63-0 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Animals KW - Embryonic and Fetal Development KW - Mice, Inbred C57BL KW - Mice KW - Plasmids KW - Female KW - RNA -- genetics KW - Pregnancy KW - Cloning, Molecular KW - RNA, Messenger -- antagonists & inhibitors KW - Yolk Sac -- metabolism KW - Methylcholanthrene -- pharmacology KW - Cytochrome P-450 Enzyme System -- genetics KW - Isoenzymes -- biosynthesis KW - Decidua -- metabolism KW - Lung -- embryology KW - Liver -- metabolism KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Lung -- metabolism KW - Isoenzymes -- genetics KW - RNA, Messenger -- biosynthesis KW - Liver -- embryology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79254327?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-09 N1 - Date created - 1989-11-09 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Anat Rec. 1987 Feb;217(2):203-19 [3578838] Mol Cell Biol. 1986 May;6(5):1471-7 [3785172] Methods Enzymol. 1987;152:649-61 [3657592] J Exp Pathol. 1987 Winter;3(1):61-74 [3681488] Science. 1968 May 3;160(3827):541-2 [5644060] J Biol Chem. 1968 Dec 10;243(23):6242-9 [4387094] Cancer Res. 1969 Oct;29(10):1763-9 [5823944] Arch Biochem Biophys. 1969 Oct;134(1):76-89 [4981257] Toxicol Appl Pharmacol. 1972 Nov;23(3):399-407 [5085454] Adv Reprod Physiol. 1971;5:1-26 [4949999] Proc Natl Acad Sci U S A. 1976 Oct;73(10):3381-5 [1068451] Mol Pharmacol. 1977 Mar;13(2):259-68 [854023] J Biol Chem. 1979 Nov 10;254(21):11015-23 [500620] Proc Natl Acad Sci U S A. 1980 Jun;77(6):3524-8 [6932035] Environ Health Perspect. 1981 Jun;39:11-22 [7016519] Proc Natl Acad Sci U S A. 1981 Nov;78(11):6991-5 [6273901] Pharmacol Rev. 1982 Jun;34(2):189-222 [6287505] Cancer Res. 1982 Dec;42(12):4875-917 [6814745] Cancer Res. 1982 Dec;42(12):5030-7 [6291746] Methods Enzymol. 1978;52:226-40 [672631] CRC Crit Rev Biochem. 1979;6(4):401-37 [378536] Mol Pharmacol. 1983 Jul;24(1):146-55 [6408394] Dev Biol. 1984 Feb;101(2):485-502 [6692991] Mol Pharmacol. 1984 Jul;26(1):117-21 [6749129] J Biol Chem. 1984 Sep 10;259(17):10705-13 [6547952] EMBO J. 1984 Aug;3(8):1881-5 [6479150] Nucleic Acids Res. 1984 Sep 25;12(18):7035-56 [6091052] Proc Natl Acad Sci U S A. 1985 May;82(10):3311-5 [3858824] Biochem Biophys Res Commun. 1985 Jul 16;130(1):396-406 [4040754] Dev Biol. 1985 Nov;112(1):177-84 [4054433] Placenta. 1986 May-Jun;7(3):263-81 [3737578] Annu Rev Biochem. 1987;56:945-93 [3304150] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Long-term follow-up of children exposed in utero to antineoplastic agents. AN - 79253198; 2678492 JF - Seminars in oncology AU - Garber, J E AD - Clinical Studies Section, National Cancer Institute, Boston, MA. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 437 EP - 444 VL - 16 IS - 5 SN - 0093-7754, 0093-7754 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Humans KW - Follow-Up Studies KW - Child KW - Adolescent KW - Male KW - Female KW - Pregnancy KW - Abnormalities, Drug-Induced -- epidemiology KW - Prenatal Exposure Delayed Effects KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79253198?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-17 N1 - Date created - 1989-11-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of arachidonic acid metabolism by pulmonary intravascular and alveolar macrophages exposed to particulate and soluble stimuli. AN - 79242173; 2552225 AB - Pulmonary intravascular macrophages, as prominent components of the pulmonary mononuclear phagocyte system, could be significant mediators of lung inflammation. We have shown that intravascular and alveolar macrophages metabolize exogenous arachidonic acid to its inflammatory metabolites via the lipoxygenase and cyclooxygenase pathways after exposure to the calcium ionophore A23187. In this study, we compare the metabolism of endogenous arachidonic acid by porcine intravascular and alveolar macrophages after exposure to soluble and particulate stimuli. Since intravascular and alveolar macrophages are exposed to various stimuli in vivo, it is essential to know the range of inflammatory mediators that these cells can generate. Alveolar macrophages attached to plastic and exposed to the various stimuli produced prostaglandin F2 alpha, 12-hydroxyheptade-catrienoic acid (HHT), hydroxyeicosatetraenoic acids (HETE), and leukotriene B4. In contrast, adherent and stimulated intravascular macrophages produced several cyclooxygenase products and lipoxygenase products including 5-HETE, 12-HETE, and leukotriene B4. Both macrophages released large amounts of arachidonic acid upon exposure to each stimulant. Intravascular macrophages that were adherent to plastic or were stimulated with glass, asbestos, or A23187 released significantly (p less than 0.05) more metabolized arachidonic acid than similarly treated alveolar macrophages. The major cyclooxygenase metabolite released by alveolar macrophages was prostaglandin 2 alpha, whereas HHT was the primary metabolite of intravascular macrophages. The major lipoxygenase metabolite released by both macrophage types was 5-HETE, but intravascular macrophages also released substantial amounts of 12-HETE and leukotriene B4. In both macrophage preparations, lipoxygenase products composed most released metabolites. After exposure to iron, asbestos, and A23187 intravascular macrophages released significantly more (p less than 0.05) lipoxygenase metabolites than alveolar macrophages. However, in alveolar macrophages, chrysotile asbestos induced greater activity by the cyclooxygenase pathway than by the lipoxygenase pathway. Both asbestos and iron spheres induced release of arachidonic acid and its metabolites, but the most potent stimulants in both macrophage preparations were A23187, zymosan, and lipopolysaccharide. We conclude that stimulated intravascular macrophages use both cyclooxygenase and lipoxygenase pathways to metabolize endogenous arachidonic acid, that these macrophages are metabolically more active than alveolar macrophages, and that both macrophage types are induced to metabolize arachidonic acid by various particulate and soluble stimuli. Furthermore, we have shown that intravascular macrophages predominantly utilize the lipoxygenase rather than cyclooxygenase pathways to metabolize endogenous arachidonic acid. JF - Laboratory investigation; a journal of technical methods and pathology AU - Bertram, T A AU - Overby, L H AU - Brody, A R AU - Eling, T E AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 457 EP - 466 VL - 61 IS - 4 SN - 0023-6837, 0023-6837 KW - Arachidonic Acids KW - 0 KW - Lipopolysaccharides KW - Asbestos KW - 1332-21-4 KW - Calcimycin KW - 37H9VM9WZL KW - Zymosan KW - 9010-72-4 KW - Iron KW - E1UOL152H7 KW - Microbial Collagenase KW - EC 3.4.24.3 KW - Index Medicus KW - Swine KW - Microbial Collagenase -- pharmacology KW - Animals KW - Phagocytosis KW - Macrophages -- cytology KW - Zymosan -- pharmacology KW - Iron -- pharmacology KW - Lipopolysaccharides -- pharmacology KW - Asbestos -- pharmacology KW - Macrophages -- physiology KW - Arachidonic Acids -- metabolism KW - Calcimycin -- pharmacology KW - Glass KW - Pulmonary Alveoli -- physiology KW - Pulmonary Alveoli -- metabolism KW - Pulmonary Alveoli -- cytology KW - Macrophages -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79242173?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-13 N1 - Date created - 1989-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of octahydromezerein and mezerein as protein kinase C activators and as mouse skin tumor promoters. AN - 79221513; 2507191 AB - Although mezerein resembles 12-O-tetradecanoylphorbol-13-acetate (TPA) in being a potent ligand for protein kinase C in vitro, its properties as a tumor promoter on mouse skin differ from those of TPA. Mezerein is a good second-stage promoter of papillomas, an inefficient complete promoter of papillomas, and an effective promoter of carcinomas. The mechanism and structural features responsible for the anomalous tumor promoting activity of mezerein are unknown. We have examined here the in vitro and in vivo activities of octahydromezerein (OHM) and compared them to those of TPA and mezerein. OHM was of interest because if it acted like mezerein it would afford a convenient route for radioactive labeling. Alternatively, if it functioned as a complete tumor promoter, it would implicate unsaturation as the critical structural feature of mezerein responsible for its altered promoting activity. Consistent with this latter possibility, we find that OHM was an effective complete tumor promoter for SENCAR mice. Moreover, the pattern and magnitude of papilloma induction, yielding a peak at 16-20 weeks followed by a decline by 30-32 weeks, resembled that for TPA; mezerein, in contrast, induced a gradual but steady increase in the number of papillomas which did not reach the OHM level by 32 weeks. The dosage of OHM for inducing a comparable degree of acute and chronic hyperplasia to that induced by mezerein was 3- to 10-fold higher. This difference agrees with the relative binding affinities to protein kinase C; the Ki for OHM was 2.7 nM, compared to 0.58 nM for mezerein. JF - Carcinogenesis AU - Sharkey, N A AU - Hennings, H AU - Yuspa, S H AU - Blumberg, P M AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, MD 20892, USA. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 1937 EP - 1941 VL - 10 IS - 10 SN - 0143-3334, 0143-3334 KW - Carcinogens KW - 0 KW - Diterpenes KW - Terpenes KW - octahydromezerein KW - 124392-15-0 KW - mezerein KW - 34807-41-5 KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Tetradecanoylphorbol Acetate -- toxicity KW - Mice, Inbred Strains KW - Animals KW - Hyperplasia KW - Enzyme Activation KW - 9,10-Dimethyl-1,2-benzanthracene -- toxicity KW - Mice KW - Female KW - Terpenes -- toxicity KW - Protein Kinase C -- metabolism KW - Carcinogens -- pharmacology KW - Skin -- drug effects KW - Papilloma -- pathology KW - Skin Neoplasms -- chemically induced KW - Skin -- pathology KW - Skin Neoplasms -- pathology KW - Terpenes -- pharmacology KW - Papilloma -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79221513?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-13 N1 - Date created - 1989-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Deficient G2 phase repair of radiation-induced chromatin damage in the SENCAR mouse. AN - 79220682; 2791207 AB - The SENCAR mouse, selectively bred for sensitivity to skin tumor induction by two-stage chemical carcinogenesis, is also genetically hypersensitive to skin carcinogenesis by high doses of UV. Skin fibroblasts from the SENCAR mouse exposed during G2 phase to radiation associated with intracellular hydroxyl radical formation, i.e. X-rays or near UV/visible light, showed a higher frequency of chromatid breaks at 2 h post-irradiation than skin fibroblasts from six other inbred strains of mice including C3H/HeN. However the level was similar to that reported previously for the BALB/cAn mouse known to be resistant to chemical carcinogenesis of skin. When exposed for 2 h to visible light (8 W/m2), chromatid breaks persisted in fibroblasts from the SENCAR mouse during the 4 h post-irradiation period, but showed an abrupt decline in C3H/HeN fibroblasts within 1 h after irradiation. Skin fibroblasts from the tumor-sensitive SENCAR mouse differed from those of the resistant BALB/cAn in response to beta-cytosine arabinoside (ara-C) an inhibitor of the repair polymerase. Ara-C added to cultures of SENCAR and BALB/cAn cells after G2 X-irradiation (68R) increased chromatid gaps 18-fold and breaks 2-fold in BALB/cAn cells but had no effect on SENCAR cells even though incorporated into DNA to the same extent. The present results suggest that the SENCAR mouse is deficient in at least two aspects of DNA repair: (i) ligation or a prior step in the repair process leading to ligation and (ii) repair endonucleolytic incision at DNA lesions induced by irradiation. JF - Carcinogenesis AU - Sanford, K K AU - Parshad, R AU - Price, F M AU - Gantt, R AU - Jones, G M AU - Tarone, R E AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 1911 EP - 1916 VL - 10 IS - 10 SN - 0143-3334, 0143-3334 KW - Chromatin KW - 0 KW - Index Medicus KW - Mice, Inbred Strains KW - Fibroblasts -- drug effects KW - Animals KW - X-Rays KW - Cells, Cultured KW - Chromatids -- radiation effects KW - Mice KW - Light KW - Fibroblasts -- cytology KW - Mice, Inbred BALB C KW - Species Specificity KW - Ultraviolet Rays KW - Skin -- radiation effects KW - DNA Repair KW - Chromatin -- radiation effects KW - Skin -- cytology KW - Interphase -- radiation effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79220682?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-13 N1 - Date created - 1989-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A case-control study of soft-tissue sarcoma. AN - 79201355; 2773915 AB - The roles of nonagricultural occupations, tobacco use, beverage consumption, medical history, and other factors in the development of soft-tissue sarcoma were examined in a population-based case-control study in Kansas. Based on 133 cases diagnosed between 1976-1982 and 948 controls, there were significant excesses associated with use of the drug chloramphenicol (odds ratio (OR) = 5.4, 95% confidence interval (Cl) 1.2-23.9) and chewing tobacco or snuff (OR = 1.8, 95% Cl 1.1-2.9). The risk associated with smokeless tobacco varied with the location of the tumors; greater risks were observed for tumors of the upper gastrointestinal tract (OR = 3.3), the lung, pleura, and thorax (OR = 3.1), and the head, neck, and face region (OR = 2.4) than other regions of the body (OR = 1.4). A nonsignificant excess was seen with the use of cholesterol-lowering drugs, such as clofibrate (OR = 1.7). Four cases reported histories of prior radiation treatment to the same area of their bodies as their tumors. Soft-tissue sarcoma was also associated with employment in woodworking occupations (OR = 1.7, 95% Cl 0.9-3.2) and risk increased with increasing duration of employment. Persons with first-degree blood relatives with a history of Hodgkin's disease, lymphoma, or cancers of the pancreas, prostate, brain, or skin were at increased risk. Many of the associations observed in this study, notably the risk of soft-tissue sarcoma with smokeless tobacco and medications such as chloramphenicol, deserve further evaluation. JF - American journal of epidemiology AU - Zahm, S H AU - Blair, A AU - Holmes, F F AU - Boysen, C D AU - Robel, R J AU - Fraumeni, J F AD - Epidemiology and Biostatistics Program, National Cancer Institute, Rockville, MD 20892. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 665 EP - 674 VL - 130 IS - 4 SN - 0002-9262, 0002-9262 KW - Chloramphenicol KW - 66974FR9Q1 KW - Index Medicus KW - Beverages KW - Chloramphenicol -- adverse effects KW - Humans KW - Wood KW - Aged KW - Tobacco, Smokeless KW - Plants, Toxic KW - Demography KW - Kansas KW - Aged, 80 and over KW - Risk Factors KW - Adult KW - Cohort Studies KW - Middle Aged KW - Occupations KW - Male KW - Soft Tissue Neoplasms -- epidemiology KW - Soft Tissue Neoplasms -- etiology KW - Sarcoma -- etiology KW - Sarcoma -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79201355?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-12 N1 - Date created - 1989-10-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Long-term efficacy and safety of omeprazole in patients with Zollinger-Ellison syndrome: a prospective study. AN - 79195497; 2777040 AB - To determine the long-term efficacy, safety, and toxicity of omeprazole, we studied 40 patients with Zollinger-Ellison syndrome given omeprazole for 6-51 mo (median 29). The mean daily dose of omeprazole required to control gastric acid secretion was 82 +/- 31 mg. Thirty-one patients required omeprazole once per day. In 9 patients acid output was not controlled by 120 mg once per day, but was controlled by 60 mg every 12 h. The daily dose of omeprazole correlated with the previous dose of histamine H2-receptor antagonist (r = 0.89, p less than 0.001), basal acid output (r = 0.43, p less than 0.01), and maximal acid output (r = 0.39, p less than 0.02) but not with serum concentration of gastrin (r = -0.32). Increases in the dose of omeprazole were required in 9 patients. Twenty-nine patients had mild peptic symptoms with acid outputs less than 10 mEq/h while taking histamine H2-receptor antagonists. Symptoms resolved completely in 23 patients and partially in 3 when taking omeprazole. Omeprazole prevented mucosal disease in all patients including 17 in whom histamine H2-receptor antagonists had produced only partial resolution despite acid output being less than 10 mEq/h and in those with symptoms during omeprazole therapy. Omeprazole therapy was not associated with any significant side effects, nor with any evidence of hematologic or biochemical toxicity. Serum concentrations of gastrin did not change significantly during therapy. In 6 patients treated with omeprazole for 1 yr there was no change in basal or maximal acid output. In all patients, gastric morphology and histopathology demonstrated no evidence of gastric carcinoid formation. These results demonstrate that with long-term treatment of up to 4 yr, omeprazole is safe, with no evidence of hematologic, biochemical, or gastric toxicity. Furthermore, omeprazole remained effective, with only 23% of patients requiring an increase in dose, and continued to control symptoms in patients who had not been entirely symptom-free despite high doses of histamine H2-receptor antagonists. Omeprazole is now the drug of choice in patients with Zollinger-Ellison syndrome. JF - Gastroenterology AU - Maton, P N AU - Vinayek, R AU - Frucht, H AU - McArthur, K A AU - Miller, L S AU - Saeed, Z A AU - Gardner, J D AU - Jensen, R T AD - Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 827 EP - 836 VL - 97 IS - 4 SN - 0016-5085, 0016-5085 KW - Omeprazole KW - KG60484QX9 KW - Abridged Index Medicus KW - Index Medicus KW - Drug Administration Schedule KW - Prospective Studies KW - Humans KW - Adult KW - Intestinal Mucosa -- pathology KW - Aged KW - Middle Aged KW - Time Factors KW - Gastric Mucosa -- pathology KW - Male KW - Female KW - Gastric Acid -- secretion KW - Zollinger-Ellison Syndrome -- metabolism KW - Zollinger-Ellison Syndrome -- drug therapy KW - Omeprazole -- adverse effects KW - Omeprazole -- therapeutic use KW - Omeprazole -- administration & dosage KW - Zollinger-Ellison Syndrome -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79195497?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-17 N1 - Date created - 1989-10-17 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - GABAA receptor complex in an experimental model of hepatic encephalopathy: evidence for elevated levels of an endogenous benzodiazepine receptor ligand. AN - 79178196; 2549194 AB - The involvement of the gamma-aminobutyric acidA (GABAA) receptor complex in the pathogenesis of hepatic encephalopathy was examined in thioacetamide-treated rats with fulminant hepatic failure. Partially purified extracts from encephalopathic rat brain were approximately three times more potent in inhibiting [3H]Ro 15-1788 binding to benzodiazepine receptors than identically prepared extracts from control rats. High levels of inhibitory activity were also found in extracts of plasma, heart, and liver from thioacetamide-treated rats. The inhibition of [3H]Ro 15-1788 binding by brain extracts appeared to be competitive and reversible and was unaffected by treatment with either proteolytic enzymes or boiling. Further, GABA significantly enhanced the potency of these extracts in inhibiting [3H]flunitrazepam binding. In contrast, no differences were found in radioligand binding to the constituent recognition sites of the GABAA receptor complex in well-washed brain membranes prepared from control and encephalopathic animals. These findings suggest that the recognition-site qualities of the constituent proteins of the GABAA receptor complex are unchanged in an experimental model of hepatic encephalopathy. However, significant elevations in the level of a substance or substances with neurochemical properties characteristic of a benzodiazepine receptor agonist may contribute to the electrophysiological and behavioral manifestations of hepatic encephalopathy. JF - Journal of neurochemistry AU - Basile, A S AU - Gammal, S H AU - Jones, E A AU - Skolnick, P AD - Laboratory of Neuroscience, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 1057 EP - 1063 VL - 53 IS - 4 SN - 0022-3042, 0022-3042 KW - Receptors, GABA-A KW - 0 KW - Thioacetamide KW - 075T165X8M KW - Flumazenil KW - 40P7XK9392 KW - Index Medicus KW - Animals KW - Reference Values KW - Flumazenil -- metabolism KW - Cerebral Cortex -- metabolism KW - Disease Models, Animal KW - Cerebellum -- metabolism KW - Rats KW - Rats, Inbred Strains KW - Kinetics KW - Binding, Competitive KW - Cell Membrane -- metabolism KW - Male KW - Receptors, GABA-A -- metabolism KW - Brain -- metabolism KW - Hepatic Encephalopathy -- metabolism KW - Hepatic Encephalopathy -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79178196?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-12 N1 - Date created - 1989-10-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of initiator-promoter-induced skin tumorigenesis in female SENCAR mice fed a vitamin A-deficient diet and reappearance of tumors in mice fed a diet adequate in retinoid or beta-carotene. AN - 79165900; 2504490 AB - Retinoids have chemopreventive activity for epithelial tumors in a variety of systems, including the two-stage tumorigenesis system of mouse skin in which only the promotion stage is inhibited. We asked whether dietary vitamin A deficiency could affect the skin tumorigenic response, prior to major changes in body weight or general health of the animals. Two regimens were tested to induce vitamin A deficiency. SENCAR mice were either (a) fed a vitamin A-deficient diet from 4 or 9 weeks of age or (b) their mothers were fed the diet from the time of birth of the experimental animals which were then weaned on the same diet. The latter regimen produced typical symptoms of vitamin A deficiency in the offspring by Weeks 12-14 and all the mice died by Week 19; the former regimen permitted sufficient accumulation of retinol and its esters to sustain life for up to 45 and 75 weeks, respectively, in the majority of mice. For our experiments, vitamin A depletion was produced by placing the mothers on the deficient diet at birth of the experimental animals. A single topical dose of 20 micrograms of 7,12-dimethylbenz(a)anthracene (DMBA) was used as the initiator at 3 weeks of age and 1 to 2 micrograms of 12-O-tetradecanoylphorbol-13-acetate (TPA) once weekly as the tumor promoter for 10 weeks (from Week 4 through 13 of the experiment). Fifty-five % of mice (n = 40) on Purina laboratory chow (mean body weight, 31.4 g) developed skin tumors (2.58 per mouse) at 12 weeks, versus 2.5% (0.05 papillomas per mouse) of mice (n = 40) kept on the purified vitamin A-deficient diet (mean body weight, 30.3 g), a 98% decrease in tumor/mouse. Retinoic acid (RA) (1-3 micrograms/g diet) supplementation after Week 12 caused a rapid tumorigenic response in 95% of the mice by week 22. This tumor response occurred to a reduced extent in the absence of continued TPA treatment up to Week 13. Even though tumor incidence increased within 1 week of RA and 95% of the mice showed the tumorigenic response, the number of tumors per mouse was about 50% of that observed in mice maintained on standard Purina diet. This was confirmed in an experiment in which the mice were maintained for life either on Purina or on the RA (3 micrograms/g) containing purified diet, the latter being the control group for the effect of vitamin A deficiency on skin tumorigenesis.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Cancer research AU - De Luca, L M AU - Shores, R L AU - Spangler, E F AU - Wenk, M L AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/10/01/ PY - 1989 DA - 1989 Oct 01 SP - 5400 EP - 5406 VL - 49 IS - 19 SN - 0008-5472, 0008-5472 KW - beta Carotene KW - 01YAE03M7J KW - Carotenoids KW - 36-88-4 KW - Tretinoin KW - 5688UTC01R KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Cocarcinogenesis KW - Mice KW - Neoplasms, Experimental -- prevention & control KW - Neoplasms, Experimental -- pathology KW - Liver -- analysis KW - Neoplasms, Experimental -- chemically induced KW - Weight Loss KW - Diet KW - Female KW - Male KW - Vitamin A Deficiency -- physiopathology KW - Vitamin A Deficiency -- mortality KW - Skin Neoplasms -- chemically induced KW - Carotenoids -- analysis KW - Tretinoin -- administration & dosage KW - Skin Neoplasms -- pathology KW - Carotenoids -- administration & dosage KW - Skin Neoplasms -- prevention & control KW - Tretinoin -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79165900?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-05 N1 - Date created - 1989-10-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pharmacokinetics of buthionine sulfoximine (NSC 326231) and its effect on melphalan-induced toxicity in mice. AN - 79165855; 2766304 AB - Intravenous doses of buthionine sulfoximine (BSO, NSC 326231), an inhibitor of glutathione synthesis, were eliminated rapidly from mouse plasma in a biexponential manner. The initial phase of the plasma concentration versus time curve had a half-life of 4.9 min and accounted for 94% of the total area under the curve. The half-life of the terminal phase of the curve was 36.7 min and the area accounted for only 6% of the total area under the curve. Plasma clearance of BSO was 28.1 ml/min/kg and the steady state volume of distribution was 280 ml/kg. The oral bioavailability of BSO, based on plasma BSO levels, was extremely low. However, comparable glutathione depletion was apparent after i.v. and p.o. doses of BSO, suggesting a rapid tissue uptake and/or metabolism of BSO. Therefore, due to the rapid elimination of BSO from mouse plasma, plasma drug levels do not directly correlate with BSO-induced tissue glutathione depletion. Administration of multiple i.v. doses of BSO to male and female mice resulted in a marked 88% depletion of liver glutathione at doses of 400-1600 mg/kg/dose. Toxicity of i.v. administered BSO was limited to a transient depression of peripheral WBC levels in female mice given six doses of 1600 mg/kg. Multiple i.v. doses of BSO of up to 800 mg/kg/dose (every 4 h for a total of six doses) did not alter the toxicity of i.v. administered melphalan. However, multiple doses of 1600 mg/kg/dose of BSO did potentiate histopathological evidence of melphalan-induced bone marrow toxicity in 30% of the mice and, additionally, the combination of BSO and melphalan produced renal tubular necrosis in 80% of the male mice. The potentiation of melphalan induced toxicity did not appear to be related to GSH depletion, since: quantitatively similar amount of GSH depletion occurred at lower dose of BSO without any increase in melphalan toxicity. JF - Cancer research AU - Smith, A C AU - Liao, J T AU - Page, J G AU - Wientjes, M G AU - Grieshaber, C K AD - Toxicology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/10/01/ PY - 1989 DA - 1989 Oct 01 SP - 5385 EP - 5391 VL - 49 IS - 19 SN - 0008-5472, 0008-5472 KW - Methionine Sulfoximine KW - 1982-67-8 KW - Buthionine Sulfoximine KW - 5072-26-4 KW - Glutathione KW - GAN16C9B8O KW - Melphalan KW - Q41OR9510P KW - Index Medicus KW - Administration, Oral KW - Animals KW - Drug Administration Schedule KW - Drug Interactions KW - Injections, Intravenous KW - Liver -- metabolism KW - Glutathione -- blood KW - Mice KW - Mice, Inbred BALB C KW - Mice, Inbred DBA KW - Half-Life KW - Premedication KW - Drug Evaluation, Preclinical KW - Methionine Sulfoximine -- blood KW - Methionine Sulfoximine -- administration & dosage KW - Methionine Sulfoximine -- toxicity KW - Melphalan -- administration & dosage KW - Methionine Sulfoximine -- pharmacology KW - Methionine Sulfoximine -- analogs & derivatives KW - Methionine Sulfoximine -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79165855?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-05 N1 - Date created - 1989-10-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Relationship between the formation of promutagenic adducts and the activation of the K-ras protooncogene in lung tumors from A/J mice treated with nitrosamines. AN - 79159208; 2670201 AB - Lung and liver tumors were induced in female A/J mice after treatment for 7 weeks (3 times/week, i.p.) with either 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) (50 mg/kg) or nitrosodimethylamine (NDMA) (3 mg/kg). Both compounds can be activated via alpha-hydroxylation to methylating agents, while NNK may also undergo hydroxylation at the N-methyl carbon to form a pyridyloxobutylated adduct. The purpose of these studies was to identify and characterize the activated oncogenes present in tumors induced by NDMA and NNK. Following transfection of high molecular weight DNA onto NIH/3T3 mouse fibroblasts, transforming genes were detected in 90% of both NNK- (10 of 11) and NDMA- (9 of 10) induced lung tumors. In contrast, transformation of NIH/3T3 fibroblasts was observed only in 40% (2 of 5) and 13% (1 of 8) of the liver tumors from NNK- and NDMA-treated mice, respectively. Southern blot analysis indicated that the transforming gene present in all lung tumors was an activated K-ras oncogene. Both rearranged bands and amplified signals were detected in the transfectants. The one transformant from the NDMA-induced liver tumor contained an activated K-ras gene. In contrast, the two liver transformants from NNK-induced tumors did not contain an activated ras or raf gene. Hybridization with oligonucleotide probes that were centered around either codon 12 or 61 of the K-ras gene were utilized to localize the mutations. Activation of this gene appeared to occur largely via a mutation in codon 12 (15 of 20 transformants) and was observed with a similar frequency in pulmonary tumors induced by either compound. The remaining mutations were found in codon 61. The specific mutation within these two codons was determined by amplifying the exon containing the base change, followed by direct sequencing. With one exception the mutation observed in codon 12 was a GC to AT transition (GGT to GAT). One transformant contained a GC to TA transversion. The activating mutation detected in codon 61 was always an AT to GC transition of the middle A (CAA to CGA). The GC to AT mutation observed in codon 12 is consistent with the formation of the O6-methylguanine adduct. Similar concentrations (23 to 32 pmol/mumol deoxyguanosine) of this promutagenic adduct were detected in lungs during treatment with either NNK or NDMA.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Cancer research AU - Belinsky, S A AU - Devereux, T R AU - Maronpot, R R AU - Stoner, G D AU - Anderson, M W AD - Laboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/10/01/ PY - 1989 DA - 1989 Oct 01 SP - 5305 EP - 5311 VL - 49 IS - 19 SN - 0008-5472, 0008-5472 KW - Codon KW - 0 KW - Nitrosamines KW - 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone KW - 7S395EDO61 KW - Dimethylnitrosamine KW - M43H21IO8R KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Neoplasms, Experimental -- chemically induced KW - Blotting, Southern KW - Neoplasms, Experimental -- analysis KW - DNA Mutational Analysis KW - Mice KW - Female KW - Genes, ras KW - Adenocarcinoma -- chemically induced KW - Transfection KW - Lung Neoplasms -- genetics KW - Gene Expression Regulation KW - Adenocarcinoma -- genetics KW - Lung Neoplasms -- chemically induced KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79159208?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-05 N1 - Date created - 1989-10-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The Structure of Attitude Strength AN - 61256476; 91X6186 AB - While many studies support the claim that strong attitudes have greater impact on cognition & behavior than do weak ones, the claim is called into question by the diversity of indicators commonly used for testing attitude strength with respect to a target object: attributed importance, intensity, extremity, or certainty of attribution, ego involvement, frequency of verbal reference, attention to relevant information, attitude accessibility, knowledge about & direct experience with target object, & affective-cognitive consistency. The interaction between these indicators is explored here through surveys of 288 Ohio State U students on abortion, capital punishment, & defense spending. Multitrait-multimethod confirmatory factor analysis of results suggests that while individual indicators can be grouped in various ways, no consistent, univocal scale of attitude strength emerges. 6 Tables, 51 References. Adapted from the source document. JF - Chung Yang Yen Chiu Yuan Min Tsu Hsueh Yen Chiu So Chi K'an/Bulletin of the Institute of Ethnology Academia Sinica AU - Chuang, Yao-chia AD - F3 No 28 Alley 122 Lane 411 Nei Hu Rd Section 1, Taipei Taiwan Y1 - 1989/10// PY - 1989 DA - October 1989 SP - 227 EP - 256 IS - 68 SN - 0001-3935, 0001-3935 KW - attitude strength, cognitive impacts, measurement problems KW - surveys KW - university students, Ohio KW - Social Attitudes KW - Cognition KW - Methodological Problems KW - Ohio KW - article KW - 0312: social psychology; personality & culture UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/61256476?accountid=14244 LA - English DB - Sociological Abstracts N1 - Date revised - 2007-04-01 N1 - Last updated - 2016-09-28 N1 - CODEN - CYMHAZ N1 - SubjectsTermNotLitGenreText - Ohio; Cognition; Social Attitudes; Methodological Problems ER - TY - JOUR T1 - Behavioral evaluation of the anti-excitotoxic properties of MK-801: comparison with neurochemical measurements. AN - 79293235; 2530473 AB - The ability of MK-801 to protect striatal neurons from the excitotoxic action of quinolinic acid was evaluated by means of apomorphine-induced rotational behavior and by measurement of striatal choline acetyltransferase (ChAT) and glutamic acid decarboxylase (GAD) activity, neurochemical markers for cholinergic and GABAergic neurons, respectively. Animals with a unilateral quinolinic acid lesion of the striatum exhibited a vigorous rotational response when challenged with apomorphine (0.5 mg/kg, s.c.) 6 days later and were found to have an 88 90% depletion of striatal ChAT and GAD activity. Treatment with a high dose of MK-801 (10 mg/kg, i.p.) prior to intrastriatal injection of quinolinic acid eliminated the subsequent rotational response to apomorphine and resulted in complete protection of striatal ChAT and GAD activity. Lower doses of MK-801 (1, 3 and 5 mg/kg, i.p.) failed to significantly reduce the rotational response to apomorphine but provided partial, dose-dependent protection of both ChAT and GAD activity. The rotational response to apomorphine correlated with the percent reduction in both ChAT activity (r = 0.57, P less than 0.0005) and GAD activity (r = 0.49, P less than 0.0005). Rotational behavior may thus provide a means to evaluate the functional integrity of the striatum. JF - Neuroscience letters AU - Susel, Z AU - Engber, T M AU - Chase, T N AD - Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892. Y1 - 1989/09/25/ PY - 1989 DA - 1989 Sep 25 SP - 125 EP - 129 VL - 104 IS - 1-2 SN - 0304-3940, 0304-3940 KW - Anticonvulsants KW - 0 KW - Dibenzocycloheptenes KW - Pyridines KW - Quinolinic Acids KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - Choline O-Acetyltransferase KW - EC 2.3.1.6 KW - Glutamate Decarboxylase KW - EC 4.1.1.15 KW - Quinolinic Acid KW - F6F0HK1URN KW - Apomorphine KW - N21FAR7B4S KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Apomorphine -- pharmacology KW - Choline O-Acetyltransferase -- metabolism KW - Male KW - Glutamate Decarboxylase -- metabolism KW - Corpus Striatum -- physiopathology KW - Dibenzocycloheptenes -- pharmacology KW - Corpus Striatum -- drug effects KW - Stereotyped Behavior -- drug effects KW - Pyridines -- antagonists & inhibitors KW - Nervous System Diseases -- physiopathology KW - Nervous System Diseases -- chemically induced KW - Dibenzocycloheptenes -- therapeutic use KW - Nervous System Diseases -- prevention & control KW - Quinolinic Acids -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79293235?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-20 N1 - Date created - 1989-12-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A single glutamic acid residue plays a key role in the transcriptional activation function of lambda repressor. AN - 79189261; 2570642 AB - Previous experiments have suggested that negative charge is an important aspect of the activating region of lambda repressor as it is for at least one class of eukaryotic transcriptional activators. Here we randomize amino acids in the activating region of repressor and assay the function of over 100 variants. We find that acidic residues at the four solvent-exposed positions on the surface of an alpha helix (helix 2 in the structure) together comprise a strong activating region. Only one of these acidic residues, however, is critical for activation, and at this position glutamate is strongly preferred to aspartate. At the three remaining positions, certain uncharged residues (different ones at each position) function as well as or better than the acidic residues. Basic residues, however, are highly detrimental to function at all four positions. Our mutagenesis studies also suggest limitations on amino acid substitutions that allow formation of the helix-turn-helix DNA binding motif found in repressor and in many other DNA binding regulatory proteins. JF - Cell AU - Bushman, F D AU - Shang, C AU - Ptashne, M AD - Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1989/09/22/ PY - 1989 DA - 1989 Sep 22 SP - 1163 EP - 1171 VL - 58 IS - 6 SN - 0092-8674, 0092-8674 KW - DNA-Binding Proteins KW - 0 KW - Glutamates KW - Repressor Proteins KW - Transcription Factors KW - Viral Proteins KW - Viral Regulatory and Accessory Proteins KW - phage repressor proteins KW - Glutamic Acid KW - 3KX376GY7L KW - Index Medicus KW - Base Sequence KW - Models, Molecular KW - Operon KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Plasmids KW - Nucleic Acid Conformation KW - Protein Conformation KW - Genes KW - Bacteriophage lambda -- genetics KW - Repressor Proteins -- physiology KW - Escherichia coli -- genetics KW - Transcription, Genetic KW - Gene Expression Regulation KW - Transcription Factors -- genetics KW - Repressor Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79189261?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-24 N1 - Date created - 1989-10-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Toxicity of levamisole and 5-fluorouracil in human colon carcinoma cells. AN - 79200100; 2778828 AB - The combination of 5-fluorouracil (5-FU) with the immunomodulator levamisole (Lev) has been clinically tested in patients with metastatic colorectal carcinoma and as adjuvant therapy following primary tumor surgery. In some studies in advanced disease, the addition of Lev to 5-FU improved the median duration of response; in the adjuvant setting, the combination was associated with improvement in the disease-free survival. We studied whether Lev was directly toxic to three human colorectal carcinoma cell lines (HCT 116, SNU-C4, and NCI-H630). We also evaluated the toxicity of Lev in combination with 5-FU in these three cell lines. Lev inhibited the growth of all three colorectal cell lines, but only at concentrations two logs above that achieved with a standard 150-mg oral dose of Lev. In cell growth studies, 500 and 1,000 microM Lev increased the toxicity of 5-FU in HCT 116 cells in an additive fashion. In clonogenic assays, continuous exposure to 10 or 100 microM Lev was minimally toxic and did not enhance the lethality associated with a 24-hour exposure to 5-FU in any of the cell lines. Lev alone at 1,000 microM decreased colony formation by 45% in HCT 116 cells. A combination of 1,000 microM Lev with 10 microM 5-FU resulted in a decrease in HCT 116 colony formation from 54% to 6% of control levels. Continuous exposure of NCI-H630 cells to 500 microM Lev decreased colony formation to 76.5% of control levels; when Lev was combined with 50 microM 5-FU, colony formation was decreased from 59.5% to 27.5% of control levels. We conclude that at concentrations achievable with conventional doses of Lev, there was no evidence of direct toxicity in these colorectal cell lines. Furthermore, an additive interaction with 5-FU was evident only at suprapharmacologic doses of Lev. JF - Journal of the National Cancer Institute AU - Grem, J L AU - Allegra, C J AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/09/20/ PY - 1989 DA - 1989 Sep 20 SP - 1413 EP - 1417 VL - 81 IS - 18 SN - 0027-8874, 0027-8874 KW - Levamisole KW - 2880D3468G KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - Clone Cells KW - Drug Administration Schedule KW - Tumor Cells, Cultured KW - Humans KW - Drug Synergism KW - Levamisole -- pharmacology KW - Colonic Neoplasms -- drug therapy KW - Fluorouracil -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79200100?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-13 N1 - Date created - 1989-10-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of immobilized, biotinylated choleragen AI protein by a 19-kilodalton guanine nucleotide-binding protein. AN - 79428308; 2514798 AB - Cholera toxin catalyzes the ADP-ribosylation that results in activation of the stimulatory guanine nucleotide-binding protein of the adenylyl cyclase system, known as Gs. The toxin also ADP-ribosylates other proteins and simple guanidino compounds and auto-ADP-ribosylates its AI protein (CTA1). All of the ADP-ribosyltransferase activities of CTAI are enhanced by 19-21-kDa guanine nucleotide-binding proteins known as ADP-ribosylation factors, or ARFs. CTAI contains a single cysteine located near the carboxy terminus. CTAI was immobilized through this cysteine by reaction with iodoacetyl-N-biotinyl-hexylenediamine and binding of the resulting biotinylated protein to avidin-agarose. Immobilized CTAI catalyzed the ARF-stimulated ADP-ribosylation of agmatine. The reaction was enhanced by detergents and phospholipid, but the fold stimulation by purified sARF-II from bovine brain was considerably less than that observed with free CTA. ADP-ribosylation of Gsa by immobilized CTAI, which was somewhat enhanced by sARF-II, was much less than predicted on the basis of the NAD:agmatine ADP-ribosyltransferase activity. Immobilized CTAI catalyzed its own auto-ADP-ribosylation as well as the ADP-ribosylation of the immobilized avidin and CTA2, with relatively little stimulation by sARF-II. ADP-ribosylation of CTA2 by free CTAI is minimal. These observations are consistent with the conclusion that the cysteine near the carboxy terminus of the toxin is not critical for ADP-ribosyltransferase activity or for its regulation by sARF-II. Biotinylation and immobilization of the toxin through this cysteine may, however, limit accessibility to Gsa or SARF-II, or perhaps otherwise reduce interaction with these proteins whether as substrates or activator. JF - Biochemistry AU - Noda, M AU - Tsai, S C AU - Adamik, R AU - Bobak, D A AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989/09/19/ PY - 1989 DA - 1989 Sep 19 SP - 7936 EP - 7940 VL - 28 IS - 19 SN - 0006-2960, 0006-2960 KW - NAD KW - 0U46U6E8UK KW - Biotin KW - 6SO6U10H04 KW - Cholera Toxin KW - 9012-63-9 KW - Poly(ADP-ribose) Polymerases KW - EC 2.4.2.30 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Cysteine KW - K848JZ4886 KW - Index Medicus KW - Enzyme Activation KW - Molecular Weight UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79428308?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-06 N1 - Date created - 1990-03-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synthetic non-peptide inhibitors of HIV protease. AN - 79227790; 2675834 AB - We have studied the inhibition of HIV protease by the antifungal antibiotic cerulenin, as well as by several related synthetic, structurally simpler analogs. The effect of these compounds on HIV protease was conveniently studied by monitoring the cleavage of an authentic single peptide bond in a synthetic nonapeptide corresponding to a natural cleavage site in HIV-1 gag precursor polyprotein. The relative inhibitory effects of these compounds have afforded an insight into the structural characteristics which impart antiprotease activity. JF - Biochemical and biophysical research communications AU - Blumenstein, J J AU - Copeland, T D AU - Oroszlan, S AU - Michejda, C J AD - Laboratory of Chemical and Physical Carcinogenesis, NCI-Frederick Cancer Research Facility MD 21701. Y1 - 1989/09/15/ PY - 1989 DA - 1989 Sep 15 SP - 980 EP - 987 VL - 163 IS - 2 SN - 0006-291X, 0006-291X KW - Antifungal Agents KW - 0 KW - Protease Inhibitors KW - Cerulenin KW - 17397-89-6 KW - Endopeptidases KW - EC 3.4.- KW - HIV Protease KW - EC 3.4.23.- KW - Index Medicus KW - AIDS/HIV KW - Endopeptidases -- metabolism KW - Hydrolysis KW - Structure-Activity Relationship KW - Protease Inhibitors -- pharmacology KW - Antifungal Agents -- pharmacology KW - Cerulenin -- pharmacology KW - Protease Inhibitors -- chemical synthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79227790?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-20 N1 - Date created - 1989-10-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Monoclonal antibodies to rat liver cytochrome P-450 2c/RLM5 that regiospecifically inhibit steroid metabolism. AN - 79215913; 2783161 AB - Hybridomas were formed from myeloma cells and spleen cells derived from BALB/c female mice immunized with purified liver microsomal cytochrome P-450 2c/RLM5 (P-450 gene IIC11) isolated from untreated adult male rats. Six hybridoma clones produced monoclonal antibodies (MAbs) of the IgM(kappa) type. All the MAbs bound strongly to P-450 2c/RLM5 when measured by radioimmunoassay, and four of the six specifically immunoprecipitated P-450 2c/RLM5 in an Ouchterlony double-immunodiffusion test. These four MAbs also bound but did not immunoprecipitate P-450 RLM3. The MAbs that precipitated P-450 2c/RLM5 neither bound nor precipitated P-450 PB-B (gene IIB1) and P-450 BNF-B (gene IA1) of rats or P-450 LM2 and P-450 LM4 of rabbits. In contrast, mouse polyclonal anti-P-450 2c/RLM5 antibody strongly immunoprecipitated P-450 RLM3 as well as P-450 2c/RLM5 and to a lesser extent P-450 PB-B and P-450 LM2. The MAbs that precipitated P-450 2c/RLM5 also inhibited by more than 90% androstenedione 16 alpha-hydroxylase activity of untreated rat microsomes, but did not inhibit microsomal 6 beta- or 7 alpha-hydroxylation. In addition, complete inhibition of both androstenedione 16 alpha-hydroxylation and testosterone 16 alpha-hydroxylation was observed in a reconstituted system with P-450 2c/RLM5. Androstenedione 6 beta-hydroxylation catalyzed by P-450 2c/RLM5 was also inhibited, whereas P-450 3-catalyzed 7 alpha-hydroxylation was not inhibited by the MAbs. P-450 2c/RLM5 catalyzed 2 alpha-, 16 alpha- and 6 beta-hydroxylation of progesterone in a reconstituted system were also inhibited by the MAb by 60-80%. These MAbs should prove useful for "reaction phenotyping," i.e. for defining the contribution of microsomal P-450 2c/RLM5 to the oxidative metabolism of endogenous steroids and other P-450 substrates in animal and human tissues. JF - Biochemical pharmacology AU - Park, S S AU - Waxman, D J AU - Lapenson, D P AU - Schenkman, J B AU - Gelboin, H V AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/09/15/ PY - 1989 DA - 1989 Sep 15 SP - 3067 EP - 3074 VL - 38 IS - 18 SN - 0006-2952, 0006-2952 KW - Antibodies, Monoclonal KW - 0 KW - Steroids KW - Androstenedione KW - 409J2J96VR KW - Progesterone KW - 4G7DS2Q64Y KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - CYP2C9 protein, human KW - EC 1.14.13.- KW - Cytochrome P-450 CYP2C9 KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - CYP2C11 protein, rat KW - CYP2C8 protein, human KW - Cytochrome P-450 CYP2C8 KW - Cytochrome P450 Family 2 KW - Steroid 16-alpha-Hydroxylase KW - Index Medicus KW - Rats KW - Antibody Specificity KW - Animals KW - Progesterone -- metabolism KW - Mice KW - Mice, Inbred BALB C KW - Androstenedione -- metabolism KW - Male KW - Female KW - Hydroxylation KW - Microsomes, Liver -- enzymology KW - Cytochrome P-450 Enzyme System -- immunology KW - Steroids -- metabolism KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79215913?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-16 N1 - Date created - 1989-10-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of rat liver microsomal and nuclear cytochrome P-450 by dietary 2-acetylaminofluorene and butylated hydroxytoluene. AN - 79215756; 2783162 AB - The influence of dietary 2-acetylaminofluorene (AAF) on the cytochrome P-450 content of rat liver microsomal and nuclear fractions was immunochemically probed with monoclonal and polyclonal antibodies to cytochromes P-450c and P-450d. Cytochrome P-450d but not P-450c was immunodetected in microsomes, nuclear envelopes, and nuclei from untreated rats. The levels of both cytochromes P-450c and P-450d were elevated after a diet of either 0.1% AAF for 1 week or 0.05% AAF for 3 weeks. However, the level of cytochrome P-450c relative to P-450d was lower after the more prolonged AAF feeding. Supplementation of AAF-containing diets with 0.3% butylated hydroxytoluene (BHT), which affords protection against AAF hepatocarcinogenesis in high-fat fed rats, protected and/or induced total (spectral) nuclear envelope cytochrome P-450 content. Immunochemical studies of liver fractions showed that BHT enhanced the AAF-dependent induction of cytochrome P-450c, but not of P-450d. This was a concerted effect of AAF + BHT since dietary BHT by itself did not affect the levels of cytochrome P-450c or P-450d as compared to control rats. Since 1- to 3-week dietary AAF had little effect on total (spectral analyses) microsomal cytochrome P-450 but markedly reduced total P-450 in nuclear envelopes, the coordinated induction of specific cytochrome P-450s in the different fractions suggests selective induction and depression of different forms of cytochrome P-450 and provides additional evidence for independent regulation of the drug-metabolizing system in nuclear envelope and microsomes. In addition, these results suggest that regulation of cytochrome P-450 may play a crucial role in the nutritional modulation of AAF hepatocarcinogenesis. JF - Biochemical pharmacology AU - Friedman, F K AU - Miller, H AU - Park, S S AU - Graham, S A AU - Gelboin, H V AU - Carubelli, R AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/09/15/ PY - 1989 DA - 1989 Sep 15 SP - 3075 EP - 3081 VL - 38 IS - 18 SN - 0006-2952, 0006-2952 KW - Antibodies, Monoclonal KW - 0 KW - Butylated Hydroxytoluene KW - 1P9D0Z171K KW - Methylcholanthrene KW - 56-49-5 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - 2-Acetylaminofluorene KW - 9M98QLJ2DL KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Immunoblotting KW - Animals KW - Enzyme Induction -- drug effects KW - Methylcholanthrene -- pharmacology KW - Diet KW - Male KW - Cell Nucleus -- enzymology KW - 2-Acetylaminofluorene -- pharmacology KW - Microsomes, Liver -- enzymology KW - Cytochrome P-450 Enzyme System -- immunology KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Butylated Hydroxytoluene -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79215756?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-16 N1 - Date created - 1989-10-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Free-radical formation by mitomycin C and its novel analogs in cardiac microsomes and the perfused rat heart. AN - 79204433; 2550081 AB - Using a spin-trapping technique, we have examined free-radical formation by mitomycin C and its analogs, BMY 25282 and BMY 25067, in rat cardiac microsomes and isolated perfused rat hearts. All three drugs stimulated 2--4-fold OH radical formation in cardiac microsomes which was inhibited by SOD and catalase. Superoxide anion radical was also detected in the presence of diethylenetetraaminopentaacetic acid. Addition of DMSO yielded methyl radicals, thus indicating the production of free OH under these conditions. Similar stimulation of OH formation (2--3-fold) in the perfusates from rat hearts was detected with all three drugs. Perfusion with catalase (550 U/ml) completely suppressed the OH signal both in the presence and absence of the drugs, thus suggesting the intermediacy of hydrogen peroxide. However, BMY 25067-induced OH formation was more sensitive to inhibition by superoxide dismutase (SOD) and the iron chelator ICRF-187. Perfusion with DMSO produced methyl radicals at the expense of OH in the presence of all three drugs. SOD and catalase inhibited DMPO-OH signals, indicating that most of the OH formation was extracellular in this setting. While mitomycin C and BMY 25067 (up to 10 microM) did not affect the heart rate, perfusion with 10 microM BMY 25282 caused acute arrhythmia and cardiac standstill within 20 min. An initial surge in OH formation (2-fold) accompanied this cardiotoxic effect. Both the arrhythmia and the free radical signal were partially blocked by SOD, catalase and ICRF-187, indicating that iron-dependent oxygen radical formation from BMY-25282 (and possibly other compounds) is involved, in part, in inducing toxic manifestations in the rat heart and possibly in clinic. JF - Biochimica et biophysica acta AU - Politi, P M AU - Rajagopalan, S AU - Sinha, B K AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/09/15/ PY - 1989 DA - 1989 Sep 15 SP - 341 EP - 348 VL - 992 IS - 3 SN - 0006-3002, 0006-3002 KW - Free Radicals KW - 0 KW - Hydroxides KW - Mitomycins KW - Superoxides KW - 11062-77-4 KW - Hydroxyl Radical KW - 3352-57-6 KW - Mitomycin KW - 50SG953SK6 KW - N(6)-((dimethylamino)methylene)mitomycin C KW - 88949-01-3 KW - N-7-(2-(nitrophenyldithio)ethyl)mitomycin C KW - 95056-36-3 KW - Catalase KW - EC 1.11.1.6 KW - Index Medicus KW - Animals KW - Perfusion KW - Catalase -- pharmacology KW - Rats, Inbred Strains KW - Rats KW - Superoxides -- metabolism KW - Heart Rate -- drug effects KW - Electron Spin Resonance Spectroscopy KW - Kinetics KW - In Vitro Techniques KW - Hydroxides -- metabolism KW - Male KW - Microsomes -- metabolism KW - Heart -- drug effects KW - Mitomycins -- pharmacology KW - Myocardium -- metabolism KW - Microsomes -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79204433?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-25 N1 - Date created - 1989-10-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phase I trial and pharmacokinetic evaluation of fazarabine in children. AN - 79166768; 2475244 AB - A phase I trial of fazarabine (1-beta-D-arabinofuranosyl-5-azacytosine, NSC 281272) administered as a 24-h continuous infusion was performed in 16 children with refractory malignancies. Dose-limiting toxicity consisting of reversible granulocytopenia and thrombocytopenia was observed in 4 of 4 solid tumor patients treated at the starting dose of 20 mg/m2/h. Subsequent patients were treated at a dose of 15 mg/m2/h which was determined to be the maximum tolerated dose. Moderate nausea and vomiting were the only other toxicities observed. Plasma steady-state concentrations of fazarabine were attained by 2-4 h in all patients and were 1.8 and 2.5 microM at the 15- and 20-mg/m2/h doses, respectively. The total body clearance of fazarabine was 571 and 550 ml/min/m2 at the 15- and 20-mg/m2/h doses, respectively. In three of four patients evaluated, fazarabine was detectable in the cerebrospinal fluid (CSF). Steady-state CSF concentrations ranged from 0.29 to 0.74 microM in these three individuals and the steady-state CSF:plasma ratios ranged from 0.22-0.25. Both the plasma and CSF steady-state concentrations were within the 0.1 to 1 microM range reported to be cytotoxic in vitro against the Molt-4 human T-lymphoblastic leukemia cell line. Based on the above, the optimal dose for phase II trials of fazarabine administered as a 24-h infusion is 15 mg/m2/h (360 mg/m2/day). JF - Cancer research AU - Heideman, R L AU - Gillespie, A AU - Ford, H AU - Reaman, G H AU - Balis, F M AU - Tan, C AU - Sato, J AU - Ettinger, L J AU - Packer, R J AU - Poplack, D G AD - Pediatric Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/09/15/ PY - 1989 DA - 1989 Sep 15 SP - 5213 EP - 5216 VL - 49 IS - 18 SN - 0008-5472, 0008-5472 KW - Antimetabolites, Antineoplastic KW - 0 KW - fazarabine KW - 5V71D8JOKK KW - Azacitidine KW - M801H13NRU KW - Index Medicus KW - Neoplasms -- drug therapy KW - Drug Evaluation KW - Infusions, Intravenous KW - Humans KW - Metabolic Clearance Rate KW - Child KW - Male KW - Female KW - Azacitidine -- therapeutic use KW - Azacitidine -- pharmacokinetics KW - Azacitidine -- adverse effects KW - Antimetabolites, Antineoplastic -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79166768?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-03 N1 - Date created - 1989-10-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Enhanced therapeutic efficacy of an immunotoxin in combination with chemotherapy against an intraperitoneal human tumor xenograft in athymic mice. AN - 79165765; 2504482 AB - A mouse IgG2b anti-pan carcinoma monoclonal antibody, NR-LU-10, was shown to bind homogeneously to ascites xenografts of both ovarian and colon carcinoma. Following linkage to a highly potent holotoxin, Pseudomonas exotoxin A (PE), NR-LU-10 demonstrated high potency and selectivity in vitro (ID50 = 100 pg/ml; elimination of greater than or equal to 4.5 logs of cells). The conjugate was evaluated for therapeutic efficacy against a human colon tumor (HT-29) transplantable in the peritoneal cavity of nude mice. Beginning 3 days after HT-29 injection, mice received either three or six i.p. injections of 0.5 micrograms of unconjugated NR-LU-10 or immunotoxin conjugate (NR-LU-10/PE) every other day. Mice that received three or six treatments of NR-LU-10 alone had median survival times (MSTs) of 39 and 40 days, respectively, which did not differ significantly from the MST observed for the untreated control groups (MST = 35 days). In contrast, treatment with three or six injections of 0.5 micrograms NR-LU-10/PE exhibited significantly increased MSTs (P = 0.002) of 50 and 60 days, respectively. Coinjection of unconjugated NR-LU-10 (20 micrograms) and 0.5 micrograms of NR-LU-10/PE blocked the therapeutic effect of the immunotoxin (MST = 33 days). The therapeutic efficacy of NR-LU-10/PE was further enhanced against HT-29 when administered i.p. during and after cytoreductive chemotherapy. The i.p. administration of 300 mg/lg of cyclophosphamide plus 100 mg/kg of the chemoprotective drug, WR-2721, 10 and 17 days posttumor cell inoculation induced a significant increase in MST from 36 days to 59 days (P = 0.002). Interestingly, groups of mice that received either two, four, or seven treatments of NR-LU-10/PE following cytoreductive therapy exhibited a further significant increase (P = 0.001) in MSTs of 89, 97, and 105 days, respectively. Therefore, the use of immunotoxin therapy following cytoreductive chemotherapy significantly prolonged survival time of mice bearing the HT-29 colon tumor over that observed with chemotherapy or NR-LU-10/PE alone. JF - Cancer research AU - Pearson, J W AU - Sivam, G AU - Manger, R AU - Wiltrout, R H AU - Morgan, A C AU - Longo, D L AD - Laboratory of Experimental Immunology, NCI-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1989/09/15/ PY - 1989 DA - 1989 Sep 15 SP - 4990 EP - 4995 VL - 49 IS - 18 SN - 0008-5472, 0008-5472 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Neoplasm 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 Transplantation KW - Animals KW - Humans KW - Antigens, Neoplasm -- analysis KW - Transplantation, Heterologous KW - Mice, Nude KW - Mice KW - Flow Cytometry KW - Pseudomonas aeruginosa KW - Tumor Stem Cell Assay KW - Male KW - Cell Line KW - Antibodies, Monoclonal -- therapeutic use KW - Colonic Neoplasms -- therapy KW - Immunotoxins -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79165765?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-03 N1 - Date created - 1989-10-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chronic carbamazepine inhibits the development of local anesthetic seizures kindled by cocaine and lidocaine. AN - 79219926; 2790457 AB - The effects of carbamazepine (CBZ) treatment on local anesthetic-kindled seizures and lethality were evaluated in different stages of the kindling process and under different methods of CBZ administration. Chronic oral CBZ inhibited the development of both lidocaine- and cocaine-induced seizures, but had little effect on the fully developed local anesthetic seizures. Chronic CBZ also decreased the incidence of seizure-related mortality in the cocaine-injected rats. Acute CBZ over a range of doses (15-50 mg/kg) had no effect on completed lidocaine-kindled or acute cocaine-induced seizures. Repeated i.p. injection of CBZ (15 mg/kg) also was without effect on the development of lidocaine- or cocaine-kindled seizures. The differential effects of CBZ depending upon stage of seizure development suggest that distinct mechanisms underlie the development versus maintenance of local anesthetic-kindled seizures. The effectiveness of chronic but not repeated, intermittent injections of CBZ suggests that different biochemical consequences result from the different treatment regimens. The possible utility of chronic CBZ in preventing the development of toxic side effects in human cocaine users is suggested by these data, but remains to be directly evaluated. JF - Brain research AU - Weiss, S R AU - Post, R M AU - Szele, F AU - Woodward, R AU - Nierenberg, J AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1989/09/11/ PY - 1989 DA - 1989 Sep 11 SP - 72 EP - 79 VL - 497 IS - 1 SN - 0006-8993, 0006-8993 KW - Anesthetics KW - 0 KW - Anticonvulsants KW - Carbamazepine KW - 33CM23913M KW - Lidocaine KW - 98PI200987 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Dose-Response Relationship, Drug KW - Male KW - Anticonvulsants -- pharmacology KW - Kindling, Neurologic -- drug effects KW - Anesthetics -- pharmacology KW - Carbamazepine -- pharmacology KW - Lidocaine -- pharmacology KW - Cocaine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79219926?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-14 N1 - Date created - 1989-11-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The CYP2D gene subfamily: analysis of the molecular basis of the debrisoquine 4-hydroxylase deficiency in DA rats. AN - 79334117; 2819073 AB - The DA rat has been proposed as an animal model for the human debrisoquine 4-hydroxylase/bufuralol 1'-hydroxylase genetic deficiency. To determine the mechanism of this deficiency, we isolated and sequenced five cDNAs in the CYP2D gene subfamily including a new IID1 allele and two cDNAs of novel P450s, designated IID3 and IID5. IID3 and IID5 cDNA-deduced amino acid sequences contained 500 and 504 residues with calculated molecular weights of 56,683 and 57,081, respectively. IID5 displayed 20 amino acid differences with the IID1, yet bore only 72% and 76% similarity to IID2 and IID3. Despite an overall nucleotide similarity of 80-98% between the 4 cDNAs, a region of 134 nucleotides of sequence exists that contains only 1 base difference. This region is probably the result of gene conversion events between the P450 IID genes. Although all IID cDNAs were expressed into immunodetectable proteins using the COS cell SV40-based expression system, only IID1 could effectively catalyze the oxidation of the prototype substrate bufuralol. Expression of a cDNA isolated in an earlier study [Gonzalez, F. J., Matsunaga, T., Nagata, K., Meyer, U. A., Nebert, D. W., Pastewka, J., Kozak, C. A., Gillette, J., Gelboin, H. V., & Hardwick, J. P. (1987) DNA 6, 149-161], previously called db1 and now designated IID1v, produced a protein with a drastically reduced activity as compared to cDNA-expressed IID1 despite only four amino acid differences between the two cDNA-deduced protein sequences.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Biochemistry AU - Matsunaga, E AU - Zanger, U M AU - Hardwick, J P AU - Gelboin, H V AU - Meyer, U A AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/09/05/ PY - 1989 DA - 1989 Sep 05 SP - 7349 EP - 7355 VL - 28 IS - 18 SN - 0006-2960, 0006-2960 KW - RNA, Messenger KW - 0 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Mixed Function Oxygenases KW - EC 1.- KW - Cytochrome P-450 CYP2D6 KW - EC 1.14.14.1 KW - Index Medicus KW - Animals KW - Gene Conversion KW - Blotting, Northern KW - Sequence Homology, Nucleic Acid KW - Biological Evolution KW - Multigene Family KW - Disease Models, Animal KW - Amino Acid Sequence KW - Rats, Inbred Strains KW - Rats KW - Alleles KW - Base Sequence KW - Blotting, Western KW - Gene Expression Regulation, Enzymologic KW - DNA -- genetics KW - Molecular Sequence Data KW - Male KW - Aging -- genetics KW - Female KW - Cytochrome P-450 Enzyme System -- genetics KW - Mixed Function Oxygenases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79334117?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-11 N1 - Date created - 1990-01-11 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - J02869; GENBANK; J02868; J02867 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - cDNA cloning and sequence and cDNA-directed expression of human P450 IIB1: identification of a normal and two variant cDNAs derived from the CYP2B locus on chromosome 19 and differential expression of the IIB mRNAs in human liver. AN - 79332559; 2573390 AB - A cDNA designated hIIB1, representing the entire coding sequence of a P450 in the IIB gene family, was isolated from a human liver lambda gt11 library by using the rat IIB1 cDNA as a probe. The hIIB1 protein, deduced from the cDNA sequence, contained 491 amino acids, had a calculated molecular weight of 56,286, and displayed 76% amino acid similarity with the rat IIB1 protein. Expression of this cDNA, using the vaccinia virus system, yielded a P450 that had a reduced CO-binding spectrum with an absorption maximum of 452 nm. The expressed human enzyme was able to catalyze the deethylation of 7-ethoxy-coumarin. Total RNA from 13 livers was probed for levels of hIIB mRNA. Two livers had high levels, four contained moderate levels, and eight contained very low, or no detectable, mRNA. These data suggest either that defective hIIB1 genes exist in humans or that the hIIB1 gene is regulated and variably induced in our liver specimens. To search for mutant mRNA transcripts, libraries were constructed from livers expressing low levels of hIIB1 mRNA. A cDNA, designated hIIB2, was isolated that was identical with the hIIB1 cDNA except for the presence of an unusual alteration of the DNA near its 5' end corresponding to the putative exon 4. This alteration was caused by a deletion of 29 bp and an insertion of 44 bp of nonhomologous DNA. This sequence replacement occurs at the junction of the third and fourth exons as predicted from the structure of the rat IIB1 gene, suggesting that a faulty splice might have given rise to the variant hIIb2 transcript.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Biochemistry AU - Yamano, S AU - Nhamburo, P T AU - Aoyama, T AU - Meyer, U A AU - Inaba, T AU - Kalow, W AU - Gelboin, H V AU - McBride, O W AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/09/05/ PY - 1989 DA - 1989 Sep 05 SP - 7340 EP - 7348 VL - 28 IS - 18 SN - 0006-2960, 0006-2960 KW - RNA, Messenger KW - 0 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Animals KW - Chromosome Deletion KW - Sequence Homology, Nucleic Acid KW - Exons KW - Multigene Family KW - Humans KW - Amino Acid Sequence KW - Cloning, Molecular KW - Rats KW - Base Sequence KW - Polymorphism, Restriction Fragment Length KW - Adult KW - Molecular Sequence Data KW - Middle Aged KW - Repetitive Sequences, Nucleic Acid KW - Mutation KW - Female KW - Male KW - Gene Expression Regulation, Enzymologic KW - Cytochrome P-450 Enzyme System -- genetics KW - DNA -- genetics KW - Chromosomes, Human, Pair 19 KW - Liver -- metabolism KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - RNA, Messenger -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79332559?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-11 N1 - Date created - 1990-01-11 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M29873; GENBANK; M29874; J02864 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Enhancement of immunotoxin efficacy by acid-cleavable cross-linking agents utilizing diphtheria toxin and toxin mutants. AN - 79176480; 2475487 AB - We have utilized a new class of acid-cleavable protein cross-linking reagents in the construction of antibody-diphtheria toxin conjugates (Srinivaschar, K., and Neville, D. M., Jr. (1989) Biochemistry 28, 2501-2509). The potency of anti-CD5 conjugates assayed by inhibition of protein synthesis on CD5 bearing cells (Jurkat) is correlated with cross-linker hydrolytic rates. The maximum increase in potency of the cleavable conjugates over non-cleavable conventional conjugates is 50-fold and is specific for the CD5 uptake route as judged by competition with excess anti-CD5. The potency of conjugates made from diphtheria toxin and the anti-high molecular weight melanoma-associated antigen (HMW-MAA) is enhanced 3-10-fold by a cleavable cross-linker. However the potency of transferrin or anti-CD3 diphtheria toxin conjugates is only minimally enhanced (2-3-fold). Mutant diphtheria toxins, CRM103 and CRM9, previously shown to express less than 1/100 of the wild type in binding affinity were substituted into these conjugates as probes for possible intracellular toxin receptor interactions. Both mutants were equally as toxic to Jurkat target cells exhibiting 1/700 the wild-type potency. CRM9 non-cleavable conjugates were equally as potent as wild-type conjugates for transferrin and anti-CD3-mediated uptake but not for anti-CD5-mediated uptake where toxicity was reduced 60-fold over the wild-type analog. The cleavable cross-linker enhanced the toxicity of anti-CD5-CRM103 and anti-CD5-CRM9 conjugates, but potency was only 1/10 that of the analogous wild-type cleavable conjugate. These data are consistent with a model in which potentiation of toxicity of the anti-CD5 and anti-high molecular weight melanoma-associated antigen conjugates by the cleavable cross-linker occurs from an enhanced intracellular toxin-toxin receptor interaction that ultimately results in increased toxin translocation to the cytosol compartment. In contrast, these data indicate that the anti-CD3 and transferrin uptake systems do not require this interaction in agreement with previous work (Johnson, V.G., Wilson, D., Greenfield, L., and Youle, R. J. (1988) J. Biol. Chem. 263, 1295-1300). JF - The Journal of biological chemistry AU - Neville, D M AU - Srinivasachar, K AU - Stone, R AU - Scharff, J AD - Laboratory of Molecular Biology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1989/09/05/ PY - 1989 DA - 1989 Sep 05 SP - 14653 EP - 14661 VL - 264 IS - 25 SN - 0021-9258, 0021-9258 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, CD5 KW - Antigens, Differentiation KW - Antigens, Neoplasm KW - Cross-Linking Reagents KW - Diphtheria Toxin KW - Immunotoxins KW - Melanoma-Specific Antigens KW - Neoplasm Proteins KW - Protein Synthesis Inhibitors KW - Transferrin KW - Index Medicus KW - Animals KW - Antigens, Differentiation -- immunology KW - Humans KW - Hydrogen-Ion Concentration KW - Melanoma -- immunology KW - Hydrolysis KW - Molecular Weight KW - Transferrin -- metabolism KW - Protein Synthesis Inhibitors -- toxicity KW - Antibodies, Monoclonal -- toxicity KW - Transferrin -- toxicity KW - Neoplasm Proteins -- metabolism KW - Catalysis KW - Immunotoxins -- toxicity KW - Diphtheria Toxin -- toxicity KW - Diphtheria Toxin -- metabolism KW - Immunotoxins -- metabolism KW - Diphtheria Toxin -- genetics KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79176480?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-11 N1 - Date created - 1989-10-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cerebral glucose utilization in rat brain during phenobarbital withdrawal. AN - 79270961; 2804629 AB - The phenobarbital withdrawal syndrome in rats is characterized by tremors, arched back, weight loss and hyperactivity. This syndrome is shown to be associated with both general and localized increases in cerebral glucose utilization. An increase in glucose utilization (significant at the P less than or equal to 0.001 level) was observed in 72% of the 57 structures examined. Increases in glucose utilization of greater than or equal to 180% of control values were noted in structures associated with the motor system (columns in the frontal sensorimotor cortex, globus pallidus, dentate nucleus of the cerebellum and ovoid areas in the cerebellar vermis), thalamic nuclei (lateral and posterior), dorsal lateral geniculate, mammillary body, cingulate cortex, locus ceruleus, and cerebellar flocculus and paraflocculus. The structures showing the greatest increase in glucose utilization were cerebellar paraflocculus (257% of control), columns in the frontal sensorimotor cortex (247% of control) and ovoid areas in the cerebellar vermis (223% of control). Areas of the brain that have been described as cell body areas for serotonergic (raphe), noradrenergic (locus ceruleus), dopaminergic (substantia nigra, zona compacta) and GABAergic (globus pallidus) neurons also showed increases in glucose utilization. The pattern of cerebral glucose utilization accompanying the phenobarbital withdrawal syndrome in rats contrasts with that for morphine withdrawal and exhibits both similarities and differences with respect to ethanol withdrawal. JF - Brain research AU - Marietta, C A AU - Wixon, H N AU - Weight, F F AU - Eckardt, M J AD - Laboratory of Physiologic and Pharmacologic Studies, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852. Y1 - 1989/09/04/ PY - 1989 DA - 1989 Sep 04 SP - 173 EP - 179 VL - 496 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Deoxyglucose KW - 9G2MP84A8W KW - Glucose KW - IY9XDZ35W2 KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Behavior, Animal -- drug effects KW - Animals KW - Female KW - Deoxyglucose -- metabolism KW - Brain -- physiopathology KW - Substance Withdrawal Syndrome -- metabolism KW - Glucose -- metabolism KW - Brain -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79270961?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-21 N1 - Date created - 1989-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Xenobiotic metabolism in human brain--presence of cytochrome P-450 and associated mono-oxygenases. AN - 79270923; 2804643 AB - The cytochromes P-450, a family of heme proteins, play an important role in the oxidation of drugs and carcinogens, as well as endogenous substrates. We report the presence of cytochrome P-450 and associated mono-oxygenase activity in human brain regions and their selective enrichment in the brainstem. Immunocytochemical studies on human medulla with antibodies raised to phenobarbital-inducible rat liver cytochrome P-450 indicate that the enzyme is primarily localized in the neuronal cell bodies and to a lesser extent in the axons. These observations indicate that the human brain could be involved in metabolism of xenobiotics and endogenous compounds, mediated through cytochrome P-450. JF - Brain research AU - Ravindranath, V AU - Anandatheerthavarada, H K AU - Shankar, S K AD - Department of Neurochemistry, National Institute of Mental Health and Neuro Sciences, Bangalore, India. Y1 - 1989/09/04/ PY - 1989 DA - 1989 Sep 04 SP - 331 EP - 335 VL - 496 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Enzyme Inhibitors KW - 0 KW - Xenobiotics KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Mixed Function Oxygenases KW - EC 1.- KW - Index Medicus KW - Humans KW - In Vitro Techniques KW - Adult KW - Enzyme Inhibitors -- pharmacology KW - Aged KW - Middle Aged KW - Brain Stem -- enzymology KW - Brain -- enzymology KW - Mixed Function Oxygenases -- metabolism KW - Brain Stem -- metabolism KW - Xenobiotics -- metabolism KW - Cytochrome P-450 Enzyme System -- metabolism KW - Brain -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79270923?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-21 N1 - Date created - 1989-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA adducts from carcinogenic and noncarcinogenic enantiomers of benzo[a]pyrene dihydrodiol epoxide. AN - 79587672; 2519824 AB - The characterization of eight benzo[a]pyrene-deoxyribonucleoside adducts derived from reaction of the anti-dihydrodiol epoxide and deoxyguanylic and deoxyadenylic acids is described. It is reported that the epoxide ring is opened by the purine amino groups to yield similar amounts of both cis and trans products. NMR data show that the 7- and 8-hydroxyl groups are pseudodiaxial in the cis products and pseudodiequatorial in the trans products, and we suggest that these products arise from reaction with the diaxial and diequatorial conformers of the dihydrodiol epoxides, respectively. The chiral nature of the interactions of these metabolites with DNA restricts the range of products formed with this macromolecule, and a trans product with deoxyguanosine is the major product formed with either enantiomer of the anti-dihydrodiol epoxide. JF - Chemical research in toxicology AU - Cheng, S C AU - Hilton, B D AU - Roman, J M AU - Dipple, A AD - BRI-Basic Research Program, NCI-Frederick Cancer Research Facility, Maryland 21701. PY - 1989 SP - 334 EP - 340 VL - 2 IS - 5 SN - 0893-228X, 0893-228X KW - Carcinogens KW - 0 KW - Deoxyadenosines KW - 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide KW - 55097-80-8 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Stereoisomerism KW - Circular Dichroism KW - Deoxyadenosines -- chemistry KW - Chromatography, High Pressure Liquid KW - Magnetic Resonance Spectroscopy KW - DNA Damage KW - Carcinogens -- chemistry KW - DNA -- chemistry KW - 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79587672?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-09 N1 - Date created - 1992-03-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Botulinum toxin therapy in hemifacial spasm: clinical and electrophysiologic studies. AN - 79500193; 2630907 AB - Three patients with idiopathic hemifacial spasm were studied clinically and electrophysiologically before and after injections of botulinum toxin into the involved periocular and facial muscles. The spasms were improved for approximately 3 months, and the effect was repeatable on reinjection. The spasms diminished only as long as the muscles were clinically weak, and spasms were observed electromyographically even though therapy eliminated the clinical spasms. Uninjected muscles continued to have spasms. Transmission of excitation from the zygomatic branch to the marginal mandibular branch of the facial nerve and vice versa in all patients was unaltered after therapy, but the amplitude of the response was decreased. The efficacy of botulinum toxin in hemifacial spasm appears to be related to the production of muscle weakness; there is no demonstrable effect on phenomena believed to be ectopic excitation or ephaptic transmission in the facial nerve. JF - Muscle & nerve AU - Geller, B D AU - Hallett, M AU - Ravits, J AD - Division of Intramural Research, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 716 EP - 722 VL - 12 IS - 9 SN - 0148-639X, 0148-639X KW - Botulinum Toxins KW - EC 3.4.24.69 KW - Index Medicus KW - Neuromuscular Junction -- drug effects KW - Humans KW - Injections, Intramuscular KW - Adult KW - Electromyography KW - Middle Aged KW - Female KW - Facial Muscles -- drug effects KW - Botulinum Toxins -- therapeutic use KW - Spasm -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79500193?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-05-08 N1 - Date created - 1990-05-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chemoprevention and modern cancer prevention. AN - 79447395; 2694155 AB - Chemoprevention is a new area of research emphasis in cancer control. The rationale is based on the accumulation of laboratory and epidemiological data indicating that various agents may halt or reverse cancer progression in animals and may reduce risks in humans. For planning purposes, research leads are submitted to a strategic system of staging with defined criteria and decision points. A research lead that enters an intervention stage must evolve through a series of phases of testing and evaluation. Human intervention clinical trials have begun to test the hypothesis that certain agents can lower cancer incidence. JF - Preventive medicine AU - Malone, W F AU - Kelloff, G J AU - Boone, C AU - Nixon, D W AD - Division of Cancer Prevention and Control, National Cancer Institute, Bethesda, Maryland 20852-4200. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 553 EP - 561 VL - 18 IS - 5 SN - 0091-7435, 0091-7435 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Clinical Trials as Topic KW - Drug Evaluation, Preclinical KW - Neoplasms -- drug therapy KW - Antineoplastic Agents -- toxicity KW - Neoplasms -- prevention & control KW - Antineoplastic Agents -- therapeutic use KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79447395?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-05 N1 - Date created - 1990-03-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Some statistical considerations for design of cancer prevention trials. AN - 79447264; 2694163 AB - Carcinogenesis is believed to occur in at least two stages, initiation and promotion, followed by a preneoplastic lesion which develops into cancer. Cancer prevention trials can be classified as primary if the intervention precedes initiation, secondary if it occurs during promotion, and tertiary if it is applied to a preneoplastic lesion. Tertiary prevention trials resemble treatment trials, but primary and secondary prevention trials may be very different in size, duration, and cost. After reviewing some basic questions which must be addressed in designing any cancer prevention trial, some special design considerations appropriate for primary and secondary prevention trials are discussed. These include the use of factorial designs, group or cluster randomization, special sample size calculations needed for large-scale trials of long duration with cancer incidence as the endpoint, and the idea of the case-cohort approach for monitoring and for subsequent exploratory analysis of trial data. JF - Preventive medicine AU - Byar, D P AD - Division of Cancer Prevention and Control, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 688 EP - 699 VL - 18 IS - 5 SN - 0091-7435, 0091-7435 KW - Index Medicus KW - Animals KW - Factor Analysis, Statistical KW - Random Allocation KW - Humans KW - Clinical Trials as Topic KW - Case-Control Studies KW - Cluster Analysis KW - Research Design -- statistics & numerical data KW - Neoplasms -- epidemiology KW - Neoplasms -- prevention & control KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79447264?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-05 N1 - Date created - 1990-03-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human CYP1A2: sequence, gene structure, comparison with the mouse and rat orthologous gene, and differences in liver 1A2 mRNA expression. AN - 79416501; 2575218 AB - We have sequenced the human CYP1A2 (cytochrome P(3)450) gene, 1,906 basepairs (bp) of the 5' flanking region, and 113 bp of the 3' flanking region. The gene spans almost 7.8 kilobases, comprising seven exons and six introns. The transcriptional start site was determined by both primer extension and S1 mapping. Including the first noncoding exon of 55 bp, the entire mRNA is 3,121 bp in length, and the open reading frame, starting with nucleotide 10 of exon 2, encodes 515 amino acids (mol wt = 58,294). Between the human CYP1A2 and CYP1A1 (cytochrome P(1)450) genes, exons 2, 4, 6, and especially 5 are strikingly conserved in both nucleotide similarity and total number of bases. Alignment of the upstream sequences and exon 1 of human CYP1A2 with that of mouse or rat CYP1A2 revealed two possibly significant regions of similarity: 1) 68% in the approximately 150 bases immediately 5' from the mRNA cap site and 2) 80% identify between the human -841 to -758 segment and the mouse -1,529 to -1,439 segment. The canonical 5-bp box (CACGC), found upstream of all mammalian CYP1A1 genes to date and believed to interact with the inducer.aromatic hydrocarbon receptor complex, was not found on either strand in the 1,906 bp of the 5' flanking region of human CYP1A2. In contrast, alignment of the upstream sequences, exon 1, and intron 1 of human CYP1A1 with that of mouse or rat CYP1A1 revealed large, highly conserved regions. Conserved regions were found in intron 1 of the human, mouse, and rat CYP1A2 gene. These data suggest that the regulatory elements controlling the CYP1A2 gene might differ in location from those controlling the CYP1A1 gene. Among 12 human liver samples, striking differences (greater than 15-fold) in the 3.3-kilobase 1A2 mRNA levels were seen. This result may reflect significant genetic differences in constitutive and/or inducible CYP1A2 gene expression that could play an important role in individual risk of environmental toxicity or cancer. JF - Molecular endocrinology (Baltimore, Md.) AU - Ikeya, K AU - Jaiswal, A K AU - Owens, R A AU - Jones, J E AU - Nebert, D W AU - Kimura, S AD - Laboratory of Developmental Pharmacology, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 1399 EP - 1408 VL - 3 IS - 9 SN - 0888-8809, 0888-8809 KW - RNA, Messenger KW - 0 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Animals KW - Blotting, Northern KW - Sequence Homology, Nucleic Acid KW - Exons KW - Humans KW - RNA, Messenger -- analysis KW - Mice KW - Cloning, Molecular KW - Rats KW - Base Sequence KW - Polymorphism, Restriction Fragment Length KW - Restriction Mapping KW - In Vitro Techniques KW - Introns KW - Molecular Sequence Data KW - Cytochrome P-450 Enzyme System -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79416501?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-15 N1 - Date created - 1990-02-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Neoplastic transformation of human epithelial cells in vitro. AN - 79359004; 2686534 AB - Efforts to investigate the progression of events that lead human cells of epithelial origin to become neoplastic in response to carcinogenic agents have been aided by the development of tissue culture systems for propagation of epithelial cells. We have recently developed an in vitro multistep model suitable for the study of human epithelial cell carcinogenesis. Primary human epidermal keratinocytes acquired indefinite lifespan in culture but did not undergo malignant conversion in response to infection with Adl2-SV40 virus. Subsequent addition of Ki-MSV, which contains a K-ras oncogene, to these cells induced morphological alterations and the acquisition of neoplastic properties. Nontumorigenic human epidermal keratinocytes immortalized by Adl2-SV40 virus (RHEK-1) were also transformed by treatment with chemical carcinogens (MNNG or 4NQO) and by X-ray irradiation. Such transformants showed morphological alterations and induced carcinomas when transplanted into nude mice. This in vitro system may be useful in assessing environmental carcinogens for human epithelial cells and in detecting new human oncogenes since ras oncogenes were not activated in these chemical--or X-ray--transformed RHEK-1 lines. Subsequently, it was found that this line could be transformed neoplastically by a variety of retroviruses containing H-ras, bas, fes, fms, erbB and src oncogenes. In addition, our recent results indicate that nontumorigenic RHEK-1 cells can be transformed following transfection with an activated human oncogene. Thus, this in vitro system may be useful in studying the interaction of a variety of carcinogenic agents and human epithelial cells. These findings demonstrate the malignant transformation of human primary epithelial cells in culture by the combined action of tumor viruses and chemical carcinogens or X-ray irradiation and support a multistep process for neoplastic conversion. Further, evidence for the multistep nature of neoplastic transformation of human epithelial cells in vitro using other model systems is presented. JF - Anticancer research AU - Rhim, J S AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892. PY - 1989 SP - 1345 EP - 1365 VL - 9 IS - 5 SN - 0250-7005, 0250-7005 KW - Index Medicus KW - Epithelial Cells KW - Cells, Cultured KW - Humans KW - Keratinocytes -- cytology KW - Retroviridae -- genetics KW - Cell Line KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79359004?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-03 N1 - Date created - 1990-01-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Time course of verapamil interaction with morphine effects on physiological parameters in rats. AN - 79344040; 2573706 AB - The effects of subcutaneous doses of morphine and verapamil on respiratory and cardiovascular parameters have been assessed in conscious rats. Verapamil (10 mg kg-1) was injected simultaneously with morphine (16 mg kg-1) or at 10, 30, or 60 min before morphine administration. Morphine induced respiratory depression, as indicated by marked hypercapnia, hypoxia and acidosis, and caused marked tachycardia. Although morphine produced only a minor and inconsistent (but statistically significant, P less than 0.01) reduction of mean arterial blood pressure, morphine potentiated verapamil-induced hypotension. Verapamil suppressed morphine-induced hypercapnia only when injected simultaneously with morphine. Verapamil alone did not affect arterial blood gases or pH, but decreased heart rate and mean arterial blood pressure. Verapamil attenuated and delayed the maximum positive chronotropic effects of morphine at all times tested. Antagonism by verapamil of respiratory depression and tachycardia produced by morphine was unrelated to morphine levels in plasma. Thus, the explanation of verapamil-morphine interactions on respiration and cardiovascular function is not pharmacokinetic. JF - The Journal of pharmacy and pharmacology AU - Della Puppa, A AU - Ford-Rice, F AU - Snyder, F R AU - Cone, E AU - London, E D AD - Neuropharmacology Laboratory, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 617 EP - 623 VL - 41 IS - 9 SN - 0022-3573, 0022-3573 KW - Carbon Dioxide KW - 142M471B3J KW - Morphine KW - 76I7G6D29C KW - Verapamil KW - CJ0O37KU29 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Oxygen Consumption -- drug effects KW - Heart Rate -- drug effects KW - Drug Interactions KW - Blood Pressure -- drug effects KW - Time Factors KW - Carbon Dioxide -- blood KW - Male KW - Morphine -- pharmacokinetics KW - Verapamil -- pharmacokinetics KW - Verapamil -- pharmacology KW - Morphine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79344040?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-08 N1 - Date created - 1990-01-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Magnetic resonance imaging studies of the brains of anesthetized rats treated with manganese chloride. AN - 79331668; 2819480 AB - An understanding of the distribution of manganese ions in the brain is of interest in connection with the development of an understanding of the neurotoxicity of this element. Information about the time dependent biodistribution of manganese ions in the brains of intact rats subsequent to single IP injections of MnCl2 has been obtained from magnetic resonance imaging (MRI) studies. The enhanced MRI contrast is based on the reduction in the spin lattice relaxation time (T1) of water protons which exchange into the coordination sphere of the manganese ions. These studies indicate rapid and significant accumulations of water accessible manganese in the ventricles, the pineal gland, and the pituitary gland. The rapid appearance of high levels of manganese in the ventricular cerebrospinal fluid indicates that manganese readily crosses the filtration barrier of the choroid plexus and is thereafter apparently absorbed by the ependymal surfaces of the ventricles and transported to the subarachnoid space. JF - Brain research bulletin AU - London, R E AU - Toney, G AU - Gabel, S A AU - Funk, A AD - National Institute of Environmental Health Sciences, NIH, Res. Triangle Park, NC 27709. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 229 EP - 235 VL - 23 IS - 3 SN - 0361-9230, 0361-9230 KW - Chlorides KW - 0 KW - Manganese Compounds KW - Manganese KW - 42Z2K6ZL8P KW - manganese chloride KW - QQE170PANO KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Magnetic Resonance Imaging KW - Animals KW - Pineal Gland -- metabolism KW - Anesthesia KW - Cerebral Ventricles -- metabolism KW - Pituitary Gland -- metabolism KW - Male KW - Blood-Brain Barrier KW - Brain -- metabolism KW - Manganese -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79331668?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-03 N1 - Date created - 1990-01-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Purification, toxicity, and antiendotoxin activity of polymyxin B nonapeptide. AN - 79330340; 2554795 AB - Polymyxin B, a relatively toxic antibiotic, has potent endotoxin-neutralizing properties that may be beneficial as adjunctive therapy in gram-negative sepsis. Polymyxin B nonapeptide (deacylated polymyxin B) is devoid of antibiotic activity but retains the capacity to disorganize the outer membrane of gram-negative bacteria. To evaluate the potential therapeutic usefulness of this derivative, we produced purified polymyxin B nonapeptide, tested its in vivo toxicity in animals, and evaluated its in vitro antiendotoxin activity. Effectiveness as an antiendotoxin agent was assessed by examining the ability of polymyxin B nonapeptide to block the enhanced release of toxic oxygen radicals induced by lipopolysaccharide in human neutrophils (priming). In vivo, at doses of 1.5 and 3.0 mg/kg, polymyxin B nonapeptide did not exhibit the neuromuscular blocking, neurotoxic, or nephrotoxic effects that were observed with polymyxin B sulfate. Both polymyxin B and polymyxin B nonapeptide inhibited lipopolysaccharide-induced neutrophil priming in a concentration-dependent manner, but the parent compound, polymyxin B, was 63 times more effective on a weight basis. The inhibitory activity of both compounds, however, diminished rapidly when they were added after the start of the lipopolysaccharide-neutrophil incubation. We conclude that polymyxin B nonapeptide is less toxic than polymyxin B and, at the doses tested, lacks the neurotoxicity and nephrotoxicity of the parent compound. Polymyxin B nonapeptide retains the antiendotoxin activity of polymyxin B but is much less potent. The findings suggest that these compounds block an early step in the neutrophil priming process, possibly lipopolysaccharide attachment to or insertion into the neutrophil membrane. JF - Antimicrobial agents and chemotherapy AU - Danner, R L AU - Joiner, K A AU - Rubin, M AU - Patterson, W H AU - Johnson, N AU - Ayers, K M AU - Parrillo, J E AD - Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 1428 EP - 1434 VL - 33 IS - 9 SN - 0066-4804, 0066-4804 KW - Indicators and Reagents KW - 0 KW - Lipopolysaccharides KW - Polymyxins KW - Superoxides KW - 11062-77-4 KW - Polymyxin B KW - 1404-26-8 KW - polymyxin B nonapeptide KW - 86408-36-8 KW - Index Medicus KW - Animals KW - Humans KW - Lipopolysaccharides -- metabolism KW - Spectrophotometry, Ultraviolet KW - Chromatography, High Pressure Liquid KW - Rats, Inbred Strains KW - Neutrophils -- drug effects KW - Neutrophils -- metabolism KW - Rats KW - Superoxides -- metabolism KW - In Vitro Techniques KW - Dogs KW - Chromatography, Thin Layer KW - Polymyxins -- isolation & purification KW - Polymyxins -- toxicity KW - Polymyxins -- metabolism KW - Polymyxins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79330340?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-12 N1 - Date created - 1989-12-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Infect Dis. 1977 Oct;136(4):469-74 [198485] J Exp Med. 1965 Aug 1;122:207-35 [14316942] Infect Immun. 1979 Mar;23(3):660-4 [222676] Am J Med. 1980 Mar;68(3):332-43 [6987870] Infect Immun. 1981 Jul;33(1):315-8 [6266967] Br J Pharmacol. 1981 Nov;74(3):701-7 [6170378] Infect Immun. 1982 May;36(2):548-57 [6282752] J Immunol Methods. 1982 Aug 13;52(3):333-40 [6290568] N Engl J Med. 1982 Nov 11;307(20):1225-30 [6752708] Biochem Biophys Res Commun. 1982 Dec 31;109(4):1129-33 [6301427] Nature. 1983 Jun 9-15;303(5917):526-8 [6406904] Rev Infect Dis. 1983 Jul-Aug;5(4):629-38 [6353525] Antimicrob Agents Chemother. 1983 Jul;24(1):107-13 [6414364] Antimicrob Agents Chemother. 1983 Jul;24(1):114-22 [6194743] J Immunol. 1984 May;132(5):2582-9 [6325539] Antimicrob Agents Chemother. 1984 Jun;25(6):701-5 [6331296] J Infect Dis. 1984 Sep;150(3):380-8 [6384378] J Exp Med. 1984 Dec 1;160(6):1656-71 [6096475] J Infect Dis. 1985 Jun;151(6):1012-8 [3889171] Antimicrob Agents Chemother. 1985 Apr;27(4):548-54 [2988430] Invest Urol. 1969 Mar;6(5):505-19 [4304849] Ann Intern Med. 1970 Jun;72(6):857-68 [5448745] J Lab Clin Med. 1971 May;77(5):802-10 [4326749] Biochem Biophys Res Commun. 1985 May 16;128(3):1364-72 [2988537] Antimicrob Agents Chemother. 1985 Jul;28(1):107-12 [2412488] FEBS Lett. 1985 Dec 2;193(2):227-30 [2998882] Infect Immun. 1971 Nov;4(5):563-6 [4343409] J Clin Invest. 1973 Mar;52(3):741-4 [4346473] J Pharmacol Exp Ther. 1973 Mar;184(3):757-65 [4347051] JAMA. 1974 Mar 4;227(9):1023-8 [4405926] Surg Gynecol Obstet. 1974 May;138(5):755-9 [4362912] N Engl J Med. 1974 Oct 3;291(14):733-4 [4851512] J Clin Invest. 1975 Jun;55(6):1357-72 [166094] J Infect Dis. 1975 Sep;132(3):316-35 [1159333] Immunochemistry. 1976 Oct;13(10):813-8 [187544] Antimicrob Agents Chemother. 1986 Mar;29(3):496-500 [3013085] Antimicrob Agents Chemother. 1986 Aug;30(2):340-1 [3021053] J Clin Invest. 1987 Sep;80(3):605-12 [3624479] J Infect Dis. 1987 Nov;156(5):706-12 [2821123] J Infect Dis. 1988 Mar;157(3):565-8 [3343526] Biochim Biophys Acta. 1959 Jul;34:255-6 [14422133] Pediatr Res. 1979 Jan;13(1):48-51 [219410] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The role of neuronal energy in the neurotoxicity of excitatory amino acids. AN - 79303906; 2572985 AB - Excitatory amino acids, acting at receptors such as the N-methyl-D-aspartate (NMDA) subtype, are good candidates for a major role in the neuronal death characteristic of Alzheimer's disease. Recent evidence from studies with cultured neurons suggests that perturbations in the energy metabolism of the neuron may be involved in the transition of NMDA agonists from neurotransmitters to neurotoxins via a mechanism that involves relief of the voltage-dependent Mg++ block of the NMDA channel. JF - Neurobiology of aging AU - Henneberry, R C AD - Laboratory of Molecular Biology, NINDS, Bethesda, MD 20892. PY - 1989 SP - 611 EP - 3; discussion 618-20 VL - 10 IS - 5 SN - 0197-4580, 0197-4580 KW - Glutamates KW - 0 KW - Receptors, N-Methyl-D-Aspartate KW - Receptors, Neurotransmitter KW - Glutamic Acid KW - 3KX376GY7L KW - Index Medicus KW - Animals KW - Humans KW - Receptors, Neurotransmitter -- metabolism KW - Glutamates -- metabolism KW - Alzheimer Disease -- metabolism KW - Glutamates -- toxicity KW - Energy Metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79303906?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-18 N1 - Date created - 1989-12-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differentiation of PC12 cells with v-src: comparison with nerve growth factor. AN - 79293162; 2810396 AB - The PC12 rat pheochromocytoma cell line is used extensively as a model to study neuronal differentiation. These cells resemble adrenal chromaffin cells, differentiating both morphologically and biochemically when cultured in the presence of dexamethasone, but develop a sympathetic neuron-like phenotype when cultured in the presence of nerve growth factor. Expression of the protein product of the v-src oncogene in PC12 cells also induces neurite outgrowth similar to that resulting from nerve growth factor treatment (Alema et al: Nature 316:557-559, 1985). It is thus possible that c-src or a src-like tyrosine kinase participates in the signal transduction pathway by which nerve growth factor acts on PC12 cells. In this study a temperature-sensitive v-src gene has been introduced into PC12 cells. When cultures of these src-transformed cells are switched from the nonpermissive (40 degrees C) to the permissive (37 degrees C) temperature they elaborate neurites. The differentiation induced by src has been compared with that induced by nerve growth factor by determining whether src-transformed PC12 cells at 37 degrees C exhibit the same biochemical alterations as those induced in PC12 cells treated with nerve growth factor. Neurite extension at 37 degrees C in v-src-transformed cells, like NGF-induced differentiation, is accompanied by an increase in the nerve growth factor-inducible large external (NILE) protein. However, neurite extension in v-src-transformed cells is not blocked by the protein kinase inhibitor K-252a, which completely blocks NGF-induced neurite extension. Likewise, EGF receptor down-regulation and the development of saxitoxin and tetanus toxin binding sites are either much reduced or completely absent in src-differentiated compared with NGF-differentiated PC12 cells. JF - Journal of neuroscience research AU - Rausch, D M AU - Dickens, G AU - Doll, S AU - Fujita, K AU - Koizumi, S AU - Rudkin, B B AU - Tocco, M AU - Eiden, L E AU - Guroff, G AD - Unit on Molecular and Cellular Neurobiology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 49 EP - 58 VL - 24 IS - 1 SN - 0360-4012, 0360-4012 KW - Amphibian Proteins KW - 0 KW - Carbazoles KW - Carrier Proteins KW - Indole Alkaloids KW - Membrane Glycoproteins KW - Nerve Growth Factors KW - Neural Cell Adhesion Molecule L1 KW - Tetanus Toxin KW - saxitoxin-binding protein, Rana catesbeiana KW - Saxitoxin KW - 35523-89-8 KW - staurosporine aglycone KW - 97161-97-2 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Animals KW - Receptor, Epidermal Growth Factor -- metabolism KW - Carrier Proteins -- metabolism KW - Cell Differentiation KW - Saxitoxin -- metabolism KW - Pheochromocytoma KW - Rats KW - Phenotype KW - Adrenal Gland Neoplasms KW - Membrane Glycoproteins -- biosynthesis KW - Binding, Competitive KW - Tetanus Toxin -- metabolism KW - Carbazoles -- pharmacology KW - Retroviridae -- genetics KW - Tumor Cells, Cultured -- cytology KW - Neurons -- cytology KW - Oncogenes -- physiology KW - Nerve Growth Factors -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79293162?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-18 N1 - Date created - 1989-12-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Influence of viral infections on body weight, survival, and tumor prevalence in Fischer 344/NCr rats on two-year studies. AN - 79293019; 2554057 AB - Sendai virus (SV), pneumonia virus of mice (PVM), and rat coronavirus/sialodacryoadenitis virus (RCV/SDAV) were common viral infections of rats in the National Cancer Institute-National Toxicology Program (NCI-NTP) studies from 1977 to 1983. Influence of these viral infections on body weight, survival, and prevalences of spontaneous tumors in the F344/NCr rats of 28 diet control groups at five different laboratories were evaluated. Tumor prevalences evaluated in this investigation included the following: leukemia and tumors of the anterior pituitary, lungs, salivary glands and Harderian glands in both sexes; adrenal pheochromocytomas in male rats; and mammary tumors in female rats. SV and PVM but not RCV/SDAV infections were associated with significant (P less than 0.05) decreases in body weights of male and female rats. Male rat groups with PVM infection had a lower prevalence of leukemia and male rat groups with RCV/SDAV infection had a higher prevalence of anterior pituitary tumors than the corresponding uninfected groups. Female rat groups with SV infection had greater survival and a higher prevalence of lung tumors than groups without SV infection. However, none of the tumor prevalence and survival differences were statistically significant when interlaboratory variability and time-related effects were taken into account. JF - Laboratory animal science AU - Rao, G N AU - Haseman, J K AU - Edmondson, J AD - Division of Toxicology Research and Testing, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 389 EP - 393 VL - 39 IS - 5 SN - 0023-6764, 0023-6764 KW - Index Medicus KW - Rats KW - Body Weight KW - Animals KW - Rats, Inbred F344 KW - Parainfluenza Virus 1, Human KW - Male KW - Female KW - Neoplasms -- veterinary KW - Respirovirus Infections -- physiopathology KW - Coronaviridae Infections -- epidemiology KW - Respirovirus Infections -- veterinary KW - Coronaviridae Infections -- physiopathology KW - Rodent Diseases -- epidemiology KW - Paramyxoviridae Infections -- veterinary KW - Neoplasms -- epidemiology KW - Coronaviridae Infections -- veterinary KW - Rodent Diseases -- physiopathology KW - Paramyxoviridae Infections -- epidemiology KW - Respirovirus Infections -- epidemiology KW - Paramyxoviridae Infections -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79293019?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-27 N1 - Date created - 1989-11-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The failure of intravenous cyclophosphamide therapy in refractory idiopathic inflammatory myopathy. AN - 79292383; 2681763 AB - Eleven patients with idiopathic inflammatory myopathy refractory to treatment with corticosteroids and other immunosuppressive agents were treated with monthly intravenous cyclophosphamide (0.75-1.357 g/m2). Six patients completed a full course of 7 infusions at which point only one patient met predefined criteria for improvement in both strength and function. Five had modest improvement in strength but did not meet the criteria for improvement. All patients have subsequently required treatment with other medications. Major complications observed during therapy included serious infections in 2 patients (streptococcal endocarditis and disseminated Mycobacterium avium intracellulare) and death in one patient in which the contribution of cyclophosphamide cannot be excluded. We conclude that intravenous cyclophosphamide as used in our study cannot be recommended for the treatment of patients with refractory inflammatory myopathy. JF - The Journal of rheumatology AU - Cronin, M E AU - Miller, F W AU - Hicks, J E AU - Dalakas, M AU - Plotz, P H AD - Arthritis and Rheumatism Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, MD 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 1225 EP - 1228 VL - 16 IS - 9 SN - 0315-162X, 0315-162X KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - Infection -- etiology KW - Infusions, Intravenous KW - Humans KW - Adult KW - Clinical Trials as Topic KW - Aged KW - Middle Aged KW - Cardiomyopathies -- chemically induced KW - Male KW - Female KW - Cyclophosphamide -- administration & dosage KW - Myositis -- drug therapy KW - Cyclophosphamide -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79292383?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-07 N1 - Date created - 1989-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human selenite metabolism: a kinetic model. AN - 79214090; 2551194 AB - A model is developed to describe the kinetics of sodium selenite metabolism in humans, based on plasma, urine, and fecal samples obtained from six subjects over a 4-wk period after a single oral 200-micrograms dose of the enriched stable isotope tracer 74Se. The model describes absorption, distributed along the gastrointestinal tract, and enterohepatic recirculation. The model includes four kinetically distinct plasma components, a subsystem consisting of the liver and pancreas, and a slowly turning-over tissue pool. For the six subjects, the ranges of mean residence times for the four plasma components are, respectively, 0.2-1.1 h, 3-8 h, 9-42 h, and 200-285 h; for the hepatopancreatic subsystem 4-41 days; and for the tissue pool 115-285 days. Approximately 84% of the administered dose was absorbed, and after 12 days approximately 65% remained in the body. The model predicts that after 90 days approximately 35% of this Se would be retained, primarily in the tissues. Separating Se metabolism into several distinct kinetic components is a first step in identifying the efficacious, nutritious, and toxic forms of the element. JF - The American journal of physiology AU - Patterson, B H AU - Levander, O A AU - Helzlsouer, K AU - McAdam, P A AU - Lewis, S A AU - Taylor, P R AU - Veillon, C AU - Zech, L A AD - Biometry Branch, National Institutes of Health, Bethesda 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - R556 EP - R567 VL - 257 IS - 3 Pt 2 SN - 0002-9513, 0002-9513 KW - Selenium KW - H6241UJ22B KW - Sodium Selenite KW - HIW548RQ3W KW - Index Medicus KW - Feces -- metabolism KW - Kinetics KW - Humans KW - Male KW - Female KW - Selenium -- blood KW - Selenium -- pharmacokinetics KW - Selenium -- urine KW - Models, Biological UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79214090?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-17 N1 - Date created - 1989-10-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Impaired production of nerve growth factor in the submandibular gland of diabetic mice. AN - 79213747; 2528912 AB - The production of nerve growth factor (NGF) in submandibular glands was examined in two kinds of diabetic mice. In genetically diabetic (C57BL/KsJ db/db) mice, which manifest marked insulin resistance and hyperglycemia, the concentration of NGF in the submandibular gland was less than one-tenth that of the nondiabetic controls. In streptozotocin-induced diabetic C57BL/KsJ mice, which show pancreatic insulitis leading to insulin deficiency and hyperglycemia, the glandular NGF concentration fell in a time-dependent manner to 26% of control level at 5 wk after the streptozotocin injection. A daily administration of insulin to the streptozotocin-induced diabetic mice restored the NGF concentration to almost the control level. The molecular size of NGF (13 kDa) in the glandular extracts of the genetically diabetic (db/db) mice in Western blots was indistinguishable from that of the control mice, but its level was reduced in the glands of the diabetic (db/db) animals. Although plasma NGF concentrations were normally below the sensitivity of the assay (less than 0.80 ng/ml) in both the control and the diabetic (db/db) mice, administration of cyclocytidine, which stimulates NGF release from the submandibular gland into the blood circulation, increased the plasma NGF level to 5.95 ng/ml in the control mice, but it failed to do so in the diabetic (db/db) mice. These findings suggest that, in diabetic mice, NGF production in the submandibular gland and its capacity to release NGF into the circulation are decreased. JF - The American journal of physiology AU - Kasayama, S AU - Oka, T AD - Laboratory of Molecular and Cellular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - E400 EP - E404 VL - 257 IS - 3 Pt 1 SN - 0002-9513, 0002-9513 KW - Insulin KW - 0 KW - Nerve Growth Factors KW - Streptozocin KW - 5W494URQ81 KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Insulin -- deficiency KW - Hyperglycemia -- metabolism KW - Mice KW - Insulin -- pharmacology KW - Islets of Langerhans -- pathology KW - Male KW - Cell Survival KW - Nerve Growth Factors -- metabolism KW - Diabetes Mellitus, Experimental -- genetics KW - Submandibular Gland -- metabolism KW - Diabetes Mellitus, Experimental -- metabolism KW - Diabetes Mellitus, Experimental -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79213747?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-18 N1 - Date created - 1989-10-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of buprenorphine in the treatment of opiate addiction. I. Physiologic and behavioral effects during a rapid dose induction. AN - 79213440; 2776393 AB - A new, rapid dose-induction procedure was used in the evaluation of buprenorphine hydrochloride (buprenorphine) as a treatment for opiate dependence. Nineteen heroin-dependent men were given buprenorphine sublingually in ascending daily doses of 2, 4, and 8 mg and then maintained on 8 mg daily. The observations of the transition from heroin to buprenorphine for the first 4 days are described. During this period, subjects reported significantly elevated ratings of "good effects" and feelings of "overall well-being" and decreased ratings of "overall sickness." Data from subscales of the Addiction Research Center Inventory indicated increasing euphoria and decreasing dysphoria and sedation after buprenorphine administration. Subjects and observers consistently identified buprenorphine as an opiate and not as an opiate antagonist. These findings indicate that a rapid dose induction with buprenorphine is acceptable to heroin-dependent persons and that it causes minimal withdrawal symptoms. JF - Clinical pharmacology and therapeutics AU - Johnson, R E AU - Cone, E J AU - Henningfield, J E AU - Fudala, P J AD - National Institute on Drug Abuse, Addiction Research Center, Francis Scott Key Medical Center, Baltimore, MD 21224. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 335 EP - 343 VL - 46 IS - 3 SN - 0009-9236, 0009-9236 KW - Buprenorphine KW - 40D3SCR4GZ KW - Abridged Index Medicus KW - Index Medicus KW - Pupil -- drug effects KW - Humans KW - Adult KW - Surveys and Questionnaires KW - Middle Aged KW - Blood Pressure -- drug effects KW - Pulse -- drug effects KW - Time Factors KW - Administration, Sublingual KW - Male KW - Buprenorphine -- therapeutic use KW - Heroin Dependence -- physiopathology KW - Buprenorphine -- administration & dosage KW - Heroin Dependence -- rehabilitation KW - Heroin Dependence -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79213440?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-20 N1 - Date created - 1989-10-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - T-type calcium channels mediate the transition between tonic and phasic firing in thalamic neurons. AN - 79212547; 2550936 AB - Thalamic neurons undergo a shift from tonic to phasic (burst) firing upon hyperpolarization. This state transition results from deinactivation of a regenerative depolarizing event referred to as the low-threshold spike. Isolated adult guinea pig thalamic (dorsal lateral geniculate) neurons exhibited low-threshold spikes that could be blocked by low concentrations of nickel but were unaffected by the dihydropyridine nimodipine. Whole-cell voltage-clamp recordings from these cells demonstrated a low-threshold, rapidly inactivating (T) Ca2+ current that manifested similar voltage dependency and time course as the low-threshold spike. Like low-threshold spikes, the T-type Ca2+ current was eliminated by nickel but was unaffected by nimodipine. In thalamic neurons, T-type Ca2+ channels underlie the low-threshold spike and, therefore, play a critical role in regulating the firing pattern of these cells. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Suzuki, S AU - Rogawski, M A AD - Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 7228 EP - 7232 VL - 86 IS - 18 SN - 0027-8424, 0027-8424 KW - Calcium Channels KW - 0 KW - Tetrodotoxin KW - 4368-28-9 KW - Nimodipine KW - 57WA9QZ5WH KW - Nickel KW - 7OV03QG267 KW - Index Medicus KW - Animals KW - Electric Conductivity KW - Nickel -- pharmacology KW - Guinea Pigs KW - Nimodipine -- pharmacology KW - In Vitro Techniques KW - Membrane Potentials KW - Tetrodotoxin -- pharmacology KW - Calcium Channels -- physiology KW - Calcium Channels -- drug effects KW - Neurons -- physiology KW - Geniculate Bodies -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79212547?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-24 N1 - Date created - 1989-10-24 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Circ Res. 1986 Aug;59(2):229-35 [2427250] J Physiol. 1989 Apr;411:161-77 [2482353] Science. 1987 Feb 6;235(4789):680-2 [2433765] Soc Gen Physiol Ser. 1987;41:167-87 [2436308] Proc Natl Acad Sci U S A. 1987 Jun;84(12):4327-31 [2438698] J Physiol. 1987 Feb;383:231-49 [2443646] J Physiol. 1987 May;386:547-70 [2445968] J Physiol. 1987 May;386:571-601 [2445969] Neurosci Lett. 1987 Oct 16;81(1-2):117-22 [3696461] J Physiol. 1987 Dec;394:149-72 [2451016] J Comp Neurol. 1975 Jan 1;159(1):45-67 [45862] Nature. 1980 Jul 24;286(5771):391-3 [7402320] J Physiol. 1981 Jun;315:569-84 [7310722] J Physiol. 1983 Apr;337:303-20 [6875932] Nature. 1984 Mar 15-21;308(5956):282-4 [6608056] J Neurophysiol. 1984 Jun;51(6):1196-219 [6737028] J Physiol. 1984 Apr;349:205-26 [6737292] J Physiol. 1984 Apr;349:227-47 [6737293] Circ Res. 1984 Sep;55(3):336-48 [6088117] Proc Natl Acad Sci U S A. 1984 Oct;81(20):6388-92 [6093100] Brain Res. 1984 Nov;320(1):1-63 [6440659] J Physiol. 1985 Feb;359:431-46 [2582115] Pflugers Arch. 1985 Apr;403(4):360-8 [2409515] Nature. 1985 Aug 1-7;316(6027):440-3 [2410796] Nature. 1985 Aug 1-7;316(6027):443-6 [2410797] J Gen Physiol. 1985 Jul;86(1):1-30 [2411846] Pflugers Arch. 1985 Jul;404(3):259-65 [2412202] J Gen Physiol. 1986 Jan;87(1):161-82 [2419479] J Neurophysiol. 1986 Mar;55(3):527-39 [2420945] Brain Res. 1986 Feb 26;366(1-2):262-71 [2421822] J Neurosci Methods. 1986 May;16(3):227-38 [3523050] Proc Natl Acad Sci U S A. 1986 Jul;83(14):5340-4 [2425366] Exp Brain Res. 1986;63(1):1-20 [3015651] J Physiol. 1987 Dec;394:173-200 [2451017] J Mol Biol. 1988 Feb 5;199(3):491-502 [2965250] Science. 1988 Apr 8;240(4849):213-5 [2451291] J Physiol. 1987 Nov;392:603-16 [2451732] Ann N Y Acad Sci. 1988;522:16-24 [2454050] Physiol Rev. 1988 Jul;68(3):649-742 [2839857] Neuroscience. 1988 May;25(2):503-12 [3399056] J Neurophysiol. 1988 Jun;59(6):1854-70 [3404208] Science. 1988 Dec 23;242(4886):1654-64 [3059497] Annu Rev Physiol. 1989;51:367-84 [2540697] J Neurophysiol. 1989 Jun;61(6):1270-83 [2501459] J Physiol. 1989 Jul;414:587-604 [2607443] Science. 1987 Jan 2;235(4784):46-52 [2432656] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mono-2-ethylhexyl phthalate, a metabolite of di-(2-ethylhexyl) phthalate, causally linked to testicular atrophy in rats. AN - 79210471; 2781553 AB - Acute testicular atrophy results when appropriate dosages of di-(2-ethylhexyl) phthalate (DEHP) or its hydrolysis product mono-2-ethylhexyl phthalate (MEHP) are given to male rats. Events thought to be involved in this pathological effect also occur in cultures of testicular cells in vitro, but require MEHP rather than DEHP. Primary cultures of hepatocytes, Sertoli cells, and Leydig cells were incubated with 14C-labeled MEHP [8 microM] for up to 24 hr. No significant reduction in viability was produced under these conditions. In contrast to the hepatocytes, which extensively metabolized MEHP to a variety of products in 1 hr, the testicular cell cultures were apparently unable to metabolize MEHP (beyond a slight hydrolysis to phthalic acid by Sertoli cells) in 18-24 hr. MEHP was efficiently taken up by hepatocytes, but much less so by testicular cells. These results, combined with related observations from the literature, support the hypothesis that MEHP itself is the metabolite of DEHP responsible for testicular atrophy in rats. JF - Toxicology and applied pharmacology AU - Albro, P W AU - Chapin, R E AU - Corbett, J T AU - Schroeder, J AU - Phelps, J L AD - National Institute of Environmental Health Sciences, Laboratory of Molecular Biophysics, Research Triangle Park, North Carolina. Y1 - 1989/09/01/ PY - 1989 DA - 1989 Sep 01 SP - 193 EP - 200 VL - 100 IS - 2 SN - 0041-008X, 0041-008X KW - Phthalic Acids KW - 0 KW - Diethylhexyl Phthalate KW - C42K0PH13C KW - mono-(2-ethylhexyl)phthalate KW - FU2EWB60RT KW - Index Medicus KW - Sertoli Cells -- drug effects KW - Rats KW - Atrophy -- chemically induced KW - Animals KW - Leydig Cells -- metabolism KW - Sertoli Cells -- metabolism KW - Liver -- drug effects KW - Cells, Cultured KW - Liver -- metabolism KW - Leydig Cells -- drug effects KW - Hydrolysis KW - Atrophy -- metabolism KW - Male KW - Diethylhexyl Phthalate -- metabolism KW - Testis -- metabolism KW - Testis -- drug effects KW - Testis -- pathology KW - Diethylhexyl Phthalate -- toxicity KW - Phthalic Acids -- metabolism KW - Diethylhexyl Phthalate -- analogs & derivatives KW - Phthalic Acids -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79210471?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-20 N1 - Date created - 1989-10-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Methylphenidate and pemoline do not cause depletion of rat brain monoamine markers similar to that observed with methamphetamine. AN - 79209688; 2551071 AB - Methylphenidate (Ritalin) and pemoline (Cylert) are central nervous system stimulants which are widely prescribed for attention deficit and other psychiatric disorders. Several other related stimulants, including amphetamine and methamphetamine, have been shown to cause long lasting decreases in monoamine markers in rat brain, characteristic of axonal degeneration. To assess the neurotoxic potential of methylphenidate and pemoline, we compared the effects of multiple injections (sc, bid for up to 4 days) of methylphenidate (21 and 50 mg/kg) and pemoline (20 and 70 mg/kg) with methamphetamine (5 and 15 mg/kg) on rat brain norepinephrine, dopamine, and serotonin levels and transport sites. While decreases were observed in all brain monoamine markers measured in rats treated with methamphetamine, no changes were observed in animals treated with methylphenidate as compared to saline-treated controls. Pemoline failed to induce significant changes in the level of monoamine transport sites; however, a wide array of changes were observed in the levels of 5-hydroxyindoleacetic acid, dopamine, and norepinephrine in various brain areas after a 3-day treatment regimen with a high dose (70 mg/kg) of pemoline. The lack of changes in monoamine transport sites following the repeated administration of high doses of methylphenidate and pemoline suggests that these drugs do not affect axonal integrity. However, the pattern of changes observed in the levels of monoamines after pemoline treatment may have relevance to the self-injurious behavior seen in these animals. JF - Toxicology and applied pharmacology AU - Zaczek, R AU - Battaglia, G AU - Contrera, J F AU - Culp, S AU - De Souza, E B AD - Neuroscience Branch, National Institute on Drug Abuse, Baltimore, Maryland 21224. Y1 - 1989/09/01/ PY - 1989 DA - 1989 Sep 01 SP - 227 EP - 233 VL - 100 IS - 2 SN - 0041-008X, 0041-008X KW - Biogenic Monoamines KW - 0 KW - Biomarkers KW - Methylphenidate KW - 207ZZ9QZ49 KW - Serotonin KW - 333DO1RDJY KW - Methamphetamine KW - 44RAL3456C KW - Pemoline KW - 7GAQ2332NK KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Behavior, Animal -- drug effects KW - Animals KW - Dose-Response Relationship, Drug KW - Synaptic Transmission -- drug effects KW - Norepinephrine -- metabolism KW - Dopamine -- metabolism KW - Biomarkers -- metabolism KW - Serotonin -- metabolism KW - Male KW - Self Mutilation -- chemically induced KW - Brain -- drug effects KW - Pemoline -- toxicity KW - Brain -- metabolism KW - Methylphenidate -- toxicity KW - Biogenic Monoamines -- metabolism KW - Methamphetamine -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79209688?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-20 N1 - Date created - 1989-10-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Organic anion and cation transport in crab urinary bladder. AN - 79209555; 2675639 AB - Crab urinary bladder, a simple, flat-sheet epithelium, is structurally and functionally analogous to vertebrate renal proximal tubule. Like proximal tubule, crab bladder plays an important role in the excretion of potentially toxic, charged metabolites and xenobiotics. Bladders from Cancer borealis secrete monovalent, organic anions and cations in vivo and in vitro. For organic cations, secretion is a two-step process, with mediated and energetically downhill uptake into cells at the serosal membrane and uphill exit at the luminal membrane. The uptake step may be driven by the electrical potential difference across the serosal membrane, the luminal step by organic cation-proton exchange. Monovalent organic anions are also secreted by a separate two-step process. Recent experiments with intact bladder tissue and isolated membrane vesicles show that (as in mammalian proximal tubule) uphill serosal uptake can be coupled indirectly to the Na+ gradient. Organic anion (p-aminohippurate; PAH) uptake is driven by exchange for certain divalent organic anions, e.g., glutarate and alpha-ketoglutarate. The divalent anion gradient (in greater than out) is in turn maintained by Na+-coupled divalent uptake. The PAH exist step at the luminal membrane is mediated and downhill; it may involve anion exchange. JF - The American journal of physiology AU - Miller, D S AU - Smith, P M AU - Pritchard, J B AD - Laboratory of Cellular and Molecular Pharmacology, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - R501 EP - R505 VL - 257 IS - 3 Pt 2 SN - 0002-9513, 0002-9513 KW - Anions KW - 0 KW - Cations KW - Index Medicus KW - Animals KW - Kidney -- metabolism KW - Biomechanical Phenomena KW - Biological Transport KW - Urinary Bladder -- metabolism KW - Brachyura -- metabolism KW - Anions -- metabolism KW - Cations -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79209555?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-17 N1 - Date created - 1989-10-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of nickel(II)acetate on distribution of calmodulin in the rat kidney. AN - 79209162; 2781596 AB - The effect of subcutaneous injection of a single dose of nickel(II)acetate (95 mumol/kg body wt.) on the distribution of calmodulin in the membrane and cytosolic fractions of kidneys of F344/NCr rats was studied with the use of radioimmunoassay. Over the first 8 h post-injection, the membrane-bound calmodulin concentration increased by 20% versus the control value of 3.84 +/- 0.54 SE micrograms/g wet tissue. That increase was then followed by a gradual decrease to the control value in 7 d. At the same time intervals, the cytosolic calmodulin concentration first decreased by 13% from the control value of 8.81 +/- 2.1 SE micrograms/g wet tissue and then slowly increased, reaching a level of 12% above the control at day 7 post-injection. Statistical analysis of the results after 8 h revealed a downward trend in the membrane-bound (P less than 0.0014) and upward trend in the cytosolic (P less than 0.0207) calmodulin concentrations until day 7. However, the total renal calmodulin calculated from the membrane/cytosolic distribution data did not show any statistically significant treatment-related differences among the mean values (13.39 micrograms/g for the nickel(II)acetate-treated rats vs. 12.56 micrograms/g wet tissue for the controls between days 1 and 7). Therefore, the observed effect of nickel(II)acetate must be attributed only to temporary transfer of calmodulin from the soluble cytosolic form into an insoluble, membrane-bound form, without any detectable influence on its degradation or synthesis rate. JF - Toxicology letters AU - Raos, N AU - Kasprzak, K S AD - Inorganic Carcinogenesis Section, National Cancer Institute, Frederick, MD 21701. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 275 EP - 282 VL - 48 IS - 3 SN - 0378-4274, 0378-4274 KW - Acetates KW - 0 KW - Calmodulin KW - Acetic Acid KW - Q40Q9N063P KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Cytosol -- analysis KW - Cell Communication -- drug effects KW - Tissue Distribution KW - Cell Membrane -- analysis KW - Male KW - Calmodulin -- metabolism KW - Calmodulin -- analysis KW - Kidney -- analysis KW - Kidney -- drug effects KW - Acetates -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79209162?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-23 N1 - Date created - 1989-10-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of hepatic metallothionein in male B6C3F1 mice exposed to hepatic tumor promoters: effects of phenobarbital, acetaminophen, sodium barbital, and di(2-ethylhexyl) phthalate. AN - 79208485; 2781555 AB - The effects of various compounds known to be hepatic tumor promoters and toxins in the male B6C3F1 mouse liver, including di(2-ethylhexyl)phthalate (DEHP), acetaminophen (ACT), barbital (BB), and phenobarbital (PB) on hepatic metallothionein (MT) concentrations were assessed after chronic exposure. From 6 weeks of age, male mice were maintained on diets containing DEHP at 12,000 or 6000 ppm, ACT at 10,000 or 5000 ppm, BB at 1,000 ppm, or drinking water with PB at 500 ppm for up to 24 weeks. MT was measured in hepatic cytosol at 0, 2, 8, and 24 weeks of exposure. DEHP proved a very effective inducer, producing elevations of MT as high as 11-fold. The increases in hepatic MT with DEHP were both dose- and time-related. ACT was likewise effective in producing hepatic MT elevations (maximum 6.7-fold) in a dose- and time-related fashion. BB and PB, however, had no effect on hepatic MT levels at any time point. While DEHP, BB, and PB treatments produced hepatomegaly, histopathological analysis at 24 weeks revealed that in both DEHP- and ACT-treated livers hepatocellular proliferation was prominent while livers exposed to BB or PB showed predominantly hepatocellular hypertrophy. Gel-filtration of DEHP-treated liver cytosol revealed that zinc was associated with the MT peak. This peak also bound cadmium in vitro and could be extracted by heat treatment and selective acetone precipitation, both typical characteristics of MT. Further confirmation of the presence of MT after DEHP treatment was obtained by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (10 to 20% acrylamide). Results indicate that some, but not all, tumor promoters can induce target organ MT and that such an induction appears associated with those promoters inducing persistent cellular hyperplasia but not those inducing cellular hypertrophy. JF - Toxicology and applied pharmacology AU - Waalkes, M P AU - Ward, J M AD - Division of Cancer Etiology, National Cancer Institute, Frederick, Maryland 21701-1013. Y1 - 1989/09/01/ PY - 1989 DA - 1989 Sep 01 SP - 217 EP - 226 VL - 100 IS - 2 SN - 0041-008X, 0041-008X KW - Carcinogens KW - 0 KW - Phthalic Acids KW - Cadmium KW - 00BH33GNGH KW - Acetaminophen KW - 362O9ITL9D KW - Barbital KW - 5WZ53ENE2P KW - Metallothionein KW - 9038-94-2 KW - Diethylhexyl Phthalate KW - C42K0PH13C KW - Zinc KW - J41CSQ7QDS KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Animals KW - Zinc -- analysis KW - Phenobarbital -- pharmacology KW - Cytosol -- analysis KW - Chromatography, Gel KW - Electrophoresis, Polyacrylamide Gel KW - Dose-Response Relationship, Drug KW - Cadmium -- analysis KW - Mice KW - Male KW - Barbital -- pharmacology KW - Liver -- ultrastructure KW - Carcinogens -- pharmacology KW - Metallothionein -- biosynthesis KW - Liver -- drug effects KW - Phthalic Acids -- pharmacology KW - Liver -- metabolism KW - Diethylhexyl Phthalate -- pharmacology KW - Acetaminophen -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79208485?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-20 N1 - Date created - 1989-10-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Amiodarone-induced complications after cardiac operation for obstructive hypertrophic cardiomyopathy. AN - 79202911; 2774719 AB - The occurrence of unanticipated and seemingly unexplicable major complications of hepatic, pulmonary, and cardiac dysfunction after palliative operation for obstructive hypertrophic cardiomyopathy prompted a review of 71 sequential patients. Fifty-five patients had been treated preoperatively with beta-blockers, calcium-channel inhibitors, or both, and 16 had received amiodarone for six to 566 days (mean time, 210 days) at total doses ranging from 8 to 175 g (mean dose, 82 g) and had drug-free intervals prior to operation of zero to 457 days (mean time, 91 days). Comparisons were made between the two treatment groups and between those with and without major complications within the amiodarone-treated group. Preoperative cardiac studies, sex, age, functional class, and type of operation were not related to outcome for the entire patient cohort. In amiodarone-treated patients, the major findings were as follows: a 50% incidence of hepatic dysfunction with a tenfold increase in concentrations of serum glutamic-oxaloacetic transaminase and serum glutamic-pyruvic transaminase; a 25% incidence of pulmonary dysfunction necessitating a fourfold increase in the number of days of ventilator support; and a 19% incidence of low cardiac output syndrome with two deaths. Only 44% of the amiodarone-treated group had no serious complications. The incidence of major complications of the liver, lungs, and heart was 2%, 0%, and 2%, respectively, in patients not treated with amiodarone. Abnormal preoperative pulmonary function studies were predictive of prolonged postoperative ventilatory support. Discontinuation of amiodarone for several months prior to operation appeared to reduce the incidence of major complications. The necessary drug-free interval required preoperatively could not be determined from this retrospective experience.(ABSTRACT TRUNCATED AT 250 WORDS) JF - The Annals of thoracic surgery AU - Kupferschmid, J P AU - Rosengart, T K AU - McIntosh, C L AU - Leon, M B AU - Clark, R E AD - Surgery Branch, NHLBI, Bethesda, MD 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 359 EP - 364 VL - 48 IS - 3 SN - 0003-4975, 0003-4975 KW - Amiodarone KW - N3RQ532IUT KW - Abridged Index Medicus KW - Index Medicus KW - Lung Diseases -- chemically induced KW - Arrhythmias, Cardiac -- etiology KW - Postoperative Complications KW - Humans KW - Chemical and Drug Induced Liver Injury KW - Adult KW - Retrospective Studies KW - Arrhythmias, Cardiac -- drug therapy KW - Cardiac Output, Low -- chemically induced KW - Male KW - Female KW - Cardiomyopathy, Hypertrophic -- surgery KW - Amiodarone -- therapeutic use KW - Cardiomyopathy, Hypertrophic -- complications KW - Amiodarone -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79202911?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-03 N1 - Date created - 1989-10-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The addition of lithium to carbamazepine. Antidepressant efficacy in treatment-resistant depression. AN - 79202083; 2505730 AB - The addition of lithium carbonate to various antidepressant agents, including heterocyclics and monoamine oxidase inhibitors, has been reported to rapidly effect an antidepressant response in otherwise treatment-unresponsive depressed patients. Fifteen depressed patients diagnosed by DSM-III criteria who had not responded to double-blind treatment with carbamazepine were treated with the blind addition of lithium to carbamazepine. Eight patients (53%) responded with a moderate to marked improvement. The time to onset of substantial clinical improvement was rapid; ie, the mean (+/- SD) was 4.1 +/- 2.4 days for lithium potentiation compared with 9.7 +/- 4.1 days in a separate group of depressed patients responding to lithium alone. Side effects during carbamazepine-lithium combination therapy were minimal. The mechanisms by which lithium appears to rapidly potentiate the effects of carbamazepine in treatment-resistant depression are discussed. JF - Archives of general psychiatry AU - Kramlinger, K G AU - Post, R M AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 794 EP - 800 VL - 46 IS - 9 SN - 0003-990X, 0003-990X KW - Antidepressive Agents KW - 0 KW - Lithium Carbonate KW - 2BMD2GNA4V KW - Carbamazepine KW - 33CM23913M KW - Lithium KW - 9FN79X2M3F KW - Abridged Index Medicus KW - Index Medicus KW - Drug Therapy, Combination KW - Psychiatric Status Rating Scales KW - Double-Blind Method KW - Humans KW - Adult KW - Clinical Trials as Topic KW - Antidepressive Agents -- therapeutic use KW - Middle Aged KW - Drug Synergism KW - Male KW - Female KW - Depressive Disorder -- psychology KW - Lithium -- therapeutic use KW - Depressive Disorder -- drug therapy KW - Carbamazepine -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79202083?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-27 N1 - Date created - 1989-09-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Quantitative approaches for assessing chromosome loss in Saccharomyces cerevisiae: general methods for analyzing downturns in dose response. AN - 79193929; 2671711 AB - Statistical methods are considered for analysis of data arising from a mitotic chromosome loss assay in Saccharomyces cerevisiae strain D61.M. The methods make use of reproducibility trial data from the assay (presented herein) and previous data, which suggest a unimodal, 'umbrella-patterned' dose response. Computer simulations are employed to illustrate the operating characteristics of the umbrella response methods. These methods are generally applicable to any toxicity assay that exhibits a downturn in dose response. Experimental design considerations are also discussed. These include applications of 2-stage sampling rules to first gauge the dose window of peak response, then test if the response deviates significantly from untreated levels. JF - Mutation research AU - Piegorsch, W W AU - Zimmermann, F K AU - Fogel, S AU - Whittaker, S G AU - Resnick, M A AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 11 EP - 29 VL - 224 IS - 1 SN - 0027-5107, 0027-5107 KW - Index Medicus KW - Alleles KW - Computer Simulation KW - Aneuploidy KW - Dose-Response Relationship, Drug KW - Mutation KW - Mathematics KW - Saccharomyces cerevisiae -- genetics KW - Chromosome Deletion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79193929?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-06 N1 - Date created - 1989-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment of localized aggressive lymphomas with combination chemotherapy followed by involved-field radiation therapy. AN - 79192604; 2788716 AB - Localized lymphomas of diffuse and aggressive histology sometimes undergo early hematogenous dissemination such that local therapies (surgery alone or followed by radiation therapy) are not curative in 100% of cases. We have treated 47 clinical stage I or IE patients with aggressive lymphoma histologies (diffuse large-cell, diffuse mixed, diffuse immunoblastic, follicular large-cell, diffuse small-non-cleaved cell) with four monthly cycles of an eight-drug combination chemotherapy program consisting of cyclophosphamide, etoposide, doxorubicin, nitrogen mustard (mechlorethamine), procarbazine, high-dose methotrexate with leucovorin rescue, and prednisone (Pro-MACE-MOPP) administered systemically followed by 40 Gy involved-field radiation therapy. Forty-five (96%) patients achieved a complete remission and no patient has relapsed with a median follow-up time of 42 months (range, 8 to 90). Both patients failing to achieve a complete remission died of lymphoma, and one patient died free of lymphoma 45 months after diagnosis during coronary artery bypass surgery unrelated to lymphoma or its treatment. Hospital admissions were necessary to manage complications on nine of 188 (5%) cycles of treatment. There were no treatment-related deaths. ProMACE-MOPP plus involved-field radiation therapy is safe and effective treatment for localized aggressive lymphoma. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Longo, D L AU - Glatstein, E AU - Duffey, P L AU - Ihde, D C AU - Hubbard, S M AU - Fisher, R I AU - Jaffe, E S AU - Gilliom, M AU - Young, R C AU - DeVita, V T AD - Medicine Branch, National Cancer Institute, Bethesda, MD. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 1295 EP - 1302 VL - 7 IS - 9 SN - 0732-183X, 0732-183X KW - Procarbazine KW - 35S93Y190K KW - Mechlorethamine KW - 50D9XSG0VR KW - Vincristine KW - 5J49Q6B70F KW - Etoposide KW - 6PLQ3CP4P3 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 - Mechlorethamine -- administration & dosage KW - Drug Administration Schedule KW - Combined Modality Therapy KW - Humans KW - Leucovorin -- administration & dosage KW - Vincristine -- administration & dosage KW - Aged KW - Doxorubicin -- administration & dosage KW - Procarbazine -- administration & dosage KW - Etoposide -- administration & dosage KW - Aged, 80 and over KW - Adult KW - Middle Aged KW - Methotrexate -- administration & dosage KW - Prednisone -- administration & dosage KW - Female KW - Male KW - Remission Induction KW - Lymphoma -- drug therapy KW - Lymphoma -- radiotherapy KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79192604?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-27 N1 - Date created - 1989-09-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Estimating Rn-induced lung cancer in the United States. AN - 79187539; 2777548 AB - The proportion of lung cancer deaths attributable to Rn among residents of single-family homes in the U.S. (approximately 70% of the housing stock) is estimated using the log-normal distribution of Rn concentrations proposed by Nero et al. (1986) and the risk model developed by the National Academy of Sciences' BEIR IV Committee. The risk model, together with the exposure distribution, predicts that approximately 14% of lung cancer deaths among such residents (about 13,300 deaths per year, or 10% of all U.S. lung cancer deaths) may be due to indoor Rn exposure. The 95% confidence interval is 7%-25%, or approximately 6600 to 24,000 lung cancer deaths. These estimated attributable risks due to Rn are similar for males and females and for smokers and nonsmokers, but higher baseline risks of lung cancer result in much larger absolute numbers of Rn-attributable cancers among males (approximately 9000) and among smokers (approximately 11,000). Because of the apparent skewness of the exposure distribution, most of the contribution to the attributable risks arises from exposure rates below 148 Bq m-3 (4 pCi L-1), i.e., below the EPA "action level." As a result, if all exposure rates that exceed 148 Bq m-3 (approximately 8% of homes) were eliminated, the models predict that the total annual lung cancer burden in the U.S. would drop by 4-5%, or by about 3800 lung cancer deaths, in contrast to a maximum reduction of 14% if all indoor Rn exposure above the 1st percentile were eliminated. JF - Health physics AU - Lubin, J H AU - Boice, J D AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 417 EP - 427 VL - 57 IS - 3 SN - 0017-9078, 0017-9078 KW - Air Pollutants KW - 0 KW - Air Pollutants, Radioactive KW - Radon KW - Q74S4N8N1G KW - Index Medicus KW - United States KW - Smoking KW - Risk KW - Humans KW - Male KW - Female KW - Lung Neoplasms -- etiology KW - Lung Neoplasms -- epidemiology KW - Neoplasms, Radiation-Induced -- etiology KW - Housing KW - Neoplasms, Radiation-Induced -- epidemiology KW - Neoplasms, Radiation-Induced -- mortality KW - Lung Neoplasms -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79187539?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-19 N1 - Date created - 1989-10-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vitro photodynamic therapy of human lung cancer. AN - 79183194; 2528031 AB - Photodynamic therapy (PDT) using a dihematoporphyrin ether (DHE) sensitizes malignant cells to damage by 630-nm light. This study investigated in vitro PDT sensitivity of human lung cancer cells (A549) and those factors which influence cell survival as determined by the colony formation assay. After incubation for 2, 4, or 6 hr with [DHE] of 2.5, 25, or 50 micrograms/ml, A549 received red light at dose rates of 0.27 or 0.09 mW/cm2 and energies of 0-250 mJ/cm2. Neither 630-nm light alone nor DHE alone affected cell survival. A dose rate of 0.27 mW/cm2 required less energy than 0.09 mW/cm2 for 90% cytotoxicity (180 mJ/cm2 vs 250 mJ/cm2, P less than 0.05). The energy required for 90% cytotoxicity with 25 micrograms/ml [DHE] was dependent on DHE incubation time (2 hr, 90% cytotoxicity not reached; 4 hr, 116 mJ/cm2; 6 hr, 69 mJ/cm2; P less than 0.05). In contrast, cellular [DHE] as measured by fluorescence, plateaued after 2 hr of incubation. Fluorescence microscopy revealed a time-dependent redistribution of fluorescence from the cell membrane to perinuclear and intracytoplasmic organelles. A 99% cytotoxicity required significantly less energy as [DHE] was increased (2.5 micrograms/ml, no cytotoxicity; 25 micrograms/ml, 243 mJ/cm2; 50 micrograms/ml, 111 mJ/cm2; P less than 0.05). Intracellular [DHE] was directly dependent on the incubating media [DHE] (2.5 micrograms/ml, 0.09 +/- 0.01 micrograms/10(6) cells; 25 micrograms/ml, 0.80 +/- 0.07 micrograms/10(6) cells; 50 micrograms/ml, 1.31 +/- 0.11 micrograms/10(6) cells; P less than 0.05). PDT cytotoxicity was inversely proportional to concentration of serum in the DHE media. These data illustrate that lung cancer in vitro is sensitive to PDT and is influenced by dose rate, energy input, and DHE environmental manipulations. These factors may be important in increasing the efficiency of PDT of thoracic malignancies in vivo. JF - The Journal of surgical research AU - Matthews, W AU - Rizzoni, W AU - Mitchell, J AU - Russo, A AU - Pass, H AD - Thoracic Oncology Section, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 276 EP - 281 VL - 47 IS - 3 SN - 0022-4804, 0022-4804 KW - Hematoporphyrins KW - 0 KW - Proteins KW - Radiation-Sensitizing Agents KW - Dihematoporphyrin Ether KW - 97067-70-4 KW - Index Medicus KW - Proteins -- pharmacology KW - Osmolar Concentration KW - Microscopy, Fluorescence KW - Tumor Cells, Cultured KW - Dose-Response Relationship, Drug KW - Humans KW - Hematoporphyrins -- metabolism KW - Hematoporphyrins -- therapeutic use KW - Environmental Exposure KW - Time Factors KW - Radiation-Sensitizing Agents -- therapeutic use KW - Carcinoma -- pathology KW - Carcinoma -- drug therapy KW - Photochemotherapy KW - Lung Neoplasms -- drug therapy KW - Carcinoma -- metabolism KW - Lung Neoplasms -- pathology KW - Lung Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79183194?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-25 N1 - Date created - 1989-09-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Passive immunization against tumor necrosis factor partially abrogates interleukin 2 toxicity. AN - 79178921; 2788701 AB - Passive immunization against TNF allowed non-tumor-bearing C3H/HEN mice and tumor-bearing C57BL/6 mice to tolerate significantly more doses of IL-2 before death (p less than 0.005 and p less than 0.001, respectively). The antitumor effect of IL-2 against both 3-d and 10-d pulmonary metastases was maintained in mice treated concurrently with neutralizing antibodies to TNF. In one experiment with 10-d pulmonary metastases, increased administration of IL-2 made possible by passive immunization against TNF significantly improved the antitumor response compared to equitoxic doses of IL-2 and control antibody. The results indicate that TNF is a mediator of IL-2 toxicity but contributes minimally to the antitumor effects of IL-2. Strategies to inhibit TNF may improve the therapeutic index of IL-2 as a neoplastic agent. JF - The Journal of experimental medicine AU - Fraker, D L AU - Langstein, H N AU - Norton, J A AD - Surgical Metabolism Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/09/01/ PY - 1989 DA - 1989 Sep 01 SP - 1015 EP - 1020 VL - 170 IS - 3 SN - 0022-1007, 0022-1007 KW - Interleukin-2 KW - 0 KW - Tumor Necrosis Factor-alpha KW - Index Medicus KW - Animals KW - Neoplasm Metastasis KW - Mice, Inbred C57BL KW - Mice KW - Female KW - Interleukin-2 -- therapeutic use KW - Tumor Necrosis Factor-alpha -- immunology KW - Immunization, Passive KW - Tumor Necrosis Factor-alpha -- physiology KW - Interleukin-2 -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79178921?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-03 N1 - Date created - 1989-10-03 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1984 Sep 28;225(4669):1487-9 [6332379] Science. 1985 Aug 30;229(4716):869-71 [3895437] J Immunol. 1985 Oct;135(4):2492-7 [3928750] J Immunol. 1985 Oct;135(4):2865-75 [2993418] J Immunol. 1986 Sep 1;137(5):1735-42 [3528289] Science. 1986 Oct 24;234(4775):470-4 [3764421] J Clin Immunol. 1988 Nov;8(6):426-36 [3265420] Ann Intern Med. 1987 Jun;106(6):817-22 [3495213] Cancer Res. 1988 Oct 15;48(20):5864-7 [3139285] Ann Intern Med. 1988 Dec 15;109(12):953-8 [3264128] N Engl J Med. 1988 Dec 22;319(25):1676-80 [3264384] J Clin Oncol. 1989 Jan;7(1):1-4 [2783337] J Clin Oncol. 1989 Jan;7(1):7-20 [2783338] N Engl J Med. 1987 Apr 9;316(15):889-97 [3493432] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Methadone treatment and acquired immunodeficiency syndrome. AN - 79177290; 2491420 AB - In light of the recent growth in public financial support for the rapid expansion of drug abuse treatment capacity, the unique effectiveness of methadone hydrochloride treatment in reducing intravenous opioid abuse and the associated sharing of injection equipment is reviewed and discussed, and its potential effect on preventing the spread of acquired immunodeficiency syndrome is examined. In addition to methadone, treatment variables that clinical research suggests are integral to effective treatment are identified. Methadone treatment is one of the most helpful means of reducing the risk of acquired immunodeficiency syndrome available, provided that programs of quality are expanded. The medical profession and universities are urged to take steps to ensure quality effort in prevention and treatment. JF - JAMA AU - Cooper, J R AD - Office of Medical and International Affairs, National Institute on Drug Abuse, Rockville, Md 20857. PY - 1989 SP - 1664 EP - 1668 VL - 262 IS - 12 SN - 0098-7484, 0098-7484 KW - Methadone KW - UC6VBE7V1Z KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Humans KW - Acquired Immunodeficiency Syndrome -- prevention & control KW - Methadone -- therapeutic use KW - Substance-Related Disorders -- rehabilitation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79177290?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-05 N1 - Date created - 1989-10-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: JAMA. 1989 Sep 22-29;262(12):1681-2 [2769924] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of target cell DNA release by the cytotoxic T lymphocyte granule protease granzyme A. AN - 79176884; 2788710 AB - The rapid breakdown of target cell DNA during CTL-mediated lysis has been difficult to explain by the granule exocytosis model of cytotoxicity. The involvement of CTL granule proteases in this process was strongly suggested by experiments in which CTL were pretreated with the serine protease inhibitor PMSF, in combination with agents that raise the pH of acidic intracellular compartments. While PMSF pretreatment alone had little effect on target lysis or DNA breakdown, the combination of PMSF and NH4Cl or monensin profoundly reduced target cell DNA release, while little effect was observed on target lysis, as measured by 51Cr release. CTL granule extracts cause release of 125I-DNA from detergent-permeabilized cells. This nuclear DNA-releasing (NDR) activity is inhibited by serine esterase inhibitors that also inhibit the granule BLT-esterase activity, and is specifically immunoabsorbed by antibodies to the CTL granule protease granzyme A. The NDR activity comigrates with BLT-esterase activity during subcellular fractionation, solubilization, gel filtration, and aprotinin-Sepharose affinity chromatography. SDS-PAGE analysis of the affinity-purified product indicates a molecular mass of 60,000 daltons under non-reducing conditions, which moves to 30,000 daltons upon reduction, consistent with previously reported behavior of granzyme A. When the purified material was reduced and alkylated, both esterase and NDR activities comigrated at 30,000 daltons upon gel filtration. Although fully lytic concentrations of purified LGL granule cytolysin alone failed to induce target cell DNA release, a combination of purified granzyme A and the cytolysin induces substantial DNA release. JF - The Journal of experimental medicine AU - Hayes, M P AU - Berrebi, G A AU - Henkart, P A AD - Experimental Immunology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/09/01/ PY - 1989 DA - 1989 Sep 01 SP - 933 EP - 946 VL - 170 IS - 3 SN - 0022-1007, 0022-1007 KW - Cytotoxins KW - 0 KW - Serine Proteinase Inhibitors KW - Ammonium Chloride KW - 01Q9PC255D KW - Phenylmethylsulfonyl Fluoride KW - 57KD15003I KW - DNA KW - 9007-49-2 KW - Monensin KW - 906O0YJ6ZP KW - Granzymes KW - EC 3.4.21.- KW - Serine Endopeptidases KW - Index Medicus KW - Animals KW - Monensin -- pharmacology KW - Mice KW - Cytotoxins -- pharmacology KW - Ammonium Chloride -- pharmacology KW - Phenylmethylsulfonyl Fluoride -- pharmacology KW - Molecular Weight KW - Cell Line KW - Serine Endopeptidases -- physiology KW - Cytoplasmic Granules -- enzymology KW - Serine Endopeptidases -- isolation & purification KW - T-Lymphocytes, Cytotoxic -- enzymology KW - DNA -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79176884?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-03 N1 - Date created - 1989-10-03 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Exp Med. 1988 Feb 1;167(2):514-27 [2450162] J Immunol. 1987 Oct 1;139(7):2398-405 [3498759] J Immunol. 1988 Aug 1;141(3):774-8 [3260910] Biochemistry. 1988 Apr 19;27(8):2641-6 [3042021] J Immunol. 1988 Oct 1;141(7):2191-4 [2844898] Nature. 1989 Jan 12;337(6203):181-4 [2521375] J Exp Med. 1989 Mar 1;169(3):765-77 [2538546] FEBS Lett. 1976 Dec 31;72(2):271-4 [16386038] Immunology. 1972 Oct;23(4):577-90 [4628464] J Immunol. 1980 Feb;124(2):870-8 [6965393] J Immunol. 1980 Mar;124(3):1028-33 [6987305] Nature. 1980 Apr 10;284(5756):555-6 [6245367] J Immunol. 1980 Sep;125(3):1256-61 [7410838] J Biol Chem. 1982 Dec 10;257(23):14300-5 [6815193] Immunol Rev. 1983;72:97-118 [6347870] Proc Natl Acad Sci U S A. 1983 Oct;80(20):6361-5 [6312454] J Immunol. 1983 Nov;131(5):2477-83 [6415172] J Immunol. 1984 Jan;132(1):38-42 [6317746] J Immunol. 1984 Jun;132(6):3197-204 [6373925] J Exp Med. 1984 Jul 1;160(1):75-93 [6736872] Nature. 1985 Apr 25-May 1;314(6013):743-5 [3873011] Adv Exp Med Biol. 1985;184:493-508 [2994413] Annu Rev Immunol. 1985;3:31-58 [3904772] J Cell Biochem. 1986;30(2):133-70 [2422185] EMBO J. 1986 Jul;5(7):1595-600 [3488903] Nature. 1986 Aug 21-27;322(6081):740-3 [3489187] Cell. 1986 Oct 24;47(2):183-94 [3094960] J Cell Biochem. 1986;32(2):151-67 [3023406] EMBO J. 1986 Dec 1;5(12):3267-74 [3545816] Nature. 1987 May 7-13;327(6117):12 [3494952] Cell. 1987 Jun 5;49(5):679-85 [3555842] Immunol Rev. 1988 Mar;103:99-109 [3292399] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inflammatory properties of human C5a and C5a des Arg/ in mast cell-depleted human skin. AN - 79176044; 2527912 AB - C5a and its degradation product, C5a des Arg, elicit immediate cutaneous inflammatory reactions after intradermal injection. Histologically, these reactions are characterized by neutrophil-rich leukocytic infiltrates, leukocytoclasis, edema, and dermal mast cell degranulation. It has not been possible to assess in vivo the relative contributions of resident mast cells and circulating leukocytes to this reaction because the accumulation of leukocytes and degranulation of mast cells occur simultaneously after injection of these anaphylatoxins. To assess the role of mast cells in these inflammatory reactions, we have examined the reactivity of human skin selectively depleted of dermal mast cells by local corticosteroid treatment. Corticosteroid-treated skin became virtually devoid of dermal mast cells within 4-6 wk as assessed by light microscopy, immunofluorescence with fluorescein-conjugated avidin, or electron microscopy. Mast cell-depleted skin demonstrated normal vasopermeability and vasodilatory responsiveness to intradermal injection of histamine, but the reactivity of these sites to the mast cell secretagogue, morphine, was absent. Moreover, no clinical reactions were detectable in mast cell-depleted human skin after intradermal challenge with 50 ng of either C5a or C5a des Arg, despite the fact that biopsies of these sites revealed substantial, neutrophil-rich infiltrates. These infiltrates were qualitatively and quantitatively identical to C5a or C5a des Arg-induced infiltrates in mast cell replete skin. This experimental approach in vivo has allowed the independent analysis of the anaphylactogenic and chemoattractant activities of human C5a and C5a des Arg in human skin, demonstrated the importance of dermal mast cells in these clinical responses, and shown that leukocytes can accumulate at these injection sites directly in response to these mediators. JF - The Journal of investigative dermatology AU - Swerlick, R A AU - Yancey, K B AU - Lawley, T J AD - Dermatology Branch, National Cancer Institute, Bethesda, Maryland. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 417 EP - 422 VL - 93 IS - 3 SN - 0022-202X, 0022-202X KW - Adrenal Cortex Hormones KW - 0 KW - Complement C5 KW - Complement C5a, des-Arginine KW - Morphine KW - 76I7G6D29C KW - Complement C5a KW - 80295-54-1 KW - Histamine KW - 820484N8I3 KW - Index Medicus KW - Drug Eruptions -- immunology KW - Adrenal Cortex Hormones -- pharmacology KW - Cell Count -- drug effects KW - Skin Tests KW - Humans KW - Biopsy KW - Drug Eruptions -- pathology KW - Mast Cells -- immunology KW - Complement C5 -- immunology KW - Skin -- immunology KW - Skin -- cytology KW - Mast Cells -- cytology KW - Complement C5 -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79176044?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-11 N1 - Date created - 1989-10-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Invest Dermatol. 1990 Apr;94(4):499 [2313120] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of murine epidermal differentiation markers is tightly regulated by restricted extracellular calcium concentrations in vitro. AN - 79172641; 2475508 AB - Epidermal differentiation is characterized by a series of coordinated morphological and biochemical changes which result in a highly specialized, highly organized, stratified squamous epithelium. Among the specific markers expressed in differentiating epidermis are (a) two early spinous cell proteins, keratins 1 and 10 (K1 and K10); and (b) two later granular cell proteins, filaggrin and a cornified envelope precursor (CE). In vitro, epidermal basal cells are selectively cultured in 0.05 mM Ca2+ medium, and terminal differentiation is induced when the Ca2+ concentration is increased to 1 mM. However, only a small fraction of the cells express the markers K1, K10, CE, or filaggrin in the higher Ca2+ medium. To explore the factors required for marker expression, cultured epidermal cells were exposed to intermediate Ca2+ concentrations and extracts were analyzed using specific antibody and nucleic acid probes for the four markers of interest. These studies revealed that marker expression was enhanced at a restricted concentration of Ca2+ in the medium of 0.10-0.16 mM. At this Ca2+ concentration, both protein and mRNA levels for each marker were substantially increased, whereas at higher or lower Ca2+ concentrations they were diminished or undetected. The percentage of cells expressing each marker was increased two- to threefold in the permissive Ca2+ medium as determined by immunofluorescence analysis. This optimal level of Ca2+ was required both to initiate and sustain marker expression. At the permissive Ca2+ concentration, expression of the markers was sequential and similar to the order of appearance in vivo. K1 was expressed within 8-12 h and K10 was expressed in the ensuing 12-24-h period. CE and filaggrin were expressed in the subsequent 24 h. Inhibition of K1 expression by cycloheximide suggested that an inducible protein was involved. Other investigators have determined that a shallow Ca2+ gradient exists in epidermis, where the basal cells and spinous cells are in a Ca2+ environment substantially below serum Ca2+ levels. These in vitro results suggest that the Ca2+ environment is a fundamental regulator of expression of epidermal differentiation markers and provide an explanation for the existence of the Ca2+ gradient in vivo. JF - The Journal of cell biology AU - Yuspa, S H AU - Kilkenny, A E AU - Steinert, P M AU - Roop, D R AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 1207 EP - 1217 VL - 109 IS - 3 SN - 0021-9525, 0021-9525 KW - Cytoskeletal Proteins KW - 0 KW - Intermediate Filament Proteins KW - Sulfur Radioisotopes KW - filaggrin KW - Keratins KW - 68238-35-7 KW - Methionine KW - AE28F7PNPL KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Blotting, Northern KW - Electrophoresis, Polyacrylamide Gel KW - Methionine -- metabolism KW - Cell Differentiation KW - Transcription, Genetic KW - Mice KW - Mice, Inbred BALB C KW - Molecular Weight KW - Animals, Newborn KW - Cells, Cultured KW - Fluorescent Antibody Technique KW - Keratins -- genetics KW - Intermediate Filament Proteins -- isolation & purification KW - Intermediate Filament Proteins -- genetics KW - Cytoskeletal Proteins -- biosynthesis KW - Epidermis -- drug effects KW - Intermediate Filament Proteins -- biosynthesis KW - Epidermis -- cytology KW - Cytoskeletal Proteins -- isolation & purification KW - Epidermis -- metabolism KW - Calcium -- pharmacology KW - Keratins -- isolation & purification KW - Keratins -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79172641?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-04 N1 - Date created - 1989-10-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 1985 Nov;45(11 Pt 2):5845-50 [2414001] Carcinogenesis. 1989 Apr;10(4):777-80 [2702726] Cell. 1986 Aug 15;46(4):583-9 [2873896] Differentiation. 1986;31(2):141-53 [2427382] J Invest Dermatol. 1986 Oct;87(4):472-6 [2428884] J Biol Chem. 1987 Apr 15;262(11):5188-96 [3558389] J Invest Dermatol. 1987 Jul;89(1):44-50 [3298447] J Invest Dermatol. 1987 Jul;89(1):51-8 [2885378] Cell. 1980 Apr;19(4):1033-42 [6155214] Proc Natl Acad Sci U S A. 1981 Jul;78(7):4097-101 [6170061] Cancer Res. 1982 Jun;42(6):2344-9 [6122503] In Vitro. 1982 Jul;18(7):633-42 [7141447] Proc Natl Acad Sci U S A. 1983 Feb;80(3):716-20 [6187003] Cell. 1983 Jul;33(3):915-24 [6191871] J Biol Chem. 1983 Oct 25;258(20):12118-21 [6688806] J Biol Chem. 1983 Nov 10;258(21):13268-72 [6195160] J Mol Biol. 1983 Nov 5;170(3):651-73 [6195345] Carcinogenesis. 1983 Nov;4(11):1413-8 [6139180] Proc Natl Acad Sci U S A. 1984 Jan;81(1):238-42 [6141559] Cell. 1984 Apr;36(4):827-34 [6200236] Biochemistry. 1984 Mar 13;23(6):1239-45 [6712945] J Cell Biol. 1984 Apr;98(4):1388-96 [6201491] Cell. 1984 May;37(1):159-70 [6202418] Differentiation. 1984;26(2):154-69 [6203803] J Biol Chem. 1984 Jul 10;259(13):8037-40 [6203901] Eur J Biochem. 1984 Jul 2;142(1):29-36 [6204871] In Vitro. 1984 Aug;20(8):652-62 [6500605] Anal Biochem. 1969 Oct 1;31(1):146-8 [5380692] Exp Cell Res. 1974 May;86(1):95-105 [4857507] Biochem Biophys Res Commun. 1976 Nov 22;73(2):470-8 [11802] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5350-4 [414220] Nature. 1978 Dec 14;276(5689):729-31 [732879] Cell. 1979 Jul;17(3):573-82 [383305] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] Cell. 1979 Nov;18(3):681-94 [42494] Cell. 1980 Jan;19(1):245-54 [6153576] Cell. 1985 Mar;40(3):685-95 [2578891] J Invest Dermatol. 1985 Jun;84(6):508-12 [3998499] Proc Natl Acad Sci U S A. 1985 Jun;82(12):4270-3 [3858880] Exp Cell Res. 1985 Aug;159(2):536-9 [2411581] J Cell Biol. 1987 Jul;105(1):427-40 [2440897] J Invest Dermatol. 1987 Oct;89(4):349-52 [3668277] J Biol Chem. 1987 Nov 15;262(32):15643-8 [3680218] Cancer Res. 1988 Jan 1;48(1):74-81 [2891434] J Invest Dermatol. 1988 Jan;90(1):37-43 [2447194] J Invest Dermatol. 1988 Mar;90(3):382-6 [2450145] Philos Trans R Soc Lond B Biol Sci. 1987 Dec 15;317(1187):525-36 [2894687] Differentiation. 1987;35(2):143-50 [2450799] Am J Pathol. 1988 Apr;131(1):171-81 [2451428] Arch Dermatol. 1988 May;124(5):709-12 [3284469] Cancer Res. 1988 Jun 1;48(11):3245-52 [2452688] Carcinogenesis. 1988 Jun;9(6):1033-8 [2453303] Lab Invest. 1988 Jun;58(6):660-6 [2454348] Cell. 1988 Aug 12;54(4):491-6 [3401924] J Biol Chem. 1988 Sep 15;263(26):13333-9 [2458346] Annu Rev Biochem. 1988;57:593-625 [3052284] J Cell Biol. 1986 May;102(5):1767-77 [2422179] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Beta-adrenergic receptor binding in brain of alcoholics. AN - 79172304; 2548890 AB - The binding of agonists and antagonists to beta-adrenergic receptors in brain tissue obtained postmortem in nonalcoholic controls and matched intoxicated and sober alcoholics was measured to assess the state of the receptors and their coupling to adenylate cyclase. Binding of antagonist, iodocyanopindolol, to cerebral cortical and cerebellar membrane preparations was not different in alcoholics compared to that in controls, suggesting that the number of beta-adrenergic receptors was not affected by chronic ethanol ingestion. Agonist binding data, however, indicated the loss of the high-affinity agonist binding state of the beta-adrenergic receptor, representing the receptor-guanine nucleotide binding protein (Gs) complex. Such changes were observed in cerebral cortex but not in cerebellum of intoxicated alcoholics. These data suggest that cerebral cortical beta-adrenergic receptors are uncoupled from adenylate cyclase in these subjects. In cerebral cortical and cerebellar membranes of sober alcoholics both the high- and low-affinity agonist binding sites were observed. These findings are similar to those seen in animal studies and suggest that the effect of chronic ethanol ingestion on beta-adrenergic receptor-adenylate cyclase coupling is brain region specific and reversible with abstinence. Ethanol-induced changes in the coupling of receptors to adenylate cyclase may contribute to the physiological and behavioral manifestations of alcohol abuse. JF - Experimental neurology AU - Valverius, P AU - Borg, S AU - Valverius, M R AU - Hoffman, P L AU - Tabakoff, B AD - Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 280 EP - 286 VL - 105 IS - 3 SN - 0014-4886, 0014-4886 KW - Receptors, Adrenergic, beta KW - 0 KW - Isoproterenol KW - L628TT009W KW - Index Medicus KW - Reference Values KW - Cerebral Cortex -- metabolism KW - Kinetics KW - Humans KW - Cell Membrane -- metabolism KW - Male KW - Isoproterenol -- pharmacology KW - Cerebellum -- metabolism KW - Receptors, Adrenergic, beta -- metabolism KW - Alcoholism -- metabolism KW - Receptors, Adrenergic, beta -- drug effects KW - Brain -- metabolism KW - Alcoholic Intoxication -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79172304?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-10 N1 - Date created - 1989-10-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lack of promoting effect of clonazepam on the development of N-nitrosodiethylamine-initiated hepatocellular tumors in mice is correlated with its inability to inhibit cell-to-cell communication in mouse hepatocytes. AN - 79169310; 2766464 AB - The tumor-promoting ability of clonazepam (CZP), a widely used benzodiazepine anticonvulsant, was investigated in an in vivo mouse liver tumor promotion assay and an in vitro mouse hepatocyte intercellular communication assay. The development of preneoplastic hepatocellular foci of cellular alteration and hepatocellular neoplasms was studied in male B6C3F1 mice initiated, at 5 weeks of age, with a single i.p. injection of N-nitrosodiethylamine (NDEA; 90 mg/kg body weight) in tricaprylin, followed by administration of either phenobarbital (PB; 0.05%) or CZP (0.068% or 0.136%) in diet beginning 2 weeks after carcinogen injection and continuing to 60 weeks of age. Several mice from each group were killed after 9, 21, 33 or 53 weeks on test diet, and portions of liver and other organs were fixed in formalin and examined histologically. Unlike PB, CZP did not promote the development of preneoplastic hepatocellular foci or neoplasms (adenomas and carcinomas) in NDEA-initiated mice. Following limited (2 weeks) dietary exposure at 0.15%, CZP was a potent inducer of hepatic P450IIB1-mediated alkoxyresorufin O-dealkylase activities. In contrast, the degree of induction in hepatic tissue from mice fed 0.136% CZP for 53 weeks was markedly lower than that in mice fed 0.05% PB for 53 weeks. In the in vitro assay, diazepam, a strong tumor promoter in mouse liver, significantly inhibited mouse hepatocyte gap junctional intercellular communication, while CZP had no significant effect on this parameter. Thus, CZP, a drug structurally related to diazepam, is inactive as a liver tumor promoter in mice. JF - Carcinogenesis AU - Diwan, B A AU - Lubet, R A AU - Nims, R W AU - Klaunig, J E AU - Weghorst, C M AU - Henneman, J R AU - Ward, J M AU - Rice, J M AD - Biological Carcinogenesis and Development Program Resources, Inc., National Cancer Institute, Frederick, MD 21701-1013. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 1719 EP - 1724 VL - 10 IS - 9 SN - 0143-3334, 0143-3334 KW - Carcinogens KW - 0 KW - Diethylnitrosamine KW - 3IQ78TTX1A KW - Clonazepam KW - 5PE9FDE8GB 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 - Aminopyrine N-Demethylase KW - EC 1.5.3.- KW - Diazepam KW - Q3JTX2Q7TU KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Animals KW - Diazepam -- pharmacology KW - Cytochrome P-450 Enzyme System -- metabolism KW - Mice KW - Mice, Inbred Strains KW - Phenobarbital -- pharmacology KW - Oxidoreductases -- metabolism KW - Aminopyrine N-Demethylase -- metabolism KW - Carcinoma -- pathology KW - Adenoma -- chemically induced KW - Adenoma -- pathology KW - Male KW - Carcinoma -- chemically induced KW - Diethylnitrosamine -- toxicity KW - Liver Neoplasms -- pathology KW - Liver -- pathology KW - Liver Neoplasms, Experimental -- pathology KW - Liver -- drug effects KW - Cell Communication -- drug effects KW - Liver Neoplasms -- chemically induced KW - Liver -- physiology KW - Clonazepam -- pharmacology KW - Clonazepam -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79169310?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-12 N1 - Date created - 1989-10-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The rat clofibrate-inducible CYP4A gene subfamily. I. Complete intron and exon sequence of the CYP4A1 and CYP4A2 genes, unique exon organization, and identification of a conserved 19-bp upstream element. AN - 79166744; 2766932 AB - The P450 CYP4A1 and CYP4A2 genes were isolated from a rat genomic library constructed in the vector lambda EMBL3 and their complete sequences were determined. The CYP4A1 and CYP4A2 genes spanned 14,144 and 10,576 bp and contained 13 and 12 exons, respectively. The CYP4A1 gene contained an additional intron that splits the exon corresponding to exon 12 of the CYP4A2 gene, resulting in a noncoding 13th exon in CYP4A1. The exon numbers of these genes were distinct among known P450 genes, and yet several intron-exon junctions along the P450 amino acid coding region were conserved with P450 genes in the CYP2, CYP11, and CYP21 gene families. On the basis of these data, the number of exons in the putative ancestral P450 gene was estimated. The evolutionary implications of this finding are discussed. No consensus TATA sequence was found upstream of either gene's transcription start site. Comparison of the CYP4A1 and CYP4A2 promoters with other genes that lack TATA boxes did not reveal any strong consensus sequence in their immediate upstream regions. However, a conserved 19-bp sequence was located at the positions of 42 and 48 bp upstream from the CYP4A1 and CYP4A2 genes' start sites, respectively. The CYP4A2 gene also contained two 378-bp direct repeats upstream from the start site; these repeats are derived from portions of the long interspersed middle repetitive element present in high copy numbers in the rat genome. JF - DNA (Mary Ann Liebert, Inc.) AU - Kimura, S AU - Hanioka, N AU - Matsunaga, E AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 30892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 503 EP - 516 VL - 8 IS - 7 SN - 0198-0238, 0198-0238 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Clofibrate KW - HPN91K7FU3 KW - Index Medicus KW - Rats KW - Animals KW - Base Sequence KW - Genetic Vectors KW - Restriction Mapping KW - Molecular Sequence Data KW - Transcription, Genetic KW - Amino Acid Sequence KW - Repetitive Sequences, Nucleic Acid KW - Cloning, Molecular KW - Promoter Regions, Genetic KW - Exons KW - Cytochrome P-450 Enzyme System -- genetics KW - Genes -- drug effects KW - Introns KW - Multigene Family -- drug effects KW - Clofibrate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79166744?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-12 N1 - Date created - 1989-10-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interindividual variation among humans in carcinogen metabolism, DNA adduct formation and DNA repair. AN - 79166450; 2670300 AB - Chemical carcinogens are generally activated enzymatically to electrophiles that form covalently bound carcinogen-DNA adducts. Detoxifying enzymes are competing with the activating enzymes for these procarcinogenic chemical substrates. Wide person-to-person variations in these two types of enzymatic activities are found. Repair rates of DNA damage caused by carcinogens also vary among individuals. These interindividual differences in the metabolism of chemical carcinogens and repair rates of carcinogen-induced DNA damage reflect acquired and inherited host factors that may influence an individual's risk for development of cancer. JF - Carcinogenesis AU - Harris, C C AD - Laboratory of Human Carcinogenesis, NCI, Bethesda, MD 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 1563 EP - 1566 VL - 10 IS - 9 SN - 0143-3334, 0143-3334 KW - Carcinogens KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Neoplasms -- pathology KW - Humans KW - Models, Biological KW - Neoplasms -- etiology KW - Cell Transformation, Neoplastic KW - DNA Repair KW - Carcinogens -- metabolism KW - DNA -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79166450?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-12 N1 - Date created - 1989-10-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The rat clofibrate-inducible CYP4A subfamily. II. cDNA sequence of IVA3, mapping of the Cyp4a locus to mouse chromosome 4, and coordinate and tissue-specific regulation of the CYP4A genes. AN - 79166082; 2766933 AB - A novel P450 cDNA, designated IVA3, was isolated from a lambda gt11 cDNA library from clofibrate-treated rat liver by screening with the lauric acid omega-hydroxylase, IVA1, cDNA probe. This cDNA encoded a protein with 507 amino acids and a calculated Mr of 58,239. The IVA3 cDNA shared 65% and 97% nucleotide and 72% and 96% DNA-deduced amino acid sequence similarities with IVA1 and IVA2, respectively. The CYP4A gene family, designated the Cyp4a locus, was mapped to mouse chromosome 4 using a panel of mouse-hamster somatic cell hybrids. Levels of the IVA mRNAs were analyzed in rat tissues and cell cultures after treatment with the hypolipidemic drug clofibrate. The IVA1, IVA2, and IVA3 mRNAs were present at very low levels in the livers of untreated rats and markedly induced in rats treated with clofibrate. Dose-response and time-course studies revealed that all three genes were regulated coordinately in liver. In contrast to the coordinate induction in liver, only the CYP4A3 gene was induced in the rat hepatoma cell line McA-RH7777. In the kidney, IVA1 and IVA3 mRNAs were present at low levels and were induced by clofibrate in a manner similar to that in liver. In contrast, the IVA2 mRNA was expressed in the kidney of untreated rats at a level similar to that of the maximally induced IVA2 mRNA in liver. These data indicate that the CYP4A1, CYP4A2, and CYP4A3 genes are regulated coordinately in liver while only CYP4A2 is activated constitutively in kidney. JF - DNA (Mary Ann Liebert, Inc.) AU - Kimura, S AU - Hardwick, J P AU - Kozak, C A AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 517 EP - 525 VL - 8 IS - 7 SN - 0198-0238, 0198-0238 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Clofibrate KW - HPN91K7FU3 KW - Index Medicus KW - Animals KW - Sequence Homology, Nucleic Acid KW - Liver -- metabolism KW - Amino Acid Sequence KW - Mice KW - DNA -- drug effects KW - Rats KW - Rats, Inbred Strains KW - Base Sequence KW - Liver -- drug effects KW - DNA -- genetics KW - Molecular Sequence Data KW - Male KW - Cytochrome P-450 Enzyme System -- genetics KW - Genes -- drug effects KW - Gene Expression Regulation KW - Multigene Family -- drug effects KW - Chromosome Mapping KW - Clofibrate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79166082?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-12 N1 - Date created - 1989-10-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Panic response to lactate administration in alcoholic and nonalcoholic patients with panic disorder. AN - 79163634; 2764173 AB - The authors administered lactate to 12 abstinent alcoholics with panic disorder, 10 nonalcoholic patients with panic disorder, and eight control subjects. They found that the alcoholic patients had fewer panic attacks in response to lactate infusion than the nonalcoholic patients. This finding was not attributable to differences in baseline anxiety or the change in plasma chemical values brought about by sodium lactate administration. The authors suggest that there may be subgroups of patients with panic disorder who need further characterization to meaningfully elucidate the pathophysiology of the disorder. JF - The American journal of psychiatry AU - George, D T AU - Nutt, D J AU - Waxman, R P AU - Linnoila, M AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 1161 EP - 1165 VL - 146 IS - 9 SN - 0002-953X, 0002-953X KW - Blood Glucose KW - 0 KW - Chlorides KW - Lactates KW - Lactic Acid KW - 33X04XA5AT KW - Sodium KW - 9NEZ333N27 KW - Calcium KW - SY7Q814VUP KW - Abridged Index Medicus KW - Index Medicus KW - Blood Pressure KW - Calcium -- blood KW - Humans KW - Hydrogen-Ion Concentration KW - Chlorides -- blood KW - Blood Glucose -- analysis KW - Adult KW - Pulse KW - Sodium -- blood KW - Female KW - Male KW - Psychological Tests KW - Lactates -- blood KW - Fear KW - Lactates -- administration & dosage KW - Anxiety Disorders -- chemically induced KW - Alcoholism -- physiopathology KW - Panic KW - Anxiety Disorders -- physiopathology KW - Alcoholism -- psychology KW - Alcoholism -- complications KW - Anxiety Disorders -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79163634?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-19 N1 - Date created - 1989-09-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Am J Psychiatry. 1990 Jun;147(6):819-20 [2343939] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sleep panic attacks: new clinical findings and theoretical implications. AN - 79161786; 2764179 AB - Forty-five panic disorder patients and 26 normal control subjects were surveyed regarding their histories of sleep panic attacks, insomnia, and vulnerability to exogenous panic stimuli. Sixty-nine percent (N = 31) of the patients reported having experienced sleep panic at some time in their lives, and 33% (N = 15) of the patients experienced recurrent sleep panic. The implications of these findings for the management of panic disorder are discussed. JF - The American journal of psychiatry AU - Mellman, T A AU - Uhde, T W AD - Section on Anxiety and Affective Disorders, NIMH, Bethesda, MD 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 1204 EP - 1207 VL - 146 IS - 9 SN - 0002-953X, 0002-953X KW - Caffeine KW - 3G6A5W338E KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Sleep Initiation and Maintenance Disorders -- complications KW - Adult KW - Caffeine -- adverse effects KW - Sleep Initiation and Maintenance Disorders -- diagnosis KW - Middle Aged KW - Sleep Initiation and Maintenance Disorders -- psychology KW - Male KW - Female KW - Sleep Wake Disorders -- diagnosis KW - Fear KW - Anxiety Disorders -- psychology KW - Anxiety Disorders -- diagnosis KW - Sleep Wake Disorders -- complications KW - Sleep Wake Disorders -- psychology KW - Panic KW - Anxiety Disorders -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79161786?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-19 N1 - Date created - 1989-09-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Am J Psychiatry. 1990 Aug;147(8):1091-2 [2115749] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Parity as a risk factor for cervical cancer. AN - 79152660; 2763994 AB - In a case-control study of 759 invasive cervical cancer patients and 1,430 controls in Colombia, Costa Rica, Mexico, and Panama conducted during 1986-1987, an association with number of pregnancies persisted after adjustment for sexual and socioeconomic variables. Risks rose steadily to 5.1 (95% confidence interval 2.7-9.7) for those with 14 or more pregnancies and a relation of risk to multiparity was observed in all four study countries. Pregnancy associations appeared to relate to the number of live births rather than to miscarriages or abortions, with multiparity relations most pronounced among premenopausal women and oral contraceptive users. Human papillomaviruses types 16 and 18, as measured by filter in situ hybridization, were not significantly associated with number of births and did not explain the strong relation of parity to risk. Our results indicate the need for further consideration of reproductive factors on cervical cancer risk, with attention given to possible mechanisms of action, including hormonal factors and cervical trauma. JF - American journal of epidemiology AU - Brinton, L A AU - Reeves, W C AU - Brenes, M M AU - Herrero, R AU - de Britton, R C AU - Gaitan, E AU - Tenorio, F AU - Garcia, M AU - Rawls, W E AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 486 EP - 496 VL - 130 IS - 3 SN - 0002-9262, 0002-9262 KW - Contraceptives, Oral KW - 0 KW - Index Medicus KW - Contraceptives, Oral -- adverse effects KW - Epidemiologic Methods KW - Risk Factors KW - Humans KW - Adult KW - Menarche KW - Middle Aged KW - Cesarean Section KW - Menopause KW - Female KW - Uterine Cervical Neoplasms -- etiology KW - Parity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79152660?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-20 N1 - Date created - 1989-09-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of magainins and cecropins on the sporogonic development of malaria parasites in mosquitoes. AN - 79141860; 2759705 AB - Magainins and cecropins are families of peptides with broad antimicrobial and antiparasitic activities derived respectively from the skin of frogs or from giant silk moths. In insects, cecropins function as part of an inducible immune system against a number of bacterial infections. When injected into anopheline mosquitoes previously infected with a variety of Plasmodium species, both magainins and cecropins disrupt sporogonic development by aborting the normal development of oocysts; sporozoites are not formed and the vector cannot transmit the parasite to another host. It may be possible to induce effective transmission-blocking immunity in the mosquito vector by the introduction and expression of genes coding for magainins, cecropins, or similarly acting parasiticidal peptides into the mosquito genome. JF - Infection and immunity AU - Gwadz, R W AU - Kaslow, D AU - Lee, J Y AU - Maloy, W L AU - Zasloff, M AU - Miller, L H AD - Malaria Section, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 2628 EP - 2633 VL - 57 IS - 9 SN - 0019-9567, 0019-9567 KW - Antimalarials KW - 0 KW - Antimicrobial Cationic Peptides KW - Insect Hormones KW - Peptides KW - Xenopus Proteins KW - magainin 1 peptide, Xenopus KW - 108433-99-4 KW - cecropin A KW - 80451-04-3 KW - Index Medicus KW - Insect Vectors -- parasitology KW - Animals KW - Dose-Response Relationship, Drug KW - Zygote -- growth & development KW - Lethal Dose 50 KW - Zygote -- drug effects KW - Microinjections KW - Plasmodium -- drug effects KW - Antimalarials -- pharmacology KW - Antimalarials -- administration & dosage KW - Plasmodium -- growth & development KW - Peptides -- administration & dosage KW - Insect Hormones -- administration & dosage KW - Insect Hormones -- pharmacology KW - Peptides -- pharmacology KW - Anopheles -- parasitology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79141860?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-15 N1 - Date created - 1989-09-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Trans R Soc Trop Med Hyg. 1968;62(6):731-65 [4389153] Annu Rev Biochem. 1970;39:841-66 [4920831] Nature. 1981 Jul 16;292(5820):246-8 [7019715] Proc Natl Acad Sci U S A. 1985 Apr;82(8):2240-3 [3857578] Eur J Biochem. 1985 Jun 18;149(3):531-5 [3839186] Science. 1986 Oct 31;234(4776):607-10 [3532325] FASEB J. 1988 Oct;2(13):2878-83 [3049204] Science. 1987 Aug 14;237(4816):779-81 [3039658] Annu Rev Microbiol. 1987;41:103-26 [3318666] Proc Natl Acad Sci U S A. 1988 Feb;85(3):910-3 [3277183] FEBS Lett. 1988 Feb 15;228(2):337-40 [3125066] Proc Natl Acad Sci U S A. 1988 Jul;85(14):5072-6 [2455891] Proc Natl Acad Sci U S A. 1987 Aug;84(15):5449-53 [3299384] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Target cell lysis by cytotoxic T lymphocytes redirected by antibody-coated polystyrene beads. AN - 79134867; 2668408 AB - Cytotoxic T lymphocytes were found to mediate rapid lysis of target cells not normally recognized in the presence of small polystyrene beads coated with a combination of anti-T3 and antitarget cell antibodies. Lysis was not seen with beads bearing one of these antibodies alone, nor with a mixture of two types of beads each coated with a single antibody. The effector cells mediating this lysis include long term allospecific human CTL, and both human and mouse CTL clones recognizing mouse class I MHC Kb Ag. TNP-modified mouse tumor cells, a human lymphoblastoid line, and human red cells were found to be good targets for this cytotoxicity. Polystyrene beads with diameters of 3 to 15 mu caused target lysis, with a dose-response curve which typically went through a maximum and declined at high bead numbers. Maximal bead-redirected lysis by CTL was less efficient than that mediated by soluble antibody heteroconjugates of the same two antibodies. Bead-redirected target lysis was calcium dependent. These results are interpreted as a form of bystander lysis induced by the beads, since the target cell membrane is not directly crosslinked to the region of CTL activation. These observations thus favor a mechanism of lysis involving the polarized secretion of a locally acting lytic agent by CTL. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Kolber, M A AU - Quinones, R R AU - Henkart, P A AD - Experimental Immunology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/09/01/ PY - 1989 DA - 1989 Sep 01 SP - 1461 EP - 1466 VL - 143 IS - 5 SN - 0022-1767, 0022-1767 KW - Antibodies KW - 0 KW - Antibodies, Monoclonal KW - Antigens, Differentiation, T-Lymphocyte KW - Polystyrenes KW - Trinitrobenzenes KW - Abridged Index Medicus KW - Index Medicus KW - Trinitrobenzenes -- immunology KW - Cytotoxicity Tests, Immunologic -- methods KW - Particle Size KW - Humans KW - Immunosorbent Techniques KW - Antigens, Differentiation, T-Lymphocyte -- immunology KW - Antibodies, Monoclonal -- physiology KW - Microspheres KW - Cell Line KW - Cytotoxicity, Immunologic KW - Antibodies -- physiology KW - T-Lymphocytes, Cytotoxic -- immunology KW - T-Lymphocytes, Cytotoxic -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79134867?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-13 N1 - Date created - 1989-09-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Current approaches to the chemotherapy of B-cell chronic lymphocytic leukemia: a review. AN - 79132052; 2667343 AB - Standard therapy has not substantially improved the outcome of patients with chronic lymphocytic leukemia (CLL). However, an increased understanding of the biology and immunology of CLL, and the availability of several new and active chemotherapy agents (eg, fludarabine, 2'-deoxycoformycin [DCF], 2-chlorodeoxyadenosine [CDA]) has stimulated enthusiasm for clinical trials. DCF induces CRs or PRs in 25% of heavily treated patients. Fludarabine has been associated with a response rate of greater than 50% in previously treated patients, and greater than 70% in untreated patients, with almost a third of these achieving a CR. Currently, phase I and II clinical trials are evaluating combinations of these drugs with each other or with conventional agents (eg, fludarabine/chlorambucil [CLB]/prednisone [P]; DCF/CLB/P; fludarabine/DCF; fludarabine/P) in previously treated patients. To facilitate comparison of these regimens, each study is adhering to the NCl-Working Group guidelines for eligibility and response criteria, and toxicity assessment. A collaborative phase III trial will then compare the most promising of these regimens with "standard" chemotherapy in previously untreated patients. The widespread availability of these clinical trials will allow clinicians ready access to the new treatments. JF - American journal of hematology AU - Cheson, B D AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/09// PY - 1989 DA - September 1989 SP - 72 EP - 77 VL - 32 IS - 1 SN - 0361-8609, 0361-8609 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Neoplasm Staging KW - Humans KW - Prognosis KW - Clinical Trials as Topic KW - Leukemia, Lymphocytic, Chronic, B-Cell -- drug therapy KW - Leukemia, Lymphocytic, Chronic, B-Cell -- pathology KW - Antineoplastic Agents -- therapeutic use KW - Leukemia, Lymphocytic, Chronic, B-Cell -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79132052?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-01 N1 - Date created - 1989-09-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Enhancement of the activity of immunotoxins by analogues of verapamil. AN - 79130092; 2788030 AB - Verapamil has been shown to enhance immunotoxin activity but only at concentrations that are too high for in vivo use. Therefore, four structural analogues of verapamil (D792, D595, D528, and Sz45) were evaluated for their ability to enhance the in vitro activity of immunotoxins made with either ricin A chain or Pseudomonas exotoxin. The following immunotoxins were used: HB21-PE and 454A12-rRTA which recognize the human transferrin receptor; and 260F9-rRTA which reacts with human ovarian carcinoma and breast carcinoma cells. The activities of the immunotoxins were determined in ovarian carcinoma cells and in KB cells using inhibition of either protein synthesis or colony formation as a measure for the cytotoxicity of the immunotoxins. Each of the four analogues enhanced the activity of ricin A-immunotoxins in a dose-dependent manner. D792 and D595 also increased the activity of IIB21-PE. Low concentrations of either Sz45 or D528 enhanced the activity of HB21-PE, but high concentrations of these two analogues either had less enhancing potency than low concentrations or even decreased the activity of HB21-PE. Specificity of enhancement by the analogues was shown by competition of the activity of the immunotoxins by the corresponding antibody and by inactivity of an irrelevant immunotoxin. The amount of enhancement ranged from 2-fold to greater than 60-fold and was dependent on the cell line and on the experimental conditions. The enhancing ability of the drugs did not correlate with their calcium-antagonistic activity. When compared with verapamil, D792 and D595 had greater enhancing potency with regard to both ricin A-immunotoxins and Pseudomonas exotoxin-immunotoxins. Greater enhancing potency and less in vivo toxicity makes D792 a candidate for use in the enhancement of immunotoxins in vivo. JF - Cancer research AU - Pirker, R AU - FitzGerald, D J AU - Raschack, M AU - Frank, Z AU - Willingham, M C AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/09/01/ PY - 1989 DA - 1989 Sep 01 SP - 4791 EP - 4795 VL - 49 IS - 17 SN - 0008-5472, 0008-5472 KW - Bacterial Toxins KW - 0 KW - Calcium Channel Blockers KW - Exotoxins KW - Immunotoxins KW - Protein Synthesis Inhibitors KW - Virulence Factors KW - Ricin KW - 9009-86-3 KW - Verapamil KW - CJ0O37KU29 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 - Exotoxins -- pharmacology KW - Humans KW - Lethal Dose 50 KW - Mice KW - Drug Synergism KW - Tumor Stem Cell Assay KW - Ricin -- pharmacology KW - Female KW - Verapamil -- analogs & derivatives KW - Tumor Cells, Cultured -- metabolism KW - Tumor Cells, Cultured -- drug effects KW - Tumor Cells, Cultured -- pathology KW - Verapamil -- pharmacology KW - Immunotoxins -- pharmacology KW - Verapamil -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79130092?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-15 N1 - Date created - 1989-09-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Cancer Res 1990 Apr 15;50(8):2546 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Functional analysis of domains II, Ib, and III of Pseudomonas exotoxin. AN - 79140177; 2503515 AB - Pseudomonas exotoxin is composed of three structural domains that are responsible for cell recognition, membrane translocation, and ADP-ribosylation. The substitution of the cell recognition domain (domain Ia) with a growth factor such as transforming growth factor alpha (TGF alpha), creates a cell-specific cytotoxic agent, TGF alpha-PE40, which kills cells bearing epidermal growth factor (EGF) receptors. We have used TGF alpha-PE40 to define the role of sequences in domains II, Ib, and III. Various mutations were made in these domains and mutant forms of TGF alpha-PE40 expressed in Escherichia coli. Mutant proteins were then tested for their ADP-ribosylation, EGF receptor-binding, and cell-killing activities. Additionally, the amino boundary of domain III, which contains the ADP-ribosylation activity, was determined by deletion analysis. Data indicate that (i) the functional amino terminus of domain III is near amino acid 400; (ii) deletion of various regions in domain II or conversion of cysteines 265 and 268 to serines results in a loss of cytotoxicity which ranged from 10-fold to more than 150-fold, indicating that domain II is essential for full expression of cytotoxicity; (iii) deletion of the amino terminus of domain Ib results in a molecule with somewhat increased cytotoxic activity, indicating that domain Ib is not essential for the cytotoxic effect of TGF alpha-PE40; and (iv) TGF alpha-PE40, produced by denaturing and refolding of insoluble material from inclusion bodies, binds better to EGF receptors and is about 10-fold more cytotoxic to cells bearing EGF receptors than is the secreted form of soluble TGF alpha-PE40. JF - The Journal of biological chemistry AU - Siegall, C B AU - Chaudhary, V K AU - FitzGerald, D J AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/08/25/ PY - 1989 DA - 1989 Aug 25 SP - 14256 EP - 14261 VL - 264 IS - 24 SN - 0021-9258, 0021-9258 KW - Exotoxins KW - 0 KW - Iodine Radioisotopes KW - Protein Synthesis Inhibitors KW - Recombinant Fusion Proteins KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Epidermal Growth Factor KW - 62229-50-9 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Recombinant Fusion Proteins -- metabolism KW - Protein Synthesis Inhibitors -- toxicity KW - Receptor, Epidermal Growth Factor -- metabolism KW - Tumor Cells, Cultured -- metabolism KW - Humans KW - Carcinoma, Squamous Cell -- metabolism KW - Amino Acid Sequence KW - Recombinant Fusion Proteins -- toxicity KW - Adenosine Diphosphate Ribose -- metabolism KW - Mutation KW - Epidermal Growth Factor -- metabolism KW - Pseudomonas aeruginosa -- metabolism KW - Exotoxins -- genetics KW - Genes, Bacterial KW - Pseudomonas aeruginosa -- genetics KW - Exotoxins -- metabolism KW - Exotoxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79140177?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-13 N1 - Date created - 1989-09-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A functional protein kinase C is required for induction of 2-5A synthetase by recombinant interferon-alpha A in Daudi cells. AN - 79131899; 2474543 AB - Treatment of Daudi B lymphoblastoid cells with interferon (IFN)-alpha or -beta has been reported (Yap, W. H., Teo, T. S., and Tan, Y. H. (1986) Science 234, 355-358) to cause a transient increase in the level of diacylglycerol, which is the endogenous activator of protein kinase C (PK-C). To assess the role for PK-C in the induction of 2-5A synthetase mRNA and activity by IFN-alpha in Daudi cells, we have examined the effects of PK-C inhibitors and activators. We have found that the PK-C inhibitor, 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H7), strongly inhibits the induction of 2-5A synthetase mRNA and activity by recombinant IFN-alpha A (rIFN-alpha A) and that this inhibition appears to be at a post-transcriptional level. The inhibition by H7 could not be attributed to a generalized decrease in macromolecular synthesis or to inhibition of the binding or internalization of rIFN-alpha A. Moreover, pretreatment of Daudi cells for 24 h with phorbol esters to down-regulate or desensitize PK-C substantially inhibited the subsequent induction of 2-5A synthetase mRNA and activity by rIFN-alpha A. These data suggest that PK-C activity is required for the induction of 2-5A synthetase by rIFN-alpha A. However, phorbol esters, which are potent PK-C activators, did not induce 2-5A synthetase. Taken together, our data indicate that a functional PK-C is required for 2-5A synthetase induction by rIFN-alpha A at a post-transcriptional level in Daudi cells but that activation of PK-C is not sufficient for induction of this enzyme. JF - The Journal of biological chemistry AU - Faltynek, C R AU - Princler, G L AU - Gusella, G L AU - Varesio, L AU - Radzioch, D AD - Biological Carcinogenesis and Development Program, National Cancer Institute, Frederick, Maryland 21701. Y1 - 1989/08/25/ PY - 1989 DA - 1989 Aug 25 SP - 14305 EP - 14311 VL - 264 IS - 24 SN - 0021-9258, 0021-9258 KW - Interferon Type I KW - 0 KW - Isoquinolines KW - Phorbol Esters KW - Piperazines KW - RNA, Messenger KW - Recombinant Proteins KW - Sulfonamides KW - RNA KW - 63231-63-0 KW - 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine KW - 84477-87-2 KW - N-(2-guanidinoethyl)-5-isoquinolinesulfonamide KW - 91742-10-8 KW - Protein Kinase C KW - EC 2.7.11.13 KW - 2',5'-Oligoadenylate Synthetase KW - EC 2.7.7.84 KW - Index Medicus KW - Protein Biosynthesis KW - Phorbol Esters -- pharmacology KW - Isoquinolines -- pharmacology KW - Humans KW - Endocytosis -- drug effects KW - Transcription, Genetic KW - Piperazines -- pharmacology KW - RNA, Messenger -- biosynthesis KW - Cell Line KW - RNA -- biosynthesis KW - Protein Kinase C -- antagonists & inhibitors KW - 2',5'-Oligoadenylate Synthetase -- genetics KW - Tumor Cells, Cultured -- drug effects KW - Interferon Type I -- pharmacology KW - Interferon Type I -- metabolism KW - Protein Kinase C -- physiology KW - 2',5'-Oligoadenylate Synthetase -- biosynthesis KW - Tumor Cells, Cultured -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79131899?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-13 N1 - Date created - 1989-09-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Combined zidovudine and interferon-alpha therapy in patients with Kaposi sarcoma and the acquired immunodeficiency syndrome (AIDS) AN - 79144463; 2757312 AB - To evaluate the toxicity and potential clinical efficacy of combined therapy with zidovudine and interferon-alpha for patients with Kaposi sarcoma and the acquired immunodeficiency syndrome (AIDS). Nonrandomized, open trial study. Outpatient clinic of a government referral-based research hospital. Volunteer sample of 39 patients with human immunodeficiency virus (HIV) infection and Kaposi sarcoma. Patients received zidovudine, 250, 100, or 50 mg orally every 4 hours; 6 weeks after interferon-alpha was begun at a dose of 5 million U/d, and the dose was increased every 2 weeks until a maximum tolerated dose was determined. Patients then received the maximum tolerated dose of the combination for a minimum of 12 weeks before formal efficacy evaluations. In the dose-escalation phase, the ability to tolerate interferon-alpha was clearly related to the zidovudine dose. Of the 13 patients receiving 250 mg of zidovudine, only 1 patient was able to tolerate at least 10 million U/d of interferon-alpha. Of the 12 patients receiving 100 mg of zidovudine, 8 tolerated 10 million U/d, 5 tolerated 15 million U/d, and none tolerated higher doses. Of the 12 patients receiving 50 mg of zidovudine, 8 tolerated 10 million U/d, 7 tolerated 15 million U/d, and 6 tolerated 20 million U/d or more. Dose-limiting toxicities included neutropenia (57%), fatigue (16%), thrombocytopenia (14%), and hepatic dysfunction (10%). Of the 22 patients who received a stable dose of both drugs for 12 weeks, 11 patients had a complete or partial tumor response and 8 showed an anti-HIV effect. Peak serum levels of interferon-alpha (32 to 250 U/mL) and zidovudine (0.40 to 3.85 microM) were in the ranges previously shown to be synergistic against HIV. Combination therapy with zidovudine and interferon-alpha can be administered to patients with HIV infection and Kaposi sarcoma in doses that effect antiviral and antitumor responses; it appears to have a potential role in managing such patients. JF - Annals of internal medicine AU - Kovacs, J A AU - Deyton, L AU - Davey, R AU - Falloon, J AU - Zunich, K AU - Lee, D AU - Metcalf, J A AU - Bigley, J W AU - Sawyer, L A AU - Zoon, K C AD - National Institute of Allergy and Infectious Diseases, Bethesda, Maryland. Y1 - 1989/08/15/ PY - 1989 DA - 1989 Aug 15 SP - 280 EP - 287 VL - 111 IS - 4 SN - 0003-4819, 0003-4819 KW - Interferon Type I KW - 0 KW - Zidovudine KW - 4B9XT59T7S KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Dose-Response Relationship, Drug KW - Combined Modality Therapy KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Leukocyte Count KW - Zidovudine -- therapeutic use KW - Interferon Type I -- adverse effects KW - Acquired Immunodeficiency Syndrome -- therapy KW - Acquired Immunodeficiency Syndrome -- complications KW - Zidovudine -- pharmacokinetics KW - Interferon Type I -- administration & dosage KW - Zidovudine -- adverse effects KW - Interferon Type I -- pharmacokinetics KW - Interferon Type I -- therapeutic use KW - Zidovudine -- administration & dosage KW - Sarcoma, Kaposi -- therapy KW - Sarcoma, Kaposi -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79144463?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-01 N1 - Date created - 1989-09-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Ann Intern Med. 1990 Feb 15;112(4):306-7 [2334482] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The male factor in the etiology of cervical cancer among sexually monogamous women. AN - 79130020; 2547727 AB - To address the hypothesis that male sexual behavior may affect the etiology of invasive cervical cancer, a case-control study was undertaken in Panama, Costa Rica, Colombia and Mexico. The study enrolled husbands of those women with invasive cervical cancer and of those age-matched controls who reported only one lifetime sexual partner. A total of 204 case and 485 control husbands (78% and 72%, respectively, of identified husbands) were interviewed, clinically examined, and had penile swabs taken for papillomavirus assays. Risk increased significantly (p = 0.005) with the number of sexual partners reported by the husband (RR = 2.0 for 26+ vs. less than 6 partners). Low educational status of the husband was also an important predictor of risk, possibly indicating the role of unmeasured aspects of sexual behavior. Visits to prostitutes, circumcision status and sexually transmitted disease histories were not important predictors of risk, but evidence from clinical examination indicated that poor genital hygiene may be involved. Human papillomavirus (HPV) expression as defined by filter in situ hybridization was detected in 20-23% of subjects and, except in the small group with both HPV types 6/11 and 16/18, was not related to risk. This may reflect sampling problems in the male or the importance of host factors which enhance viral carcinogenicity in the female. JF - International journal of cancer AU - Brinton, L A AU - Reeves, W C AU - Brenes, M M AU - Herrero, R AU - Gaitan, E AU - Tenorio, F AU - de Britton, R C AU - Garcia, M AU - Rawls, W E AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/08/15/ PY - 1989 DA - 1989 Aug 15 SP - 199 EP - 203 VL - 44 IS - 2 SN - 0020-7136, 0020-7136 KW - DNA, Viral KW - 0 KW - Index Medicus KW - Educational Status KW - DNA, Viral -- analysis KW - Risk Factors KW - Humans KW - Papillomaviridae -- genetics KW - Circumcision, Male KW - Male KW - Female KW - Uterine Cervical Neoplasms -- etiology KW - Sexual Behavior UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79130020?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-20 N1 - Date created - 1989-09-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vitro neoplastic progression of rat tracheal epithelial cells transformed by diverse carcinogens. AN - 79081162; 2472879 AB - Preneoplastic transformants were isolated from primary rat tracheal epithelial cells after treatment with (a) mutagenic concentrations of the alkylating agent N-methyl-N-nitro-N'-nitrosoguanidine, (b) nonmutagenic concentrations of the DNA hypomethylating agent 5-azacytidine, or (c) after arising spontaneously. We have addressed the question of whether preneoplastic transformants induced by different carcinogens differ in their ability to progress to the immortal stage and to become neoplastic. Spontaneous transformants occurred with a very low frequency, and 5-azacytidine induced preneoplastic transformants half as efficiently as N-methyl-N-nitro-N'-nitrosoguanidine. However, no phenotypic differences could be detected between the 70 preneoplastic colonies isolated from the 3 groups; colony size, cell density, and clonogenicity were not statistically different. Clones from all 3 groups became immortal and further progressed to become neoplastic with similar frequencies. The level of expression of the oncogenes H-ras, K-ras, and raf was also similar in all 3 groups. These experiments indicated that there was no difference in the ability of spontaneous transformants or those induced by N-methyl-N-nitro-N'-nitrosoguanidine or 5-azacytidine to progress to become immortal or neoplastic. This suggests that whereas the nature of the carcinogen influenced the frequency of the initial transforming event, progression to the neoplastic stage was independent of the nature of the transforming insult. JF - Cancer research AU - Walker, C AU - Nettesheim, P AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/08/15/ PY - 1989 DA - 1989 Aug 15 SP - 4427 EP - 4430 VL - 49 IS - 16 SN - 0008-5472, 0008-5472 KW - Carcinogens KW - 0 KW - Methylnitronitrosoguanidine KW - 12H3O2UGSF KW - Azacitidine KW - M801H13NRU KW - Index Medicus KW - Rats KW - Animals KW - Precancerous Conditions -- genetics KW - Precancerous Conditions -- chemically induced KW - Epithelium -- pathology KW - Precancerous Conditions -- pathology KW - Epithelium -- drug effects KW - Cell Transformation, Neoplastic -- pathology KW - Tracheal Neoplasms -- chemically induced KW - Trachea -- pathology KW - Cell Transformation, Neoplastic -- chemically induced KW - Tracheal Neoplasms -- pathology KW - Trachea -- drug effects KW - Tracheal Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79081162?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-23 N1 - Date created - 1989-08-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evidence of alpha 1-adrenergic----protein kinase C----Na+/H+ antiporter-dependent increase in pinealocyte intracellular pH. Role in the adrenergic stimulation of cGMP accumulation. AN - 79121370; 2568991 AB - The regulation of intracellular pH (pHi) in isolated rat pinealocytes was studied using the fluorescent pH indicator 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. Resting pHi was 7.09 when the extracellular pH (pHe) was 7.2. Treatment of pinealocytes with the physiological regulator of pineal function, norepinephrine, resulted in a concentration-dependent increase in pHi. Further analysis indicated that norepinephrine is probably acting via an alpha 1-adrenergic----[Ca2+]i----Ca2+/phospholipid- dependent protein kinase (protein kinase C) mechanism to activate the Na+/H+ antiporter, thereby causing cytoplasmic alkalization. A potential influence of cytosolic alkalization on the responsiveness of cyclic nucleotides to adrenergic agonists was also studied. Five analogs of the antiporter inhibitor amiloride reduced norepinephrine stimulation of cGMP accumulation with the same relative potency as they act on the antiporter. In contrast, although inhibitory effects of these compounds on cAMP accumulation were detectable, they occurred at 10-100-fold higher concentrations, and the relative potency of these inhibitors did not indicate they were acting via the antiporter. These findings provide evidence that 1) alpha 1-adrenergic receptor activation increases pinealocyte pHi through Ca2+----protein kinase C-dependent activation of the Na+/H+ antiporter; and 2) norepinephrine stimulation of cGMP accumulation is pHi-dependent. It would appear that alpha 1-adrenergic regulation of pHi via the Na+/H+ antiporter may be of general importance in the control of cGMP accumulation. JF - The Journal of biological chemistry AU - Ho, A K AU - Chik, C L AU - Weller, J L AU - Cragoe, E J AU - Klein, D C AD - Section on Neuroendocrinology, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1989/08/05/ PY - 1989 DA - 1989 Aug 05 SP - 12983 EP - 12988 VL - 264 IS - 22 SN - 0021-9258, 0021-9258 KW - Adrenergic alpha-Agonists KW - 0 KW - Adrenergic alpha-Antagonists KW - Carrier Proteins KW - Receptors, Adrenergic, alpha KW - Sodium-Hydrogen Antiporter KW - 5H-amiloride KW - 1203-87-8 KW - Phenylephrine KW - 1WS297W6MV KW - Amiloride KW - 7DZO8EB0Z3 KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinase C KW - EC 2.7.11.13 KW - Cyclic GMP KW - H2D2X058MU KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Potassium KW - RWP5GA015D KW - Calcium KW - SY7Q814VUP KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Cytosol -- physiology KW - Animals KW - Adrenergic alpha-Agonists -- pharmacology KW - Enzyme Activation KW - Norepinephrine -- pharmacology KW - Hydrogen-Ion Concentration KW - Amiloride -- pharmacology KW - Amiloride -- analogs & derivatives KW - Rats KW - Calcium -- metabolism KW - Cyclic AMP -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Potassium -- pharmacology KW - Adrenergic alpha-Antagonists -- pharmacology KW - Phenylephrine -- pharmacology KW - Protein Kinase C -- metabolism KW - Cyclic GMP -- metabolism KW - Carrier Proteins -- antagonists & inhibitors KW - Carrier Proteins -- physiology KW - Protein Kinase C -- physiology KW - Pineal Gland -- physiology KW - Receptors, Adrenergic, alpha -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79121370?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-07 N1 - Date created - 1989-09-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The cardiovascular response of normal humans to the administration of endotoxin. AN - 79091176; 2664516 AB - Marked abnormalities in cardiovascular function accompany septic shock, and bacterial endotoxin is believed to be one of the principal mediators of these abnormalities. To evaluate the cardiovascular effects of endotoxemia in humans, we measured hemodynamic variables in nine normal subjects given an intravenous bolus dose of endotoxin (Escherichia coli, 4 ng per kilogram of body weight) and in six normal subjects given a bolus dose of saline, before and three hours after administration. All the subjects then underwent volume loading with normal saline (mean, 2217 ml) during the fourth and fifth hours after administration of the bolus, and the measurements were repeated. Three hours after the administration of endotoxin and before volume loading, the cardiac index had increased by 53 percent and the heart rate by 36 percent (both changes were significant; P less than or equal to 0.008), and the systemic vascular-resistance index had decreased by 46 percent (P = 0.004). After volume loading (five hours after the administration of endotoxin), the left ventricular ejection fraction decreased by 1 percent of the base-line value in the subjects given endotoxin, but increased by 14 percent in the controls (P = 0.008). The left ventricular end-diastolic and end-systolic volume indexes increased by 18 percent (P = 0.07) and 24 percent (P = 0.042), respectively. Left ventricular performance, as measured by the ratio of the peak systolic pressure to the end-systolic volume index, was depressed (a decrease of 0.90 in the subjects given endotoxin vs. an increase of 0.76 in the controls; P = 0.024). We conclude that the administration of endotoxin to normal subjects causes a depression of left ventricular function that is independent of changes in left ventricular volume or vascular resistance. The changes in function are similar to those observed in septic shock and suggest that endotoxin is a major mediator of the cardiovascular dysfunction in this condition. JF - The New England journal of medicine AU - Suffredini, A F AU - Fromm, R E AU - Parker, M M AU - Brenner, M AU - Kovacs, J A AU - Wesley, R A AU - Parrillo, J E AD - Critical Care Medicine Department, National Institutes of Health, Bethesda, MD 20892. Y1 - 1989/08/03/ PY - 1989 DA - 1989 Aug 03 SP - 280 EP - 287 VL - 321 IS - 5 SN - 0028-4793, 0028-4793 KW - Endotoxins KW - 0 KW - Tumor Necrosis Factor-alpha KW - Calcium KW - SY7Q814VUP KW - Abridged Index Medicus KW - Index Medicus KW - Calcium -- blood KW - Humans KW - Vascular Resistance -- drug effects KW - Heart Rate -- drug effects KW - Adult KW - Escherichia coli KW - Tumor Necrosis Factor-alpha -- analysis KW - Shock, Septic -- physiopathology KW - Blood Pressure -- drug effects KW - Toxemia -- physiopathology KW - Stroke Volume -- drug effects KW - Female KW - Male KW - Hemodynamics -- drug effects KW - Heart -- drug effects KW - Endotoxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79091176?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-15 N1 - Date created - 1989-08-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: N Engl J Med. 1989 Dec 28;321(26):1828-30 [2594042] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pathologic anatomy of the dilated cardiomyopathies. AN - 79119785; 2756900 AB - Dilated cardiomyopathies are characterized by systolic pump failure and by dilatation of the ventricular cavity. Thus, they differ from the other 2 main types of cardiomyopathies, namely, hypertrophic cardiomyopathy and restrictive/obliterative cardiomyopathy. The term dilated cardiomyopathy designates a number of heterogeneous syndromes: idiopathic dilated cardiomyopathy, alcoholic cardiomyopathy, postpartal cardiomyopathy, infantile cardiomyopathy with histiocytoid change in cardiac muscle cells, anthracycline cardiomyopathy, Keshan disease, and several ultrastructurally distinct abnormalities, some of which maybe familial. The pathologic features of these syndromes are reviewed in detail. JF - The American journal of cardiology AU - Ferrans, V J AD - National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989/08/02/ PY - 1989 DA - 1989 Aug 02 SP - 9C EP - 11C VL - 64 IS - 6 SN - 0002-9149, 0002-9149 KW - Antibiotics, Antineoplastic KW - 0 KW - Selenium KW - H6241UJ22B KW - Abridged Index Medicus KW - Index Medicus KW - Selenium -- deficiency KW - Infant KW - Cardiomyopathy, Alcoholic -- pathology KW - Puerperal Disorders -- pathology KW - Myocardium -- pathology KW - Humans KW - Female KW - Antibiotics, Antineoplastic -- adverse effects KW - Pregnancy KW - Cardiomyopathy, Dilated -- etiology KW - Cardiomyopathy, Dilated -- chemically induced KW - Cardiomyopathy, Dilated -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79119785?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-30 N1 - Date created - 1989-08-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 4-Ipomeanol: a novel investigational new drug for lung cancer. AN - 79089842; 2664191 AB - 4-Ipomeanol (IPO) is the first agent to undergo preclinical development at the National Cancer Institute (NCI) based principally on a specific biochemical-biological rationale for clinical investigation as an antineoplastic agent targeted against lung cancer. This disease-specific development of IPO was initially stimulated by observations that the compound was activated by metabolism, preferentially within the mammalian lung, specifically within bronchiolar Clara cells, and that its predominant toxicity was to the lung in most species. IPO is inactive or only minimally active against most conventional antitumor test systems. However, some human lung cancer cell lines, as well as a variety of fresh human lung tumor biopsy specimens, have been shown to be capable of mediating the in situ biotransformation of IPO to a potentially cytotoxic intermediate. In this report, the biochemistry, metabolism, preclinical pharmacology, and toxicology of IPO are reviewed and the clinical development plans for this unique and challenging new agent are presented. JF - Journal of the National Cancer Institute AU - Christian, M C AU - Wittes, R E AU - Leyland-Jones, B AU - McLemore, T L AU - Smith, A C AU - Grieshaber, C K AU - Chabner, B A AU - Boyd, M R AD - Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/08/02/ PY - 1989 DA - 1989 Aug 02 SP - 1133 EP - 1143 VL - 81 IS - 15 SN - 0027-8874, 0027-8874 KW - Antineoplastic Agents KW - 0 KW - Terpenes KW - 4-ipomeanol KW - 32954-58-8 KW - Index Medicus KW - Drug Evaluation KW - Animals KW - Humans KW - Drug Evaluation, Preclinical KW - Terpenes -- toxicity KW - Lung Neoplasms -- drug therapy KW - Terpenes -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79089842?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-22 N1 - Date created - 1989-08-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: J Natl Cancer Inst 1990 Sep 5;82(17):1434 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of excitatory amino acid receptors by group IIB metal cations in cultured mouse hippocampal neurones. AN - 79547738; 2561788 AB - 1. Responses to the excitatory amino acids kainate, quisqualate, N-methyl-D-aspartate (NMDA), L-glutamate and L-aspartate were recorded in mouse hippocampal neurones in cell culture, using the whole-cell configuration of the patch clamp technique. Agonists were applied rapidly from an array of flow pipes each of 250 microns diameter, positioned within 100 microns of the nerve cell body. 2. Responses to NMDA, L-aspartate and to low concentrations of L-glutamate, recorded with glycine in the extracellular fluid, were strongly antagonized by 50 microM-zinc. Responses to kainate, quisqualate, and in glycine-free solution, responses to L-glutamate, were potentiated by 50 microM-zinc, but partially antagonized by 1 mM-zinc. On average, with 50 microM-zinc, responses to NMDA were reduced to 0.19 times control, while responses to kainate and quisqualate were increased to 1.09 and 1.14 times control. With 1 mM-zinc responses to kainate and quisqualate were reduced to 0.54 and 0.42 times control. 3. Cadmium had a similar, though less potent action, and at 50 microM antagonized responses to NMDA but potentiated responses to kainate and quisqualate. On average, with 50 microM-cadmium, responses to NMDA were reduced to 0.39 times control, while responses to kainate and quisqualate were increased to 1.08 and 1.15 times control. With 1 mM-cadmium responses to NMDA were reduced to 0.04 times control while responses to kainate and quisqualate were reduced to 0.79 and 0.60 times control. Mercury was neurotoxic and increased the leakage current; however, no reduction of the response to NMDA was produced by 5 microM-mercury. 4. The equilibrium dissociation constant (Kd) for zinc antagonism of responses to NMDA, estimated from fit of a single binding site adsorption isotherm, was 13 microM; cadmium was about 4 times less potent than zinc. These effects of zinc and cadmium were nearly voltage independent. In contrast the antagonism of responses to NMDA by 150 microM-magnesium was highly voltage dependent, such that the Kd for magnesium increased e-fold per 17.6 mV depolarization. 5. The potency of zinc as an NMDA antagonist did not vary with the concentration of NMDA, and was not greatly influenced by a 1000-fold variation in the concentration of the NMDA-modulator glycine. This suggests that zinc acts as a non-competitive antagonist, and does not directly interfere with the binding of NMDA to the agonist recognition site nor with the binding of glycine to an allosteric site on the NMDA receptor complex.(ABSTRACT TRUNCATED AT 400 WORDS) JF - The Journal of physiology AU - Mayer, M L AU - Vyklicky, L AU - Westbrook, G L AD - Laboratory of Developmental Neurobiology, NICHD, National Institutes of Health, Bethesda, MD 20892. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 329 EP - 350 VL - 415 SN - 0022-3751, 0022-3751 KW - Amino Acids KW - 0 KW - Cations, Divalent KW - Glutamates KW - Receptors, Amino Acid KW - Receptors, Cell Surface KW - Receptors, Glutamate KW - Receptors, Neurotransmitter KW - Mercury KW - FXS1BY2PGL KW - Zinc KW - J41CSQ7QDS KW - Glycine KW - TE7660XO1C KW - Index Medicus KW - Animals KW - Drug Interactions KW - Mercury -- pharmacology KW - Receptors, Neurotransmitter -- drug effects KW - Mice KW - Zinc -- pharmacology KW - Glutamates -- physiology KW - Cells, Cultured KW - Glycine -- pharmacology KW - Mice, Inbred C57BL KW - Membrane Potentials -- drug effects KW - Hippocampus -- physiology KW - Neurons -- physiology KW - Amino Acids -- physiology KW - Receptors, Cell Surface -- drug effects KW - Cations, Divalent -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79547738?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-09-04 N1 - Date created - 1990-09-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Brain Res. 1987 Sep 15;420(2):313-23 [3676764] Nature. 1987 Aug 13-19;328(6131):640-3 [3039375] J Physiol. 1988 May;399:227-45 [2457088] J Physiol. 1988 May;399:247-66 [2457089] Proc Natl Acad Sci U S A. 1988 Sep;85(17):6547-50 [2842779] Eur J Pharmacol. 1988 Jun 22;151(1):103-12 [2843387] Neurosci Lett. 1988 Jul 8;89(3):313-8 [2458553] J Neurophysiol. 1988 Aug;60(2):645-63 [2902200] Proc Natl Acad Sci U S A. 1989 Feb;86(4):1411-5 [2537497] J Physiol. 1989 Aug;415:351-65 [2561789] J Physiol. 1979 Oct;295:139-70 [42780] Neuroscience. 1980;5(12):2325-7 [6970348] Annu Rev Pharmacol Toxicol. 1981;21:165-204 [6112965] J Membr Biol. 1982;64(1-2):55-66 [6276548] Nature. 1982 Mar 25;296(5855):357-9 [6278324] J Physiol. 1982 Oct;331:577-97 [6296371] Nature. 1984 Feb 2-8;307(5950):462-5 [6320006] J Physiol. 1984 Sep;354:29-53 [6148411] Exp Brain Res. 1984;57(1):158-66 [6151515] J Physiol. 1985 Apr;361:65-90 [2580984] Brain Res. 1985 May 20;334(2):281-6 [2859913] Biophys J. 1986 Mar;49(3):607-18 [2421791] Neurosci Lett. 1986 May 23;66(3):305-10 [2425291] Nature. 1987 Feb 5-11;325(6104):529-31 [2433595] J Neurochem. 1987 Jun;48(6):1699-708 [2883254] Prog Neurobiol. 1987;28(3):197-276 [2883706] Science. 1987 May 1;236(4801):589-93 [2883728] J Physiol. 1987 Dec;394:501-27 [2451020] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Captopril and capsaicin modify opioid withdrawal in the morphine-dependent rat. AN - 79453267; 2482512 AB - The involvement of neurokinins, especially substance P, in the opiate withdrawal syndrome was studied by treating rats with drugs that have been reported to increase (captopril) or decrease (capsaicin) tissue levels of substance P. Preliminary experiments with captopril (0.1, 0.3, 1 or 3 mg/kg, SC) showed that the 0.3 mg/kg dose enhanced some of the naloxone-precipitated withdrawal signs. Captopril alone had no effect in the morphine-dependent rat. On experimental days, either saline or captopril (0.3 mg/kg) was injected (SC) immediately before naloxone in morphine-dependent rats that were pretreated (4 to 10 days before the morphine pellet implantation) with either capsaicin (125 mg/kg, SC) or the capsaicin vehicle (N = 8 for each of 4 groups). Capsaicin treatment inhibited the following withdrawal signs: rhinorrhea, lacrimation and salivation. Captopril increased the occurrence of these secretory responses in vehicle-treated but not in capsaicin-treated animals. Other withdrawal signs were not altered by either captopril or capsaicin treatment. The results support the conclusion that substance P and related neurokinins may be involved in the expression of some signs of opioid withdrawal. JF - Pharmacology, biochemistry, and behavior AU - Sharpe, L G AU - Jaffe, J H AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 899 EP - 902 VL - 33 IS - 4 SN - 0091-3057, 0091-3057 KW - Substance P KW - 33507-63-0 KW - Naloxone KW - 36B82AMQ7N KW - Morphine KW - 76I7G6D29C KW - Captopril KW - 9G64RSX1XD KW - Capsaicin KW - S07O44R1ZM KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Naloxone -- pharmacology KW - Animals KW - Dose-Response Relationship, Drug KW - Male KW - Substance Withdrawal Syndrome -- physiopathology KW - Substance P -- physiology KW - Captopril -- pharmacology KW - Capsaicin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79453267?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-06 N1 - Date created - 1990-03-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Specific polypeptide differences in normal versus malignant breast tissue by two-dimensional electrophoresis. AN - 79279255; 2806203 AB - High resolution two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) in combination with computer-assisted densitometry was used to analyze 800-1000 silver stained postmitochrondrial and 600-800 cytosolic polypeptides extracted from malignant and nonmalignant human breast tissues. The 2D-PAGE patterns of polypeptides from malignant and normal tissues were similar, although both qualitative and quantitative polypeptide differences were noted. Six cytosolic polypeptides (pI/molecular mass x 10(-3), 5.20/80, 5.75/43, 6.20/40, 5.43/35, 5.46/34.5, and 5.50/34 were detected exclusively in malignant tissues. One constitutive polypeptide, p52 (7.25/52), was not detected in tumor samples. Marked quantitative differences in spot density were noted in polypeptides localized mainly in the molecular weight ranges of 22-40 kDa and pI of 5.65-7.00. An overall increase in polypeptide expression was noted in this region of 2D-PAGE gels of malignant tissues as compared to normal. Twenty-two acidic and 19 polypeptides separated under nonequilibrium isoelectric focusing conditions were significantly increased in tumor samples while one polypeptide was decreased. One polypeptide, p24 (6.15/24), was expressed in greatest concentrations in tumors which also expressed the greatest estrogen receptor content. Expression of p24 was markedly reduced in normal tissue and in malignant tissues expressing low levels of estrogen and progesterone receptors. No significant differences in the expression of the Yb and Ya subunits of glutathione-S-transferases (GST)-A, -B and ligandin were observed between normal and malignant breast tissue. None of the Yp subunits of the placental isoform of GST were detected in either normal or malignant breast tissues. JF - Electrophoresis AU - Wirth, P J AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. PY - 1989 SP - 543 EP - 554 VL - 10 IS - 8-9 SN - 0173-0835, 0173-0835 KW - Antibodies, Monoclonal KW - 0 KW - Neoplasm Proteins KW - Peptides KW - Receptors, Estrogen KW - Receptors, Progesterone KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Index Medicus KW - Animals KW - Liver -- enzymology KW - Humans KW - Biopsy KW - Receptors, Estrogen -- analysis KW - Glutathione Transferase -- analysis KW - Receptors, Progesterone -- analysis KW - Rats KW - Blotting, Western KW - Automatic Data Processing KW - Mitochondria -- analysis KW - Densitometry KW - Electrophoresis, Gel, Two-Dimensional -- methods KW - Peptides -- analysis KW - Breast Neoplasms -- analysis KW - Neoplasm Proteins -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79279255?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-04 N1 - Date created - 1989-12-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ethanol: an enhancer of transplantation antigen expression. AN - 79259507; 2478042 AB - Major histocompatibility antigens (MHC) play a pivotal role in the immune response. Abnormal expression of MHC antigens has been correlated with aberrant regulation of the immune response. Studies on the effect of ethanol on class I MHC antigens demonstrate that ethanol significantly enhances their cell surface expression in a variety of cell lines in vitro. These changes in cell surface levels reflect increased intracellular protein synthesis and increased steady state mRNA levels. The effective ethanol concentrations (0.1-1.0%) are physiologically attainable. Measurement of class I MHC antigens on peripheral blood lymphocytes in a population of acutely ethanol-intoxicated patients showed a highly significant increase relative to controls. The possibility that the elevated levels of MHC antigens induced by ethanol may play a role in the evolution of ethanol-related disease is discussed. JF - Alcoholism, clinical and experimental research AU - Singer, D S AU - Parent, L J AU - Kolber, M A AD - Experimental Immunology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 480 EP - 484 VL - 13 IS - 4 SN - 0145-6008, 0145-6008 KW - Histocompatibility Antigens Class I KW - 0 KW - Histocompatibility Antigens Class II KW - Ethanol KW - 3K9958V90M KW - RNA KW - 63231-63-0 KW - Index Medicus KW - Teratoma -- genetics KW - Animals KW - Histocompatibility Antigens Class II -- genetics KW - Ovarian Neoplasms -- genetics KW - Dose-Response Relationship, Drug KW - Humans KW - Aged KW - Mice KW - Adult KW - Mice, Inbred C3H KW - Middle Aged KW - Lymphocytes -- drug effects KW - Cell Line KW - Female KW - Male KW - RNA -- genetics KW - Major Histocompatibility Complex -- drug effects KW - Ethanol -- pharmacokinetics KW - Ethanol -- pharmacology KW - Alcoholic Intoxication -- immunology KW - Histocompatibility Antigens Class I -- genetics KW - Gene Expression Regulation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79259507?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-09 N1 - Date created - 1989-11-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reproductive toxicity of 2,2-bis(bromomethyl)-1,3-propanediol in a continuous breeding protocol in Swiss (CD-1) mice. AN - 79231768; 2792593 AB - The effect of 2,2-bis(bromomethyl)-1,3-propanediol (BMP) on reproduction in Swiss CD-1 mice was evaluated by use of a continuous breeding protocol. BMP was administered in the feed at 0.1, 0.2, and 0.4% concentrations. Both male and female F0 mice (20 pairs per treatment group, 40 pairs of control animals) were dosed 7 days prior to and during a 98-day cohabitation period. Although the fertility index was unchanged in the high-dose group, BMP exposure significantly decreased the numbers of litters per pair, pups born alive per litter, and pup weight when adjusted for litter size. Crossover mating between treated and control F0 animals indicated a specific effect only on female reproductive capacity. At the highest dose, BMP caused a body weight decrease in the F0 animals of both sexes with no effect on relative organ weights. Sperm concentration, motility, morphology, and estrual cyclicity were unaffected by BMP exposure. Histopathology in the F0 animals revealed specific kidney lesions in both sexes; males were more sensitive than females. The last litter born in the 98-day breeding phase was reared to age 74 days and then mated to nonsiblings of the same treatment group. The effect of high-dose BMP exposure on F1 fertility, body and organ weights, sperm parameters, and estrual cyclicity was the same as that for the F0 animals, with the exception of the lack of renal lesions seen in the F1 females. These data show that BMP impaired fertility in female mice in both generations in the absence of an effect on reproductive organ weights and estrual cyclicity. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Treinen, K A AU - Chapin, R E AU - Gulati, D K AU - Mounce, R AU - Morris, L Z AU - Lamb, J C AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 245 EP - 255 VL - 13 IS - 2 SN - 0272-0590, 0272-0590 KW - Flame Retardants KW - 0 KW - Propylene Glycols KW - 2,2-bis(bromomethyl)-1,3-propanediol KW - 3296-90-0 KW - Index Medicus KW - Eating -- drug effects KW - Animals KW - Kidney Diseases -- pathology KW - Mice, Inbred ICR KW - Kidney -- pathology KW - Mice KW - Estrus -- drug effects KW - Spermatozoa -- drug effects KW - Body Weight -- drug effects KW - Female KW - Male KW - Kidney Diseases -- chemically induced KW - Organ Size -- drug effects KW - Propylene Glycols -- toxicity KW - Flame Retardants -- toxicity KW - Fertility -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79231768?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-28 N1 - Date created - 1989-10-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Commentary on "Are there location/cage/systematic nontreatment effects in long-term rodent studies? A question revisited". AN - 79229558; 2792589 JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Haseman, J K AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 189 EP - 192 VL - 13 IS - 2 SN - 0272-0590, 0272-0590 KW - Index Medicus KW - Animals KW - Research Design KW - Toxicology -- standards KW - Animals, Laboratory -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79229558?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-28 N1 - Date created - 1989-10-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Barbital sodium, a tumor promoter for kidney tubules, urinary bladder, and liver of the F344 rat, induces persistent increases in levels of DNA synthesis in renal tubules but not in urinary bladder epithelium or hepatocytes. AN - 79227657; 2792600 AB - The nephrotoxicity of barbital sodium (NaBB), a renal and urinary bladder tumor promoter, was investigated in male F344/NCr rats. In an 8-week toxicity study, NaBB was administered to 6-week-old male rats for 8 weeks at dietary levels of 16,000, 8000, 4000, 2000, 1000, or 0 ppm. Rats tolerated NaBB at levels of 4000 ppm and below with no weight depression or mortality. Liver-to-body weight ratios, however, were significantly increased at 4000 ppm, and toxic renal lesions were observed histologically. Light microscopic studies of male rats fed 1000 ppm NaBB for 2-52 weeks or 4000 or 8000 ppm for 8 weeks revealed elevated levels of DNA synthesis in renal tubular cells as measured with tritiated thymidine autoradiography or 5-bromo-2'-deoxyuridine immunohistochemistry that were associated with degenerative and regenerative nephrotoxic lesions. Increased labeling indices of urothelium and hepatocytes were not seen in rats exposed to 1000 ppm NaBB which is effective as a bladder and liver tumor promoter at these doses. These studies provide evidence for the chronic nephrotoxicity and renal tubular hyperplasia induced by NaBB in F344 rats, which are associated with the tumor-promoting activity of NaBB at the doses studied. Hyperplasia in the urinary bladder or liver was not found, however, for this bladder and liver tumor promoter. The conflicting findings in liver, bladder, and kidney are discussed. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Hagiwara, A AU - Diwan, B A AU - Ward, J M AD - Division of Cancer Etiology, National Cancer Institute, Frederick, Maryland. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 332 EP - 340 VL - 13 IS - 2 SN - 0272-0590, 0272-0590 KW - Barbiturates KW - 0 KW - Barbital KW - 5WZ53ENE2P KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Urinary Bladder -- pathology KW - Animals KW - Liver -- pathology KW - Kidney Tubules -- pathology KW - Cell Nucleus -- ultrastructure KW - Cell Nucleus -- drug effects KW - Rats KW - Rats, Inbred F344 KW - Epithelial Cells KW - Immunohistochemistry KW - Time Factors KW - Male KW - Organ Size -- drug effects KW - Kidney Neoplasms -- chemically induced KW - Liver Neoplasms, Experimental -- physiopathology KW - Liver Neoplasms, Experimental -- chemically induced KW - Barbiturates -- toxicity KW - DNA -- biosynthesis KW - Barbital -- toxicity KW - Urinary Bladder Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79227657?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-28 N1 - Date created - 1989-10-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nerve growth factor and phorbol esters increase the number of choline acetyltransferase-positive cells in two morphologically distinct classes of basal forebrain neurons in primary cultures. AN - 79213722; 2776295 AB - Nerve growth factor (NGF) has been shown to be active in the CNS as a neurotrophic agent. Cholinergic neurons of the basal forebrain are one cell type in the CNS which have been identified as a target for NGF. When dissociated cell cultures from the basal forebrain were treated for 7 days with NGF (20 ng/100 microliters), the number of choline acetyltransferase (ChAT)-immunopositive cells was increased from 30 +/- 6 to 58 +/- 3. Cholinergic cells taken from the basal forebrain exhibit 3 different morphologies: stellate, pyramidal, and bipolar. The NGF treatment was found to increase the number of stellate cells from 7 +/- 2 to 23 +/- 2 and the number of pyramidal cells from 14 +/- 2 to 26 +/- 2, but had no effect on the number of bipolar cells. The activation of protein kinase C by phorbol 12-myristate, 13-acetate (TPA) also increased the number of ChAT-positive cells in a dose-dependent manner. A maximal increase was observed with 10 ng/ml of TPA which increased the number of positive cells from a basal level of 21 +/- 4 to 42 +/- 4. As was the case with NGF, only the stellate and pyramidal cells were affected by the phorbol ester treatment. In co-addition experiments, the cultures were treated with 10 ng/100 of NGF and 10 ng/ml of TPA, with the result that there was no further increase in the number of immunopositive cells over the NGF controls. These results suggest that the mechanisms by which NGF and TPA increase the number of ChAT-positive cells are interactive at some point. The effect of TPA at the higher doses of NGF was distinctly different. When cells were treated with 20 ng/100 microliters of NGF and 0.05-50 ng/ml of TPA, the NGF response was down-regulated to the level of the vehicle-treated controls. JF - Brain research. Developmental brain research AU - Alderson, R F AU - Hua, Z W AU - Hersh, L B AD - Laboratory of Developmental Neurobiology, NICHD, Bethesda, MD 20892. Y1 - 1989/08/01/ PY - 1989 DA - 1989 Aug 01 SP - 229 EP - 241 VL - 48 IS - 2 SN - 0165-3806, 0165-3806 KW - Nerve Growth Factors KW - 0 KW - Choline O-Acetyltransferase KW - EC 2.3.1.6 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Cell Survival -- drug effects KW - Cells, Cultured KW - Mice, Inbred C57BL KW - Mice KW - Immunohistochemistry KW - Male KW - Female KW - Frontal Lobe -- cytology KW - Nerve Growth Factors -- pharmacology KW - Frontal Lobe -- drug effects KW - Cholinergic Fibers -- cytology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cholinergic Fibers -- drug effects KW - Choline O-Acetyltransferase -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79213722?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-19 N1 - Date created - 1989-10-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cancer and other mortality patterns among United States furniture workers. AN - 79204269; 2775670 AB - Cause specific mortality was investigated among 36,622 members of a national furniture workers' union who were first employed in unionised shops between 1946 and 1962. Overall mortality for each race and sex group was less than expected when compared with United States death rates (white men SMR = 0.8, black men SMR = 0.7, white women SMR = 0.8, black women SMR = 0.5); however, raised risks were observed among white men employed in specific types of furniture industries and followed up for 20 or more years after first employment. Lymphatic and haematopoietic cancers were significantly raised (SMR = 1.8) among wood furniture workers followed up for at least 20 years due to excess deaths from leukaemia (SMR = 2.0) and non-Hodgkin's lymphoma (SMR = 2.0). Mortality from acute myeloid leukaemia was particularly high in this group (SMR = 4.7) based on six observed cases. Metal furniture workers followed up for at least 20 years experienced a significant excess of all cancers combined (SMR = 1.6), with non-significant increases in cancers of the lung, stomach, and colorectum. This group also had non-significant excesses of liver cirrhosis, arteriosclerotic heart disease, and cerebrovascular disease. Nasal cancer was not found to be significantly raised in this cohort, though the average follow up period may not have been sufficient to detect an excess risk for this uncommon tumour. JF - British journal of industrial medicine AU - Miller, B A AU - Blair, A E AU - Raynor, H L AU - Stewart, P A AU - Zahm, S H AU - Fraumeni, J F AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 508 EP - 515 VL - 46 IS - 8 SN - 0007-1072, 0007-1072 KW - Index Medicus KW - United States KW - Humans KW - Cohort Studies KW - Residence Characteristics KW - Male KW - Female KW - Cause of Death KW - Interior Design and Furnishings KW - Neoplasms -- epidemiology KW - Occupational Diseases -- epidemiology KW - Facility Design and Construction UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79204269?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-23 N1 - Date created - 1989-10-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Occup Med. 1986 Jun;28(6):425-33 [3723215] Am J Epidemiol. 1986 Oct;124(4):569-77 [3752051] J Occup Med. 1987 Sep;29(9):734-40 [3316543] Am J Ind Med. 1988;13(1):5-41 [3344755] Int J Cancer. 1988 Mar 15;41(3):354-8 [3346099] Cancer Res. 1988 Apr 1;48(7):1960-4 [3349470] Lancet. 1967 Jul 15;2(7507):136-7 [4165646] Lancet. 1967 Nov 4;2(7523):988-9 [4167528] Comput Biomed Res. 1974 Aug;7(4):325-32 [4850570] Am J Epidemiol. 1976 Feb;103(2):226-35 [1251836] J Occup Med. 1976 Mar;18(3):165-8 [1255276] Cancer. 1976 Oct;38(4):1591-601 [991080] J Occup Med. 1976 Dec;18(12):797-801 [993873] J Natl Cancer Inst. 1976 Nov;57(5):1193-5 [1003549] Br J Prev Soc Med. 1976 Dec;30(4):225-30 [1009272] Cancer Res. 1977 Oct;37(10):3473-4 [908001] J Natl Cancer Inst. 1977 Oct;59(4):1147-85 [903993] Z Gesamte Hyg. 1978 Mar;24(3):174-7 [654358] Lancet. 1978 Sep 16;2(8090):626-7 [80546] Lancet. 1979 Jan 6;1(8106):1-4 [83461] Arch Environ Health. 1978 Nov-Dec;33(6):300-7 [736613] J Occup Med. 1980 Jan;22(1):25-9 [7354410] Am J Epidemiol. 1980 Feb;111(2):183-93 [7355881] Int J Epidemiol. 1979 Dec;8(4):375-82 [541161] J Toxicol Environ Health. 1980 Sep-Nov;6(5-6):1267-73 [7463519] Br J Cancer. 1981 Feb;43(2):169-76 [7470379] Scand J Work Environ Health. 1980 Sep;6(3):201-5 [6937825] Occup Health Saf. 1981 Jul;50(7):23-5, 28, 30 passim [7243152] Am J Ind Med. 1980;1(2):159-65 [7342763] Am J Ind Med. 1984;6(3):185-205 [6475965] Am J Ind Med. 1984;6(3):207-30 [6475966] Scand J Work Environ Health. 1984 Aug;10(4):211-7 [6494840] Am Ind Hyg Assoc J. 1984 Dec;45(12):809-11 [6549104] Br J Ind Med. 1985 Jun;42(6):403-5 [4005193] Am J Epidemiol. 1986 Feb;123(2):235-49 [3946373] Br J Ind Med. 1986 Feb;43(2):84-90 [3947573] Cancer. 1982 Jul 15;50(2):364-71 [7083144] Am J Ind Med. 1983;4(4):565-75 [6869381] Br J Cancer. 1983 Aug;48(2):217-25 [6882662] Am J Ind Med. 1984;5(5):343-57 [6720695] Am J Epidemiol. 1984 Jun;119(6):896-906 [6731431] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Colchicine administered into the area of the nucleus basalis decreases cortical nicotinic cholinergic receptors labelled by [3H]-acetylcholine. AN - 79201180; 2779754 AB - Lesions in the nucleus basalis in the rat are known to decrease presynaptic markers for acetylcholine, including levels of cholineacetyltransferase (CHAT), high affinity uptake of choline and levels of acetylcholinesterase. Effects of lesions of the nucleus basalis on populations of nicotinic and muscarinic receptors are less well understood. After bilateral injection of the neurotoxic agent, colchicine into the nucleus basalis in the rat, levels of CHAT in the cerebral cortex were reduced 44%. Muscarinic cholinergic [( 3H]QNB) and dopaminergic [( 3H]spiroperidol) binding was not changed in the cortex, hippocampus or striatum. However, significant decreases in nicotinic binding sites, labelled by [( 3H]acetylcholine), were observed in the frontal cortex of nucleus basalis treated animals; scatchard plot analysis indicated a significant decrease in the number, but not affinity, of nicotinic binding sites. Colchicine injected into the nucleus basalis had no effect on the binding of [3H]acetylcholine in the hippocampus, but decreased binding of [3H]acetylcholine in the striatum. Subsequent experiments, in which colchicine was administered into the striatum at a site above the nucleus basalis had no significant effect on nicotinic binding in the striatum or frontal cortex. These results support the hypothesis that degeneration of the nucleus-basalis-cortical cholinergic pathway results in a loss of presynaptic nicotinic binding sites in the cortex as well as in the striatum (through transsynaptic degeneration of the cortico-striatal pathway). JF - Neuropharmacology AU - Tilson, H A AU - Schwartz, R D AU - Ali, S F AU - McLamb, R L AD - Laboratory of Molecular and Integrative Neuroscience, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 855 EP - 861 VL - 28 IS - 8 SN - 0028-3908, 0028-3908 KW - Receptors, Cholinergic KW - 0 KW - Receptors, Muscarinic KW - Spiperone KW - 4X6E73CJ0Q KW - Quinuclidinyl Benzilate KW - 6581-06-2 KW - Choline O-Acetyltransferase KW - EC 2.3.1.6 KW - Acetylcholine KW - N9YNS0M02X KW - Colchicine KW - SML2Y3J35T KW - Index Medicus KW - Animals KW - Membranes -- metabolism KW - Choline O-Acetyltransferase -- metabolism KW - Corpus Striatum -- enzymology KW - Hippocampus -- drug effects KW - Rats KW - Rats, Inbred F344 KW - Body Weight -- drug effects KW - Corpus Striatum -- drug effects KW - Hippocampus -- enzymology KW - Male KW - Receptors, Muscarinic -- metabolism KW - Cerebral Cortex -- drug effects KW - Colchicine -- pharmacology KW - Receptors, Cholinergic -- drug effects KW - Cerebral Cortex -- metabolism KW - Cerebral Cortex -- enzymology KW - Acetylcholine -- pharmacology KW - Colchicine -- administration & dosage KW - Olivary Nucleus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79201180?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-20 N1 - Date created - 1989-10-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Degradation and disposal of some antineoplastic drugs. AN - 79201124; 2550609 AB - Bulk quantities and pharmaceutical preparations of the antineoplastic drugs carmustine (BCNU), lomustine (CCNU), chlorozotocin, N-[2-chloroethyl]-N'-[2,6-dioxo-3-piperidinyl]-N-nitrosourea (PCNU), methyl CCNU, mechlorethamine, melphalan, chlorambucil, cyclophosphamide, ifosfamide, uracil mustard, and spiromustine may be degraded using nickel-aluminum alloy in KOH solution. The drugs are completely destroyed and only nonmutagenic reaction mixtures are produced. Destruction of cyclophosphamide in tablets requires refluxing in HCl before the nickel-aluminum alloy reduction. Streptozotocin, chlorambucil, and mechlorethamine may be degraded using an excess of saturated sodium bicarbonate solution. The nitrosourea drugs BCNU, CCNU, chlorozotocin, PCNU, methyl CCNU, and streptozotocin were also degraded using hydrogen bromide in glacial acetic acid. The drugs were completely destroyed but some of the reaction mixtures were mutagenic and the products were found to be, in some instances, the corresponding mutagenic, denitrosated compounds. JF - Journal of pharmaceutical sciences AU - Lunn, G AU - Sansone, E B AU - Andrews, A W AU - Hellwig, L C AD - Environmental Control and Research Program, Program Resources, Inc., NCI-Frederick Cancer Research Facility, MD 21701. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 652 EP - 659 VL - 78 IS - 8 SN - 0022-3549, 0022-3549 KW - Acetates KW - 0 KW - Antineoplastic Agents KW - Bicarbonates KW - Mutagens KW - Nitrosourea Compounds KW - Thiosulfates KW - Mechlorethamine KW - 50D9XSG0VR KW - Nickel KW - 7OV03QG267 KW - Sodium Bicarbonate KW - 8MDF5V39QO KW - Sodium KW - 9NEZ333N27 KW - Aluminum KW - CPD4NFA903 KW - Index Medicus KW - Animals KW - Salmonella -- genetics KW - Chemistry KW - Nitrosourea Compounds -- analysis KW - Nitrosourea Compounds -- toxicity KW - Chromatography, High Pressure Liquid KW - Magnetic Resonance Spectroscopy KW - Rats KW - Oxidation-Reduction KW - Mutagenicity Tests KW - Mechlorethamine -- analysis KW - Chemical Phenomena KW - In Vitro Techniques KW - Antineoplastic Agents -- toxicity KW - Antineoplastic Agents -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79201124?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-25 N1 - Date created - 1989-10-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cerebrospinal fluid quinolinic acid concentrations are increased in acquired immune deficiency syndrome. AN - 79196059; 2528321 AB - Dementia and brain atrophy are established features of a large proportion of patients with acquired immune deficiency syndrome (AIDS). To investigate a potential mechanism for atrophy in AIDS, we measured the concentration of the endogenous neurotoxin quinolinic acid in the cerebrospinal fluid of 10 patients with AIDS and found that they had 3-fold higher quinolinic acid concentrations than 9 age-matched control subjects: 53.8 +/- 10.7 pmol/ml versus 18.4 +/- 3.4 pmol/ml, respectively (p less than 0.005). It remains to be determined whether increased brain quinolinic acid concentrations are involved in the pathogenesis of the neuropathology of AIDS. JF - Annals of neurology AU - Heyes, M P AU - Rubinow, D AU - Lane, C AU - Markey, S P AD - Laboratory of Neurophysiology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 275 EP - 277 VL - 26 IS - 2 SN - 0364-5134, 0364-5134 KW - Pyridines KW - 0 KW - Quinolinic Acids KW - Tryptophan KW - 8DUH1N11BX KW - Quinolinic Acid KW - F6F0HK1URN KW - Index Medicus KW - AIDS/HIV KW - Humans KW - Adult KW - Male KW - Female KW - Pyridines -- cerebrospinal fluid KW - Quinolinic Acids -- cerebrospinal fluid KW - Tryptophan -- metabolism KW - Acquired Immunodeficiency Syndrome -- cerebrospinal fluid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79196059?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-03 N1 - Date created - 1989-10-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Bendectin and human congenital malformations. AN - 79194076; 2772850 AB - The relationship between Bendectin exposure during the first trimester of pregnancy and the occurrence of congenital malformations was prospectively studied in 31,564 newborns registered in the Northern California Kaiser Permanente Birth Defects Study. The odds ratio for any major malformation and Bendectin use was 1.0 (95% confidence interval 0.8-1.4). There were 58 categories of congenital malformations; three of them were statistically associated with Bendectin exposure (microcephaly--odds ratio = 5.3, 95% confidence interval = 1.8-15.6; congenital cataract--odds ratio = 5.3, 95% confidence interval = 1.2-24.3; lung malformations (ICD-8 codes 484.4-484.8)--odds ratio = 4.6, 95% confidence interval = 1.9-10.9). This is exactly the number of associations that would be expected by chance. An independent study (the Collaborative Perinatal Project) was used to determine whether vomiting during pregnancy in the absence of Bendectin use was associated with these three malformations. Two of the three (microcephaly and cataract) had strong positive associations with vomiting in the absence of Bendectin use. We conclude that there is no increase in the overall rate of major malformations after exposure to Bendectin and that the three associations found between Bendectin and individual malformations are unlikely to be causal. JF - Teratology AU - Shiono, P H AU - Klebanoff, M A AD - National Institute of Child Health and Human Development, Prevention Research Program, Bethesda, Maryland 20892. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 151 EP - 155 VL - 40 IS - 2 SN - 0040-3709, 0040-3709 KW - Drug Combinations KW - 0 KW - Pyridines KW - dicyclomine, doxylamine, pyridoxine drug combination KW - Dicyclomine KW - 4KV4X8IF6V KW - Doxylamine KW - 95QB77JKPL KW - Pyridoxine KW - KV2JZ1BI6Z KW - Index Medicus KW - Vomiting KW - Humans KW - Pregnancy KW - Urogenital Abnormalities KW - Digestive System Abnormalities KW - Pregnancy Trimester, First KW - Prospective Studies KW - Central Nervous System -- abnormalities KW - Drug Combinations -- adverse effects KW - Lung -- abnormalities KW - Female KW - Head -- abnormalities KW - Heart Defects, Congenital -- chemically induced KW - Pyridoxine -- adverse effects KW - Abnormalities, Drug-Induced -- etiology KW - Pyridines -- adverse effects KW - Doxylamine -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79194076?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-04 N1 - Date created - 1989-10-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Teratology 1990 Feb;41(2):250-1 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transmembrane signals mediating adrenocorticotropin release from mouse anterior pituitary cells. AN - 79189587; 2550296 AB - The effect of arginine vasopressin (AVP) and corticotropin releasing factor (CRF) an adrenocorticotropin (ACTH) secretion, phosphatidylinositol breakdown and cAMP accumulation was examined in primary cultures of mouse anterior pituitary cells. AVP and CRF added alone stimulated ACTH secretion in a dose-dependent manner. At 10(-8) M concentration of peptide, AVP and CRF stimulated ACTH secretion 2.8- and 4.6-fold, respectively. AVP and CRF added in combination at equal doses gave an additive effect. CRF enhanced cAMP accumulation, but AVP had no effect on basal or CRF-induced cAMP accumulation. Both forskolin (10(-5) M) and 8-bromo-cAMP (10(-3) M) increased ACTH secretion in these cells by 2.8- and 1.7-fold, respectively. AVP induced the breakdown of phosphoinositides, and CRF alone, or in combination with AVP did not modify this effect. Phorbol 12-myristate 13-acetate (10(-7) M), dioctanoylglycerol (10(-4) M) and phospholipase C (100 mU/ml) also stimulated ACTH secretion in these cells by 4.2-, 2.4-, and 3.7-fold, respectively. Depletion of intracellular and extracellular Ca2+ decreased ACTH secretion, but had no significant effect on CRF-induced cAMP accumulation. However, AVP-induced phosphoinositide breakdown was dependent on extracellular Ca2+. These results indicate that CRF stimulates ACTH secretion via the cAMP-dependent pathway and AVP via the phosphoinositide breakdown-phospholipase C pathway. In the presence of AVP and CRF, both pathways appear to operate independently to produce an additive effect on ACTH secretion. JF - Molecular and cellular endocrinology AU - Castro, M G AU - Gusovsky, F AU - Loh, Y P AD - Section on Cellular Neurobiology, Laboratory of Neurochemistry and Neuroimmunology, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 165 EP - 173 VL - 65 IS - 1-2 SN - 0303-7207, 0303-7207 KW - Diglycerides KW - 0 KW - Phosphatidylinositols KW - 1,2-dioctanoylglycerol KW - 1069-87-0 KW - Arginine Vasopressin KW - 113-79-1 KW - Colforsin KW - 1F7A44V6OU KW - 8-Bromo Cyclic Adenosine Monophosphate KW - 23583-48-4 KW - Egtazic Acid KW - 526U7A2651 KW - Adrenocorticotropic Hormone KW - 9002-60-2 KW - Corticotropin-Releasing Hormone KW - 9015-71-8 KW - Cyclic AMP KW - E0399OZS9N KW - Type C Phospholipases KW - EC 3.1.4.- KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Phosphatidylinositols -- metabolism KW - Animals KW - Mice KW - 8-Bromo Cyclic Adenosine Monophosphate -- pharmacology KW - Corticotropin-Releasing Hormone -- pharmacology KW - Arginine Vasopressin -- pharmacology KW - Colforsin -- pharmacology KW - Diglycerides -- pharmacology KW - Cells, Cultured KW - Calcium -- physiology KW - Cyclic AMP -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Type C Phospholipases -- pharmacology KW - Egtazic Acid -- pharmacology KW - Male KW - Adrenocorticotropic Hormone -- metabolism KW - Pituitary Gland, Anterior -- metabolism KW - Pituitary Gland, Anterior -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79189587?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-23 N1 - Date created - 1989-10-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molindone hydrochloride: a review of laboratory and clinical findings. AN - 79172263; 2671060 AB - Molindone hydrochloride, a dihydroindolone neuroleptic, is structurally distinct from other classes of neuroleptics. Molindone exhibits many similarities to other neuroleptics, including dopamine receptor blockade, antipsychotic efficacy, and extrapyramidal side effects. Despite these similarities, molindone also has atypical properties and inhibits the enzyme monoamine oxidase in vitro and in vivo. Several studies have shown that molindone causes less dopamine receptor supersensitivity than other neuroleptics and thus may be less likely to cause tardive dyskinesia. It also appears to have a greater effect on mesolimbic and mesocortical dopamine neurons than on those in the nigrostriatal dopamine system. Clinically, molindone has a tendency to cause weight loss and may have less effect on seizure threshold than conventional antipsychotic agents. The authors review the laboratory and clinical data on molindone and discuss the relevance of atypical research findings to the clinical characteristics of this antipsychotic agent. JF - Journal of clinical psychopharmacology AU - Owen, R R AU - Cole, J O AD - Clinical Neuroscience Branch, National Institute of Mental Health, Bethesda, Maryland. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 268 EP - 276 VL - 9 IS - 4 SN - 0271-0749, 0271-0749 KW - Indoles KW - 0 KW - Receptors, Dopamine KW - Molindone KW - RT3Y3QMF8N KW - Index Medicus KW - Receptors, Dopamine -- drug effects KW - Behavior, Animal -- drug effects KW - Animals KW - Humans KW - Adult KW - Substantia Nigra -- drug effects KW - Corpus Striatum -- drug effects KW - Schizophrenia -- drug therapy KW - Child KW - Indoles -- therapeutic use KW - Molindone -- therapeutic use KW - Molindone -- adverse effects KW - Psychotic Disorders -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79172263?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-27 N1 - Date created - 1989-09-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prevention and treatment of endotoxin and sepsis lethality with recombinant human tumor necrosis factor. AN - 79158659; 2669193 AB - Tumor necrosis factor (TNF) is a macrophage product released in response to endotoxin that has been implicated as a cause of the toxicity and lethality seen in septic shock. Previous work suggests that tolerance to nutritional and lethal effects of TNF occur after repeated exposure to recombinant tumor necrosis factor (rTNF). In this study pretreatment of rats with a single low intravenous dose of rTNF prevented subsequent death when a lethal dose of rTNF was administered 24 hours later (tolerance or tachyphylaxis). Pretreatment with rTNF also afforded protection against the lethal effects of either endotoxin or cecal ligation and puncture when rats were challenged 24 hours later. Recombinant TNF injected 6 hours after cecal ligation and puncture initially resulted in a significant survival advantage for treated animals. When this experiment was repeated with a different lot of rTNF, however, the therapeutic benefit of rTNF was not obtained until the dose was decreased by a factor of 10. Protection against the lethal effects of cecal ligation and puncture did not occur when rTNF was given 24 hours after the insult. A single low dose of rTNF can result in tolerance or tachyphylaxis to the lethal effects of TNF. The results suggest that the early administration of low-dose rTNF may be useful in the prevention and treatment of the lethality of sepsis. JF - Surgery AU - Sheppard, B C AU - Fraker, D L AU - Norton, J A AD - Surgical Metabolism Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 156 EP - 61; discussion 161-2 VL - 106 IS - 2 SN - 0039-6060, 0039-6060 KW - Endotoxins KW - 0 KW - Recombinant Proteins KW - Tumor Necrosis Factor-alpha KW - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Drug Tolerance KW - Animals KW - Rats, Inbred F344 KW - Tachyphylaxis KW - Male KW - Bacterial Infections -- therapy KW - Escherichia coli KW - Tumor Necrosis Factor-alpha -- therapeutic use KW - Endotoxins -- pharmacology KW - Bacterial Infections -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79158659?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-08 N1 - Date created - 1989-09-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interleukin 7 is a T-cell growth factor. AN - 79158585; 2788279 AB - Interleukin 7 (IL-7) is a 25-kDa cytokine which was purified and its corresponding cDNA was cloned based upon its ability to stimulate the proliferation of pre-B cells. It has been shown that IL-7 can also function as a costimulator with Con A for the proliferation of T lymphocytes by inducing the production of interleukin 2 (IL-2). We demonstrate here that IL-7 in combination with phorbol 12-myristate 13-acetate can directly drive the proliferation of purified T cells and that this response is not inhibited by cyclosporine A or by antibodies to IL-2 and IL-4. Stimulation of T cells with phorbol myristate acetate and IL-2, IL-4, or IL-7 prepared T cells to respond to any of the three lymphokines. Although T cells activated in vitro by anti-CD3 or allogeneic cells failed to proliferate when challenged with IL-7, T cells primed in vivo to the same stimuli demonstrated a significant proliferative response when restimulated in vitro with IL-7. IL-7 can, therefore, function both as a growth factor for T cells in an IL-2-independent manner and as a competence factor for the induction of lymphokine responsiveness. The ability to induce IL-7 responsiveness via stimulation of the T-cell receptor complex in vivo, but not in vitro, raises the possibility that IL-7 may play a role in T-cell growth and differentiation in vivo. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Chazen, G D AU - Pereira, G M AU - LeGros, G AU - Gillis, S AU - Shevach, E M AD - Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 5923 EP - 5927 VL - 86 IS - 15 SN - 0027-8424, 0027-8424 KW - Antibodies, Monoclonal KW - 0 KW - Interleukin-7 KW - Interleukins KW - Recombinant Proteins KW - Concanavalin A KW - 11028-71-0 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Recombinant Proteins -- pharmacology KW - Mice KW - Mice, Inbred BALB C KW - DNA Replication -- drug effects KW - Cells, Cultured KW - Mice, Inbred C57BL KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Lymph Nodes -- drug effects KW - Concanavalin A -- pharmacology KW - Female KW - Lymph Nodes -- immunology KW - Lymphocyte Activation -- drug effects KW - T-Lymphocytes -- cytology KW - Interleukins -- pharmacology KW - T-Lymphocytes -- drug effects KW - Interleukins -- immunology KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79158585?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-12 N1 - Date created - 1989-09-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Immunol. 1979 Jun;122(6):2491-7 [87465] J Exp Med. 1989 Mar 1;169(3):707-16 [2522498] J Immunol. 1981 Dec;127(6):2488-95 [6170707] J Exp Med. 1982 Mar 1;155(3):914-23 [6977612] Immunol Rev. 1983;74:29-56 [6195085] Proc Natl Acad Sci U S A. 1984 Aug;81(16):5214-8 [6332315] Hybridoma. 1982;1(2):125-31 [6821397] Nature. 1985 May 23-29;315(6017):333-6 [2582266] Annu Rev Immunol. 1985;3:133-57 [3933529] Proc Natl Acad Sci U S A. 1986 Aug;83(15):5654-8 [3090545] J Exp Med. 1986 Sep 1;164(3):709-22 [3489060] J Exp Med. 1987 Jan 1;165(1):157-72 [3098893] J Immunol. 1987 Feb 15;138(4):1121-9 [3543122] Proc Natl Acad Sci U S A. 1987 Mar;84(5):1374-8 [2950524] Proc Natl Acad Sci U S A. 1987 Nov;84(21):7629-33 [3499611] J Exp Med. 1988 Mar 1;167(3):988-1002 [3258354] J Exp Med. 1988 Apr 1;167(4):1417-27 [2965738] Nature. 1988 Jun 9;333(6173):571-3 [3259677] J Immunol. 1988 Jul 15;141(2):369-76 [2838547] J Immunol. 1988 Jul 15;141(2):504-11 [3133410] Transplantation. 1988 Aug;46(2 Suppl):53S-60S [3136567] J Immunol. 1988 Dec 1;141(11):3868-74 [3263438] Proc Natl Acad Sci U S A. 1989 Jan;86(1):302-6 [2643102] Immunol Rev. 1979;47:63-90 [398327] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Structural requirements for anthracycline-induced cardiotoxicity and antitumor effects. AN - 79155940; 2763305 AB - By employing rat cardiac myocytes in culture and mouse L-1210 leukemia cells, we have compared different anthracycline analogs with respect to their ability to kill cardiac myocytes and tumor cells. Anthracyclines induced a decrease in cellular ATP and glutathione from both cardiac myocytes and L-1210 cells in a time- and concentration-dependent fashion. Moreover, the decrease in ATP in cardiac myocytes was followed by release of the cytoplasmic enzyme lactic acid dehydrogenase and of adenine nucleotides after anthracycline treatment. At very low concentrations of anthracyclines, at which ATP and glutathione were not affected, the drugs induced complete cessation of the growth of L-1210 cells. Some structural alterations in the anthracycline molecule resulted in parallel changes in antitumor activity and in cardiotoxicity. But other structural alterations resulted in dissimilar changes in antitumor activity and cardiotoxicity. Although the results indicate that the structural requirements for inducing cardiotoxicity and antitumor activity may be different, they also indicate that the mechanisms by which anthracycline causes cell death in tumor cells and cardiac myocytes may be the same. JF - Toxicology and applied pharmacology AU - Singh, Y AU - Ulrich, L AU - Katz, D AU - Bowen, P AU - Krishna, G AD - Section on Drug Tissue Interaction, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 9 EP - 23 VL - 100 IS - 1 SN - 0041-008X, 0041-008X KW - Doxorubicin KW - 80168379AG KW - Daunorubicin KW - ZS7284E0ZP KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Cells, Cultured KW - Lethal Dose 50 KW - Cell Division -- drug effects KW - Mice KW - Leukemia L1210 -- drug therapy KW - Structure-Activity Relationship KW - Daunorubicin -- pharmacology KW - Doxorubicin -- analogs & derivatives KW - Doxorubicin -- pharmacology KW - Daunorubicin -- toxicity KW - Heart -- drug effects KW - Doxorubicin -- toxicity KW - Daunorubicin -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79155940?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-13 N1 - Date created - 1989-09-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mapping and insertional mutagenesis of a vaccinia virus gene encoding a 13,800-Da secreted protein. AN - 79154992; 2763467 AB - The objective of this study was to identify and characterize the gene encoding a protein of approximately 12 kDa that is secreted from cells infected with the vaccinia virus. The absence of this protein from the medium of cells infected with a spontaneous deletion mutant (6/2) suggested that the open reading frame (ORF) was located within a 12,800-base pair segment near the left end of the genome (G. Kotwal and B. Moss, Nature (London) 335, 176-178, 1988). Antibody to the 12-kDa protein immunoprecipitated an appropriate size in vitro translation product of mRNA that hybridized to a DNA segment containing an ORF (N1L) that could encode a 13.8-kDa polypeptide. The similarity in the sizes of the in vitro translation product and the secreted protein was consistent with the absence of processing. Transcriptional analysis revealed major and minor early RNA start sites preceding the N1L ORF as well as a late RNA start site with an atypical TAAAAT sequence. The N1L gene was interrupted by replacing a segment of the ORF with the Escherichia coli beta-galactosidase gene. When two-dimensional polyacrylamide gel electrophoretic patterns of [35S]methionine-labeled proteins secreted from cells infected with parental and recombinant viruses were compared, a spot missing from the latter corresponded in molecular weigh and isoelectric point with that predicted from the N1L ORF. The latter analysis revealed the presence of other secreted proteins of similar molecular weight but different isoelectric points that also appear to map within the left end of the vaccinia genome. The recombinant virus was attenuated as judged by the increased intracranial LD50 for mice but nevertheless induced antibody and cytotoxic responses after intradermal and intraperitoneal injections. Relative to the parental virus, the recombinant was also more attenuated for immunodeficient nude mice, based on their survival time after infection. JF - Virology AU - Kotwal, G J AU - Hügin, A W AU - Moss, B AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 579 EP - 587 VL - 171 IS - 2 SN - 0042-6822, 0042-6822 KW - N1L protein, Vaccinia virus KW - 0 KW - RNA, Messenger KW - Viral Proteins KW - Index Medicus KW - Base Sequence KW - DNA Mutational Analysis KW - Restriction Mapping KW - Isoelectric Point KW - Molecular Sequence Data KW - Transcription, Genetic KW - Amino Acid Sequence KW - RNA, Messenger -- genetics KW - Molecular Weight KW - Viral Proteins -- genetics KW - Vaccinia virus -- genetics KW - Genes, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79154992?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-12 N1 - Date created - 1989-09-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular cloning, characterization, and expression of human ADP-ribosylation factors: two guanine nucleotide-dependent activators of cholera toxin. AN - 79147644; 2474826 AB - ADP-ribosylation factors (ARFs) are small guanine nucleotide-binding proteins that enhance the enzymatic activities of cholera toxin. Two ARF cDNAs, ARF1 and ARF3, were cloned from a human cerebellum library. Based on deduced amino acid sequences and patterns of hybridization of cDNA and oligonucleotide probes with mammalian brain poly(A)+ RNA, human ARF1 is the homologue of bovine ARF1. Human ARF3, which differs from bovine ARF1 and bovine ARF2, appears to represent a newly identified third type of ARF. Hybridization patterns of human ARF cDNA and clone-specific oligonucleotides with poly(A)+ RNA are consistent with the presence of at least two, and perhaps four, separate ARF messages in human brain. In vitro translation of ARF1, ARF2, and ARF3 produced proteins that behaved, by SDS/PAGE, similar to a purified soluble brain ARF. Deduced amino acid sequences of human ARF1 and ARF3 contain regions, similar to those in other G proteins, that are believed to be involved in GTP binding and hydrolysis. ARFs also exhibit a modest degree of homology with a bovine phospholipase C. The observations reported here support the conclusion that the ARFs are members of a multigene family of small guanine nucleotide-binding proteins. Definition of the regulation of ARF mRNAs and of function(s) of recombinant ARF proteins will aid in the elucidation of the physiologic role(s) of ARFs. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Bobak, D A AU - Nightingale, M S AU - Murtagh, J J AU - Price, S R AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, Bethesda, MD 20892. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 6101 EP - 6105 VL - 86 IS - 16 SN - 0027-8424, 0027-8424 KW - RNA, Messenger KW - 0 KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Poly A KW - 24937-83-5 KW - RNA KW - 63231-63-0 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 - ARF4 protein, human KW - Index Medicus KW - Animals KW - Base Sequence KW - Sequence Homology, Nucleic Acid KW - Humans KW - Poly A -- genetics KW - Molecular Sequence Data KW - Brain -- metabolism KW - Amino Acid Sequence KW - Nucleic Acid Hybridization KW - Adenosine Diphosphate Ribose -- metabolism KW - RNA -- genetics KW - GTP-Binding Proteins -- metabolism KW - DNA -- metabolism KW - DNA -- genetics KW - GTP-Binding Proteins -- genetics KW - Cloning, Molecular KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79147644?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-19 N1 - Date created - 1989-09-19 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M25204; GENBANK; M25203 N1 - SuppNotes - Cited By: Anal Biochem. 1983 Jul 1;132(1):6-13 [6312838] Proc Natl Acad Sci U S A. 1988 Oct;85(20):7652-6 [3174659] J Cyclic Nucleotide Protein Phosphor Res. 1983-1984;9(6):435-48 [6396323] J Biol Chem. 1986 Jun 15;261(17):7906-11 [3086320] Proc Natl Acad Sci U S A. 1987 May;84(10):3107-11 [3106961] Proc Natl Acad Sci U S A. 1987 Aug;84(15):5139-42 [3110784] Annu Rev Biochem. 1987;56:779-827 [3304147] Nature. 1970 Aug 15;227(5259):680-5 [5432063] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4 [388439] Proc Natl Acad Sci U S A. 1983 Mar;80(5):1194-8 [6219389] Methods Enzymol. 1987;152:337-42 [3309564] J Biol Chem. 1988 Feb 5;263(4):1768-72 [3123477] Science. 1988 Jan 29;239(4839):487-91 [2448875] J Biol Chem. 1988 Feb 25;263(6):2577-80 [2830256] Nature. 1988 Mar 17;332(6161):269-72 [2831461] Adv Enzymol Relat Areas Mol Biol. 1988;61:303-79 [3128060] Proc Natl Acad Sci U S A. 1988 Apr;85(8):2444-8 [3162770] FASEB J. 1988 May;2(8):2356-67 [2452111] Cell. 1988 Jun 3;53(5):669-71 [2836065] J Biol Chem. 1988 Jun 15;263(17):8282-7 [3131341] J Biol Chem. 1988 Jul 15;263(20):9926-32 [3133371] J Biol Chem. 1988 Nov 25;263(33):17255-7 [3141419] J Biol Chem. 1988 Dec 15;263(35):18965-71 [3143720] Anal Biochem. 1989 May 1;178(2):239-42 [2751085] Proc Natl Acad Sci U S A. 1988 Jul;85(13):4620-4 [3133654] Proc Natl Acad Sci U S A. 1988 Aug;85(15):5488-91 [3135549] Oncogene. 1988 Aug;3(2):201-4 [3045729] Nucleic Acids Res. 1988 Aug 11;16(15):7583-600 [2970625] J Biol Chem. 1984 May 25;259(10):6228-34 [6327671] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutagenesis of phi X174 am3 cs70 incorporated into the genome of mouse L-cells. AN - 79139944; 2761552 AB - The objective of our work with phi X174 has been to develop a shuttle vector that can be used comparatively in bacterial cells, different types of mammalian cells, and possibly in the various tissues of transgenic mice, with a constant mechanism for detection and analysis of mutations independent of any host-cell type. Toward that end, we have efficiently rescued phi X174 am3 cs70 that is host-silent and stably integrated into the genome of mouse L-cells. The particular mouse L-cell line contains tandem arrays, single copies, and fragments of phi X that, upon restriction enzyme excision, can result in 5 potentially active copies per diploid genome. The excised phi X DNA is recovered by column chromatography, ligated, and transfected into highly competent spheroplasts. The Rescue Efficiency, defined as the number of viable phages produced out of the total number of potentially recoverable copies, is approx. 10(-3). The Recovery Ratio, defined as the Rescue Efficiency for chromosomally-integrated phage DNA divided by the Rescue Efficiency for phi X am3 cs70, is close to one. Mouse L-cells containing the integrated phi X174 am3 cs70 were treated with 20 mM ethyl methanesulfonate. The reversion frequency of am3 among progeny phages rescued from treated cells was 1.4 X 10(-5) (193 revertants in 1.4 X 10(7) phages). This is significantly higher than the 5.8 X 10(-7) reversion frequency of am3 (7 revertants in 1.2 X 10(7) phages) among progeny phages rescued from untreated cells. JF - Mutation research AU - Burkhart, J G AU - Malling, H V AD - Laboratory of Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 125 EP - 134 VL - 213 IS - 2 SN - 0027-5107, 0027-5107 KW - DNA, Viral KW - 0 KW - Index Medicus KW - L Cells (Cell Line) KW - Animals KW - Mutagenicity Tests KW - Electrophoresis, Agar Gel KW - Chromatography, Liquid KW - Mice KW - DNA, Viral -- isolation & purification KW - Genetic Vectors KW - Bacteriophages -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79139944?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-13 N1 - Date created - 1989-09-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prophylactic zidovudine after occupational exposure to the human immunodeficiency virus: an interim analysis. AN - 79126680; 2760486 AB - Note from Dr. Merle A. Sande--Health care workers are at risk of acquiring human immunodeficiency virus (HIV) infection subsequent to accidental sticks with needles contaminated with blood from infected patients. The risk is small but real. Postexposure management is critically important, but few solid data are available. Can zidovudine (AZT, azidothymidine) prevent infection? How soon after exposure must the drug be given? At what dosage? For how long? Two leading authorities were asked to discuss this problem and to offer recommendations. Both have developed programs in their institutions, Dr. David K. Henderson at the Warren Grant Magnuson Clinical Center at the National Institutes of Health and Dr. Julie L. Gerberding at the University of California, San Francisco. JF - The Journal of infectious diseases AU - Henderson, D K AU - Gerberding, J L AD - Hospital Epidemiology Service, Warren G. Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 321 EP - 327 VL - 160 IS - 2 SN - 0022-1899, 0022-1899 KW - Zidovudine KW - 4B9XT59T7S KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Humans KW - Zidovudine -- therapeutic use KW - Acquired Immunodeficiency Syndrome -- prevention & control KW - Zidovudine -- adverse effects KW - Occupational Diseases -- prevention & control KW - Health Manpower UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79126680?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-08 N1 - Date created - 1989-09-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Systemic therapy for small-cell lung cancer: old themes replayed, new ones awaited. AN - 79123363; 2547029 JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Viallet, J AU - Ihde, D C AD - National Cancer Institute Bethesda, MD. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 985 EP - 987 VL - 7 IS - 8 SN - 0732-183X, 0732-183X KW - Mitomycins KW - 0 KW - Mitomycin KW - 50SG953SK6 KW - Etoposide KW - 6PLQ3CP4P3 KW - Lomustine KW - 7BRF0Z81KG KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Cisplatin KW - Q20Q21Q62J KW - Altretamine KW - Q8BIH59O7H KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Etoposide -- administration & dosage KW - Humans KW - Mitomycins -- administration & dosage KW - Altretamine -- administration & dosage KW - Doxorubicin -- administration & dosage KW - Lomustine -- administration & dosage KW - Methotrexate -- administration & dosage KW - Cisplatin -- administration & dosage KW - Lung Neoplasms -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Carcinoma, Small Cell -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79123363?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-29 N1 - Date created - 1989-08-29 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Clin Oncol. 1990 Jul;8(7):1282-3 [2162913] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparative tumorigenicity of N-nitroso-2-hydroxymorpholine, N-nitrosodiethanolamine and N-nitrosomorpholine in A/J mice and F344 rats. AN - 79120487; 2752522 AB - N-Nitroso-2-hydroxymorpholine (NHMOR), a genotoxic metabolite of the environmental carcinogens N-nitrosomorpholine (NMOR) and N-nitrosodiethanolamine (NDELA), was assayed for tumorigenicity in A/J mice and F344 rats. Groups of female mice were given NHMOR, NMOR or NDELA in the drinking water over a 10-week period; total doses were 53-55 mumol/mouse. The experiment was terminated after 30 weeks. Whereas NMOR was a potent tumorigen, inducing 20.3 lung tumors/mouse, NHMOR and NDELA were only weakly tumorigenic, giving 1.2 and 1.4 lung tumors/mouse respectively. Groups of female F344 rats were also given these three nitrosamines in drinking water for 50 weeks, as follows: NHMOR, total dose 0.6 mmol/rat; NHMOR, 1.2 mmol; NMOR, 1.1 mmol and NDELA, 5.6 mmol. The experiment was terminated after 120 weeks. NMOR was a potent carcinogen, inducing liver tumors in 100% of the rats. NDELA gave hepatocellular tumors in 70% of the rats. NHMOR was inactive even at the higher dose. The results of this study do not support the hypothesis that NHMOR is a proximate carcinogen of NDELA or NMOR. JF - Carcinogenesis AU - Hecht, S S AU - Lijinsky, W AU - Kovatch, R M AU - Chung, F L AU - Saavedra, J E AD - NCI-Frederick Cancer Research Facility, MD 21701. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 1475 EP - 1477 VL - 10 IS - 8 SN - 0143-3334, 0143-3334 KW - Carcinogens KW - 0 KW - Nitrosamines KW - N-nitrosodiethanolamine KW - 30YI1289VY KW - Diethylnitrosamine KW - 3IQ78TTX1A KW - N-nitrosomorpholine KW - 3L25FO7FN7 KW - N-nitroso-2-hydroxymorpholine KW - 67587-52-4 KW - Index Medicus KW - Thyroid Neoplasms -- chemically induced KW - Animals KW - Adenocarcinoma -- chemically induced KW - Liver Neoplasms -- chemically induced KW - Hemangiosarcoma -- chemically induced KW - Mice KW - Structure-Activity Relationship KW - Adenocarcinoma -- pathology KW - Rats KW - Mice, Inbred A KW - Rats, Inbred F344 KW - Liver Neoplasms -- pathology KW - Liver Neoplasms, Experimental -- pathology KW - Hemangiosarcoma -- pathology KW - Thyroid Neoplasms -- pathology KW - Lung Neoplasms -- chemically induced KW - Species Specificity KW - Female KW - Lung Neoplasms -- pathology KW - Diethylnitrosamine -- toxicity KW - Diethylnitrosamine -- analogs & derivatives KW - Nitrosamines -- toxicity KW - Carcinogens -- toxicity KW - Neoplasms, Experimental -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79120487?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-31 N1 - Date created - 1989-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vitro processing of dengue virus structural proteins: cleavage of the pre-membrane protein. AN - 79118137; 2501515 AB - Processing of dengue virus structural proteins was assessed in vitro. RNA transcripts for cell-free translation were prepared from cloned DNA (dengue virus type 4, strain 814669 genome) encoding capsid, pre-membrane (prM), and the first 23 amino acids of envelope (E). Processing of a 33-kilodalton precursor polypeptide encoded by wild-type RNA transcripts occurred only in the presence of added microsomal membranes. Under these conditions, cleavage at the capsid-prM and prM-E sites and glycosylation of prM occurred in association with translocation. Amino acid sequence analysis confirmed that translation initiated at the predicted N terminus of the capsid and that capsid-prM cleavage occurred at the predicted site for the action of signal peptidase following a candidate signal sequence (hydrophobic residues 100 to 113) in the dengue virus precursor. Mutations were introduced into the dengue virus DNA template by site-directed mutagenesis, altering nucleotide sequences encoding the capsid and the candidate signal for prM. The phenotypes of the mutants were deduced by analysis of the products of cell-free translation of the respective RNA transcripts. The resulting observations confirmed that cleavage at the capsid-prM and prM-E sites is effected entirely by signal peptidase and that the candidate signal is required for translocation. JF - Journal of virology AU - Markoff, L AD - Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 3345 EP - 3352 VL - 63 IS - 8 SN - 0022-538X, 0022-538X KW - DNA, Viral KW - 0 KW - Glycoproteins KW - Protein Precursors KW - Protein Sorting Signals KW - RNA, Viral KW - Viral Proteins KW - Viral Structural Proteins KW - Glycoside Hydrolases KW - EC 3.2.1.- KW - Mannosyl-Glycoprotein Endo-beta-N-Acetylglucosaminidase KW - EC 3.2.1.96 KW - Index Medicus KW - Protein Biosynthesis KW - Protein Precursors -- metabolism KW - Protein Sorting Signals -- genetics KW - Glycoside Hydrolases -- metabolism KW - Capsid -- genetics KW - Transcription, Genetic KW - Amino Acid Sequence KW - Precipitin Tests KW - Glycoproteins -- metabolism KW - Restriction Mapping KW - RNA, Viral -- genetics KW - DNA, Viral -- genetics KW - Mutation KW - Viral Proteins -- genetics KW - Protein Processing, Post-Translational KW - Viral Proteins -- metabolism KW - Dengue Virus -- genetics KW - Dengue Virus -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79118137?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-18 N1 - Date created - 1989-08-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Virology. 1972 Jul;49(1):283-9 [4625020] J Immunol. 1967 Aug;99(2):291-6 [4961907] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Virology. 1978 Sep;89(2):423-37 [568848] Virology. 1981 Mar;109(2):418-27 [6259820] Virology. 1981 Apr 15;110(1):26-34 [7210510] Biochem J. 1981 Jun 1;195(3):639-44 [7316978] J Biol Chem. 1982 Oct 25;257(20):12180-90 [6896877] J Mol Biol. 1983 Jun 5;166(4):477-535 [6864790] Methods Enzymol. 1983;100:468-500 [6225933] Proc Natl Acad Sci U S A. 1985 Jul;82(14):4648-52 [3895223] Science. 1985 Aug 23;229(4715):726-33 [4023707] Virology. 1985 Sep;145(2):227-36 [2992152] Virology. 1985 May;143(1):224-9 [2998002] Cell. 1986 Jan 31;44(2):283-92 [3943125] J Mol Biol. 1986 Feb 5;187(3):309-23 [3009829] FEBS Lett. 1986 May 12;200(2):314-6 [3635477] Nucleic Acids Res. 1986 Jun 11;14(11):4683-90 [3714490] Virology. 1986 Nov;155(1):77-88 [3022479] Virology. 1986 Dec;155(2):365-77 [3024394] Virology. 1987 Feb;156(2):293-304 [3027980] Arch Virol. 1987;92(3-4):273-91 [3813888] Virology. 1987 Jun;158(2):348-60 [3035787] Adv Virus Res. 1987;33:45-90 [3035906] Virology. 1987 Aug;159(2):217-28 [3039728] Virology. 1987 Aug;159(2):237-43 [2441520] J Mol Biol. 1987 Jun 5;195(3):621-36 [2821280] Virology. 1987 Nov;161(1):262-7 [3672932] J Virol. 1987 Dec;61(12):4019-22 [3316711] J Gen Virol. 1988 Jan;69 ( Pt 1):1-21 [2826659] J Gen Virol. 1988 Jan;69 ( Pt 1):23-34 [2826667] Virology. 1988 Jan;162(1):167-80 [2827375] Virology. 1973 Feb;51(2):454-65 [4632654] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanisms of hypertension in the elderly. AN - 79110123; 2666486 AB - It has long been recognized that, with advancing age, basal systolic blood pressure increases within the clinically "normal" range in many individuals. Likewise, the prevalence of clinical hypertension, either systolic plus diastolic or isolated systolic, also increases with age. This report reviews the purported mechanisms underlying these types of hypertension and discusses age-associated changes in the cardiovascular system of normotensive individuals that could plausibly interact with these pathophysiologic mechanisms of hypertension. JF - Journal of the American Geriatrics Society AU - Lakatta, E G AD - Laboratory of Cardiovascular Science, National Institute on Aging, Baltimore, Maryland 21224. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 780 EP - 790 VL - 37 IS - 8 SN - 0002-8614, 0002-8614 KW - Sodium, Dietary KW - 0 KW - Index Medicus KW - Animals KW - Sodium, Dietary -- adverse effects KW - Humans KW - Hemodynamics KW - Autonomic Nervous System -- physiopathology KW - Aging -- physiology KW - Hypertension -- physiopathology KW - Hypertension -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79110123?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-06 N1 - Date created - 1989-09-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effect of intravenous interleukin-2 on brain water content. AN - 79107071; 2787395 AB - Parenteral treatment with interleukin-2 (IL-2) is effective against certain advanced cancers outside the central nervous system. Prior to commencement of Phase II trials in patients with brain tumors, the neurological and neuroradiological features of 10 patients treated with intravenous administration of repeated doses of IL-2 were studied. Three patients had malignant gliomas, and seven patients had extracranial cancer without evidence of intracranial metastasis. All were treated with intravenous doses of 10(5) U/kg three times daily for up to 5 days. The patients with gliomas received cranial computerized axial tomography (CT) scans before IL-2 therapy was initiated and during the later stages of treatment. The patients with extracranial cancer underwent T2-weighted magnetic resonance (MR) imaging before and later during therapy. After two to 11 doses of IL-2, the patients with gliomas had marked neurological deterioration that was associated with a mild to marked increase in peritumoral edema and mass effect visible on CT scans. With cessation of treatment and appropriate supportive care, all returned to their pretreatment state. The patients with extracranial cancer were either neurologically unchanged or underwent minor transient changes in mental status (lethargy and confusion). In these patients, the MR signal intensity was quantified and compared in eight anatomic regions of interest. In six of the seven patients, there were increases in gray and white matter signal intensity consistent with increased cerebral water content. The percentage changes (means +/- standard error of the means) were 12.6% +/- 7.3% in the gray matter and 17.0% +/- 6.2% in the white matter. This study demonstrates that treatment with a high parenteral dose of IL-2 is not tolerated by patients with gliomas due to increased cerebral edema. In patients with extracranial cancer but no brain disease, parenteral IL-2 induces an increase in the cerebral water content of both gray and white matter. JF - Journal of neurosurgery AU - Saris, S C AU - Patronas, N J AU - Rosenberg, S A AU - Alexander, J T AU - Frank, J AU - Schwartzentruber, D J AU - Rubin, J T AU - Barba, D AU - Oldfield, E H AD - Clinical Neurosurgery Section, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 169 EP - 174 VL - 71 IS - 2 SN - 0022-3085, 0022-3085 KW - Interleukin-2 KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Injections, Intravenous KW - Humans KW - Brain Chemistry -- drug effects KW - Interleukin-2 -- adverse effects KW - Interleukin-2 -- administration & dosage KW - Glioma -- drug therapy KW - Brain Neoplasms -- drug therapy KW - Interleukin-2 -- therapeutic use KW - Brain Edema -- chemically induced KW - Brain Neoplasms -- metabolism KW - Glioma -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79107071?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-23 N1 - Date created - 1989-08-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in the dog: effect of pargyline pretreatment. AN - 79104408; 2568405 AB - Adult beagle dogs of either sex were injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-HCl (2.5 mg/kg, i.v.) alone or after pretreatment with pargyline (5.0 mg/kg, s.c., twice), with pargyline alone, or were uninjected. Groups were killed 2 h, 3 weeks, or 3 months after injection, and several brain areas were assayed for biogenic amines and their synthetic and degradative enzymes. MPTP caused a massive and permanent loss of striatal dopamine, tyrosine hydroxylase, and 3,4-dihydroxyphenylalanine decarboxylase activities and the loss of cells within the substantia nigra pars compacta. Dopamine and norepinephrine also were depleted to various degrees in cortex, olfactory bulb, and hypothalamus; however, dopamine beta-hydroxylase activity in cortex was normal. There was no cell loss in the ventral tegmental area or locus ceruleus. The activities of monoamine oxidase (MAO)-A and MAO-B in cortex and caudate were not affected by MPTP. Despite a permanent loss of the nigrostriatal system, the dogs exhibited only a transient hypokinesia lasting 1-2 weeks. Pargyline pretreatment prevented the loss of striatal dopamine and cells from the substantia nigra, but did not prevent a prolonged but reversible decrease in the concentration of dopamine metabolites. It is argued that this apparent inhibition of MAO is due not to suicide inactivation of the enzyme by MPTP, but to reversible inhibition by accumulation of the pyridinium metabolite, 1-methyl-4-phenylpyridinium, selectivity in aminergic terminals. JF - Journal of neurochemistry AU - Johannessen, J N AU - Chiueh, C C AU - Bacon, J P AU - Garrick, N A AU - Burns, R S AU - Weise, V K AU - Kopin, I J AU - Parisi, J E AU - Markey, S P AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1989/08// PY - 1989 DA - August 1989 SP - 582 EP - 589 VL - 53 IS - 2 SN - 0022-3042, 0022-3042 KW - Pyridines KW - 0 KW - 3,4-Dihydroxyphenylacetic Acid KW - 102-32-9 KW - Pargyline KW - 9MV14S8G3E KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Tyrosine 3-Monooxygenase KW - EC 1.14.16.2 KW - Monoamine Oxidase KW - EC 1.4.3.4 KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Animals KW - Tyrosine 3-Monooxygenase -- metabolism KW - Brain -- drug effects KW - Dopamine -- metabolism KW - Brain -- metabolism KW - Tissue Distribution KW - Behavior, Animal -- drug effects KW - 3,4-Dihydroxyphenylacetic Acid -- metabolism KW - Norepinephrine -- metabolism KW - Brain -- pathology KW - Dogs KW - Monoamine Oxidase -- metabolism KW - Female KW - Male KW - Pargyline -- pharmacology KW - Pyridines -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79104408?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-25 N1 - Date created - 1989-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human peripheral lymphocyte growth regulation and response to phorbol esters is linked to synthesis and phosphorylation of the cytosolic protein, prosolin. AN - 79080235; 2745978 AB - Prosolin is a major cytosolic protein (Mr 18400, isoelectric point 5.9) first reported in HL-60 promyelocytic leukemia cells. It is rapidly phosphorylated (15 to 30 min) in response to TPA treatment as an early event in a sequence that leads to cessation of cell proliferation and to differentiation of promyelocytes into monocytes. In our study we examined the expression of prosolin in human peripheral lymphocytes and investigated the effects of TPA treatment on prosolin phosphorylation and on lymphocyte proliferation. Prosolin was not expressed in resting PBL but was induced after 24 to 36 h of PHA stimulation, simultaneously with induction of DNA synthesis. In rapidly proliferating (IL-2 dependent) PBL prosolin was a major cytosolic component, comprising 0.5% of total cytosolic protein, of which approximately 28% was phosphorylated. Expression of prosolin decreased again when either mitogen-induced or IL-2-dependent proliferation diminished during extended periods in culture. Thus, expression of prosolin is correlated with periods when PBL are cycling through S-phase. TPA treatment of IL-2-dependent PBL at the peak of their growth caused phosphorylation of about two-thirds of preexisting unphosphorylated prosolin within 1 h. This was accompanied by cessation of cell proliferation, as indicated by measurements of TdR incorporation. Although TPA has well known mitogenic effects in lymphocytes during initial activation, this result shows that it exerts an antiproliferative effect in rapidly dividing PBL. It is suggested that increased phosphorylation of prosolin may be an initiating event in the antiproliferative response to TPA, which would occur only in proliferating lymphocytes expressing prosolin. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Cooper, H L AU - McDuffie, E AU - Braverman, R AD - Cell and Molecular Physiology Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/08/01/ PY - 1989 DA - 1989 Aug 01 SP - 956 EP - 963 VL - 143 IS - 3 SN - 0022-1767, 0022-1767 KW - Neoplasm Proteins KW - 0 KW - Phosphoproteins KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Phosphorylation KW - Humans KW - Cell Division -- drug effects KW - Cell Differentiation -- drug effects KW - Lymphocyte Activation -- drug effects KW - Cytosol -- physiology KW - Neoplasm Proteins -- biosynthesis KW - Lymphocytes -- immunology KW - Phosphoproteins -- biosynthesis KW - Neoplasm Proteins -- isolation & purification KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Lymphocytes -- metabolism KW - Lymphocytes -- physiology KW - Phosphoproteins -- isolation & purification KW - Neoplasm Proteins -- metabolism KW - Phosphoproteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79080235?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-18 N1 - Date created - 1989-08-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cadmium carcinogenesis in male Wistar [Crl:(WI)BR] rats: dose-response analysis of effects of zinc on tumor induction in the prostate, in the testes, and at the injection site. AN - 79066342; 2743314 AB - The ability of zinc acetate to modify the carcinogenic effects of CdCl2 in male Wistar [Crl:(WI)BR] rats was studied over a 2-year period. Groups of rats received a single s.c. injection of Cd (30.0 mumol/kg) in the dorsal thoracic midline or i.m. in the right thigh at time 0. Zinc was given in three separate s.c. doses of 0.1, 0.3, or 1.0 mmol/kg (at -6, 0, and +18 h relative to cadmium) in the lumbosacral area or p.o. at 100 ppm in the drinking water (-2 to +100 weeks). Cadmium treatments (s.c.) resulted in the appearance of tumors at the injection site and in the testes. The incidence of s.c. injection site tumors (mostly mixed sarcomas) was markedly reduced by high dose (1.0 mmol/kg) s.c. zinc (50% reduction) and was almost abolished by p.o. zinc (92% reduction). Testicular tumors (mostly Leydig cell adenomas) induced by s.c. cadmium were reduced in a dose-related fashion by zinc and were found to be highly dependent on the ability of zinc to prevent the chronic degenerative effects of cadmium in the testes. Oral zinc had no effect on s.c. cadmium-induced testicular tumors, while i.m. cadmium alone did not induce these tumors. In rats in which s.c. cadmium-induced testicular tumors and chronic degenerative effects were prevented by zinc (1.0 mmol/kg, s.c.), a marked elevation in prostatic tumors (exclusively adenomas) occurred (control, 9.6%; cadmium plus high zinc 29.6%). Cadmium given i.m., which did not result in testicular tumors or degeneration, also induced an elevated incidence (42.3%) of prostatic tumors, again indicating a dependence on testicular function. Prostatic tumor incidence was also significantly elevated (25.0%) in rats receiving 1.0 mmol/kg zinc, s.c., in combination with i.m. cadmium. These results indicate that zinc inhibition of cadmium carcinogenesis is a complex phenomenon, depending not only on dose and route but also on the target site in question. JF - Cancer research AU - Waalkes, M P AU - Rehm, S AU - Riggs, C W AU - Bare, R M AU - Devor, D E AU - Poirier, L A AU - Wenk, M L AU - Henneman, J R AD - Inorganic Carcinogenesis Section, National Cancer Institute, Frederick, Maryland. Y1 - 1989/08/01/ PY - 1989 DA - 1989 Aug 01 SP - 4282 EP - 4288 VL - 49 IS - 15 SN - 0008-5472, 0008-5472 KW - Cadmium KW - 00BH33GNGH KW - Metallothionein KW - 9038-94-2 KW - Zinc KW - J41CSQ7QDS KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Metallothionein -- biosynthesis KW - Dose-Response Relationship, Drug KW - Injections, Subcutaneous KW - Male KW - Zinc -- pharmacology KW - Sarcoma, Experimental -- prevention & control KW - Sarcoma, Experimental -- chemically induced KW - Skin Neoplasms -- chemically induced KW - Testicular Neoplasms -- prevention & control KW - Prostatic Neoplasms -- chemically induced KW - Cadmium -- toxicity KW - Prostatic Neoplasms -- prevention & control KW - Testicular Neoplasms -- chemically induced KW - Skin Neoplasms -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79066342?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-25 N1 - Date created - 1989-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vivo activity against HIV and favorable toxicity profile of 2',3'-dideoxyinosine. AN - 79123347; 2502840 AB - The purine analog 2',3'-dideoxyinosine (ddI), which has anti-retroviral activity in vitro was administered for up to 42 weeks to 26 patients with acquired immunodeficiency syndrome (AIDS) or severe AIDS-related complex (ARC). Ten of these individuals were AZT-intolerant. Eight dose regimens were studied. The drug was orally bioavailable and penetrated into the cerebrospinal fluid (CSF). Comparatively little evidence of an effect against human immunodeficiency virus (HIV) was seen at the lowest four doses. However, patients in the four highest dose groups (ddI at 1.6 milligrams per kilogram intravenously and then greater than or equal to 3.2 milligrams per kilogram orally at least every 12 hours or higher) had increases in their circulating CD4+ T cells (P less than 0.0005), increased CD4/CD8 T cell ratios (P less than 0.01), and, where evaluable, more than an 80% decrease in serum HIV p24 antigen (P less than 0.05). The patients also had evidence of improved immunologic function, had reduced viremic symptomatology, and gained a mean of 1.6 kilogram with these comparatively infrequent dosing schedules (every 8 or 12 hours). The most notable adverse effects directly attributable to ddI administration at the doses used in this study included increases in serum uric acid (due to hypoxanthine release) and mild headaches and insomnia. These results suggest that serious short-term toxicity at therapeutic doses is not an inherent feature in the profile of agents with clinical anti-HIV activity. Further controlled studies to define the safety and efficacy of this agent may be worth considering. JF - Science (New York, N.Y.) AU - Yarchoan, R AU - Mitsuya, H AU - Thomas, R V AU - Pluda, J M AU - Hartman, N R AU - Perno, C F AU - Marczyk, K S AU - Allain, J P AU - Johns, D G AU - Broder, S AD - Clinical Oncology Program, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/07/28/ PY - 1989 DA - 1989 Jul 28 SP - 412 EP - 415 VL - 245 IS - 4916 SN - 0036-8075, 0036-8075 KW - Antiviral Agents KW - 0 KW - Dideoxynucleosides KW - HIV Antigens KW - HIV Core Protein p24 KW - Retroviridae Proteins KW - Didanosine KW - K3GDH6OH08 KW - Index Medicus KW - AIDS/HIV KW - Molecular Structure KW - Retroviridae Proteins -- analysis KW - Dose-Response Relationship, Drug KW - Humans KW - Clinical Trials as Topic KW - Leukocyte Count KW - Biological Availability KW - HIV Antigens -- analysis KW - Hypersensitivity, Delayed KW - Immunity, Cellular KW - Adult KW - Middle Aged KW - T-Lymphocytes -- immunology KW - Male KW - Female KW - Antiviral Agents -- therapeutic use KW - HIV -- drug effects KW - AIDS-Related Complex -- immunology KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Dideoxynucleosides -- therapeutic use KW - Antiviral Agents -- cerebrospinal fluid KW - Dideoxynucleosides -- pharmacology KW - AIDS-Related Complex -- drug therapy KW - Antiviral Agents -- pharmacology KW - Acquired Immunodeficiency Syndrome -- immunology KW - Dideoxynucleosides -- adverse effects KW - Antiviral Agents -- adverse effects KW - Dideoxynucleosides -- cerebrospinal fluid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79123347?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-30 N1 - Date created - 1989-08-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of calcium entry by the tumor promoter thapsigargin in parotid acinar cells. Evidence that an intracellular calcium pool and not an inositol phosphate regulates calcium fluxes at the plasma membrane. AN - 79092643; 2663854 AB - The depletion of an inositol 1, 4,5-trisphosphate-sensitive intracellular Ca2+ pool has been proposed to be the signal for Ca2+ entry in agonist-activated cells. Consistent with this idea, thapsigargin, which releases intracellular Ca2+ without inositol phosphate formation, has been reported to activate Ca2+ entry in certain cells. We now report the effects of thapsigargin on Ca2+ entry in parotid acinar cells. In fura-2-loaded parotid acinar cells, thapsigargin caused a sustained elevation of [Ca2+], but did not increase inositol phosphate formation. In the absence of extracellular Ca2+, the increase in [Ca2+], was transient, suggesting that thapsigargin activates both the release of Ca2+ from intracellular stores and the entry of Ca2+ from the extracellular space. In the absence of extracellular Ca2+, pretreatment with methacholine, an agonist believed to mobilize Ca2+ through the production of inositol 1,4,5-trisphosphate, inhibited but did not completely block the response to thapsigargin; likewise, pretreatment with thapsigargin inhibited the response to methacholine. In permeabilized cells, thapsigargin gradually released Ca2+, whereas inositol 1,4,5-trisphosphate caused a rapid and transient discharge of Ca2+. The simultaneous addition of thapsigargin with inositol 1,4,5-trisphosphate evoked a maximum Ca2+ release similar to that for inositol 1,4,5-trisphosphate alone, but the reuptake seen with inositol 1,4,5-trisphosphate alone was abolished. In intact cells, methacholine and thapsigargin together produced a greater initial release of Ca2+ than either alone, but they were not additive in the sustained phase of Ca2+ mobilization. These results demonstrate that the mechanisms for activation of Ca2+ entry by thapsigargin and methacholine are the same and are consistent with the idea that entry is initiated by the depletion of the intracellular inositol 1,4,5-trisphosphate-sensitive Ca2+ pool. The results also indicate that, in contrast to previously proposed models, Ca2+ entry into agonist-activated cells occurs directly across the plasma membrane to the cytoplasm rather than through a cycle of uptake and release by the intracellular Ca2+ pool. JF - The Journal of biological chemistry AU - Takemura, H AU - Hughes, A R AU - Thastrup, O AU - Putney, J W AD - Laboratory of Cellular and Molecular Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/07/25/ PY - 1989 DA - 1989 Jul 25 SP - 12266 EP - 12271 VL - 264 IS - 21 SN - 0021-9258, 0021-9258 KW - Carcinogens KW - 0 KW - Ethers KW - Inositol Phosphates KW - Methacholine Compounds KW - Plant Extracts KW - Sugar Phosphates KW - Methacholine Chloride KW - 0W5ETF9M2K KW - Inositol KW - 4L6452S749 KW - Ionomycin KW - 56092-81-0 KW - Thapsigargin KW - 67526-95-8 KW - Inositol 1,4,5-Trisphosphate KW - 85166-31-0 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Ethers -- pharmacology KW - Cell Membrane -- drug effects KW - Methacholine Compounds -- pharmacology KW - Inositol -- metabolism KW - Models, Biological KW - Biological Transport -- drug effects KW - Rats KW - Cells, Cultured KW - Kinetics KW - Cell Membrane Permeability KW - Cell Membrane -- metabolism KW - Signal Transduction KW - Calcium -- metabolism KW - Plant Extracts -- pharmacology KW - Carcinogens -- pharmacology KW - Sugar Phosphates -- metabolism KW - Parotid Gland -- drug effects KW - Inositol Phosphates -- metabolism KW - Sugar Phosphates -- pharmacology KW - Parotid Gland -- metabolism KW - Parotid Gland -- cytology KW - Inositol Phosphates -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79092643?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-18 N1 - Date created - 1989-08-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Thirteen-week toxicity study of n-hexane in B6C3F1 mice after inhalation exposure. AN - 79107275; 2749745 AB - B6C3F1 mice were exposed to n-hexane 6 h/day, 5 days/week for 13 weeks at concentrations of 0, 500, 1000, 4000, and 10,000 ppm and at 1000 ppm 22 h/day, 5 days/week for 13 weeks (1000C group). Toxicological endpoints assessed included clinical signs, body and organ weight changes, gross and histopathology, neuropathology, and a battery of neurobehavioral tests. All mice survived the treatment. Exposure-related effects of n-hexane included sneezing at 10,000 ppm and body weight gain depression at 1000C and 10,000 ppm. Histopathologic changes included mild inflammatory, erosive and regenerative lesions in the olfactory and respiratory epithelium of the nasal cavity at 1000C, 4000, and 10,000 ppm. The only neurobehavioral parameter affected was a decrease in locomotor activity in female mice at 1000C and 10,000 ppm. In teased fiber preparations of tibial nerve, paranodal axonal swellings were observed at 1000C or at 10,000 ppm, but not in the control groups. The severity of the peripheral nerve lesion was mild. These studies show that n-hexane has minimal toxicity to the nervous system and respiratory system of mice. JF - Toxicology AU - Dunnick, J K AU - Graham, D G AU - Yang, R S AU - Haber, S B AU - Brown, H R AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/07/17/ PY - 1989 DA - 1989 Jul 17 SP - 163 EP - 172 VL - 57 IS - 2 SN - 0300-483X, 0300-483X KW - Hexanes KW - 0 KW - n-hexane KW - 2DDG612ED8 KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Reference Values KW - Turbinates -- pathology KW - Sex Factors KW - Dose-Response Relationship, Drug KW - Turbinates -- drug effects KW - Mice KW - Administration, Inhalation KW - Male KW - Female KW - Hexanes -- administration & dosage KW - Hexanes -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79107275?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-23 N1 - Date created - 1989-08-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pyrethroids: involvement of sodium channels in effects on inositol phosphate formation in guinea pig synaptoneurosomes. AN - 79099299; 2546657 AB - The effects of pyrethroids were studied on phosphoinositide breakdown in guinea pig synaptoneurosomes. Similar to other agents that activate voltage-dependent sodium channels, type I and type II pyrethroids stimulated phosphoinositide breakdown. Type II pyrethroids, like deltamethrin and fenvalerate, were more potent and, at least for deltamethrin, more efficacious than type I pyrethroids, like allethrin, resmethrin and permethrin. The effects of type II pyrethroids could be partially inhibited by the sodium channel blocker tetrodotoxin. The effects of allethrin and resmethrin were not affected by 5 microM tetrodotoxin. Stimulation of phosphoinositide breakdown by fenvalerate was additive to the stimulation elicited by the receptor agonists carbamylcholine and norepinephrine, but not to the stimulation elicited by sodium channel agents (batrachotoxin, scorpion venom and pumiliotoxin B). Stimulation by allethrin was not additive to the stimulation elicited either by receptor agonists or sodium channel agents. A submaximal concentration of allethrin, a type I pyrethroid, did not greatly affect the dose-dependent stimulation elicited by a type II pyrethroid, deltamethrin, while a higher concentration of allethrin prevented further stimulation by type II pyrethroids. A local anesthetic, dibucaine, which inhibits sodium channel activation, inhibited phosphoinositide breakdown induced by type II, but not by type I pyrethroids, except at higher concentrations. Thus, type II pyrethroids appear to stimulate phosphoinositide breakdown in synaptoneurosomes in a manner analogous to other sodium channel agents, while type I pyrethroids elicit phosphoinositide breakdown by a different mechanism, probably not involving sodium channels. JF - Brain research AU - Gusovsky, F AU - Secunda, S I AU - Daly, J W AD - Laboratory of Bioorganic Chemistry, NIDDK, Bethesda, MD 20892. Y1 - 1989/07/17/ PY - 1989 DA - 1989 Jul 17 SP - 72 EP - 78 VL - 492 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Inositol Phosphates KW - 0 KW - Insecticides KW - Nitriles KW - Pyrethrins KW - Sodium Channels KW - Sugar Phosphates KW - decamethrin KW - 2JTS8R821G KW - fenvalerate KW - Z6MXZ39302 KW - Index Medicus KW - Animals KW - Synaptosomes -- drug effects KW - Guinea Pigs KW - Insecticides -- pharmacology KW - Synaptosomes -- metabolism KW - Sugar Phosphates -- metabolism KW - Cerebral Cortex -- drug effects KW - Cerebral Cortex -- metabolism KW - Inositol Phosphates -- metabolism KW - Sodium Channels -- metabolism KW - Pyrethrins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79099299?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-31 N1 - Date created - 1989-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Radiation dose and breast cancer risk in patients treated for cancer of the cervix. AN - 79091660; 2744900 AB - The relationship between breast cancer and radiation treatment for cervical cancer was evaluated in an international study of 953 women who subsequently developed breast cancer and 1,806 matched controls. Radiation doses to the breast (average 0.31 Gy) and ovaries (average 32 Gy) were reconstructed for exposed subjects on the basis of their original radiotherapy records. Overall, 88% of the breast cancer cases and 89% of the controls received radiation treatment [relative risk (RR) = 0.88; 95% confidence interval (CI) = 0.7-1.2]. Among women with intact ovaries (561 cases, 1,037 controls), radiotherapy was linked to a significant 35% reduction in breast cancer risk, attributable in all likelihood to the cessation of ovarian function. Ovarian doses of 6 Gy were sufficient to reduce breast cancer risk but larger doses did not reduce risk further. This saturation-type response is probably due to the killing of a critical number of ovarian cells. Cervical cancer patients without ovaries (145 cases, 284 controls) were analyzed separately because such women are at especially low natural risk for breast cancer development. In theory, any effect of low-dose breast exposure, received incidentally during treatment for cervical cancer, should be more readily detectable. Among women without ovaries, there was a slight increase in breast cancer risk (RR = 1.07; 95% CI = 0.6-2.0), and a suggestion of a dose response with the RR being 1.0, 0.7, 1.5 and 3.1 for breast doses of 0, 0.01-0.24, 0.25-0.49 and 0.50+ Gy, respectively. However, this trend of increasing RR was not statistically significant. If low-dose radiation increases the risk of breast cancer among women over age 40 years, it appears that the risk is much lower than would be predicted from studies of younger women exposed to higher doses. JF - International journal of cancer AU - Boice, J D AU - Blettner, M AU - Kleinerman, R A AU - Engholm, G AU - Stovall, M AU - Lisco, H AU - Austin, D F AU - Bosch, A AU - Harlan, L AU - Krementz, E T AU - Latouret, H B AU - Merril, J A AU - Petters, L J AU - Schulz, M D AU - Wactawski, J AU - Storm, H H AU - Björkholm, E AU - Pettersson, F AU - Bell, C M AU - Coleman, M P AU - Fraser, P AU - Neal, F E AU - Prior, P AU - Choi, N W AU - Hislop, T G AU - Koch, M AU - Kreiger, N AU - Robb, D AU - Robson, D AU - Thomson, D H AU - Lochmüller, H AU - von Fournier, D AU - Frischkorn, R AU - Kjørstad, K E AU - Rimpela, A AU - Pejovic, M H AU - Kirn, V P AU - Stankusova, H AU - Pisani, P AU - Sigurdsson, K AU - Hutchison, G B AU - MacMahon, B AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/07/15/ PY - 1989 DA - 1989 Jul 15 SP - 7 EP - 16 VL - 44 IS - 1 SN - 0020-7136, 0020-7136 KW - Index Medicus KW - Ovary -- radiation effects KW - Age Factors KW - Risk Factors KW - Radiotherapy Dosage KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Dose-Response Relationship, Radiation KW - Female KW - Neoplasms, Radiation-Induced -- etiology KW - Breast Neoplasms -- etiology KW - Uterine Cervical Neoplasms -- radiotherapy KW - Radiotherapy -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79091660?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-16 N1 - Date created - 1989-08-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Int J Cancer 1991 Jul;127(1):118 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A single amino acid substitution in HLA-A2 can alter the selection of the cytotoxic T lymphocyte repertoire that responds to influenza virus matrix peptide 55-73. AN - 79066477; 2472444 AB - Previous studies have demonstrated that certain amino acid substitutions in the alpha two domain at positions 152 and 156 in the alpha two helix of the HLA-A2 molecule can affect presentation of the influenza virus matrix peptide M1 55-73 without abolishing binding of the M1 peptide. HLA-A2.1-restricted M1 55-73 peptide-specific CTL lines obtained from almost all HLA-A2.1+ individuals fail to recognize the M1 peptide presented by site-directed mutants of HLA-A2 that have either a Val----Ala or Val----Gln substitution at position 152 or a Leu----Trp substitution at position 156. Only one HLA-A2+ individual (donor Q66, HLA-A2,-B53,-B63) has been found who is able to generate a unique repertoire of HLA-A2-restricted M1 peptide-specific CTL that can recognize peptide presented by HLA-A2 mutants with either an Ala or Gln substitution at position 152 or a Trp substitution at position 156. These Q66 M1 peptide-specific CTL could be selected by stimulation with M1 peptide-pulsed transfectants that express the mutant HLA-A2 gene with the Trp substitution at 156. To determine if the presence of the unique CTL repertoire could be attributed to a variant HLA-A2 molecule in Q66, sequences were determined from polymerase chain reaction-amplified segments of the HLA-A2 RNA. Two different HLA-A2 genes were found expressed in Q66 cells: one is identical to HLA-A2.1 and the other is identical to HLA-A2.2F (Gln----Arg at position 43, Val----Leu at position 95, and Leu----Trp at position 156). These results demonstrate that a different CTL repertoire specific for HLA-A2 plus the M1 55-73 peptide is generated in an individual that expresses both HLA-A2.1 and HLA-A2.2F compared to individuals who express HLA-A2.1 alone, and that the unique repertoire can be selected by the presence of an HLA-A2 molecule with a single amino acid substitution at position 156. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Shimojo, N AU - Cowan, E P AU - Engelhard, V H AU - Maloy, W L AU - Coligan, J E AU - Biddison, W E AD - Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892. Y1 - 1989/07/15/ PY - 1989 DA - 1989 Jul 15 SP - 558 EP - 564 VL - 143 IS - 2 SN - 0022-1767, 0022-1767 KW - Antigens, Viral KW - 0 KW - Epitopes KW - HLA-A Antigens KW - HLA-A2 Antigen KW - Peptide Fragments KW - Viral Matrix Proteins KW - Abridged Index Medicus KW - Index Medicus KW - Base Sequence KW - Humans KW - Antigens, Viral -- immunology KW - Adult KW - Molecular Sequence Data KW - Cytotoxicity Tests, Immunologic KW - Amino Acid Sequence KW - Antigen-Presenting Cells -- immunology KW - Epitopes -- immunology KW - Mutation KW - Cell Line KW - T-Lymphocytes, Cytotoxic -- classification KW - Influenza A virus -- immunology KW - T-Lymphocytes, Cytotoxic -- immunology KW - HLA-A Antigens -- immunology KW - Peptide Fragments -- immunology KW - Viral Matrix Proteins -- immunology KW - HLA-A Antigens -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79066477?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-31 N1 - Date created - 1989-07-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of endogenous cytokine-mRNA in circulating peripheral blood mononuclear cells by IL-2 administration to cancer patients. AN - 79064984; 2661690 AB - The lymphokine IL-2 plays a central role in immune regulation. Recent clinical trials have shown that when administered systemically either alone, or in combination with lymphokine-activated killer cells, IL-2 can cause regression of metastatic tumors in some patients with a variety of otherwise refractory cancers. To evaluate the mechanism of in vivo action of IL-2, as well as the toxicity associated with its administration, we have studied the in vivo cytokine-mRNA expression of circulating PBMC in cancer patients undergoing treatment with high dose IL-2. Before IL-2 administration, we found low level or no evidence of cytokine-mRNA expression in PBMC. After IL-2 infusion, circulating PBMC showed enhanced proliferative activity and contained significant levels of mRNA for TNF-alpha and IL-6 as well as mRNA for the p55 IL-2R, Tac, but no mRNA coding for granulocyte-monocyte-CSF and TNF-beta (lymphotoxin). IL-1 beta mRNA was expressed at very low levels in circulating PBMC after IL-2 infusion. Each of these cytokine -mRNA was, however, inducible in vitro by stimulation of PBMC with IL-2 alone. The results of these in vivo studies suggest that IL-2 may be a physiologic inducer of TNF and IL-6 which, because of their pleiotropic effects, may be important endogenous signals in the body's immune response and account for some of the physiologic changes seen in patients receiving high dose IL-2. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Kasid, A AU - Director, E P AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/07/15/ PY - 1989 DA - 1989 Jul 15 SP - 736 EP - 739 VL - 143 IS - 2 SN - 0022-1767, 0022-1767 KW - Biological Factors KW - 0 KW - Cytokines KW - Interleukin-2 KW - Interleukin-6 KW - Interleukins KW - RNA, Messenger KW - Receptors, Interleukin-2 KW - Recombinant Proteins KW - Tumor Necrosis Factor-alpha KW - Abridged Index Medicus KW - Index Medicus KW - Receptors, Interleukin-2 -- blood KW - Lymphocyte Activation KW - Drug Administration Schedule KW - Interleukins -- blood KW - Humans KW - Tumor Necrosis Factor-alpha -- blood KW - Recombinant Proteins -- administration & dosage KW - Interleukin-2 -- blood KW - Interleukin-2 -- administration & dosage KW - Leukocytes, Mononuclear -- metabolism KW - Biological Factors -- metabolism KW - RNA, Messenger -- isolation & purification KW - RNA, Messenger -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79064984?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-31 N1 - Date created - 1989-07-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Current concepts in the idiopathic inflammatory myopathies: polymyositis, dermatomyositis, and related disorders. AN - 79061530; 2662848 AB - Idiopathic inflammatory myopathy, a category encompassing polymyositis, dermatomyositis, and a number of other disorders, is very uncommon, but has been the focus of intense study in the Arthritis and Rheumatism Branch of the National Institute of Arthritis and Musculoskeletal and Skin Diseases for the past several years. We describe the clinical picture, stressing the need for biopsy to ensure correct diagnosis. It is especially important to recognize the treatment-resistant variant, inclusion body myositis. The extraskeletal manifestations, particularly the cardiopulmonary, oropharyngeal, gastrointestinal, and endocrine involvement, are described. The cardiopulmonary involvement, especially interstitial lung disease, arrhythmias, and cardiac failure, may dominate the clinical picture. The known causes are varied, and include drugs, toxins, and some infectious agents, however, in most cases a cause cannot yet be identified. Circumstantial evidence suggests that picornaviruses may initiate some cases in humans, and a very similar disease in mice caused by a picornavirus is actively under study. Studies of autoantibodies and cellular immune function support a central role for disordered immunity in the pathogenesis. The myositis-specific autoantibodies, especially those directed at certain enzymes important in protein synthesis (the aminoacyl-transfer RNA synthetases), are found in a clinically distinct subset of patients. Although most patients respond initially to corticosteroids, cytotoxic drugs are sometimes added when steroid toxicity or refractoriness develops. We describe several newer therapies under study for such cases and outline future directions in research. JF - Annals of internal medicine AU - Plotz, P H AU - Dalakas, M AU - Leff, R L AU - Love, L A AU - Miller, F W AU - Cronin, M E AD - National Institutes of Health, Bethesda, MD 20892. Y1 - 1989/07/15/ PY - 1989 DA - 1989 Jul 15 SP - 143 EP - 157 VL - 111 IS - 2 SN - 0003-4819, 0003-4819 KW - Autoantibodies KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Cell Movement KW - Animals KW - Neoplasms -- complications KW - Autoantibodies -- metabolism KW - Humans KW - Disease Models, Animal KW - Antibody Formation KW - Lymphocytes -- physiology KW - Dermatomyositis -- pathology KW - Myositis -- immunology KW - Myositis -- therapy KW - Dermatomyositis -- etiology KW - Myositis -- physiopathology KW - Myositis -- pathology KW - Myositis -- etiology KW - Dermatomyositis -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79061530?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-04 N1 - Date created - 1989-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of bryostatins and retinoic acid on phorbol ester- and diacylglycerol-induced squamous differentiation in human tracheobronchial epithelial cells. AN - 79033509; 2567623 AB - Previous studies have shown that normal human tracheobronchial epithelial (HBE) cells undergo squamous differentiation upon treatment with phorbol 12-myristate 13-acetate (PMA). In this study, we report that induction of this differentiation program is accompanied by an increase in the accumulation of cholesterol sulfate and in transglutaminase type I activity, two markers of squamous differentiation. Several carcinoma cell lines did not exhibit an increase in these differentiation markers after PMA-treatment and appear to have acquired a defect in the mechanism that triggers differentiation. The diacylglycerol analogue, didecanoylglycerol (diC10), was also able to induce squamous differentiation. Bryostatin 1, another activator of protein kinase C, did not induce terminal cell division or increase cholesterol sulfate accumulation or transglutaminase type I activity. Bryostatin 1 not only failed to inhibit cell proliferation and to induce differentiation but antagonized the PMA- and diC10-induced commitment to terminal differentiation. The bryostatin blocked both the PMA-induced terminal cell division as well as the expression of the two differentiation markers. Retinoids were found not to affect the PMA-induced commitment to terminal cell division but did inhibit the expression of the differentiated phenotype. Our results indicate that the bryostatins and retinoids affect the multistep process of squamous differentiation in tracheobronchial epithelial cells at two different stages. JF - Cancer research AU - Jetten, A M AU - George, M A AU - Pettit, G R AU - Rearick, J I AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 22709. Y1 - 1989/07/15/ PY - 1989 DA - 1989 Jul 15 SP - 3990 EP - 3995 VL - 49 IS - 14 SN - 0008-5472, 0008-5472 KW - Antineoplastic Agents KW - 0 KW - Bryostatins KW - Diglycerides KW - Glycerides KW - Lactones KW - Macrolides KW - Sulfates KW - bryostatin 1 KW - 37O2X55Y9E KW - Tretinoin KW - 5688UTC01R KW - bryostatin 2 KW - 87745-28-6 KW - Transglutaminases KW - EC 2.3.2.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Sulfates -- metabolism KW - Transglutaminases -- metabolism KW - Epithelial Cells KW - Cells, Cultured KW - Kinetics KW - Humans KW - Organ Culture Techniques KW - Epithelium -- drug effects KW - Tretinoin -- pharmacology KW - Diglycerides -- pharmacology KW - Bronchi -- cytology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Trachea -- cytology KW - Bronchi -- drug effects KW - Trachea -- drug effects KW - Cell Differentiation -- drug effects KW - Antineoplastic Agents -- pharmacology KW - Glycerides -- pharmacology KW - Lactones -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79033509?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-03 N1 - Date created - 1989-08-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Augmentation of antitumor efficacy by the combination of recombinant tumor necrosis factor and chemotherapeutic agents in vivo. AN - 79033146; 2736513 AB - We evaluated the in vivo antitumor effects of the combination of recombinant human tumor necrosis factor (rhTNF) and three chemotherapeutic agents in an established murine tumor model. C57BL/6 mice bearing a subdermal weakly immunogenic 3-methylcholanthrene-induced sarcoma (MCA-106) received one i.v. dose of cyclophosphamide (Cy) (100 mg/kg), doxorubicin (5 mg/kg), or 5-fluorouracil (75 mg/kg) on either Day 8, 10, or 12. All animals received one i.v. dose of rhTNF (4 or 6 micrograms/mouse) on Day 10. The most effective time for administration of the chemotherapeutic agent was determined to be 48 h following rhTNF administration of all agents tested. The combined results of four separate experiments evaluating tumor size on Day 28 following tumor inoculation revealed that the groups treated with 4 or 6 micrograms of rhTNF and Cy (on Day 12) had tumor size reductions of 70 and 94%, respectively, compared to untreated controls (P2 less than 0.005). Mice treated with Cy alone, or with 4 or 6 micrograms of rhTNF alone had tumor size reductions of 30, 35, and 41%, respectively, compared to untreated controls (P2 less than 0.02). Analysis of cure rates demonstrates that the combination of Cy with 4 or 6 micrograms tumor necrosis factor cured 35 and 48% of the animals, respectively (P2 less than 0.01), compared to 10, 0, and 14% of mice treated with single agent Cy, 4 micrograms rhTNF, or 6 micrograms rhTNF, respectively. The timing of Cy and TNF administration was critical since administration of Cy prior to or concurrent with rhTNF was not effective in reducing tumor area or increasing cure rates over those achieved with either agent alone. Mice treated with doxorubicin alone had an increase in tumor size of 139 +/- 29% over untreated controls (P2 less than 0.05) on Day 28 following tumor inoculation and none were cured. In contrast, mice treated with doxorubicin plus 4 or 6 micrograms rhTNF exhibited early reductions in tumor size such that on Day 28 the average tumor areas were decreased by 66 +/- 34% (P2 less than 0.05) and 73 +/- 1% (P2 less than 0.02) of untreated controls with cure rates of 29% and 43% (P2 less than 0.02), respectively. However, the combination of 6 micrograms rhTNF plus doxorubicin led to substantial lethal toxicity with only 29% of mice surviving treatment. 5-Fluorouracil alone resulted in an increase in tumor area of 164% (P2 less than 0.05) over that of untreated controls on Day 28 following tumor inoculation.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Cancer research AU - Krosnick, J A AU - Mulé, J J AU - McIntosh, J K AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/07/15/ PY - 1989 DA - 1989 Jul 15 SP - 3729 EP - 3733 VL - 49 IS - 14 SN - 0008-5472, 0008-5472 KW - Recombinant Proteins KW - 0 KW - Tumor Necrosis Factor-alpha KW - Methylcholanthrene KW - 56-49-5 KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - Animals KW - Mice, Inbred C57BL KW - Mice KW - Drug Evaluation, Preclinical KW - Recombinant Proteins -- therapeutic use KW - Recombinant Proteins -- administration & dosage KW - Female KW - Sarcoma, Experimental -- drug therapy KW - Fluorouracil -- therapeutic use KW - Fluorouracil -- administration & dosage KW - Cyclophosphamide -- administration & dosage KW - Cyclophosphamide -- therapeutic use KW - Tumor Necrosis Factor-alpha -- administration & dosage KW - Sarcoma, Experimental -- chemically induced KW - Sarcoma, Experimental -- pathology KW - Doxorubicin -- therapeutic use KW - Doxorubicin -- administration & dosage KW - Tumor Necrosis Factor-alpha -- therapeutic use KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79033146?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-03 N1 - Date created - 1989-08-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evaluation of the transplacental tumorigenicity of the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in mice. AN - 79032291; 2736518 AB - The transplacental tumorigenicity of the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) was assessed in three strains of mice: A/J; C3H/He x C57BL/6 F1 (hereafter called C3B6F1); and Swiss outbred [Cr:NIH(S)]. NNK (100 mg/kg) was administered i.p. on Days 14, 16, and 18 of gestation to A/J and C3H/He mice and on Days 15, 17 and 19 of gestation to the Swiss mice. The effects of postnatal treatment with tumor-promoting agents, including 0.05% sodium barbital in the drinking water until death or a single dose of Aroclor 1254 (a mixture of polychlorinated biphenyls, PCB) given on Postnatal Day 8 or 56, were also examined. Progeny were sacrificed at age 24 wk (A/J) or 72 wk (C3B6F1 and Swiss). Significant incidences of tumors occurred in the lungs of strain A/J progeny and in the livers of male C3B6F1 and Swiss progeny. Lung tumor incidence was 8 of 34 (24%) in the female offspring of the A/J mice treated with NNK, compared with 1 of 39 (3%) in controls (P less than 0.05). A 2-fold difference in lung tumor incidence in male offspring of NNK-treated (4 of 23, 13%) versus control (3 of 48, 6%) A/J mice was not of statistical significance. However, the incidence of lung tumors in NNK-exposed progeny A/J mice in both sexes combined (12 of 66, 18%) was also significantly greater than in controls (4 of 87, 5%). The incidence of liver tumors in the male C3B6F1 mice exposed transplacentally to NNK was 12 of 30 (40%) compared to 8 of 46 (17%) in controls (P less than 0.05). No effects of postnatal sodium barbital or PCB were observed on transplacental NNK tumorigenicity in C3B6F1 mice. The combined incidence of liver carcinoma in male mice in all NNK-treated groups (13 of 141, 9%) was significantly greater (P less than 0.05) than in controls (5 of 144, 3%). In male Swiss mice exposed transplacentally to NNK, the incidence of liver tumors was 3 of 57 (5%) compared to 0 of 35 controls, and postnatal treatment with PCB on Day 56 caused a significant increase (5 of 26, 19%) (P less than 0.05) in the incidence of NNK-induced liver tumors. The combined incidence of liver tumors in the male offspring of the Swiss mice treated with NNK, with or without PCB, was 8 of 83 (10%) which was significantly greater (P less than 0.05) than in controls (0 of 66).(ABSTRACT TRUNCATED AT 400 WORDS) JF - Cancer research AU - Anderson, L M AU - Hecht, S S AU - Dixon, D E AU - Dove, L F AU - Kovatch, R M AU - Amin, S AU - Hoffmann, D AU - Rice, J M AD - Division of Cancer Etiology, National Cancer Institute, Frederick, Maryland 21701. Y1 - 1989/07/15/ PY - 1989 DA - 1989 Jul 15 SP - 3770 EP - 3775 VL - 49 IS - 14 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 - Animals KW - Fetus -- drug effects KW - Mice, Inbred C57BL KW - Mice, Inbred C3H KW - Mice KW - Placenta -- physiology KW - Neoplasms, Experimental -- pathology KW - Male KW - Female KW - Pregnancy KW - Plants, Toxic KW - Nitrosamines -- toxicity KW - Maternal-Fetal Exchange KW - Liver Neoplasms, Experimental -- pathology KW - Tobacco KW - Carcinogens -- toxicity KW - Lung Neoplasms -- chemically induced KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79032291?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-03 N1 - Date created - 1989-08-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The use of native T7 DNA polymerase for site-directed mutagenesis. AN - 79150903; 2668888 JF - Nucleic acids research AU - Bebenek, K AU - Kunkel, T A AD - Laboratory of Molecular Genetics, NIEHS, Research Triangle Park, NC 27709. Y1 - 1989/07/11/ PY - 1989 DA - 1989 Jul 11 SP - 5408 VL - 17 IS - 13 SN - 0305-1048, 0305-1048 KW - DNA KW - 9007-49-2 KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - Index Medicus KW - T-Phages -- enzymology KW - Escherichia coli -- enzymology KW - DNA Replication KW - DNA -- chemical synthesis KW - Mutation KW - DNA-Directed DNA Polymerase -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79150903?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-11 N1 - Date created - 1989-09-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1971 Apr 25;246(8):2692-701 [4928650] J Biol Chem. 1974 Sep 10;249(17):5668-76 [4606459] J Biol Chem. 1987 Nov 25;262(33):16212-23 [3316214] J Biol Chem. 1983 Sep 25;258(18):11174-84 [6309835] Science. 1985 Apr 19;228(4697):291-7 [3838593] J Biol Chem. 1981 Apr 25;256(8):4087-94 [6971292] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Recognition properties of peptides hydropathically complementary to residues 356-375 of the c-raf protein. AN - 79064060; 2472393 AB - Two peptides with hydropathic complementarity to residues 356-375 of the c-raf protein were synthesized to determine if they recognize the raf-(356-375) peptide as well as the entire protein. One peptide was deduced from the complementary mRNA for the raf protein corresponding to residues 356-375, whereas the other was deduced solely from the amino acid sequence of the 20-mer segment using a computer program able to generate peptide sequences with hydropathic complementarity to a given sequence. Specific binding of both peptides to the raf 20-mer segment was demonstrated when either the raf 20-mer peptide or the complementary peptides were immobilized on a column. Binding affinities were in the millimolar-micromolar range. Identical binding properties were observed with peptides synthesized with either all D- or all L-amino acids, suggesting a lack of conformational dependence. Binding was also unaffected by the presence of 8 M urea or detergents, was dependent on solvent characteristics of pH and ionic strength, and was abolished by the presence of competing peptides in the eluting buffer. Recognition between raf complementary peptides was accompanied by spectral changes in the far and near UV region, as monitored by circular dichroism. Proteolytic degradation was retarded by the binding of these peptides. Once immobilized on a column, these peptides proved useful for the isolation by affinity chromatography of a recombinant c-raf protein from an Escherichia coli crude cell extract. JF - The Journal of biological chemistry AU - Fassina, G AU - Roller, P P AU - Olson, A D AU - Thorgeirsson, S S AU - Omichinski, J G AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/07/05/ PY - 1989 DA - 1989 Jul 05 SP - 11252 EP - 11257 VL - 264 IS - 19 SN - 0021-9258, 0021-9258 KW - Peptide Fragments KW - 0 KW - Proto-Oncogene Proteins KW - RNA, Complementary KW - RNA, Messenger KW - RNA KW - 63231-63-0 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Proto-Oncogene Proteins c-raf KW - EC 2.7.11.1 KW - Trypsin KW - EC 3.4.21.4 KW - Index Medicus KW - Software KW - Sequence Homology, Nucleic Acid KW - Circular Dichroism KW - Amino Acid Sequence KW - Chromatography, High Pressure Liquid KW - Binding Sites KW - Chromatography, Affinity KW - Adenosine Triphosphate -- metabolism KW - Binding, Competitive KW - Molecular Sequence Data KW - Trypsin -- metabolism KW - Protein Conformation KW - Peptide Fragments -- metabolism KW - Proto-Oncogene Proteins -- isolation & purification KW - Proto-Oncogene Proteins -- metabolism KW - Proto-Oncogene Proteins -- genetics KW - Escherichia coli -- analysis KW - Peptide Fragments -- chemical synthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79064060?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-02 N1 - Date created - 1989-08-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mammalian topoisomerase II activity is modulated by the DNA minor groove binder distamycin in simian virus 40 DNA. AN - 79045841; 2544590 AB - DNA topoisomerases II are nuclear enzymes that have been identified recently as targets for some of the most active anticancer drugs. Antitumor topoisomerase II inhibitors such as teniposide (VM-26) produce enzyme-induced DNA cleavage and inhibition of enzyme activity. By adding to such reactions distamycin, a compound whose effects on DNA have been extensively characterized, we investigated the effects of drug binding upon topoisomerase II-mediated DNA cleavage induced by VM-26. We have found a correspondence between distamycin binding (determined by footprinting analysis) and topoisomerase II-mediated cleavage of SV40 DNA (determined by sequencing gel analysis). Distamycin binding potentiated the cleavage of specific sites in the near proximity of distamycin-binding sites (within at least 25 base pairs), which indicates that DNA secondary structure is involved in topoisomerase II-DNA interactions. That distamycin potentiated cleavage only at sites that were recognized in the absence of distamycin and suppressed cleavage directly at distamycin-binding sites indicates that topoisomerase II recognizes DNA on the basis of primary sequence. In addition, distamycin stimulated topoisomerase II-mediated DNA relaxation and antagonized the inhibitory effect of VM-26. These results show that the DNA sequence-specific binding of distamycin produces local and propagated effects in the DNA which markedly affect topoisomerase II activity. JF - The Journal of biological chemistry AU - Fesen, M AU - Pommier, Y AD - Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/07/05/ PY - 1989 DA - 1989 Jul 05 SP - 11354 EP - 11359 VL - 264 IS - 19 SN - 0021-9258, 0021-9258 KW - DNA, Viral KW - 0 KW - Distamycins KW - Pyrroles KW - Teniposide KW - 957E6438QA KW - DNA Restriction Enzymes KW - EC 3.1.21.- KW - DNA Topoisomerases, Type II KW - EC 5.99.1.3 KW - Index Medicus KW - Animals KW - Drug Interactions KW - Base Sequence KW - Electrophoresis KW - Tumor Cells, Cultured KW - Molecular Sequence Data KW - Leukemia L1210 -- enzymology KW - Mice KW - Repetitive Sequences, Nucleic Acid KW - Nucleic Acid Conformation -- drug effects KW - Teniposide -- pharmacology KW - Binding Sites KW - Distamycins -- metabolism KW - Simian virus 40 -- genetics KW - DNA Topoisomerases, Type II -- metabolism KW - Pyrroles -- pharmacology KW - Distamycins -- pharmacology KW - DNA, Viral -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79045841?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-02 N1 - Date created - 1989-08-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of MPP+ on the release of serotonin and 5-hydroxyindoleacetic acid from rat striatum in vivo. AN - 79280488; 2478372 AB - A procedure utilizing brain dialysis was employed to investigate the effects of 1-methyl-4-phenylpyridinium ion (MPP+), the major metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), on the in vivo release of 5-hydroxytryptamine (5-HT) from the rat striatum. MPP+ (10(-5)-10(-2) M) was administered through the microdialysis probe and dialysates were collected and assayed for monoamines and their metabolites by a high performance liquid chromatography coupled with an electrochemical detector (HPLC-EC). In addition to a dopamine (DA) releasing action, MPP+ caused a cumulatively dose-dependent increase in the release of 5-HT while concomitantly producing a decrease in the efflux of 5-hydroxyindoleacetic acid (5-HIAA). This MPP+-induced increase in the 5-HT release, may play an important role in the acute 5-HT syndrome seen in animals after MPTP. JF - European journal of pharmacology AU - Miyake, H AU - Chiueh, C C AD - Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1989/07/04/ PY - 1989 DA - 1989 Jul 04 SP - 49 EP - 55 VL - 166 IS - 1 SN - 0014-2999, 0014-2999 KW - Biogenic Monoamines KW - 0 KW - Neurotoxins KW - 3,4-Dihydroxyphenylacetic Acid KW - 102-32-9 KW - Serotonin KW - 333DO1RDJY KW - Hydroxyindoleacetic Acid KW - 54-16-0 KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Homovanillic Acid KW - X77S6GMS36 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Anesthesia KW - Dose-Response Relationship, Drug KW - 3,4-Dihydroxyphenylacetic Acid -- metabolism KW - Homovanillic Acid -- metabolism KW - Biogenic Monoamines -- metabolism KW - Male KW - Hydroxyindoleacetic Acid -- metabolism KW - Corpus Striatum -- metabolism KW - Neurotoxins -- pharmacology KW - Corpus Striatum -- drug effects KW - Serotonin -- metabolism KW - 1-Methyl-4-phenylpyridinium -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79280488?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-01 N1 - Date created - 1989-12-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - cDNA-directed expression of human thyroid peroxidase. AN - 79121013; 2753139 AB - A human thyroid peroxidase cDNA, hTPO-1 [(1987) Proc. Natl. Acad. Sci. USA 84, 5555-5559], was expressed in human Hep G2 cells using a vaccinia virus cDNA-expression system. When examined by immunoblot analysis, the level of hTPO-1 protein expression reached a maximum approx. 24 h after infection and remained at a similar level up to 72 h post-infection. The expressed protein was enzymatically active as measured by guaiacol oxidation. Monoclonal antibody-assisted immunoaffinity column chromatography was used for partial purification of vaccinia-expressed hTPO-1, resulting in more than 300-fold higher specific activity and a measurable difference spectrum of the hTPO-1 (Fe3+)-CN complex. JF - FEBS letters AU - Kimura, S AU - Kotani, T AU - Ohtaki, S AU - Aoyama, T AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/07/03/ PY - 1989 DA - 1989 Jul 03 SP - 377 EP - 380 VL - 250 IS - 2 SN - 0014-5793, 0014-5793 KW - Guaiacol KW - 6JKA7MAH9C KW - DNA KW - 9007-49-2 KW - Peroxidases KW - EC 1.11.1.- KW - Index Medicus KW - Oxidation-Reduction KW - Blotting, Western KW - Humans KW - Guaiacol -- pharmacology KW - DNA -- metabolism KW - Peroxidases -- genetics KW - Thyroid Gland -- enzymology KW - Gene Expression Regulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79121013?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-07 N1 - Date created - 1989-09-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Perineurial permeability and endoneurial edema during Wallerian degeneration of the frog peripheral nerve. AN - 85251153; pmid-2475214 AB - Perineurial permeabilities to [3H]sucrose and [14C]dextran (MW = 70,000), and water content, conduction velocity (CV) and maximum amplitude (MAP) of the compound action potential, were determined in Wallerian degenerated nerves (sciatic or tibial) of the frog and compared with values in the contralateral uncut nerves. Three days after transection of the lumbosacral plexuses, about 2 cm proximal to the sciatic nerve, mean water content of the sciatic nerve was significantly higher than in the contralateral uncut nerve. After 10 days, the degenerating sciatic nerve showed significant increases in the mean perineurial permeabilities to [3H]sucrose and [14C]dextran when compared to values in the contralateral nerve. Means MAP's and CV's were significantly decreased. At 21 days and after, no compound action potential was detected and perineurial permeability and nerve water content had increased further. Decreases in mean MAP's and CV's and permeability increases of the perineurium were less in degenerating tibial nerves than in degenerating sciatic nerves. It is concluded that following transection, (1) Wallerian degeneration produces an irreversible increase in perineurial permeability, (2) the increase of perineurial permeability follows a proximodistal gradient, and (3) the frog peripheral nerve develops endoneurial edema during Wallerian degeneration as do degenerated nerves of mammals. JF - Brain Research AU - Wadhwani, K C AU - Latker, C H AU - Balbo, A AU - Rapoport, S I AD - Laboratory of Neurosciences, National Institute on Aging, Bethesda, MD 20892. PY - 1989 SP - 231 EP - 239 VL - 493 IS - 2 SN - 0006-8993, 0006-8993 KW - Peripheral Nerves KW - Rana pipiens KW - Sucrose KW - Animal KW - Action Potentials KW - Time Factors KW - Female KW - Dextrans KW - Nerve Degeneration KW - Wallerian Degeneration KW - Cell Membrane Permeability UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85251153?accountid=14244 LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - A study of proteins in the auditory system of rabbits using two-dimensional gels: identification of glial fibrillary acidic protein and vitamin D-dependent calcium binding protein. AN - 85246732; pmid-2776001 AB - Two-dimensional gel electrophoresis and computerized optical densitometry were employed to compare the relative content of proteins across major auditory brain regions in rabbits. Areas examined included the dorsal and ventral cochlear nuclei which receive the primary afferents from the organ of Corti, the lateral superior olivary nucleus which has strong reciprocal relationships with the cochlear nucleus, and the successively more rostral projections of the auditory pathways to inferior colliculus, medial geniculate and auditory cortex. Twelve proteins demonstrated significant decreases and 5 proteins significant increases in content at successively more rostral levels of the auditory system, including 2 proteins which were highly localized to the cochlear nuclei and 2 proteins greatest in amounts in the auditory cortex. One protein which was localized to the cochlear nuclei and lateral superior olive (molecular weight (MW) = 50.3, isoelectric point (pI) = 5.7) was identified as the glial fibrillary acidic protein by reaction of specific antisera on blots. Antisera to the vitamin D-dependent calcium binding protein reacted specifically with one protein (MW = 27.2, pI = 4.8) which was greatest in amount in the lateral superior olive (LSO) versus other auditory regions examined. The significance of these findings rests in the potential for identifying specific markers for cellular elements that are important in auditory function and which might be lost as a consequence of developmental abnormalities or other traumas. JF - Brain Research AU - Winsky, L AU - Harvey, J A AU - McMaster, S E AU - Jacobowitz, D M AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD 20892. PY - 1989 SP - 136 EP - 146 VL - 493 IS - 1 SN - 0006-8993, 0006-8993 KW - Auditory Cortex KW - Calcium-Binding Protein, Vitamin D-Dependent KW - Immunoblotting KW - Inferior Colliculus KW - Support, U.S. Gov't, P.H.S. KW - Auditory Pathways KW - Animal KW - Rabbits KW - Glial Fibrillary Acidic Protein KW - Geniculate Bodies KW - Electrophoresis, Gel, Two-Dimensional KW - Cochlear Nerve KW - Olivary Nucleus KW - Male KW - Brain Chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85246732?accountid=14244 LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Fast in vitro movement of outer hair cells in an external electric field: effect of digitonin, a membrane permeabilizing agent. AN - 85142361; pmid-2793606 AB - Isolated outer hair cells from the organ of Corti show elongation and contraction in response to an externally applied ac electric field as well as to a direct current injection into these cells. This is thought to be the basis of the positive feedback mechanism for fine tuning of the mammalian hearing organ. To test whether the mechanical response depends on the intracellular electric field or on the membrane potential, we used digitonin to shunt the membrane resistance. We observed that the application of digitonin abolished the cellular response of the outer hair cells to an ac external electric field (5-30 Hz). Coinciding with the abolition of the cellular response, the nuclear matrix started to oscillate synchronous to the external field, indicating an appreciable increase of the intracellular electric field. If the intracellular electric field was the regulating factor of the motile response, the initiation of the movement of the nuclear matrix would have been accompanied by an enhancement of the cellular movement. Our observation is therefore consistent with the interpretation that the (local) membrane potential, and not the intracellular electric field, regulates the hair cell movement. JF - Hearing Research AU - Iwasa, Kuni H AU - Kachar, B AD - National Institute on Deafness and Other Communication Disorders PY - 1989 SP - 247 EP - 254 VL - 40 IS - 3 SN - 0378-5955, 0378-5955 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85142361?accountid=14244 LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - The Fenton degradation as a nonenzymatic model for microsomal denitrosation of N-nitrosodimethylamine. AN - 79587036; 2519780 AB - The microsomal metabolism of the carcinogen N-nitrosodimethylamine (NDMA) was suggested to be initiated by hydrogen atom abstraction to form an alpha-nitrosamino radical, which either oxidizes further to an alpha-hydroxy nitrosamine as the initial product of the activating dealkylation pathway or fragments to the nitric oxide radical and N-methylformaldimine as the first step of the presumably inactivating denitrosation route. To examine the chemistry of the alpha-nitrosamino radical in a nonenzymatic setting, we exposed NDMA to the Fenton reagent, which is known to be capable of abstracting hydrogen atoms from organic species. The products observed were those expected of a denitrosation model. Solutions containing 13 mM [14C]NDMA, 15 mM FeSO4, 15 mM H2O2, and 7.5 mM H2SO4 were kept at 4-10 degrees C for 1 h and then basified to yield methylamine (3.2 +/- 0.5 mM, mean +/- SD, n = 8), formaldehyde (3.1 +/- 0.9 mM), and unreacted nitrosamine (10.2 +/- 0.7 mM) as the only radioactive species detected, with total nitrate/nitrite also being found at a level of 2.8 +/- 0.5 mM. N-Methylformaldiminium ion was identified as an intermediate. The parallels between these results and those seen in the microsomal reaction support the hypothesis that the alpha-nitrosamino radical is a common intermediate in enzymatic denitrosation versus dealkylation of NDMA.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Chemical research in toxicology AU - Heur, Y H AU - Streeter, A J AU - Nims, R W AU - Keefer, L K AD - Chemistry Section, National Cancer Institute, Frederick Cancer Research Facility, Maryland 21701. PY - 1989 SP - 247 EP - 253 VL - 2 IS - 4 SN - 0893-228X, 0893-228X KW - Imines KW - 0 KW - Nitroso Compounds KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Dimethylnitrosamine KW - M43H21IO8R KW - Index Medicus KW - Mass Spectrometry KW - Cytochrome P-450 Enzyme System -- metabolism KW - Models, Biological KW - Imines -- metabolism KW - Chromatography, High Pressure Liquid KW - Magnetic Resonance Spectroscopy KW - Catalysis KW - Nitroso Compounds -- metabolism KW - Microsomes -- metabolism KW - Dimethylnitrosamine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79587036?accountid=14244 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 - Medication effect on lymphocyte morphology in schizophrenia. AN - 79571913; 2577275 AB - Past studies on the occurrence of atypical lymphocytes in the blood of individuals with schizophrenia are contradictory; some researchers have argued that such cells are a genetic marker of the disease while others have explained the cells simply as an effect of antipsychotic drugs. The present study blindly measured atypical lymphocytes in 14 schizophrenics on medication for at least 6 weeks and off medication for at least 4 weeks, ten Huntington's disease patients on antipsychotic medication, and ten normal controls. The patients with schizophrenia (P less than 0.05) and those with Huntington's disease (P less than 0.02) both had significantly more atypical lymphocytes than the normal controls. However no difference was found in the percentage of atypical lymphocytes in patients with schizophrenia on and off medication. The authors cite the need for studies of first-admission, never-tested patients to definitively settle this question. JF - Schizophrenia research AU - Torrey, E F AU - Upshaw, Y D AU - Suddath, R AD - Twin Study Unit, NIMH Neurosciences Center, St. Elizabeths Hospital, Washington, DC 20032. PY - 1989 SP - 385 EP - 390 VL - 2 IS - 4-5 SN - 0920-9964, 0920-9964 KW - Antipsychotic Agents KW - 0 KW - Index Medicus KW - Huntington Disease -- blood KW - Humans KW - Adult KW - Huntington Disease -- drug therapy KW - Cell Nucleus -- drug effects KW - Huntington Disease -- psychology KW - Male KW - Female KW - Antipsychotic Agents -- administration & dosage KW - Schizophrenia -- blood KW - Schizophrenic Psychology KW - Schizophrenia -- drug therapy KW - Antipsychotic Agents -- adverse effects KW - Lymphocytes -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79571913?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-08 N1 - Date created - 1991-03-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanisms of arsenic-induced cell transformation. AN - 79565723; 2484623 AB - Arsenic is a well-established carcinogen in humans, but there is little evidence for its carcinogenicity in animals and it is inactive as an initiator or tumor promoter in two-stage models of carcinogenicity in mice. Studies with cells in culture have provided some possible mechanisms by which arsenic and arsenical compounds may exert a carcinogenic activity. Sodium arsenite and sodium arsenate were observed to induce morphological transformation of Syrian hamster embryo cells in a dose-dependent manner. The trivalent sodium arsenite was greater than tenfold more potent than the pentavalent sodium arsenate. The compounds also exhibited toxicity; however, transformation was observed at nontoxic as well as toxic doses. At low doses, enhanced colony forming efficiency of the cells was observed. To understand the mechanism of arsenic-induced transformation, the genetic effects of the two arsenicals were examined over the same doses that induced transformation. No arsenic-induced gene mutations were detected at two genetic loci. However, cell transformation and cytogenetic effects, including endoreduplication, chromosome aberrations, and sister chromatid exchanges, were induced by the arsenicals with similar dose responses. These results support a possible role for chromosomal changes in arsenic-induced transformation. The two arsenic salts also induced another form of mutation-gene amplification. Both sodium arsenite and sodium arsenate induced a high frequency of methotrexate-resistant 3T6 cells, which were shown to have amplified copies of the dihydrofolate reductase gene.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Biological trace element research AU - Barrett, J C AU - Lamb, P W AU - Wang, T C AU - Lee, T C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1989 SP - 421 EP - 429 VL - 21 SN - 0163-4984, 0163-4984 KW - Arsenic KW - N712M78A8G KW - Index Medicus KW - Animals KW - Humans KW - Arsenic -- toxicity KW - Cell Transformation, Neoplastic -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79565723?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-11-02 N1 - Date created - 1990-11-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Neoplastic transformation of BALB/3T3 cells by metals and the quest for induction of a metastatic phenotype. AN - 79565032; 2484630 AB - In the mouse embryo cell line BALB/3T3 Clone A31-1-1, dose-dependent morphologic neoplastic transformation was obtained with NaAsO2, Na2HAsO4, CdCl2, and K2CrO4. Cellular uptake was four fold higher for As3+ than for As5+, and As5- was metabolized to As3+ in cytosol. Cytotoxicity and transformation rates were four fold higher for As3+ than As5+, but when correlated to cellular As burden they were equivalent. As3+ appears responsible for the transforming activity. The foci transformed by metals (or by other carcinogens) gave rise to tumorigenic cell lines (sc sarcomas in nude mice), none of which, however, induced metastases when tested by sc or by iv injection in nude mice. Thus carcinogens change this aneuploid cell line from a preneoplastic stage to the expression of malignant growth but not of metastatic activity. Metastatic and type IV collagenolytic activities can be induced by transfection of the c-Ha-ras oncogene and inhibited by the Ad2-E1a gene (so far shown in other cell types). It remains to be seen whether metal or other carcinogens can induce the nonmetastatic phenotype to become metastatic. The molecular mechanisms of metal carcinogenesis, studied in cell culture systems, in combination with other factors or oncogenes, may reveal the effect of individual metal carcinogens on discrete steps of the complex process of carcinogenesis. JF - Biological trace element research AU - Saffiotti, U AU - Bertolero, F AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, MD 20892. PY - 1989 SP - 475 EP - 482 VL - 21 SN - 0163-4984, 0163-4984 KW - Arsenates KW - 0 KW - Arsenites KW - Chromates KW - Metals KW - Potassium Compounds KW - Sodium Compounds KW - Cadmium KW - 00BH33GNGH KW - sodium arsenite KW - 48OVY2OC72 KW - potassium chromate(VI) KW - 5P0R38CN2X KW - sodium arsenate KW - 7631-89-2 KW - Cadmium Chloride KW - J6K4F9V3BA KW - Arsenic KW - N712M78A8G KW - Index Medicus KW - Phenotype KW - Animals KW - Arsenic -- toxicity KW - Cell Survival -- drug effects KW - Chromates -- toxicity KW - Cadmium -- toxicity KW - Arsenates -- toxicity KW - Mice KW - Mice, Inbred BALB C KW - Cell Transformation, Neoplastic -- pathology KW - Neoplasm Metastasis KW - Cell Transformation, Neoplastic -- drug effects KW - Metals -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79565032?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-11-02 N1 - Date created - 1990-11-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tissue susceptibility factors in cadmium carcinogenesis. Correlation between cadmium-induction of prostatic tumors in rats and an apparent deficiency of metallothionein. AN - 79550489; 2484631 AB - Recently, in two separate studies we have observed cadmium (Cd)-induction of prostatic tumors (PT) in rats. Cd (sc or im) at doses nontoxic to the testes markedly increased PT formation (2.5 mumols/kg, sc, 8 PT/29 exposed, 28%; 30 mumols/kg, im, 11/26, 42%; control 14/127, 11%). The administration of zinc (Zn; 1 mmol/kg, sc, at -6, 0 and +18 h) to prevent testicular toxicity and tumors from Cd (30 mumols/kg, sc, 0 h) also resulted in an elevated incidence of PT (8/27, 30%). The nature of the metal-binding proteins in the prostate has not been defined, although metallothionein (MT), a low Mr Cd-binding protein that confers tolerance to Cd, is deficient in other target tissues of Cd carcinogenesis, such as the rat testes. Using a technique that extracts MT from liver, a low-Mr Cd-binding protein was extracted from both ventral (VP) and dorsal prostate (DP) and isolated by gel filtration. In contrast to the two forms of rat MT, reverse phase HPLC of VP and DP extract eluted 1 and 5 forms, respectively. The amino acid compositions of the VP and DP proteins were quite distinct from MT, with much less cys than MT and the presence of residues not found in MT (leu, tyr, phe). Thus Cd-induction of PT appears to be dependent on functional testes and, as is the case with Cd-induced testicular formation, appears to be associated with a deficiency of MT. JF - Biological trace element research AU - Waalkes, M P AU - Perantoni, A AU - Rehm, S AD - Division of Cancer Etiology, National Cancer Institute, Frederick, MD 21701-1013. PY - 1989 SP - 483 EP - 490 VL - 21 SN - 0163-4984, 0163-4984 KW - Carcinogens KW - 0 KW - Cadmium KW - 00BH33GNGH KW - Metallothionein KW - 9038-94-2 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Testis -- metabolism KW - Chromatography, Gel KW - Testicular Neoplasms -- chemically induced KW - Male KW - Chromatography, High Pressure Liquid KW - Testicular Neoplasms -- metabolism KW - Prostatic Neoplasms -- metabolism KW - Metallothionein -- deficiency KW - Prostatic Neoplasms -- chemically induced KW - Cadmium -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79550489?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-11-02 N1 - Date created - 1990-11-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Subchronic toxicology studies of hexachloro-1,3-butadiene (HCBD) in B6C3F1 mice by dietary incorporation. AN - 79506498; 2632770 AB - Two-week repeated-dose and 13-week subchronic studies of HCBD were conducted in B6C3F1 mice. Groups of five mice/sex received 0, 30, 100, 300, 1,000, or 3,000 ppm HCBD in feed for 15 days. Toxic responses, primarily in the higher dose groups, included abnormal clinical signs (lethargy, hunched posture, rough coat, sensitivity to light, and/or incoordination), mortality (all mice in the top two dose groups died by day 7), body and organ weight depression, and gross and histopathological changes. The most prevalent microscopic lesion, seen in all HCBD-treated mice of both sexes, was renal tubular cell necrosis and/or regeneration. Regeneration was seen only in the lower dose groups. Thirteen-week studies were conducted in which groups of 10 mice/sex received 0, 1, 3, 10, 30, or 100 ppm HCBD in feed. No treatment-related clinical signs or mortality were observed. Body weight gain was reduced in the 30- and 100-ppm males (-49 and -56, respectively), and the 100-ppm females (-47). Significant reduction in kidney weights was seen in the 30- and 100-ppm males and 100-ppm females. A treatment-related increase in tubular cell regeneration in the renal cortex occurred in both male and female mice. This lesion was characterized by an increase both in number and basophilic staining intensity of the tubular epithelial cells. Regeneration was seen in the outer stripe of the outer medulla and extended into the medullary rays (pars recta); severity increased with dose. Female mice were more susceptible to the toxicity of HCBD than male mice. Although no adverse effects were observed at the 10-ppm level for male mice in the subchronic study, the regenerative lesion was present in female mice at 1 ppm, the lowest dose administered. JF - Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer AU - Yang, R S AU - Abdo, K M AU - Elwell, M R AU - Levy, A C AU - Brennecke, L H AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1989 SP - 323 EP - 332 VL - 9 IS - 4 SN - 0731-8898, 0731-8898 KW - Butadienes KW - 0 KW - Environmental Pollutants KW - hexachlorobutadiene KW - CQ8AAO9MO1 KW - Index Medicus KW - Animals KW - Kidney Diseases -- pathology KW - Kidney Diseases -- physiopathology KW - Environmental Pollutants -- toxicity KW - Kidney -- pathology KW - Kidney Tubules -- pathology KW - Sex Characteristics KW - Kidney Tubules -- physiopathology KW - Mice KW - Organ Size KW - Necrosis KW - Regeneration KW - Mice, Inbred C57BL KW - Mice, Inbred C3H KW - Epithelium -- pathology KW - Female KW - Male KW - Kidney Diseases -- chemically induced KW - Butadienes -- toxicity KW - Butadienes -- administration & dosage KW - Diet UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79506498?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-05-17 N1 - Date created - 1990-05-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The Lexington addicts, 1971-1972: demographic characteristics, drug use patterns, and selected infectious disease experience. AN - 79387769; 2599682 AB - The demographics, drug habits, and medical complications of a cohort of 1,129 addicts treated at Lexington in the period 1971-1972 were studied. These patients, admitted from 41 different states, had a mean period of addiction of 5.4 years. Over one-third of the sample had engaged in pimping or prostitution, and there were no differences by gender in terms of involvement. Eight-eight percent had shared injection equipment, and surprisingly, 78% admitted to some effort at sterilizing their "works." Hepatitis was the most common associated medical condition: 87% had serologic markers of hepatitis B virus (HBV) infection, 60% had evidence of hepatitis A virus (HAV) exposure, and 47% had abnormal liver function parameters. Gynecomastia was evident in 2% of male subjects. Thirteen percent of the sample had a reactive VDRL assay, but 64% of these were biologically false positive. Subtle abnormalities of immune function were also observed; 18% of the patients had recent unexplained weight loss, 6% had lymphadenopathy, 8% had leukopenia, and 2% had lymphocytopenia. We conclude that both HBV and HAV were important infectious disease risks in these addicts, and that many evidenced deficiencies in immune function well before AIDS became a major public health concern. JF - The International journal of the addictions AU - Lange, W R AU - Ball, J C AU - Pfeiffer, M B AU - Snyder, F R AU - Cone, E J AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 609 EP - 626 VL - 24 IS - 7 SN - 0020-773X, 0020-773X KW - Street Drugs KW - 0 KW - Index Medicus KW - AIDS/HIV KW - Age Factors KW - Sex Factors KW - Humans KW - Cross-Sectional Studies KW - Risk Factors KW - Adult KW - Cohort Studies KW - Incidence KW - Kentucky KW - Middle Aged KW - Adolescent KW - Heroin Dependence -- complications KW - Female KW - Male KW - Opioid-Related Disorders -- epidemiology KW - Communicable Diseases -- epidemiology KW - Substance Abuse, Intravenous -- epidemiology KW - Substance Abuse, Intravenous -- complications KW - Communicable Diseases -- transmission KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79387769?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-06 N1 - Date created - 1990-02-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tripelennamine interactions with the psychotomimetic sigma agonist N-allylnormetazocine. AN - 79348876; 2555824 AB - The pharmacological effects of individual and combined intravenous doses of the antihistamine tripelennamine and the psychotomimetic sigma benzomorphan opioid derivative, N-allylnormetazocine (NANM), on nociceptive reflexes, autonomic parameters and behavior were assessed in the chronic spinal dog. NANM (1.65 mg/kg, IV) produced antinociception, mydriasis, tachycardia, hyperthermia and behavioral signs of canine delirium. Tripelennamine (1.25 mg/kg, IV) produced antinociception, mydriasis and tachycardia without affecting behavior. The combined effects of the two drugs were additive except for heart rate. However, tripelennamine did not antagonize any of the physiological effects or the signs of canine delirium produced by NANM. The findings are inconsistent with the hypothesis that tripelennamine antagonizes the psychotomimetic NANM-like effects of pentazocine to make pentazocine-tripelennamine combinations (T's and Blues) more desirable as a heroin substitute. JF - Pharmacology, biochemistry, and behavior AU - Vaupel, D B AD - Neuropharmacology Laboratory, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 717 EP - 720 VL - 33 IS - 3 SN - 0091-3057, 0091-3057 KW - Hallucinogens KW - 0 KW - Receptors, Opioid KW - Receptors, sigma KW - Tripelennamine KW - 3C5ORO99TY KW - SK&F 10047 KW - 7619-35-4 KW - Phenazocine KW - J0ND6N0AQC KW - Index Medicus KW - Animals KW - Sensory Thresholds -- drug effects KW - Drug Interactions KW - Autonomic Nervous System -- drug effects KW - Dogs KW - Female KW - Tripelennamine -- pharmacology KW - Behavior, Animal -- drug effects KW - Pain -- physiopathology KW - Phenazocine -- analogs & derivatives KW - Phenazocine -- pharmacology KW - Hallucinogens -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79348876?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-29 N1 - Date created - 1989-12-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pregnenolone sulfate antagonizes barbiturate-induced hypnosis. AN - 79347655; 2587612 AB - The potential influence of the neurosteroid pregnenolone sulfate (PrS) on barbiturate-induced hypnosis was tested in rats. PrS, when injected intracerebroventricularly or intraperitoneally, significantly shortened the sleep-time produced by pentobarbital. The results suggest an important physiological and pharmacological role for PrS in the regulation of CNS excitability. JF - Pharmacology, biochemistry, and behavior AU - Majewska, M D AU - Bluet-Pajot, M T AU - Robel, P AU - Baulieu, E E AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 701 EP - 703 VL - 33 IS - 3 SN - 0091-3057, 0091-3057 KW - pregnenolone sulfate KW - 04Y4D91RG0 KW - Pregnenolone KW - 73R90F7MQ8 KW - Pentobarbital KW - I4744080IR KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Injections, Intraperitoneal KW - Animals KW - Rats, Inbred F344 KW - Drug Interactions KW - Dose-Response Relationship, Drug KW - Male KW - Injections, Intraventricular KW - Pregnenolone -- pharmacology KW - Hypnosis, Anesthetic KW - Pregnenolone -- administration & dosage KW - Pentobarbital -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79347655?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-29 N1 - Date created - 1989-12-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Novel pyrrolidines in the venom of the ant Monomorium indicum. AN - 79284494; 2809607 AB - New 2,5-dialkylpyrrolidines found in the venom of Monomorium indicum include trans-2-butyl-5-(4-pentenyl)pyrrolidine [1], trans-2-butyl-5-(6-heptenyl)pyrrolidine [4], trans-5-(5-hexenyl)-2-(4-pentenyl)pyrrolidine [6], trans-5-(6-heptenyl)-2-(5-hexenyl)pyrrolidine [8], and trans-5-heptyl-2-hexylpyrrolidine [16], whose structures were confirmed by synthesis. The concomitance of five previously reported trans-2,5-dialkyl-pyrrolidines along with small amounts of the cis isomers and N-methyl analogues makes the venom of M. indicum the most qualitatively diverse blend of alkaloids reported from an ant to date. The toxicities to termites of four of these alkaloids were determined. JF - Journal of natural products AU - Jones, T H AU - Blum, M S AU - Escoubas, P AU - Musthak Ali, T M AD - Laboratory of Chemistry, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. PY - 1989 SP - 779 EP - 784 VL - 52 IS - 4 SN - 0163-3864, 0163-3864 KW - Ant Venoms KW - 0 KW - Arthropod Venoms KW - Pyrrolidines KW - Index Medicus KW - Animals KW - Insects KW - Magnetic Resonance Spectroscopy KW - Pyrrolidines -- analysis KW - Ant Venoms -- analysis KW - Pyrrolidines -- isolation & purification KW - Pyrrolidines -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79284494?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-20 N1 - Date created - 1989-12-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Through the centuries with food and drink, for better or worse. AN - 79232577; 2676718 JF - Allergy proceedings : the official journal of regional and state allergy societies AU - Cohen, S G AU - Saavedra-Delgado, A M AD - National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. PY - 1989 SP - 281 EP - 290 VL - 10 IS - 4 SN - 1046-9354, 1046-9354 KW - Index Medicus KW - History of medicine KW - Bible KW - Humans KW - Foodborne Diseases -- history KW - History, Ancient KW - Food Hypersensitivity -- history UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79232577?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-21 N1 - Date created - 1989-11-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Metabolite-based internal doses used in a risk assessment of benzene. AN - 79226281; 2792038 AB - Risk assessments of benzene have been based upon both human and animal studies. In this paper, metabolite information is used to construct an internal dose (a surrogate of the biologically effective dose) for a given administered dose. The relationship between the administered dose and this internal dose is nonlinear and is well described by a Michaelis-Menten function. The administered doses from the National Toxicology Program's rodent carcinogenicity study of benzene are transformed into internal doses, and these internal doses are used in conjunction with a multistage model to compare previous estimated virtually safe doses (VSD) associated with small added health risks. The ratio of VSD for the administered dose risk assessment to the VSD from the internal dose risk assessment was approximately 1.0 for the F344/N rats and ranged from 2.5 to 5.0 for B6C3F1 mice in the National Toxicology Program study. For an occupational exposure of 1 ppm, a risk estimate of 0.7 excess cancers/1000 exposed with an upper bound of 3.5/1000 was obtained for a total metabolite internal dose risk assessment. Risk estimates based upon internal doses constructed from levels of the toxic metabolites of benzene are also presented. The implication of a dose-rate study of benzene metabolism for risk assessment is discussed, and finally, suggestions for better characterization of the dose-response function for benzene are provided. JF - Environmental health perspectives AU - Bailer, A J AU - Hoel, D G AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 177 EP - 184 VL - 82 SN - 0091-6765, 0091-6765 KW - Carcinogens KW - 0 KW - Benzene KW - J64922108F KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Administration, Oral KW - Risk KW - Animals KW - Rats, Inbred F344 KW - Dose-Response Relationship, Drug KW - Humans KW - Mice KW - Models, Biological KW - Mathematics KW - Benzene -- administration & dosage KW - Benzene -- metabolism KW - Benzene -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79226281?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-02 N1 - Date created - 1989-11-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Lancet. 1977 Jul 9;2(8028):76-8 [69157] Arch Environ Health. 1978 Jan-Feb;33(1):3-10 [629594] J Environ Pathol Toxicol. 1978 Sep-Oct;1(1):163-79 [722184] Am J Ind Med. 1981;2(3):217-45 [7345926] Science. 1983 Mar 4;219(4588):1032-7 [6823565] J Toxicol Clin Toxicol. 1982 Aug;19(6-7):781-805 [7161853] Am J Ind Med. 1983;4(5):589-630 [6353911] Toxicol Appl Pharmacol. 1987 Feb;87(2):325-36 [3824388] N Engl J Med. 1987 Apr 23;316(17):1044-50 [3561457] Am J Epidemiol. 1988 Mar;127(3):419-39 [3277397] Environ Health Perspect. 1989 Jul;82:9-17 [2792053] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Multifunctional receptor model for dioxin and related compound toxic action: possible thyroid hormone-responsive effector-linked site. AN - 79225864; 2551666 AB - Molecular/theoretical modeling studies have revealed that thyroid hormones and toxic chlorinated aromatic hydrocarbons of environmental significance (for which dioxin or TCDD is the prototype) have similar structural properties that could be important in molecular recognition in biochemical systems. These molecular properties include a somewhat rigid, sterically accessible and polarizable aromatic ring and size-limited, hydrophobic lateral substituents, usually contained in opposite adjoining rings of a diphenyl compound. These molecular properties define the primary binding groups thought to be important in molecular recognition of both types of structures in biochemical systems. Similar molecular reactivities are supported by the demonstration of effective specific binding of thyroid hormones and chlorinated aromatic hydrocarbons with four different proteins, enzymes, or receptor preparations that are known or suspected to be involved in the expression of thyroid hormone activity. These binding interactions represent both aromatic-aromatic (stacking) and molecular cleft-type recognition processes. A multiple protein or multifunctional receptor-ligand binding mechanism model is proposed as a way of visualizing the details and possible role of both the stacking and cleft type molecular recognition factors in the expression of biological activity. The model suggests a means by which hormone-responsive effector-linked sites (possible protein-protein-DNA complexes) can maintain highly structurally specific control of hormone action. Finally, the model also provides a theoretical basis for the design and conduct of further biological experimentation on the molecular mechanism(s) of action of toxic chlorinated aromatic hydrocarbons and thyroid hormones. JF - Environmental health perspectives AU - McKinney, J D AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 323 EP - 336 VL - 82 SN - 0091-6765, 0091-6765 KW - Dioxins KW - 0 KW - Hydrocarbons, Chlorinated KW - Receptors, Aryl Hydrocarbon KW - Receptors, Drug KW - Thyroid Hormones KW - Index Medicus KW - Molecular Structure KW - Animals KW - Models, Molecular KW - Computer Graphics KW - Models, Chemical KW - Dioxins -- metabolism KW - Receptors, Drug -- metabolism KW - Hydrocarbons, Chlorinated -- toxicity KW - Hydrocarbons, Chlorinated -- metabolism KW - Thyroid Hormones -- metabolism KW - Dioxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79225864?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-02 N1 - Date created - 1989-11-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochemistry. 1981 Nov 24;20(24):6781-9 [6274379] J Biol Chem. 1982 Jan 25;257(2):930-8 [6274872] Annu Rev Pharmacol Toxicol. 1982;22:517-54 [6282188] Int Rev Cytol Suppl. 1983;15:17-48 [6189802] Proc Natl Acad Sci U S A. 1983 Sep;80(18):5749-52 [6310591] J Biol Chem. 1984 Jan 25;259(2):980-5 [6319394] Biochemistry. 1984 Jan 17;23(2):340-9 [6365163] Biochem Pharmacol. 1984 Mar 15;33(6):833-9 [6324800] J Clin Invest. 1985 Jan;75(1):147-54 [3965501] Life Sci. 1985 Feb 18;36(7):695-703 [3881642] Mol Pharmacol. 1985 Feb;27(2):271-6 [2982091] J Med Chem. 1985 Mar;28(3):375-81 [3919186] J Med Chem. 1986 Nov;29(11):2149-53 [3783576] J Med Chem. 1986 Dec;29(12):2451-7 [3097319] J Biol Chem. 1985 May 25;260(10):6481-7 [3922975] Science. 1985 Jul 5;229(4708):23-8 [3892686] Environ Health Perspect. 1985 May;60:57-68 [2992928] Toxicology. 1985 Oct;37(1-2):51-63 [3933144] Environ Health Perspect. 1985 Sep;61:41-53 [2998749] Environ Health Perspect. 1985 Sep;61:5-10 [2998750] J Med Chem. 1986 May;29(5):641-8 [3009810] Biochem Biophys Res Commun. 1986 Apr 14;136(1):294-9 [3707577] Toxicol Appl Pharmacol. 1986 Jun 15;84(1):45-55 [3715868] Toxicol Lett. 1986 May;31(2):151-8 [3012826] Annu Rev Pharmacol Toxicol. 1986;26:371-99 [3013079] Endocrinology. 1986 Sep;119(3):1076-82 [3732155] Proc Natl Acad Sci U S A. 1986 Aug;83(16):5774-8 [2874556] J Biol Chem. 1986 Sep 5;261(25):11613-22 [3745159] Toxicol Appl Pharmacol. 1986 Sep 30;85(3):301-12 [3094194] Science. 1986 Nov 28;234(4780):1081-6 [3775377] J Clin Endocrinol Metab. 1968 Mar;28(3):386-92 [4171084] Biochemistry. 1969 Apr;8(4):1554-7 [4241490] Endocrinology. 1974 Sep;95(3):897-903 [4369384] J Biol Chem. 1974 Nov 10;249(21):6796-805 [4607556] J Biol Chem. 1976 Aug 25;251(16):4936-46 [956169] Endocrinology. 1977 Jul;101(1):292-6 [862558] J Clin Invest. 1977 Sep;60(3):555-62 [197120] Nature. 1977 Jul 14;268(5616):115-20 [201845] Recent Prog Horm Res. 1978;34:437-75 [216059] Cancer Res. 1979 Aug;39(8):3172-6 [455301] J Biol Chem. 1979 Sep 10;254(17):8534-9 [224057] J Biol Chem. 1980 Nov 10;255(21):10271-8 [6253468] Cancer Res. 1980 Oct;40(10):3616-20 [6108157] Endocr Rev. 1980 Spring;1(2):140-66 [6263601] Biochemistry. 1986 Oct 7;25(20):6335-42 [3024707] Nature. 1986 Dec 18-31;324(6098):635-40 [2879242] Nature. 1986 Dec 18-31;324(6098):641-6 [2879243] Endocrinology. 1987 Mar;120(3):1089-96 [3803311] J Med Chem. 1987 Jan;30(1):79-86 [3100800] Biochem J. 1986 Dec 1;240(2):621-2 [3101675] Biochem Pharmacol. 1987 Jan 15;36(2):283-91 [3814171] Science. 1987 Mar 20;235(4795):1478-84 [3823899] Toxicol Appl Pharmacol. 1987 Feb;87(2):337-50 [3824389] Environ Health Perspect. 1986 Dec;70:137-47 [3830099] Endocrinology. 1987 May;120(5):1742-9 [3106010] Annu Rev Pharmacol Toxicol. 1987;27:87-111 [3034142] Cancer Res. 1987 Jun 15;47(12):3052-6 [3581059] Biochem Pharmacol. 1987 Apr 15;36(8):1361-5 [3036167] Toxicol Appl Pharmacol. 1987 Jun 30;89(2):165-74 [3111013] Pharmacol Rev. 1987 Jun;39(2):147-61 [3303065] Chem Biol Interact. 1987;64(1-2):39-60 [3690723] J Med Chem. 1988 Feb;31(2):357-62 [2828621] Science. 1988 May 13;240(4854):889-95 [3283939] Proc Natl Acad Sci U S A. 1988 Jun;85(12):4128-32 [3380784] Science. 1988 Jun 24;240(4860):1759-64 [3289117] J Theor Biol. 1987 Nov 21;129(2):231-41 [3138502] Nature. 1961 Mar 4;189:729-32 [13763782] J Med Pharm Chem. 1962 Nov;91:1307-15 [14056463] Mayo Clin Proc. 1964 Aug;39:560-8 [14198023] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Multiple-site carcinogenicity of benzene in Fischer 344 rats and B6C3F1 mice. AN - 79225763; 2676495 AB - Toxicology and carcinogenesis studies of benzene (CAS No. 71-43-2; greater than 99.7% pure) were conducted in groups of 60 F344/N rats and 60 B6C3F1 mice of each sex for each of three exposure doses and vehicle controls. These composite studies on benzene were designed and conducted because of large production volume and widespread human exposure, because of the epidemiologic association with leukemia, and because previous experiments were considered inadequate or inconclusive for determining carcinogenicity in laboratory animals. Using the results from 17-week studies, doses for the 2-year studies were selected based on clinical observations (tremors in higher dosed mice), on clinical pathologic findings (lymphoid depletion in rats and leukopenia in mice), and on body weight effects. Doses of 0, 50, 100, or 200 mg/kg body weight benzene in corn oil were administered by gavage to male rats, 5 days per week, for 103 weeks. Doses of 0, 25, 50, or 100 mg/kg benzene in corn oil were administered by gavage to female rats and to male and female mice for 103 weeks. Ten animals in each of the 16 groups were killed at 12 months, and necropsies were performed. Hematologic profiles were performed at 3-month intervals. For the 2-year studies, mean body weights of the top dose groups of male rats and of both sexes of mice were lower than those of the controls. Survivals of the top dose group of rats and mice of each sex were reduced; however, at week 92 for rats and week 91 for mice, survival was greater than 60% in all groups; most of the dosed animals that died before week 103 had neoplasia. Compound-related nonneoplastic or neoplastic effects on the hematopoietic system, Zymbal gland, forestomach, and adrenal gland were found both for rats and mice. Further, the oral cavity was affected in rats, and the lung, liver, Harderian gland, preputial gland, ovary, and mammary gland were affected in mice. Under the conditions of these 2-year gavage studies, there was clear evidence of carcinogenicity of benzene in male F344/N rats, female F344/N rats, male B6C3F1 mice, and female B6C3F1 mice. In male rats, benzene caused increased incidences of Zymbal gland carcinomas, squamous cell papillomas and squamous cell carcinomas of the oral cavity, and squamous cell papillomas and squamous cell carcinomas of the skin. In female rats, benzene caused increased incidences of Zymbal gland carcinomas and squamous cell papillomas and squamous cell carcinomas of the oral cavity.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Environmental health perspectives AU - Huff, J E AU - Haseman, J K AU - DeMarini, D M AU - Eustis, S AU - Maronpot, R R AU - Peters, A C AU - Persing, R L AU - Chrisp, C E AU - Jacobs, A C AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 125 EP - 163 VL - 82 SN - 0091-6765, 0091-6765 KW - Carcinogens KW - 0 KW - Mutagens KW - Benzene KW - J64922108F KW - Index Medicus KW - Rats KW - Hematologic Diseases -- chemically induced KW - Animals KW - Rats, Inbred F344 KW - Neoplasms, Experimental -- chemically induced KW - Dose-Response Relationship, Drug KW - Body Weight -- drug effects KW - Mice KW - Neoplasms, Experimental -- pathology KW - Male KW - Female KW - Benzene -- administration & dosage KW - Benzene -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79225763?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-02 N1 - Date created - 1989-11-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Environ Health Perspect. 1989 Jul;82:43-9 [2792050] Environ Health Perspect. 1989 Jul;82:9-17 [2792053] Environ Health Perspect. 1989 Jul;82:97-108 [2792054] Biochem J. 1953 May;54(2):231-8 [13058864] Cancer. 1961 Nov-Dec;14:1306-15 [14008628] Mutat Res. 1975 Dec;31(6):347-64 [768755] Schweiz Med Wochenschr. 1982 Dec 11;112(50):1858-9 [7156970] Cancer Res. 1983 Mar;43(3):1330-4 [6825102] Mutat Res. 1983 Mar;119(3):355-60 [6828070] Carcinogenesis. 1983;4(3):291-5 [6339095] Environ Res. 1983 Feb;30(1):16-25 [6832104] Helv Med Acta. 1971 Dec;36(1):59-66 [5140811] J Natl Cancer Inst. 1973 Aug;51(2):703-5 [4765384] CRC Crit Rev Toxicol. 1975 Jun;3(3):265-88 [1097190] Cancer Res. 1975 Dec;35(12):3651-5 [1192426] J Natl Cancer Inst. 1975 Dec;55(6):1329-36 [1547] J Natl Cancer Inst. 1976 Jun;56(6):1237-42 [994224] Ann N Y Acad Sci. 1976;271:143-51 [1069497] Mutat Res. 1977 Jan;42(1):19-31 [191747] J Toxicol Environ Health Suppl. 1977;2:23-36 [342714] J Toxicol Environ Health Suppl. 1977;2:69-105 [342717] Mutat Res. 1978;47(2):75-97 [415231] Arch Environ Health. 1978 Jan-Feb;33(1):3-10 [629594] Mutat Res. 1978 May;57(2):163-7 [96337] Toxicology. 1978 Sep;11(1):55-63 [705804] Ann N Y Acad Sci. 1978 Sep 29;298:124-40 [360906] Mol Pharmacol. 1978 Sep;14(5):920-9 [714029] Mutat Res. 1978 Sep;58(1):29-34 [362193] Toxicol Appl Pharmacol. 1978 Oct;46(1):9-18 [725954] Environ Health Perspect. 1978 Dec;27:11-20 [367762] Mutat Res. 1978 Nov;58(2-3):313-6 [370577] J Natl Cancer Inst. 1979 Apr;62(4):957-74 [285297] CRC Crit Rev Biochem. 1979;6(4):401-37 [378536] Tex Rep Biol Med. 1978;37:153-61 [752975] Toxicol Appl Pharmacol. 1979 Jul;49(3):417-23 [473208] Cancer Res. 1979 Oct;39(10):4152-9 [383281] Mol Gen Genet. 1979 Jul 2;174(1):39-46 [384160] Life Sci. 1979 Aug 13;25(7):567-72 [502750] Cancer Res. 1980 Apr;40(4):1189-93 [7357548] Experientia. 1980 Mar 15;36(3):297-9 [7371785] Mutat Res. 1980 Feb;77(2):149-55 [6990240] Proc Natl Acad Sci U S A. 1980 Apr;77(4):2148-52 [6929542] Chem Biol Interact. 1980 May;30(2):241-5 [7389002] Mutat Res. 1980 Jul;76(1):1-50 [6993936] Chem Biol Interact. 1980 Dec;33(1):1-17 [7438288] J Natl Cancer Inst. 1981 Jan;66(1):163-9 [6935456] Am Ind Hyg Assoc J. 1980 Sep;41(9):616-23 [7457381] Chem Biol Interact. 1981 Jan;33(2-3):285-99 [7460069] Med Lav. 1979 Sep-Oct;70(5):352-7 [554913] Toxicology. 1980;15(3):219-232 [7008261] Mutat Res. 1980 Oct;74(5):379-87 [7207475] J Environ Pathol Toxicol. 1980 Nov;4(5-6):123-31 [7012268] Mutat Res. 1980 Nov;79(3):203-12 [7012602] Environ Mutagen. 1981;3(1):11-32 [7021142] Environ Mutagen. 1981;3(4):429-44 [7021147] Environ Health Perspect. 1984 Dec;58:385-92 [6525993] Mutat Res. 1983 Mar;116(3-4):217-38 [6339893] Science. 1983 Jul 15;221(4607):227-36 [6336310] Cancer Res. 1983 Aug;43(8):3660-2 [6305491] Environ Mutagen. 1983;5(2):223-6 [6407826] Drug Metab Rev. 1983;14(3):559-607 [6347595] Toxicol Appl Pharmacol. 1983 Jul;69(3):363-8 [6879607] Mutat Res. 1983 Oct;113(6):467-79 [6621578] Environ Health Perspect. 1983 Oct;52:75-82 [6653540] Mutat Res. 1984 Mar;135(3):203-9 [6708961] Mutat Res. 1984 Mar;135(3):225-43 [6424008] Carcinogenesis. 1984 Jun;5(6):827-32 [6722989] Toxicol Pathol. 1984;12(2):126-35 [11478313] Natl Cancer Inst Monogr. 1968 Jun;28:173-80 [5671401] Acta Med Biol (Niigata). 1970 Mar;17(4):285-91 [5431869] Mutat Res. 1981 Oct;85(5):335-45 [7029261] Environ Mutagen. 1980;2(1):43-50 [7327159] J Toxicol Environ Health. 1981 Jul-Aug;8(1-2):251-80 [7328708] Mutat Res. 1981 Oct;90(2):91-109 [6799819] Mutat Res. 1981 Nov;90(3):273-8 [7329437] Cancer Lett. 1981 Dec;14(3):251-60 [7199376] Chem Biol Interact. 1982 Mar 15;39(2):129-38 [7060224] Mutat Res. 1981 Dec;90(4):399-409 [7038461] Toxicol Lett. 1982 Oct;13(3-4):169-73 [6959383] Toxicol Appl Pharmacol. 1984 Sep 15;75(2):358-61 [6474468] Prog Clin Biol Res. 1985;163B:295-300 [3983155] Cancer Res. 1985 Jun;45(6):2471-7 [3986787] Mutat Res. 1985 May-Jun;143(1-2):55-9 [4000143] Am J Ind Med. 1985;7(5-6):403-13 [3890530] Am J Ind Med. 1985;7(5-6):415-46 [4003403] Mutat Res. 1985 Nov;154(3):153-81 [3930957] J Natl Cancer Inst. 1985 Nov;75(5):975-84 [3863995] J Invest Dermatol. 1985 Dec;85(6):522-6 [4067326] Mol Pharmacol. 1985 Dec;28(6):560-6 [4079912] Environ Mutagen. 1986;8(1):29-40 [3943496] J Natl Cancer Inst. 1986 Feb;76(2):283-9 [3456066] Toxicol Lett. 1985 Dec;29(2-3):161-7 [2418539] Arch Toxicol Suppl. 1985;8:425-30 [3868373] Mutat Res. 1986 May;160(3):259-66 [3960039] Mol Pharmacol. 1986 Jul;30(1):42-7 [3724744] Toxicol Appl Pharmacol. 1986 Sep 30;85(3):464-77 [3764927] Toxicology. 1986 Dec 15;42(2-3):171-81 [3798466] Toxicol Appl Pharmacol. 1987 Feb;87(2):325-36 [3824388] N Engl J Med. 1987 Apr 23;316(17):1044-50 [3561457] Mutat Res. 1987 Jun;188(2):135-40 [3587261] Toxicol Ind Health. 1986 Dec;2(4):445-51 [3590199] Mutat Res. 1987 Jul;179(1):23-31 [3037363] Arch Toxicol. 1987;60(1-3):61-4 [3619644] Toxicol Lett. 1987 Sep;38(1-2):123-33 [3307023] Crit Rev Toxicol. 1987;18(2):141-59 [3311642] Mutat Res. 1987 Dec;192(4):239-46 [3317033] Environ Health Perspect. 1987 Oct;74:229-35 [3691430] Jpn J Cancer Res. 1987 Nov;78(11):1144-9 [3121550] Am J Epidemiol. 1988 Mar;127(3):419-39 [3277397] Mutagenesis. 1987 May;2(3):235-8 [3325750] Mutat Res. 1988 Feb;204(2):203-6 [3278211] Oncogene. 1987 Mar;1(1):59-69 [3438083] Mutat Res. 1988 Jun;203(3):155-76 [2836728] Toxicol Appl Pharmacol. 1988 Jun 15;94(1):128-40 [3376110] Ann N Y Acad Sci. 1988;534:427-40 [3389672] Mutat Res. 1981 Nov;90(3):261-72 [6799821] Environ Health Perspect. 1989 Jul;82:109-24 [2792037] Environ Health Perspect. 1989 Jul;82:193-7 [2676498] Environ Health Perspect. 1989 Jul;82:207-13 [2792042] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Estrogen-induced expression of mouse lactate dehydrogenase-A gene. AN - 79219671; 2676196 AB - The synthesis of lactate dehydrogenase-A isoenzyme was shown to increase significantly in the uterus of immature mice treated by diethylstilbestrol. The expression of the mouse LDH-A promoter and cat fusion gene in Chinese hamster ovary cells was also induced by 17 beta-estradiol and diethylstilbestrol. JF - Cell biology international reports AU - Li, S S AU - Hou, E W AD - Laboratory of Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 619 EP - 624 VL - 13 IS - 7 SN - 0309-1651, 0309-1651 KW - Estrogens KW - 0 KW - Isoenzymes KW - Recombinant Fusion Proteins KW - Diethylstilbestrol KW - 731DCA35BT KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - Index Medicus KW - Animals KW - Cricetulus KW - Mice KW - Plasmids KW - Uterus -- metabolism KW - Recombinant Fusion Proteins -- metabolism KW - Mice, Inbred Strains KW - Ovary -- metabolism KW - Uterus -- cytology KW - Promoter Regions, Genetic -- drug effects KW - Ovary -- cytology KW - Transfection KW - Recombinant Fusion Proteins -- genetics KW - Diethylstilbestrol -- pharmacology KW - Escherichia coli KW - Female KW - Cricetinae KW - Gene Expression -- drug effects KW - Estrogens -- pharmacology KW - Gene Expression Regulation, Enzymologic -- drug effects KW - L-Lactate Dehydrogenase -- genetics KW - L-Lactate Dehydrogenase -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79219671?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-30 N1 - Date created - 1989-10-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evidence for a decline with age in behavioral responsivity to the serotonin agonist, m-chlorophenylpiperazine, in healthy human subjects. AN - 79197910; 2772095 AB - The functional significance of alterations in brain serotonin (5HT) associated with normal aging in both animals and humans is largely unknown. Using the effects of the 5HT agonist, m-chlorophenylpiperazine (m-CPP), as a measure of central serotonergic responsivity, we compared the behavioral and neuroendocrine responses of older normal volunteers (mean age +/- SD = 62.4 +/- 4.12) to those of younger normal volunteers (mean age +/- SD = 31.6 +/- 5.52). When m-CPP was administered intravenously, older subjects showed decreased behavioral responses but similar neuroendocrine responses, compared to younger subjects. The decreased behavioral responsivity was unrelated to pharmaco-kinetic differences between the groups, since m-CPP plasma levels were similar in both groups. This report is the first in vivo study in humans to demonstrate decreased behavioral responsivity with age following serotonergic stimulation, and may indicate a functionally less responsive 5HT subsystem in older subjects. JF - Psychiatry research AU - Lawlor, B A AU - Sunderland, T AU - Hill, J L AU - Mellow, A M AU - Molchan, S E AU - Mueller, E A AU - Jacobsen, F M AU - Murphy, D L AD - Section on Clinical Neuropharmacology, NIMH Bethesda, MD 20892. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 1 EP - 10 VL - 29 IS - 1 SN - 0165-1781, 0165-1781 KW - Piperazines KW - 0 KW - Receptors, Serotonin KW - Prolactin KW - 9002-62-4 KW - 1-(3-chlorophenyl)piperazine KW - REY0CNO998 KW - Hydrocortisone KW - WI4X0X7BPJ KW - Index Medicus KW - Prolactin -- blood KW - Age Factors KW - Substance-Related Disorders -- blood KW - Aged, 80 and over KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Male KW - Hydrocortisone -- blood KW - Female KW - Receptors, Serotonin -- drug effects KW - Piperazines -- pharmacokinetics KW - Arousal -- drug effects KW - Brain -- drug effects KW - Piperazines -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79197910?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-27 N1 - Date created - 1989-09-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A phase I trial of recombinant human interferon-gamma in patients with Kaposi's sarcoma and the acquired immunodeficiency syndrome (AIDS). AN - 79182993; 2549086 AB - A Phase I study of recombinant interferon-gamma (rIFN-gamma) was conducted to determine the toxicity and pharmacokinetics of this lymphokine in acquired immunodeficiency syndrome (AIDS) patients with Kaposi's sarcoma (KS). Sixteen patients with AIDS/KS were entered into a fixed-dose trial at either 0.001, 0.01, 0.1, or 1.0 mg/m2 of rIFN-gamma. rIFN-gamma was initially administered either as a single 24-hr continuous iv infusion or as a single im injection, followed 4 days later by a 10-day course of daily therapy by the same route. Following a 1-week washout period, this sequence of administration was then repeated, with the drug given by the alternate route. Pharmacokinetic analysis of the 1.0-mg/m2 group revealed that peak serum levels of up to 153 U/ml occurred 2-4 hr after im injection and that steady-state levels of up to 40 U/ml were reached approximately 7-12 hr after beginning iv infusion. Dose-related toxicities in this trial included fever, headache, fatigue, nausea, and hepatitis, all of which were most severe at the two highest doses. Dose-dependent depression of the total white blood-cell (WBC) count, affecting both granulocytes and lymphocytes, was the most common laboratory abnormality. Natural killer (NK)-cell activity was slightly enhanced at a dose of 0.1 mg/m2 but suppressed at 1.0 mg/m2 of drug; monocyte-mediated cytotoxicity, in contrast, was significantly increased only at the highest dose. No dose-related changes were noted in KS lesions, HLA-DR expression by peripheral blood mononuclear cells, lymphocyte blastogenesis, or the ability to culture cytomegalovirus (CMV) from body fluids. We conclude that a maximally tolerated dose (MTD) for this drug is in the range of 0.1-1.0 mg/m2 and that at least modest evidence of systemic immunomodulation may be seen when rIFN-gamma is given at doses at or near this MTD. JF - Journal of clinical immunology AU - Lane, H C AU - Davey, R T AU - Sherwin, S A AU - Masur, H AU - Rook, A H AU - Manischewitz, J F AU - Quinnan, G V AU - Smith, P D AU - Easter, M E AU - Fauci, A S AD - Laboratory of Immunoregulation, NIAID, Bethesda, Maryland 20892. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 351 EP - 361 VL - 9 IS - 4 SN - 0271-9142, 0271-9142 KW - Adjuvants, Immunologic KW - 0 KW - Recombinant Proteins KW - Interferon-gamma KW - 82115-62-6 KW - Index Medicus KW - AIDS/HIV KW - Leukocyte Count -- drug effects KW - Drug Evaluation -- methods KW - Humans KW - Adult KW - Middle Aged KW - Cytotoxicity, Immunologic -- drug effects KW - Adolescent KW - Male KW - Killer Cells, Natural -- drug effects KW - Cytomegalovirus -- drug effects KW - Sarcoma, Kaposi -- drug therapy KW - Interferon-gamma -- toxicity KW - Interferon-gamma -- administration & dosage KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Interferon-gamma -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79182993?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-12 N1 - Date created - 1989-10-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - TPA-induced neurite formation in a neuroblastoma cell line (SH-SY5Y) is associated with increased IGF-I receptor mRNA and binding. AN - 79180347; 2770453 AB - The neuroblastoma cell line SH-SY5Y was cultured in the presence of TPA for three days. Increased neurite formation was noted as early as 24 hours after TPA was added. These changes were associated with an increase in IGF-I receptor binding as well as increased mRNA for the IGF-I receptor. JF - Brain research. Molecular brain research AU - Ota, A AU - Shen-Orr, Z AU - Roberts, C T AU - LeRoith, D AD - Section of Molecular and Cellular Physiology, NIDDK, Bethesda, MD 20892. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 69 EP - 76 VL - 6 IS - 1 SN - 0169-328X, 0169-328X KW - RNA, Messenger KW - 0 KW - Somatomedins KW - Insulin-Like Growth Factor I KW - 67763-96-6 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Binding, Competitive KW - Cell Differentiation -- drug effects KW - Insulin-Like Growth Factor I -- genetics KW - Tumor Cells, Cultured -- cytology KW - Tumor Cells, Cultured -- metabolism KW - RNA, Messenger -- metabolism KW - Tumor Cells, Cultured -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Insulin-Like Growth Factor I -- metabolism KW - Dendrites -- physiology KW - Somatomedins -- metabolism KW - Neuroblastoma KW - Dendrites -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79180347?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-04 N1 - Date created - 1989-10-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - An 18-mer peptide derived from the retinal S antigen induces uveitis and pinealitis in primates. AN - 79169405; 2475283 AB - S-antigen, a photoreceptor cell protein, induces a predominantly T-cell mediated autoimmune uveitis in many vertebrate animals, including primates. Because of this activity and the finding of immune responses to S antigen in patients with uveitis, this protein has been implicated in the pathogenesis of uveitis in humans. Peptide M, an 18-amino acid component of S antigen, has previously been shown to be highly uveitopathogenic in rats and guinea pigs. We report here that peptide M is immunopathogenic in some monkeys, producing inflammatory changes in eyes and pineal glands similar to those induced by native S antigen. Monkeys with disease also developed intense immune responses to peptide M, measured by the lymphocyte proliferation assay. In addition, lymphocytes from these monkeys reacted against whole S antigen. Furthermore, lymphocytes from certain monkeys immunized with whole S antigen responded well against peptide M, thus indicating that this peptide is an immunodominant epitope in these animals. Two of the four monkeys immunized with peptide M did not develop disease. Lymphocytes from these two animals did not respond in culture against the peptide. Following immunization with the whole protein, these monkeys were capable, however, of developing cellular immunity against S antigen and one of them developed disease. The possible involvement of peptide M in the pathogenesis of uveitis in humans is discussed. JF - Clinical and experimental immunology AU - Hirose, S AU - Singh, V K AU - Donoso, L A AU - Shinohara, T AU - Kotake, S AU - Tanaka, T AU - Kuwabara, T AU - Yamaki, K AU - Gery, I AU - Nussenblatt, R B AD - Laboratory of Immunology, National Eye Institute, Bethesda, MD 20892. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 106 EP - 111 VL - 77 IS - 1 SN - 0009-9104, 0009-9104 KW - Antigens KW - 0 KW - Epitopes KW - Eye Proteins KW - Peptide Fragments KW - peptide M, retinal S antigen KW - Index Medicus KW - Lymphocyte Activation KW - Animals KW - Macaca KW - Inflammation -- etiology KW - Inflammation -- immunology KW - Eye Proteins -- toxicity KW - Peptide Fragments -- toxicity KW - Uveitis -- immunology KW - Antigens -- toxicity KW - Uveitis -- etiology KW - Pineal Gland UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79169405?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-25 N1 - Date created - 1989-09-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Ophthalmol. 1982 Aug;94(2):147-58 [6956239] Curr Top Eye Res. 1980;2:215-302 [7344837] Clin Immunol Immunopathol. 1983 Apr;27(1):81-95 [6872352] Invest Ophthalmol Vis Sci. 1984 Aug;25(8):977-80 [6204954] J Immunol. 1982 Sep;129(3):1209-11 [6179999] Biol Cell. 1984;52(2):195-8 [6241493] Science. 1985 May 17;228(4701):891-3 [2988124] J Immunol. 1986 Jan;136(2):511-5 [2416808] FEBS Lett. 1986 Feb 3;196(1):23-8 [3080338] Invest Ophthalmol Vis Sci. 1986 Aug;27(8):1296-300 [3488297] Nature. 1986 Nov 20-26;324(6094):258-60 [2431317] Curr Eye Res. 1986 Dec;5(12):995-1004 [3492336] Immunol Rev. 1986 Dec;94:5-21 [2948901] Arch Ophthalmol. 1987 Jun;105(6):838-40 [3495256] Proc Natl Acad Sci U S A. 1987 Jul;84(13):4577-80 [2955411] Curr Eye Res. 1987 Jul;6(7):909-19 [3621983] Curr Eye Res. 1987 Sep;6(9):1151-9 [2444394] Proc Natl Acad Sci U S A. 1987 Oct;84(20):6975-9 [3478675] Exp Eye Res. 1987 Nov;45(5):695-702 [3428394] Curr Eye Res. 1988 Jan;7(1):87-92 [3258805] FEBS Lett. 1988 Jul 4;234(1):39-43 [3164688] J Immunol. 1977 Dec;119(6):1949-58 [334977] J Immunol. 1978 Feb;120(2):563-9 [304460] Invest Ophthalmol Vis Sci. 1978 Aug;17(8):774-83 [355185] Am J Ophthalmol. 1980 Feb;89(2):173-9 [7355973] Cell Immunol. 1981 Mar 1;58(2):257-68 [6452218] Arch Ophthalmol. 1981 Jun;99(6):1090-2 [7236108] Invest Ophthalmol Vis Sci. 1981 Nov;21(5):669-80 [7298272] J Fr Ophtalmol. 1981;4(6-7):465-72 [7299063] Ophthalmic Res. 1982;14(4):249-55 [6813787] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Influence of viral infections on body weight, survival, and tumor prevalence of B6C3F1 (C57BL/6N x C3H/HeN) mice in carcinogenicity studies. AN - 79164121; 2767355 AB - Sendai virus (SV), mouse hepatitis virus (MHV), and pneumonia virus of mice (PVM) are common viral infections of mice. Influence of these viral infections on the prevalence of liver tumors, lung tumors, and lymphoma is of concern in chemical carcinogenicity studies. Body weight, survival, and tumor prevalence of B6C3F1 mice with and without viral infections in 33 male and 34 female untreated control groups and 32 male and 32 female low- and high-dose groups of 2-year chemical carcinogenicity studies were evaluated. In male mice, the SV infection was associated with significantly (p less than 0.05) higher survival of control, low-dose, and high-dose groups, and higher prevalence of liver tumors and lymphoma. The increases in tumor prevalence are possibly due to an increase in the survival of male mice that had SV infection. However, when interlaboratory variability and time-related effects were taken into account, the number of significant effects was consistent with the expected false-positive rate inherent to the statistical procedures. The MHV and PVM infections did not cause consistent changes in body weight, survival, and tumor prevalences in the control and chemical treatment groups of male mice. Viral infections did not cause consistent increases or decreases in body weight, survival, or tumor prevalence in the control and chemical treatment groups of female B6C3F1 mice. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Rao, G N AU - Piegorsch, W W AU - Crawford, D D AU - Edmondson, J AU - Haseman, J K AD - National Toxicology Program-Division of Toxicology Research and Testing, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 156 EP - 164 VL - 13 IS - 1 SN - 0272-0590, 0272-0590 KW - Index Medicus KW - Body Weight KW - Animals KW - Sex Factors KW - Carcinogenicity Tests KW - Mice KW - Diet KW - Male KW - Female KW - Neoplasms, Experimental -- complications KW - Neoplasms, Experimental -- chemically induced KW - Virus Diseases -- physiopathology KW - Virus Diseases -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79164121?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-10 N1 - Date created - 1989-10-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Training under Superfund. AN - 79156854; 2763316 JF - Toxicology and industrial health AU - Dement, J AD - NIEHS, Research Triangle Park, North Carolina. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 103 EP - 10; discussion 111-4 VL - 5 IS - 4 SN - 0748-2337, 0748-2337 KW - Hazardous Waste KW - 0 KW - Index Medicus KW - United States KW - United States Environmental Protection Agency KW - Hazardous Waste -- adverse effects KW - Humans KW - Environmental Exposure KW - Training Support KW - Occupational Medicine -- education UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79156854?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-14 N1 - Date created - 1989-09-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Experience of the National Cancer Institute. AN - 79156426; 2763325 JF - Toxicology and industrial health AU - Ringen, K AD - National Cancer Institute, Special Populations Studies Branch. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 97 EP - 101; discussion 111-4 VL - 5 IS - 4 SN - 0748-2337, 0748-2337 KW - Index Medicus KW - United States KW - Risk Factors KW - Humans KW - National Institutes of Health (U.S.) KW - Environmental Exposure KW - Research KW - Male KW - Female KW - Occupational Medicine -- trends KW - Neoplasms -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79156426?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-14 N1 - Date created - 1989-09-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - NIEHS training in environmental toxicology. AN - 79153793; 2763320 JF - Toxicology and industrial health AU - Rall, D P AD - NIEHS, Research Triangle Park, North Carolina. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 35 EP - 7; discussion 79-84 VL - 5 IS - 4 SN - 0748-2337, 0748-2337 KW - Saccharin KW - FST467XS7D KW - Index Medicus KW - United States KW - Rats KW - Animals KW - Humans KW - National Institutes of Health (U.S.) KW - Environmental Exposure KW - Saccharin -- adverse effects KW - Male KW - Urinary Bladder Neoplasms -- chemically induced KW - Education, Medical, Continuing KW - Occupational Medicine -- education UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79153793?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-14 N1 - Date created - 1989-09-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular and genetic organization of the suppressor of sable and minute (1) 1B region in Drosophila melanogaster. AN - 79136042; 2503417 AB - Recessive mutations at the suppressor of sable [su(s)] locus in Drosophila melanogaster result in suppression of second site mutations caused by insertions of the mobile element 412. In order to determine whether su(s) mutations might have other phenotypes, a saturation mapping of the su(s) region was carried out. The screen yielded 76 mutations that comprise ten genetic complementation groups ordered distal to proximal as follows: l(1)1Bh, l(1)1Bi, M(1)1B, su(s), l(1)1Bk, l(1)1Ca, mul, tw, l(1)lDa and brc. Twenty-three of the mutations are su(s) alleles, and all are suppressors of the 412-insertion-caused v1 allele. Although the screen could have detected su(s) mutations causing sex-specific dominant lethality or sterility as well as all types of recessive lethality or sterility, the only other phenotype observed was male sterility that is enhanced by cold temperature. This type of sterility is exhibited only by alleles induced by base-substitution-causing mutagens. Genetic functions of the poly(A+) messages transcribed from the su(s) microregion were identified by the reintroduction of cloned sequences into embryos by P element transformation. su(s) function has been attributed to a 5-kb message. The segment of DNA encoding only this 5-kb message rescues both the suppression and cold-sensitive male sterility phenotypes of su(s). Minute (1) 1B has been provisionally identified as encoding a 3.5-kb message; lethal (1)1Bi encodes a 1-kb message; and lethal (1)1Bk encodes a 4-kb message. The possible functions of su(s) and M(1)1B are discussed. JF - Genetics AU - Voelker, R A AU - Huang, S M AU - Wisely, G B AU - Sterling, J F AU - Bainbridge, S P AU - Hiraizumi, K AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 625 EP - 642 VL - 122 IS - 3 SN - 0016-6731, 0016-6731 KW - Index Medicus KW - Phenotype KW - Animals KW - Alleles KW - Transformation, Genetic KW - Genetic Complementation Test KW - Transcription, Genetic KW - Infertility, Male -- genetics KW - Mutation KW - Genes, Lethal KW - Chromosome Mapping KW - Male KW - Female KW - Drosophila melanogaster -- genetics KW - Suppression, Genetic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79136042?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-18 N1 - Date created - 1989-09-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Mol Cell Biol. 1986 May;6(5):1520-8 [3023894] Mol Cell Biol. 1986 Jan;6(1):47-53 [3023836] EMBO J. 1987 Dec 20;6(13):4095-104 [2832151] EMBO J. 1987 Dec 20;6(13):4105-11 [3443103] EMBO J. 1988 Apr;7(4):1081-6 [2841109] Genetics. 1962 Jul;47:807-17 [14454469] Genetics. 1969 Jul;62(3):781-95 [5384490] Genetics. 1977 Feb;85(2):259-72 [405273] Biochemistry. 1980 Apr 1;19(7):1425-33 [6770897] Genetics. 1981 Nov-Dec;99(3-4):461-80 [6806144] Mutat Res. 1982 Feb 22;92(1-2):107-15 [6806646] Cell. 1982 Oct;30(3):817-23 [6814765] Proc Natl Acad Sci U S A. 1983 Mar;80(6):1678-82 [6300868] Mutat Res. 1983 Feb;107(2):187-201 [6408464] Cell. 1983 Aug;34(1):59-73 [6309412] Genetics. 1983 Jul;104(3):433-48 [6411520] Cell. 1984 Aug;38(1):135-46 [6088058] Proc Natl Acad Sci U S A. 1984 Oct;81(19):6090-4 [6435123] Mol Cell Biol. 1984 Dec;4(12):2643-52 [6084810] Cell. 1985 Jun;41(2):429-37 [2985277] Mutat Res. 1985 Jun-Jul;150(1-2):261-75 [3923338] Science. 1985 Aug 9;229(4713):558-61 [2992080] Nature. 1985 Oct 10-16;317(6037):555-8 [4047173] Genetics. 1985 Nov;111(3):495-515 [2414153] Proc Natl Acad Sci U S A. 1986 Jan;83(2):404-8 [3001735] Mutat Res. 1986 Aug;162(1):47-54 [3014321] Genetics. 1986 Aug;113(4):869-95 [3091446] Genetics. 1986 Nov;114(3):819-40 [3098623] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A human rel proto-oncogene cDNA containing an Alu fragment as a potential coding exon. AN - 79131720; 2666912 AB - Two rel-containing cDNA clones were isolated from a library derived from the Daudi human cell line, which is known to express c-rel mRNA. Clone #1 appeared to contain the entire c-rel coding sequence, which differs from v-rel in having three additional N-terminal residues and 111 additional C-terminal residues. In addition, Clone #1 had an internal 32 amino acid exon not found in v-rel or in turkey c-rel. Clone #2 was truncated at its 5' end and did not contain this new exon. Analysis of a genomic clone of human c-rel revealed that the new exon was a portion of an inverted Alu repeat. The occurrence of potential splice sites and of open reading frames in the inverted consensus Alu sequence suggests that the incorporation of Alu fragments as potential coding exons could be a relatively common event in human mRNAs. Whether such messages can be translated is unknown: antiserum raised against a peptide at the predicted C-terminus of the c-rel protein precipitated p82hc-rel, but antiserum raised against a peptide located in the Alu exon did not. JF - Oncogene AU - Brownell, E AU - Mittereder, N AU - Rice, N R AD - Laboratory of Molecular Virology and Carcinogenesis, NCI-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 935 EP - 942 VL - 4 IS - 7 SN - 0950-9232, 0950-9232 KW - Proto-Oncogene Proteins KW - 0 KW - Proto-Oncogene Proteins c-rel KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Protein Biosynthesis KW - Base Sequence KW - Humans KW - Molecular Sequence Data KW - Proto-Oncogene Proteins -- analysis KW - Exons KW - DNA -- analysis KW - Repetitive Sequences, Nucleic Acid KW - Proto-Oncogenes KW - Proto-Oncogene Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79131720?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-07 N1 - Date created - 1989-09-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential effects of acute and repeated electrically and chemically induced seizures on [3H]Nimodipine and [125I]omega-conotoxin GVIA binding in rat brain. AN - 79126886; 2753000 AB - [3H]Nimodipine and high-affinity [125I]omega-conotoxin GVIA (CgTX) binding were investigated in membranes from rat cerebral cortex, cerebellum, and hippocampus after electrically and chemically induced seizures. Animals were decapitated 30 min after a single electroconvulsive shock (ECS) or lidocaine-induced seizure and 24 h after the last of 10 once-daily ECS or six once-daily lidocaine-induced seizures. After a single ECS, [3H]nimodipine and [125I]CgTX binding sites decreased in cerebral cortex (by 10% and 17%, respectively). A downregulation of [3H]nimodipine binding sites in hippocampus occurred after single and repeated lidocaine-induced seizures (by 24% and 11%, respectively), whereas [125I]CgTX binding remained unaltered. An earlier report on changes in [3H]nitrendipine binding after chronic ECS in cortex and hippocampus was not confirmed. JF - Epilepsia AU - Gleiter, C H AU - Cain, C J AU - Weiss, S R AU - Post, R M AU - Marangos, P J AD - Laboratory of Clinical Studies, D.I.C.B.R., National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland. PY - 1989 SP - 487 EP - 492 VL - 30 IS - 4 SN - 0013-9580, 0013-9580 KW - Calcium Channel Blockers KW - 0 KW - Iodine Radioisotopes KW - Mollusk Venoms KW - Tritium KW - 10028-17-8 KW - Nimodipine KW - 57WA9QZ5WH KW - omega-Conotoxin GVIA KW - 92078-76-7 KW - Lidocaine KW - 98PI200987 KW - Index Medicus KW - Animals KW - Cerebral Cortex -- metabolism KW - Hippocampus -- metabolism KW - Binding Sites KW - Cerebellum -- metabolism KW - Rats KW - Rats, Inbred Strains KW - Electroshock KW - Male KW - Seizures -- chemically induced KW - Calcium Channel Blockers -- metabolism KW - Nimodipine -- metabolism KW - Seizures -- etiology KW - Mollusk Venoms -- metabolism KW - Seizures -- metabolism KW - Brain -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79126886?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-01 N1 - Date created - 1989-09-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chromosome aberrations in peripheral lymphocytes and radiation dose to active bone marrow in patients treated for cancer of the cervix. AN - 79121270; 2787917 AB - An international study of cervical cancer patients reported a doubling of the risk for leukemia following radiotherapy. To evaluate the extent of residual chromosome damage in circulating T-cell lymphocytes in this population, approximately 200 metaphases were examined from each of 96 irradiated and 26 nonirradiated cervical cancer patients treated more than 17 years ago (average 23 years). Radiation dose averaged over the total red bone marrow was estimated to be 8.1 Gy. The type and frequency of stable and unstable chromosome aberrations were quantified in 24,117 metaphases. Unstable aberrations did not differ significantly between irradiated and nonirradiated patients (P greater than 0.5). Stable aberrations (i.e., translocations, inversions, or chromosomes with deleted segments), however, were significantly higher among irradiated (2.8 per 100 cells) compared to nonirradiated (0.7 per 100 cells) women (P less than 10(4). The frequency of these stable aberrations was found to increase significantly with increasing dose to the bone marrow. These data indicate that a direct relationship between radiation dose and extent of damage to somatic cells persists in populations and can be detected many years after partial-body radiation exposure. The stable aberration rate in irradiated cervical cancer patients was 50 to 75% lower than those observed 25 years or more after radiation exposure in atomic bomb survivors and in ankylosing spondylitis patients treated with radiotherapy. The average marrow dose was only 1 Gy in the examined atomic bomb survivors and 3.5 Gy in the ankylosing spondylitis patients. It appears, then, that a very high dose delivered to the pelvic cavity in fractionated doses resulted in far fewer persistent stable aberrations than lower doses delivered either in acute whole-body exposure or in fractionated doses to the spinal column and sacroiliac joints. The higher radiation dose and the concentration of that dose in a smaller area of the body appear to be responsible for the lower rate of persistent aberrations observed in cervical cancer patients. JF - Radiation research AU - Kleinerman, R A AU - Littlefield, L G AU - Tarone, R E AU - Machado, S G AU - Blettner, M AU - Peters, L J AU - Boice, J D AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 176 EP - 190 VL - 119 IS - 1 SN - 0033-7587, 0033-7587 KW - Index Medicus KW - Space life sciences KW - Chromosome Deletion KW - Humans KW - Chromosome Inversion KW - Translocation, Genetic KW - Female KW - Bone Marrow KW - Radiation Dosage KW - Chromosome Aberrations KW - T-Lymphocytes -- radiation effects KW - Uterine Cervical Neoplasms -- radiotherapy KW - Uterine Cervical Neoplasms -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79121270?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-28 N1 - Date created - 1989-08-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alcoholism treatment in general hospitals. AN - 79118004; 2502688 AB - This article examines recent developments in the role of general hospitals in providing treatment for alcoholism. It employs data on 5,000 U.S. short-term general hospitals and on all patients discharged from a subsample of 400 of these hospitals in the years 1980 through 1985. The article describes the growth in alcoholism treatment resources in short-term hospitals (1980-85) and examines linked hospital and patient data for the 400 hospitals in the subsample to describe patient diagnoses and resource use (1980 and 1985). Patients are classified by the stage of their alcohol problem, and hospital use is examined for patients in different stages. JF - Journal of studies on alcohol AU - Wallen, J AU - Noble, J A AD - Division of Clinical Research and Prevention, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 301 EP - 305 VL - 50 IS - 4 SN - 0096-882X, 0096-882X KW - Index Medicus KW - United States KW - Cross-Sectional Studies KW - Alcohol Withdrawal Delirium -- rehabilitation KW - Diagnosis-Related Groups KW - Humans KW - Substance-Related Disorders -- rehabilitation KW - Health Resources -- utilization KW - Bed Occupancy KW - Alcoholism -- rehabilitation KW - Hospitals, General -- utilization KW - Alcoholism -- epidemiology KW - Alcoholism -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79118004?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-31 N1 - Date created - 1989-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The biochemical toxicity of perfluorodecanoic acid in the mouse is different from that of 2,3,7,8-tetrachlorodibenzo-p-dioxin. AN - 79106164; 2749739 AB - Perfluorodecanoic acid (PFDA) is an industrial surfactant that has been reported to produce signs of toxicity in rats similar to those due to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). In order to characterize the biochemical toxicity of PFDA in the mouse and to determine whether PFDA toxicity is mediated by the Ah locus, congenic female C57BL/6J mice differing only at the Ah locus (normal homozygous responsive Ahb/b, heterozygous responsive Ahb/d, and homozygous nonresponsive Ahd/d) were administered a single oral dose of PFDA. The wild type (Ahb/b) mice were killed 2, 7, 14, or 30 days after administration of 0, 40, 80, 100, 120, or 160 mg PFDA/kg. Mice from the other two congenic strains were killed 30 days after dosing with 0, 40, 80, or 160 mg/kg. PFDA produced a 2.5-fold increase in absolute liver weight, a 5- to 15-fold increase in hepatic fatty acyl Co-A oxidase activity, and a 70% decrease in hepatic ethoxyresorufin O-deethylase (EROD) activity. These effects were dose and time dependent. Total hepatic lipids were increased at an early time point and at the lowest dose. At later time periods and/or higher doses, the lipid concentration was decreased approximately 20% from that of controls. Hepatic protein concentrations were depressed approximately 25% from control levels 30 days after treatment. There was little difference in any of these parameters between responsive (Ahb/b, Ahb/d) and nonresponsive (Ahd/d) mice. These results suggest that the Ah allele has little effect in regulating the toxicity of PFDA in the mouse and that the biochemical response to PFDA in the mouse is markedly different from that of TCDD. Furthermore, the biochemical response to PFDA in the mouse is different from that reported in the rat. JF - Toxicology and applied pharmacology AU - Brewster, D W AU - Birnbaum, L S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 544 EP - 554 VL - 99 IS - 3 SN - 0041-008X, 0041-008X KW - Decanoic Acids KW - 0 KW - Dioxins KW - Fluorocarbons KW - Lipids KW - Polychlorinated Dibenzodioxins KW - Proteins KW - perfluorodecanoic acid KW - 335-76-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Oxidoreductases KW - EC 1.- KW - Cytochrome P-450 CYP1A1 KW - EC 1.14.14.1 KW - Acyl-CoA Oxidase KW - EC 1.3.3.6 KW - Index Medicus KW - Cytochrome P-450 Enzyme System -- analysis KW - Animals KW - Body Weight -- drug effects KW - Mice, Inbred C57BL KW - Oxidoreductases -- analysis KW - Proteins -- analysis KW - Mice KW - Species Specificity KW - Female KW - Organ Size -- drug effects KW - Lipids -- analysis KW - Polychlorinated Dibenzodioxins -- toxicity KW - Fluorocarbons -- toxicity KW - Dioxins -- toxicity KW - Decanoic Acids -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79106164?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-18 N1 - Date created - 1989-08-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Calcium-dependent effects of maitotoxin on phosphoinositide breakdown and on cyclic AMP accumulation in PC12 and NCB-20 cells. AN - 79104223; 2546052 AB - The marine dinoflagellate toxin maitotoxin (MTX) stimulates phosphoinositide breakdown in pheochromocytoma PC12 cells and in neuroblastoma hybrid NCB-20 cells. In both cell lines, the stimulation of phosphoinositide breakdown by MTX is dependent on extracellular calcium, but it is not reduced by organic or inorganic calcium channel blockers. In PC12 cells, the maximal stimulation of phosphoinositide breakdown occurs at 1.5 mM [Ca2+]o, whereas in NCB-20 cells the maximal stimulation is observed at 2.5-4.5 mM [Ca2+]o. Phosphoinositide breakdown is known to lead to formation of both inositol phosphates and diacylglycerols. The latter, through stimulation of protein kinase C, would, like phorbol esters, be expected to augment cyclic AMP accumulation in PC12 cells and to inhibit receptor-mediated cyclic AMP accumulation in NCB-20 cells. MTX does potentiate forskolin-induced accumulation of cyclic AMP in PC12 cells and does inhibit prostaglandin E2-induced accumulation of cyclic AMP in NCB-20 cells. The effects of MTX on accumulation of cyclic AMP are calcium dependent and the concentrations of calcium required for maximal responses are the same as the ones required for maximal stimulation of phosphoinositide breakdown. MTX increases intracellular calcium in both cell lines, as measured by calcium-quin2 fluorescence. But the effects of MTX on forskolin- and prostaglandin E2-mediated cyclic AMP accumulation are not mimicked by a calcium ionophore and are not blocked by nifedipine, a calcium channel blocker. Translocation of protein kinase C occurs after treatment with MTX in both cell lines; the protein kinase C activity and content are reduced in the cytosol and increased in membranes after exposure to either MTX or a phorbol ester. The results confirm previous studies on the heterogeneous input of protein kinase C to cyclic AMP-generating systems performed with phorbol esters and demonstrate the utility of MTX as a unique tool for studies of systems that involve second messengers generated through stimulation of phosphoinositide breakdown. JF - Molecular pharmacology AU - Gusovsky, F AU - Yasumoto, T AU - Daly, J W AD - Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 44 EP - 53 VL - 36 IS - 1 SN - 0026-895X, 0026-895X KW - Marine Toxins KW - 0 KW - Oxocins KW - Phosphatidylinositols KW - maitotoxin KW - 9P59GES78D KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinase C KW - EC 2.7.11.13 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats KW - Protein Kinase C -- metabolism KW - Animals KW - Tumor Cells, Cultured -- metabolism KW - Adrenal Gland Neoplasms -- metabolism KW - Biological Transport KW - Pheochromocytoma -- metabolism KW - Cricetinae KW - Marine Toxins -- pharmacology KW - Phosphatidylinositols -- metabolism KW - Cyclic AMP -- metabolism KW - Calcium -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79104223?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-22 N1 - Date created - 1989-08-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human NADPH-P450 oxidoreductase: complementary DNA cloning, sequence and vaccinia virus-mediated expression and localization of the CYPOR gene to chromosome 7. AN - 79102409; 2501655 AB - The cDNA containing the full coding sequence of human NADPH-P450 oxidoreductase was isolated and completely sequenced. The cDNA contained 2398 base pairs, including 9 and 358 base pairs of 5' and 3' noncoding sequences, respectively. The human NADPH-P450 oxidoreductase protein deduced from the cDNA has 677 amino acids, with a calculated molecular weight of 76,656. The cDNA nucleotide and deduced amino acid sequences displayed 83 and 92% similarities, respectively, with those of the rat NADPH-P450 oxidoreductase. By use of somatic cell hybrids, the NADPH-P450 oxidoreductase gene was regionally localized to human chromosome 7 (7p15-q35). The levels of NADPH-P450 oxidoreductase protein and mRNA were analyzed in 13 human liver specimens and less than 3-fold variation was found among the different livers. The NADPH-P450 oxidoreductase cDNA was inserted into vaccinia virus and expressed in cell culture. The cDNA-expressed enzyme was active in reducing the electron acceptor cytochrome c. In addition, the NADPH-P450 oxidoreductase stimulated the enzymatic activity of vaccinia virus-expressed human P3(450) when both recombinant viruses were used to coinfect human cells in culture. An approximate equal mole level of NADPH-P450 oxidoreductase and P3(450) was required to achieve maximal activity for both ethoxycoumarin O-deethylase and aryl hydrocarbon hydroxylase. JF - Molecular pharmacology AU - Yamano, S AU - Aoyama, T AU - McBride, O W AU - Hardwick, J P AU - Gelboin, H V AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 83 EP - 88 VL - 36 IS - 1 SN - 0026-895X, 0026-895X KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - NADPH-Ferrihemoprotein Reductase KW - EC 1.6.2.4 KW - Index Medicus KW - Rats KW - Animals KW - Base Sequence KW - Humans KW - Molecular Sequence Data KW - Chromosome Mapping KW - Cloning, Molecular KW - Cytochrome P-450 Enzyme System -- analysis KW - NADPH-Ferrihemoprotein Reductase -- genetics KW - Vaccinia virus -- enzymology KW - Cytochrome P-450 Enzyme System -- genetics KW - DNA -- analysis KW - Chromosomes, Human, Pair 7 KW - NADPH-Ferrihemoprotein Reductase -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79102409?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-22 N1 - Date created - 1989-08-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fine specificity of xenogeneic antigen recognition by human T cells. AN - 79101857; 2473552 AB - T cell mediated responses play a role in xenograft as well as allograft rejection. In vitro T cell responses to xenogeneic antigens are characterized by T cell recognition of polymorphic determinants of gene products encoded by the major histocompatibility complex of the stimulating cells, but little is known of the fine specificity of this recognition of xenogeneic antigens and its comparability to allogeneic antigen recognition. In order to study the fine specificity of human CTL in the recognition of xenogeneic antigens, long-term lines or clones were established from a secondary mixed lymphocyte response in which the stimulator cells were H-2b murine splenocytes. By comparing the ability of a series of target cells derived from congenic recombinant mouse strains to be lysed by these CTL, it was demonstrated that all isolated lines specifically lysed target cells expressing H-2b or T1a/Qa-1b products. Of the effector populations specific for H-2b cell surface molecules, all recognized class I products with Kb specificity predominating when evaluated for their ability to lyse in vivo-derived class I mutants or cells transfected with class I genes. These human xenoreactive CTL were able to distinguish wild type Kb molecules from those altered by amino acid changes confined to a single molecular domain of Kb. These findings demonstrate that xenogeneic antigen recognition by human T cells is characterized by a fine specificity of antigen recognition comparable to the specificity of recognition of major histocompatibility complex-encoded molecules by murine CTL across allogeneic differences. JF - Transplantation AU - Gress, R E AU - Nathenson, S G AU - Lucas, P J AD - Experimental Immunology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 93 EP - 98 VL - 48 IS - 1 SN - 0041-1337, 0041-1337 KW - Epitopes KW - 0 KW - H-2 Antigens KW - Histocompatibility Antigens Class I KW - Q surface antigens KW - Index Medicus KW - Animals KW - Humans KW - Lymphocyte Culture Test, Mixed KW - Histocompatibility Antigens Class I -- immunology KW - Mice, Inbred C57BL KW - Mice, Inbred C3H KW - Cytotoxicity Tests, Immunologic KW - Mice KW - Histocompatibility Antigens Class I -- genetics KW - Cell Line KW - Genes, MHC Class I KW - H-2 Antigens -- genetics KW - T-Lymphocytes, Cytotoxic -- transplantation KW - Epitopes -- genetics KW - Transplantation, Heterologous KW - H-2 Antigens -- immunology KW - T-Lymphocytes, Cytotoxic -- immunology KW - Epitopes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79101857?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-18 N1 - Date created - 1989-08-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Action of phorbol esters, bryostatins, and retinoic acid on cholesterol sulfate synthesis: relation to the multistep process of differentiation in human epidermal keratinocytes. AN - 79098650; 2473132 AB - This study examines the action of phorbol 12-myristate 13-acetate (PMA) on the synthesis of cholesterol sulfate in cultured normal and transformed human epidermal keratinocytes and assesses the antagonistic effects by retinoids and bryostatins on PMA action in relation to the multistep program of squamous differentiation. Treatment of normal human epidermal keratinocytes (NHEK) with PMA induces terminal cell division (irreversible growth-arrest) and causes a time- and dose-dependent increase in the incorporation of Na2(35)SO4 into cholesterol sulfate, a marker for squamous cell differentiation. This stimulation in sulfate incorporation appears specific for cholesterol sulfate and is due to increased levels of cholesterol sulfotransferase activity. The increase in cholesterol sulfate accumulation parallels the increase in transglutaminase type I, another marker for squamous differentiation. Several transformed NHEK cell lines do not exhibit increased levels of cholesterol sulfate and transglutaminase type I activity after PMA treatment, indicating that they acquired defects in the regulation of squamous differentiation. Bryostatins 1 and 2, and several diacylglycerol analogues neither inhibit cell proliferation nor increase cholesterol sulfate synthesis or transglutaminase activity, indicating that these agents do not induce terminal differentiation. In contrast, the bryostatins block the increase in cholesterol sulfate and transglutaminase activity as well as the commitment to terminal cell division by PMA. Bryostatin 1 inhibits the commitment to terminal cell division and the accumulation of cholesterol sulfate significantly even when added 8 h after PMA administration. Retinoids inhibit cholesterol sulfate accumulation and the increase in transglutaminase activity by PMA but do not affect the commitment to terminal cell division. In summary, phorbol esters induce in NHEK cells a program of squamous differentiation. This process of differentiation consists of the commitment to terminal cell division and expression of a squamous phenotype. Expression of this phenotype is accompanied by an accumulation of cholesterol sulfate and increased cholesterol sulfotransferase activity. Bryostatins 1 and 2 and retinoic acid affect this differentiation process at different stages. JF - The Journal of investigative dermatology AU - Jetten, A M AU - George, M A AU - Pettit, G R AU - Herald, C L AU - Rearick, J I AD - Cell Biology Group, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 108 EP - 115 VL - 93 IS - 1 SN - 0022-202X, 0022-202X KW - Bryostatins KW - 0 KW - Cholesterol Esters KW - Diglycerides KW - Lactones KW - Macrolides KW - bryostatin 1 KW - 37O2X55Y9E KW - Tretinoin KW - 5688UTC01R KW - Keratins KW - 68238-35-7 KW - bryostatin 2 KW - 87745-28-6 KW - cholesteryl sulfate KW - KU576NT9O9 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Diglycerides -- pharmacology KW - Humans KW - Cell Differentiation KW - Cell Line, Transformed KW - Tretinoin -- pharmacology KW - Cholesterol Esters -- biosynthesis KW - Epidermis -- cytology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Lactones -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79098650?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-25 N1 - Date created - 1989-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Gestational trophoblastic disease: a case-control study from the People's Republic of China. AN - 79092903; 2546427 AB - A case-control study involving 331 patients with complete hydatidiform mole and 662 community controls matched to the cases on age and timing of pregnancy was conducted in Beijing, China. A history of a term birth was associated with reduced risk (odds ratio = 0.6, 95% confidence interval 0.4 to 0.9), with some evidence of further decrease with multiple births. Previous spontaneous abortions were not related to risk, although those with a prior induced abortion were at elevated risk, particularly if two or more abortions were involved (odds ratio = 2.8, 95% confidence interval 1.4 to 5.7). A history of having sought medical advice for infertility was associated with reduced risk (odds ratio = 0.5, 95% confidence interval 0.2 to 0.8), but those who reported use of herbal medicines during a first trimester of a previous pregnancy were at excess risk (odds ratio = 2.2, 95% confidence interval 1.3 to 3.6). In addition, a statistically significant trend in risk was observed with years of oral contraceptive use (odds ratio = 2.6, 95% confidence interval 0.9 to 6.9 for greater than or equal to 4 years of use). Dietary habits and family histories of cancer or trophoblastic disease were not related to risk in this study. JF - American journal of obstetrics and gynecology AU - Brinton, L A AU - Wu, B Z AU - Wang, W AU - Ershow, A G AU - Song, H Z AU - Li, J Y AU - Bracken, M B AU - Blot, W J AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 121 EP - 127 VL - 161 IS - 1 SN - 0002-9378, 0002-9378 KW - Contraceptives, Oral KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Contraceptives, Oral -- adverse effects KW - Infertility KW - Age Factors KW - Intrauterine Devices KW - Humans KW - Adult KW - Reproduction KW - Diet KW - Female KW - China KW - Pregnancy KW - Pregnancy Complications, Neoplastic KW - Uterine Neoplasms -- chemically induced KW - Uterine Neoplasms -- etiology KW - Trophoblastic Neoplasms -- etiology KW - Trophoblastic Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79092903?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-17 N1 - Date created - 1989-08-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Incineration and monitoring of low-level 35S wastes at a biological research institution. AN - 79092323; 2745082 JF - Health physics AU - Hamrick, P E AU - Wall, B E AU - Simon, S L AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 191 EP - 194 VL - 57 IS - 1 SN - 0017-9078, 0017-9078 KW - Air Pollutants, Radioactive KW - 0 KW - Radioactive Waste KW - Sulfates KW - Sulfur Radioisotopes KW - sodium sulfate KW - 0YPR65R21J KW - Methionine KW - AE28F7PNPL KW - Index Medicus KW - Hot Temperature KW - Equipment Contamination KW - Filtration -- instrumentation KW - Air Pollutants, Radioactive -- analysis KW - Refuse Disposal -- methods KW - Radioactive Waste -- analysis KW - Refuse Disposal -- instrumentation KW - Radiation Monitoring KW - Sulfur Radioisotopes -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79092323?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-17 N1 - Date created - 1989-08-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Infectious papillomavirus in the vapor of warts treated with carbon dioxide laser or electrocoagulation: detection and protection. AN - 79090607; 2545749 AB - Papillomavirus DNA has been reported recently in the vapor (smoke plume) derived from warts treated with carbon dioxide laser; this raises concerns for operator safety. We therefore have studied a group of human and bovine warts to define further the potential risk of wart therapy and to test whether a surgical mask could reduce exposure. Half of each wart was treated with carbon dioxide laser and the other half with electrocoagulation. The vapor produced by each form of therapy was collected with a dry filter vacuum apparatus and analyzed for the presence of papillomavirus. Vapor from human plantar warts was analyzed for the presence of human papillomavirus DNA, because there is no infectivity assay for human papillomavirus. Of plantar warts treated, five of eight laser-derived vapors and four of seven electrocoagulation-derived vapors were positive for human papillomavirus DNA. Greater amounts of papillomavirus DNA were usually recovered in the laser vapor than in the electrocoagulation vapor from the same wart. Bioassay readily detected infectious bovine papillomavirus in the vapor from bovine warts treated with either modality; more virus was present in laser-derived material. A surgical mask was found capable of removing virtually all laser- or electrocoagulation-derived virus, strongly suggesting that such masks can protect operators from potential inhalation exposure to papillomavirus. JF - Journal of the American Academy of Dermatology AU - Sawchuk, W S AU - Weber, P J AU - Lowy, D R AU - Dzubow, L M AD - Laboratory of Cellular Oncology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 41 EP - 49 VL - 21 IS - 1 SN - 0190-9622, 0190-9622 KW - Air Pollutants, Occupational KW - 0 KW - DNA, Viral KW - Carbon Dioxide KW - 142M471B3J KW - Index Medicus KW - Animals KW - Cattle KW - Humans KW - Air Pollutants, Occupational -- isolation & purification KW - Environmental Exposure KW - Cattle Diseases -- surgery KW - Volatilization KW - DNA, Viral -- isolation & purification KW - Nucleic Acid Hybridization KW - Bovine papillomavirus 1 -- isolation & purification KW - Cell Transformation, Viral KW - Masks KW - Papillomaviridae -- isolation & purification KW - Laser Therapy KW - Air Microbiology KW - Warts -- surgery KW - Electrocoagulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79090607?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-22 N1 - Date created - 1989-08-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Elevation of pi class glutathione S-transferase activity in human breast cancer cells by transfection of the GST pi gene and its effect on sensitivity to toxins. AN - 79088298; 2747627 AB - Increased expression of the glutathione S-transferase (GST; E.C.2.5.1.18) pi class isozyme is associated with both malignant transformation and drug resistance, as well as with decreased estrogen receptor content in breast cancer. In order to further characterize the role of this enzyme in drug resistance, we cloned the cDNA encoding the human isozyme GST pi and developed two eukaryotic expression vectors using this cDNA and either the human metallothionein IIa or cytomegalovirus immediate-early promoters. These GST pi expression vectors were cotransfected with pSV2neo into drug-sensitive MCF-7 human breast cancer cells, which have low amounts of GST activity and which do not express GST pi. The transfected cells were selected for G418 resistance and individual clones were screened for GST activity. Three clones that demonstrated increased GST activity were selected for further study. Immunoprecipitation studies demonstrated that the increase in GST activity in these clones was due to expression of GST pi. Although the total GST activity of the positive clones was increased as much as 15-fold over that in wild-type MCF-7 cells, there was no change in glutathione peroxidase activity, as measured using cumene hydroperoxide as a substrate. Immunoblot studies revealed that the increased GST enzyme produced in the transfected cells was identical in size to endogenous GST pi. Southern blot analysis demonstrated the incorporation of the GST pi expression vector into the genome of the positive clones and Northern blot analysis showed that the transfected genes made a hybrid GST pi RNA that was slightly larger than the endogenous GST pi RNA. Primer extension studies demonstrated that this increase in length corresponded to the added length of the 5' leader sequence of the expression vector. The effect of increased GST pi activity on the sensitivity of the transfected clones to several cytotoxic agents was assessed by colony-forming assay. The transfected clones were slightly more resistant (1.3-4.1-fold) to benzo(a)pyrene and its toxic metabolite benzo(a)pyrene-(anti)-7,8-dihydrodiol-9,10-epoxide, as well as to ethacrynic acid (3.1-to 4.4-fold). Although increased GST pi expression is found in MCF-7 cells selected for doxorubicin resistance, the transfected clones were not consistently more resistant to doxorubicin than control cells. In addition, the transfected cells were not resistant to either melphalan or (cis)-platinum, even though conjugation with glutathione is known to play a role in the detoxification of both of these drugs.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Molecular pharmacology AU - Moscow, J A AU - Townsend, A J AU - Cowan, K H AD - Medicine Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 22 EP - 28 VL - 36 IS - 1 SN - 0026-895X, 0026-895X KW - Isoenzymes KW - 0 KW - Doxorubicin KW - 80168379AG KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Ethacrynic Acid KW - M5DP350VZV KW - Index Medicus KW - Doxorubicin -- pharmacology KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Ethacrynic Acid -- toxicity KW - Drug Resistance KW - Female KW - Isoenzymes -- analysis KW - Glutathione Transferase -- physiology KW - Transfection KW - Glutathione Transferase -- genetics KW - Glutathione Transferase -- analysis KW - Breast Neoplasms -- enzymology KW - Isoenzymes -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79088298?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-22 N1 - Date created - 1989-08-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Oncogenes and their applications in epidemiologic studies. AN - 79071593; 2662757 JF - American journal of epidemiology AU - Taylor, J A AD - National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 6 EP - 13 VL - 130 IS - 1 SN - 0002-9262, 0002-9262 KW - Carcinogens KW - 0 KW - Index Medicus KW - Neoplasms -- diagnosis KW - Humans KW - Prognosis KW - Data Collection KW - Neoplasms -- therapy KW - Neoplasms -- genetics KW - Neoplasms -- etiology KW - Oncogenes KW - Epidemiologic Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79071593?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-04 N1 - Date created - 1989-08-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Am J Epidemiol. 1990 Jun;131(6):1099-100 [2140491] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The National Cancer Institute's Smoking, Tobacco, and Cancer Program. AN - 79063695; 2737004 JF - Chest AU - Cullen, J W AD - Division of Cancer Prevention and Control, National Cancer Institute, Bethesda, Md 20892-3100. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 9S EP - 13S VL - 96 IS - 1 Suppl SN - 0012-3692, 0012-3692 KW - Abridged Index Medicus KW - Index Medicus KW - United States KW - Life Style KW - Behavior Therapy KW - Humans KW - Male KW - Female KW - National Institutes of Health (U.S.) KW - Tobacco Use Disorder -- prevention & control KW - Neoplasms -- prevention & control KW - Smoking -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79063695?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-03 N1 - Date created - 1989-08-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phenytoin withdrawal and seizure frequency. AN - 79062969; 2739918 AB - We withdrew phenytoin from 17 inpatients maintained on combination therapy with carbamazepine for complex partial seizures and analyzed seizure occurrence in relation to plasma levels and time from initiation of withdrawal. The ratio of maximum to mean weekly seizure frequency did not vary with initial level or rate of withdrawal. The week with most frequent seizures began a median of 10 days after phenytoin levels became undetectable, and mean daily seizure frequency was higher at undetectable than at falling levels for the entire 2- to 10-week study period. Four patients had a total of 6 clusters of generalized tonic-clonic seizures; only 2 occurred while levels were falling and the other 4 at 3, 9, 28, and 42 days after reaching undetectable levels. Our data argue against the occurrence of withdrawal seizures in these patients and suggest that worsening of seizures following phenytoin discontinuation more likely reflects loss of therapeutic drug effect than a true abstinence phenomenon. JF - Neurology AU - Bromfield, E B AU - Dambrosia, J AU - Devinsky, O AU - Nice, F J AU - Theodore, W H AD - Clinical Epilepsy Section, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 905 EP - 909 VL - 39 IS - 7 SN - 0028-3878, 0028-3878 KW - Carbamazepine KW - 33CM23913M KW - Phenytoin KW - 6158TKW0C5 KW - Diazepam KW - Q3JTX2Q7TU KW - Abridged Index Medicus KW - Index Medicus KW - Drug Therapy, Combination KW - Diazepam -- therapeutic use KW - Humans KW - Adult KW - Middle Aged KW - Carbamazepine -- therapeutic use KW - Male KW - Female KW - Epilepsy, Temporal Lobe -- physiopathology KW - Epilepsy -- physiopathology KW - Epilepsy -- chemically induced KW - Substance Withdrawal Syndrome KW - Epilepsy, Temporal Lobe -- chemically induced KW - Phenytoin -- therapeutic use KW - Phenytoin -- blood KW - Phenytoin -- adverse effects KW - Epilepsy -- drug therapy KW - Epilepsy, Temporal Lobe -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79062969?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-03 N1 - Date created - 1989-08-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Zidovudine in patients with human immunodeficiency virus (HIV) infection and Kaposi sarcoma. A phase II randomized, placebo-controlled trial. AN - 79060863; 2735626 AB - To evaluate the toxicity, effects on immune function, antitumor effects, antiretroviral effects, and pharmacokinetics of zidovudine therapy in patients with early human immunodeficiency virus (HIV) infection and Kaposi sarcoma. Randomized, double-blind, placebo-controlled trial. National Institutes of Health, a referral-based research institution (single site). Physician-referred volunteer patients with HIV infection, Kaposi sarcoma, CD4+ lymphocyte counts greater than 0.2 x 10(9)/L, and no systemic symptoms or history of opportunistic infection. Of 41 patients enrolled, 4 had not met all entry criteria and were therefore not evaluable. Patients were randomized to one of four treatment groups for an initial 12-week treatment period: oral placebo (9 patients); zidovudine, 250 mg orally every 4 hours (9 patients); zidovudine, 0.5 mg/kg body weight intravenously every 4 hours (9 patients); and zidovudine, 2.5 mg/kg intravenously every 4 hours (10 patients). After at least 12 weeks of therapy at their assigned dose, patients were treated with oral zidovudine, generally 250 mg every 4 hours, with a mean 42-week follow-up. Anemia and granulocytopenia were the major toxicities. Significant increases in platelet counts and declines in serum HIV antigen and IgG and IgM levels occurred in treated patients. Treated patients were more likely than those on placebo to clear HIV from the cerebrospinal fluid. There were no differences in tumor progression or CD4+ or CD8+ lymphocyte counts among the groups. Zidovudine was well tolerated and had antiretroviral activity in patients with early HIV infection and Kaposi sarcoma but it had no significant effect on the extent of Kaposi sarcoma or on immune function. JF - Annals of internal medicine AU - Lane, H C AU - Falloon, J AU - Walker, R E AU - Deyton, L AU - Kovacs, J A AU - Masur, H AU - Banks, S AU - Kirk, L E AU - Baseler, M W AU - Salzman, N P AD - National Institutes of Health, Bethesda, Maryland. Y1 - 1989/07/01/ PY - 1989 DA - 1989 Jul 01 SP - 41 EP - 50 VL - 111 IS - 1 SN - 0003-4819, 0003-4819 KW - Zidovudine KW - 4B9XT59T7S KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Leukocyte Count -- drug effects KW - HIV -- drug effects KW - Drug Evaluation KW - Prospective Studies KW - Double-Blind Method KW - Random Allocation KW - Humans KW - Anemia -- chemically induced KW - Adult KW - Granulocytes -- drug effects KW - Middle Aged KW - Male KW - Zidovudine -- therapeutic use KW - Sarcoma, Kaposi -- drug therapy KW - Acquired Immunodeficiency Syndrome -- complications KW - Zidovudine -- pharmacokinetics KW - Zidovudine -- adverse effects KW - Acquired Immunodeficiency Syndrome -- immunology KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Sarcoma, Kaposi -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79060863?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-18 N1 - Date created - 1989-07-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Ann Intern Med 1990 Mar 1;112(5):388 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Quality control procedure for 6-[18F]fluoro-L-DOPA: a presynaptic PET imaging ligand for brain dopamine neurons. AN - 79060242; 2500503 AB - The goal of the current study was to establish a quality control procedure for clinical use of 6-[18F]fluoro-L-DOPA (6-[18F]-DOPA) as a selective presynaptic positron emission tomographic (PET) imaging ligand for brain dopamine neurons. A high performance liquid chromatographic procedure using a 5-mu C-18 reverse phase column and ion-pairing mobile phase was used for the quantification of 6-[18F]-DOPA. The radiochemical purity of 6-[18F]-DOPA was measured by 18F radioactivity in HPLC fractions while the chemical purity was determined by an amperometric electrochemical detector with a sensitivity of 25 pg. Quality control of eight consecutive batches of highly purified 6-[18F]-DOPA sample used in a pre-clinical trial revealed that the chemical and/or radiochemical purity of the PET imaging ligand, 6-[18F]-DOPA was greater than 97 +/- 0.5% with a specific activity of 365 +/- 31 mCi/mmol. The knowledge and assurance of radiochemical purity of PET ligands are essential for the interpretation of clinical PET imaging results. The assurance of such quality control would enable comparisons of 6-[18F]-DOPA/PET data obtained from various medical centers using different radiopharmaceutical procedures. JF - Journal of nuclear medicine : official publication, Society of Nuclear Medicine AU - Chen, J J AU - Huang, S J AU - Finn, R D AU - Kirk, K L AU - Francis, B E AU - Adams, H R AU - Cohen, R M AU - Chiueh, C C AD - Clinical Brain Imaging Section, National Institute of Mental Health, Bethesda, Maryland 20892-1000. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 1249 EP - 1256 VL - 30 IS - 7 SN - 0161-5505, 0161-5505 KW - Pyrogens KW - 0 KW - fluorodopa F 18 KW - 2C598205QX KW - Dihydroxyphenylalanine KW - 63-84-3 KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Drug Stability KW - Humans KW - Electrochemistry KW - Quality Control KW - Chromatography, High Pressure Liquid KW - Dihydroxyphenylalanine -- standards KW - Dihydroxyphenylalanine -- analysis KW - Tomography, Emission-Computed KW - Dopamine -- metabolism KW - Brain -- metabolism KW - Brain -- diagnostic imaging KW - Dihydroxyphenylalanine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79060242?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-10 N1 - Date created - 1989-08-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Nucl Med. 1990 Dec;31(12):2076-7 [2125067] J Nucl Med. 1991 May;32(5):894-5 [1902510] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Testosterone selectively influences protein kinase-C-coupled secretion of proluteinizing hormone-releasing hormone-derived peptides. AN - 79057134; 2661212 AB - LHRH and GnRH-associated peptide (GAP) are two major pro-LHRH-derived peptides which are secreted from median eminence (ME) nerve terminals in vitro. The purpose of the present experiment was to determine whether manipulation of gonadal steroid levels in vivo influenced selectively the in vitro secretion of LHRH and GAP under basal or K+ and phorbol ester (PDBu) stimulation. Secretion of both peptides under each of these three conditions was reduced at least 2-fold in 2-week orchidectomized (ORDX) rats relative to the level in intact controls. Tissue stores of LHRH and GAP were also depressed in the ME of ORDX relative to control rats. When the data were expressed in terms of the percentage of peptide secreted per ME, both groups secreted similar percentages of the peptides into the medium under basal and K+-stimulated conditions. Interestingly, PDBu-activated secretion of LHRH and GAP remained depressed in ORDX animals. The nerve terminals from ORDX animals were not susceptible to a more rapid depletion of releasable peptides, since both groups secreted similar percentages of the peptides during repeated K+ depolarization. By comparison, protein kinase C (PKC)-coupled secretion from ORDX rats was selectively affected, since secretion of pro-LHRH-derived peptides became even more depressed with successive activation with PDBu. Immediate replacement with testosterone after ORDX fully restored the peptide levels in tissue and the LHRH and GAP secretory response to PKC activation. Since testosterone influenced both tissue stores and PDBu-stimulated secretion of LHRH and GAP, this steroid may selectively regulate biosynthesis and secretion of pro-LHRH-derived peptides through activation of the metabolic cascade involving the PKC system. JF - Endocrinology AU - Wetsel, W C AU - Negro-Vilar, A AD - Reproductive Neuroendocrinology Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 538 EP - 547 VL - 125 IS - 1 SN - 0013-7227, 0013-7227 KW - Protein Precursors KW - 0 KW - gonadotropin releasing hormone associated peptide KW - 124375-77-5 KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Testosterone KW - 3XMK78S47O KW - Protein Kinase C KW - EC 2.7.11.13 KW - Potassium KW - RWP5GA015D KW - Abridged Index Medicus KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Median Eminence -- secretion KW - Potassium -- pharmacology KW - Male KW - Phorbol 12,13-Dibutyrate -- pharmacology KW - Orchiectomy KW - Protein Kinase C -- metabolism KW - Testosterone -- pharmacology KW - Protein Precursors -- secretion KW - Gonadotropin-Releasing Hormone -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79057134?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-02 N1 - Date created - 1989-08-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential DNA sequence deletions from chromosomes 3, 11, 13, and 17 in squamous-cell carcinoma, large-cell carcinoma, and adenocarcinoma of the human lung. AN - 79051537; 2567993 AB - Activation of protooncogenes and inactivation of putative tumor suppressor genes are genetic lesions considered to be important in lung carcinogenesis. Fifty-four cases of non-small-cell lung cancer (23 adenocarcinomas, 23 squamous-cell carcinomas, and 8 large-cell carcinomas) were examined for loss of DNA sequences at 13 polymorphic genetic loci. Loss of heterozygosity was seen more frequently in squamous-cell carcinoma than in adenocarcinoma. The loss of DNA sequences from the short arm of chromosome 17 (D17S1 locus) was detected in 8 of 9 heterozygous cases of squamous-cell carcinoma and in only 2 of 11 heterozygous cases of adenocarcinomas. Furthermore, in 7 of these 8 squamous-cell carcinomas, loss of heterozygosity from chromosome 17 was accompanied by loss of DNA sequences from chromosome 11. The spectrum of allelic sequences lost from chromosome 11 was, however, similar in every type of carcinoma studied, and the data show two regions commonly deleted from chromosome 11 (11pter-p15.5 and 11p13-q13) that may have a role in the pathogenesis of all these types of non-small-cell bronchogenic carcinoma. Loss of DNA sequences from chromosome 3 was seen in 16 of 31 cases where the constitutive DNA was heterozygous-i.e., informative. These data included only 6 of 16 cases where loss of heterozygosity involved a chromosomal locus previously shown to be lost consistently in small-cell lung cancer (DNF15S2). Loss of heterozygosity at the chromosome 13q locus, D13S3, was seen in 9 of 21 informative cases, and in 2 cases, both adenocarcinomas, duplication of the intact DNA sequences suggested the possibility that mitotic recombination had occurred. Frequent DNA sequence deletions, including those from chromosome 17, in squamous-cell carcinomas may reflect the extensive mutagenic and clastogenic effects of tobacco smoke that may lead to inactivation of putative tumor-suppressor genes. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Weston, A AU - Willey, J C AU - Modali, R AU - Sugimura, H AU - McDowell, E M AU - Resau, J AU - Light, B AU - Haugen, A AU - Mann, D L AU - Trump, B F AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 5099 EP - 5103 VL - 86 IS - 13 SN - 0027-8424, 0027-8424 KW - Index Medicus KW - Heterozygote Detection KW - Polymorphism, Restriction Fragment Length KW - Humans KW - Proto-Oncogenes KW - Chromosomes, Human, Pair 17 KW - Chromosomes, Human, Pair 3 KW - Chromosome Deletion KW - Carcinoma, Squamous Cell -- genetics KW - Lung Neoplasms -- genetics KW - Adenocarcinoma -- genetics KW - Chromosomes, Human, Pair 13 KW - Carcinoma, Small Cell -- genetics KW - Chromosomes, Human, Pair 11 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79051537?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-10 N1 - Date created - 1989-08-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Mol Biol. 1975 Nov 5;98(3):503-17 [1195397] Nature. 1986 Oct 16-22;323(6089):643-6 [2877398] Nature. 1983 Oct 13-19;305(5935):641-3 [6312329] Cancer Genet Cytogenet. 1985 Feb 15;15(3-4):335-47 [2982476] Nature. 1985 Jul 25-31;316(6026):330-4 [2991766] Annu Rev Genet. 1986;20:231-51 [2880556] Science. 1987 Mar 13;235(4794):1394-9 [3823889] Am J Hum Genet. 1987 May;40(5):413-20 [2883892] Nature. 1987 Jun 25-Jul 1;327(6124):721-4 [2885753] Proc Natl Acad Sci U S A. 1987 Aug;84(15):5419-23 [3037550] Nature. 1987 Aug 13-19;328(6131):616-9 [2886919] N Engl J Med. 1987 Oct 29;317(18):1109-13 [2821398] Nature. 1987 Oct 1-7;329(6138):451-4 [2821400] Nature. 1987 Oct 15-21;329(6140):645-7 [3657988] Science. 1987 Oct 9;238(4824):193-7 [2889267] Cancer Res. 1987 Nov 1;47(21):5518-27 [2889524] Nature. 1987 Dec 10-16;330(6148):578-81 [2825033] Cancer Res. 1988 Feb 1;48(3):682-5 [2891438] Nature. 1988 Jan 21;331(6153):273-7 [2827040] Proc Natl Acad Sci U S A. 1987 Dec;84(24):9252-6 [2892196] Proc Natl Acad Sci U S A. 1987 Dec;84(24):9275-9 [2892198] Jpn J Cancer Res. 1987 Dec;78(12):1302-8 [2892820] Proc Natl Acad Sci U S A. 1988 Mar;85(5):1571-5 [2894030] Nature. 1988 Mar 3;332(6159):85-7 [2894610] Science. 1988 Jul 15;241(4863):353-7 [2838909] J Clin Invest. 1988 Aug;82(2):502-7 [2900253] Oncogene Res. 1988;3(4):401-8 [3067190] Science. 1989 Apr 14;244(4901):217-21 [2649981] Mol Carcinog. 1988;1(3):151-60 [2855021] Proc Natl Acad Sci U S A. 1985 Sep;82(18):6216-20 [2994066] Nature. 1985 Nov 28-Dec 4;318(6044):377-80 [2999610] Proc Natl Acad Sci U S A. 1985 Dec;82(24):8592-6 [3001710] Annu Rev Biochem. 1986;55:831-54 [3017198] Nature. 1986 Aug 14-20;322(6080):644-7 [3092103] Hum Genet. 1981;57(3):300-6 [6114032] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cardiac morphologic and functional changes induced by epirubicin chemotherapy. AN - 79048174; 2738625 AB - Cardiac toxicity was evaluated in 24 patients who received epirubicin as a single chemotherapeutic agent, in doses of either 30 mg/m2 every week (11 patients) or 90 mg/m2 every 3 weeks (13 patients). The total doses of epirubicin ranged from 180 mg/m2 to 918 mg/m2 (mean, 491 +/- 187). No patient had prior heart disease, hypertension, mediastinal irradiation, or chemotherapy with other anthracycline agents. None of the patients developed overt heart failure, significant arrhythmias, ECG alterations, or roentgenographic changes in heart size. There was no significant change in the mean value of echocardiographic percent fractional shortening before and after epirubicin therapy. Patients receiving epirubicin doses less than 450 mg/m2 had minimal hemodynamic disturbances; however, no cut-off point separating two significantly different subpopulations could be demonstrated. Endomyocardial biopsy was performed on all patients; 20 biopsies were evaluable. Histologic and ultrastructural changes were similar to those caused by other anthracycline agents. A strong correlation was demonstrated between total dose of epirubicin and pathologic change as quantified using the Billingham scale (r = .7, P = .0006). A cut-off point beyond which there was a probability of increased pathologic damage was statistically defined at 450 mg/m2 of epirubicin. Severe pathologic alterations and moderate hemodynamic changes were observed in only one patient, who received 918 mg/m2 of epirubicin. Patients who are expected to receive epirubicin in excess of 450 mg/m2 should be monitored for cardiac toxicity, and continuation of epirubicin therapy beyond 900 mg/m2 should be based on the results of monitoring. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Dardir, M D AU - Ferrans, V J AU - Mikhael, Y S AU - el-Grindy, M S AU - el-Aasar, A B AU - el-Zawahry, H M AU - Alling, D W AU - Banks, S M AU - el-Mawla, N G AD - Ultrastructure Section, National Heart, Lung and Blood Institute, Bethesda, MD. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 947 EP - 958 VL - 7 IS - 7 SN - 0732-183X, 0732-183X KW - Epirubicin KW - 3Z8479ZZ5X KW - Index Medicus KW - Breast Neoplasms -- drug therapy KW - Humans KW - Adult KW - Urinary Bladder Neoplasms -- drug therapy KW - Middle Aged KW - Male KW - Female KW - Epirubicin -- therapeutic use KW - Heart Diseases -- chemically induced KW - Epirubicin -- adverse effects KW - Heart Diseases -- physiopathology KW - Heart Diseases -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79048174?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-01 N1 - Date created - 1989-08-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fluorouracil and high-dose leucovorin in previously treated patients with metastatic breast cancer. AN - 79047814; 2661735 AB - The efficacy and toxicity of leucovorin 500 mg/m2 administered intravenously (IV) over 30 minutes daily for five days followed in one hour by fluorouracil (5-FU) 375 mg/m2 administered IV daily for five days, each given every 3 weeks, was assessed in 54 previously treated patients with metastatic breast cancer. An overall objective response rate of 24% was achieved (95% confidence interval, 13% to 38%), with an additional 56% of patients maintaining stable disease. Eleven of 12 patients who responded had received previous 5-FU therapy. Toxicity of this regimen included grade 3 diarrhea in 13%, grade 3 or 4 mucositis in 33%, grade 3 or 4 granulocytopenia in 65%, and grade 3 or 4 thrombocytopenia in 19%. Delay of treatment was required for hematologic toxicity in 44 patients. Thirty-eight patients required dose reductions due to toxicity. Biochemical evaluation of tumor biopsy specimens obtained from 17 patients used as their own controls with and without leucovorin was performed. These studies reveal an increased stabilization of the 5-fluorodeoxyuridylate (FdUMP)-thymidylate synthase (TS) folate ternary complex with the addition of leucovorin. There was a 71% +/- 14% occupancy or inhibition of the enzyme with the use of both 5-FU and leucovorin, v 30% +/- 13% for 5-FU alone (P2 less than .037). The percent TS bound in responding patients was substantially higher than in those patients with progressive disease. Finally, the mean total tumor TS pre-therapy in seven patients was 31 fmol/mg compared with a mean of 81 fmol/mg in these same seven patients 24 hours after therapy. This 2.6-fold increase suggests that there is an induction of the enzyme, TS, with 5-FU treatment. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Swain, S M AU - Lippman, M E AU - Egan, E F AU - Drake, J C AU - Steinberg, S M AU - Allegra, C J AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 890 EP - 899 VL - 7 IS - 7 SN - 0732-183X, 0732-183X KW - Thymidylate Synthase KW - EC 2.1.1.45 KW - Leucovorin KW - Q573I9DVLP KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - Fluorouracil -- administration & dosage KW - Leucovorin -- administration & dosage KW - Humans KW - Adult KW - Neoplasm Metastasis KW - Clinical Trials as Topic KW - Aged KW - Middle Aged KW - Fluorouracil -- metabolism KW - Thymidylate Synthase -- metabolism KW - Leucovorin -- metabolism KW - Menopause KW - Female KW - Breast Neoplasms -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Breast Neoplasms -- enzymology KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79047814?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-01 N1 - Date created - 1989-08-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Family history of alcoholism in violent offenders and impulsive fire setters. AN - 79047318; 2472125 AB - Fifty-six of 58 violent offenders and impulsive fire setters fulfilled the DSM-III criteria for alcohol abuse. Information necessary for evaluation of family history of alcoholism was obtained on 54 subjects. Forty-four of the 54 subjects had first- or second-degree blood relatives with alcoholism. Thirty-five had alcoholic fathers. Subjects with alcoholic fathers had a lower mean cerebrospinal fluid 5-hydroxyindoleacetic acid concentration and were more often impulsive than subjects without alcoholic fathers. JF - Archives of general psychiatry AU - Linnoila, M AU - De Jong, J AU - Virkkunen, M AD - Laboratory of Clinical Studies, DICBR, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Md 20892. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 613 EP - 616 VL - 46 IS - 7 SN - 0003-990X, 0003-990X KW - Hydroxyindoleacetic Acid KW - 54-16-0 KW - Abridged Index Medicus KW - Index Medicus KW - Sex Factors KW - Humans KW - Adult KW - Fathers -- psychology KW - Hydroxyindoleacetic Acid -- cerebrospinal fluid KW - Male KW - Female KW - Disruptive, Impulse Control, and Conduct Disorders -- genetics KW - Firesetting Behavior -- genetics KW - Firesetting Behavior -- cerebrospinal fluid KW - Impulsive Behavior -- cerebrospinal fluid KW - Criminal Psychology KW - Impulsive Behavior -- genetics KW - Alcoholism -- genetics KW - Violence KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79047318?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-27 N1 - Date created - 1989-07-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of CD3- large granular lymphocyte functions by agonist and antagonists of protein kinase C: effects on NK and lymphokine-activated killer activity and production of IFN-gamma. AN - 79044957; 2543702 AB - The biochemical mechanisms involved in the activation and killing of tumor targets by large granular lymphocytes (LGL) have not yet been clearly defined. This laboratory has investigated these processes by analyzing the effects of protein kinase C (PKC) inhibitors (1-(5-isoquinolinesulfonyl)2-methyl-piperazine-dihydrochloride and retinol) on LGL cytotoxicity and IFN-gamma production. We now report that PKC inhibitors block the LGL functions of 1) NK activity, 2) IFN-gamma production, and 3) LAK activity induced by IL-2. Complete inhibition of cytotoxic activity occurs rapidly because only 2.5 h treatment of the LGL with the inhibitors was required. However, the inhibition of NK activity by the PKC inhibitors could be reversed by IL-2 or the synthetic diacylglycerol, L-gamma-1-oleyl-2-acetol-sn-3-glycerol (OAG), but not by IFN-alpha. The reversal of inhibition observed with OAG indicates that, in these studies, (1-(5-isoquinolinesulfonyl)2-methyl-piperazine-dihydrochloride is inhibiting PKC activity and not the activity of other cellular kinases. Furthermore, inhibition of LGL functional activity with PGE2 could not be reversed with OAG, supporting the contention that PG inhibition of NK activity is mediated by a pathway that does not directly involve PKC. These results indicate, in addition to IL-2-mediated events, that basal NK activity is under PKC regulatory control. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Ortaldo, J R AU - Young, H A AU - Varesio, L AD - Laboratory of Experimental Immunology, National Cancer Institute, Frederick, MD 21701-1013. Y1 - 1989/07/01/ PY - 1989 DA - 1989 Jul 01 SP - 366 EP - 371 VL - 143 IS - 1 SN - 0022-1767, 0022-1767 KW - Antigens, CD3 KW - 0 KW - Antigens, Differentiation, T-Lymphocyte KW - Diglycerides KW - Interleukin-2 KW - Isoquinolines KW - Piperazines KW - Receptors, Antigen, T-Cell KW - Vitamin A KW - 11103-57-4 KW - Interferon-gamma KW - 82115-62-6 KW - 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine KW - 84477-87-2 KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinase C KW - EC 2.7.11.13 KW - Dinoprostone KW - K7Q1JQR04M KW - Abridged Index Medicus KW - Index Medicus KW - Isoquinolines -- pharmacology KW - Dinoprostone -- pharmacology KW - Diglycerides -- pharmacology KW - Humans KW - Vitamin A -- pharmacology KW - Cytotoxicity Tests, Immunologic KW - Cyclic AMP -- physiology KW - Piperazines -- pharmacology KW - Protein Kinase C -- metabolism KW - Lymphocyte Activation -- drug effects KW - Protein Kinase C -- antagonists & inhibitors KW - Interferon-gamma -- biosynthesis KW - Cytotoxicity, Immunologic -- drug effects KW - Killer Cells, Natural -- metabolism KW - Killer Cells, Natural -- immunology KW - Killer Cells, Natural -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79044957?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-21 N1 - Date created - 1989-07-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effective pharmacotherapy of alcoholic amnestic disorder with fluvoxamine. Preliminary findings. AN - 79027836; 2472126 AB - Ten patients with alcoholic chronic organic brain disease were categorized as having alcohol amnestic disorder, or Korsakoff's psychosis (n = 6), dementia associated with alcoholism (n = 3), or compensated alcoholic liver disease (n = 1). All patients had severe deficits in memory for recently acquired information (episodic memory). Patients with alcohol dementia also showed global intellectual decline, including decreased performance on measures of semantic (knowledge) memory and reduction in levels of cerebrospinal fluid somatostatin. In a 4-week double-blind crossover design, the serotonin-uptake blocker fluvoxamine maleate (100 to 200 mg/d) was found to improve episodic memory in only the patients with alcohol amnestic disorder. These improvements in memory were significantly correlated with reductions in levels of cerebrospinal fluid 5-hydroxyindoleacetic acid, suggesting that facilitation of serotonergic neurotransmission may ameliorate the episodic memory failure in patients with alcohol amnestic disorder. JF - Archives of general psychiatry AU - Martin, P R AU - Adinoff, B AU - Eckardt, M J AU - Stapleton, J M AU - Bone, G A AU - Rubinow, D R AU - Lane, E A AU - Linnoila, M AD - Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 617 EP - 621 VL - 46 IS - 7 SN - 0003-990X, 0003-990X KW - Oximes KW - 0 KW - Serotonin Antagonists KW - Somatostatin KW - 51110-01-1 KW - Hydroxyindoleacetic Acid KW - 54-16-0 KW - Fluvoxamine KW - O4L1XPO44W KW - Abridged Index Medicus KW - Index Medicus KW - Somatostatin -- cerebrospinal fluid KW - Double-Blind Method KW - Memory -- drug effects KW - Humans KW - Clinical Trials as Topic KW - Aged KW - Hydroxyindoleacetic Acid -- cerebrospinal fluid KW - Wechsler Scales KW - Middle Aged KW - Psychoses, Alcoholic -- blood KW - Psychoses, Alcoholic -- psychology KW - Psychoses, Alcoholic -- drug therapy KW - Female KW - Male KW - Serotonin Antagonists -- therapeutic use KW - Oximes -- blood KW - Oximes -- therapeutic use KW - Serotonin Antagonists -- blood KW - Alcohol Amnestic Disorder -- psychology KW - Alcohol Amnestic Disorder -- cerebrospinal fluid KW - Alcohol Amnestic Disorder -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79027836?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-27 N1 - Date created - 1989-07-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Arch Gen Psychiatry. 1990 Oct;47(10):978-9 [2121117] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lung cancer risk, occupational exposure, and the debrisoquine metabolic phenotype. AN - 79025808; 2731181 AB - The risk of lung cancer in smokers was examined based on the debrisoquine metabolic phenotype and on exposure to occupational lung carcinogens, specifically asbestos and polycyclic aromatic hydrocarbons. Extensive metabolizers of debrisoquine are at a 4-fold increased risk for lung cancer compared to poor metabolizers, after adjustment for age, sex, and smoking (pack-years), when only occupationally unexposed subjects are considered. Increased risk related to the debrisoquine metabolic phenotype was greatest for squamous and small cell histologies, and least for the adenocarcinoma subtype. Men with a history of exposure to occupational carcinogens had significantly increased risk of lung cancer (relative risk = 2.8), after adjustment for age and smoking. Considering the combined effect of the high risk extensive metabolizers debrisoquine metabolic phenotype and likely occupational exposure to asbestos, the relative excess risk for lung cancer was 18-fold. This finding is consistent with a synergism in risk between the ability to extensively metabolize debrisoquine and occupational exposure to lung carcinogens in male smokers. Debrisoquine phenotyping has potential for identifying carcinogen-exposed workers at high risk of lung cancer. JF - Cancer research AU - Caporaso, N AU - Hayes, R B AU - Dosemeci, M AU - Hoover, R AU - Ayesh, R AU - Hetzel, M AU - Idle, J AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/07/01/ PY - 1989 DA - 1989 Jul 01 SP - 3675 EP - 3679 VL - 49 IS - 13 SN - 0008-5472, 0008-5472 KW - Isoquinolines KW - 0 KW - Polycyclic Compounds KW - Asbestos KW - 1332-21-4 KW - Debrisoquin KW - X31CDK040E KW - Index Medicus KW - Oxidation-Reduction KW - Smoking KW - Risk Factors KW - Humans KW - Lung Diseases, Obstructive -- epidemiology KW - Male KW - Female KW - Lung Neoplasms -- epidemiology KW - Debrisoquin -- metabolism KW - Isoquinolines -- metabolism KW - Occupational Diseases -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79025808?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-27 N1 - Date created - 1989-07-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Conditions associated with hepatocellular carcinoma. AN - 79018332; 2542707 AB - The most important condition associated with hepatocellular carcinoma is chronic hepatitis B virus infection. This article summarizes the information linking hepatocellular carcinoma with conditions other than hepatitis B virus infection. JF - The Medical clinics of North America AU - Lisker-Melman, M AU - Martin, P AU - Hoofnagle, J H AD - Liver Diseases Section, National Institutes of Health, Bethesda, Maryland. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 999 EP - 1009 VL - 73 IS - 4 SN - 0025-7125, 0025-7125 KW - Aflatoxins KW - 0 KW - Androgens KW - Estrogens KW - Thorium Dioxide KW - 9XA7X17UQC KW - Abridged Index Medicus KW - Index Medicus KW - Thorium Dioxide -- adverse effects KW - Hepatitis, Chronic KW - Hepatitis C -- complications KW - Humans KW - Androgens -- adverse effects KW - Estrogens -- adverse effects KW - Male KW - Female KW - Aflatoxins -- adverse effects KW - Liver Diseases -- complications KW - Carcinoma, Hepatocellular -- etiology KW - Liver Neoplasms -- chemically induced KW - Metabolic Diseases -- complications KW - Liver Diseases -- classification KW - Liver Neoplasms -- etiology KW - Carcinoma, Hepatocellular -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79018332?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-07 N1 - Date created - 1989-07-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of the human T-cell leukemia virus type I long terminal repeat by 12-O-tetradecanoylphorbol-13-acetate and by tax (p40x) occurs through similar but functionally distinct target sequences. AN - 79017752; 2786091 AB - One potent transcriptional activator of human T-cell leukemia virus type I (HTLV-I) is virally encoded protein Tax (p40x). p40x trans-activates HTLV-I through the long terminal repeat (LTR) by using a triply repeated 21-base-pair sequence as the target. In this report we have characterized the induction of the HTLV-I LTR by 12-O-tetradecanoylphorbol-13-acetate (TPA). By assaying progressively deleted mutations in the HTLV-I LTR, we have delimited a 60-base-pair sequence in the LTR which is capable of conferring TPA responsiveness, but not p40x responsiveness, to heterologous promoters in a position-independent fashion. This HTLV-I TPA-responsive element is specifically recognized by preexisting factors from uninfected cells. We show that activation of this sequence by phorbol ester does not require de novo cellular protein synthesis. When the HTLV-I LTR was simultaneously activated by both Tax and TPA, an additive effect was seen. This suggests the use of distinct regulatory pathways by the two respective trans-activators. JF - Journal of virology AU - Radonovich, M AU - Jeang, K T AD - Laboratory of Molecular Virology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 2987 EP - 2994 VL - 63 IS - 7 SN - 0022-538X, 0022-538X KW - HTLV-I Antigens KW - 0 KW - Trans-Activators KW - Transcription Factors KW - Cycloheximide KW - 98600C0908 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - AIDS/HIV KW - HeLa Cells -- metabolism KW - Base Sequence KW - Transcription, Genetic -- drug effects KW - Humans KW - Cycloheximide -- pharmacology KW - Genes -- drug effects KW - Molecular Sequence Data KW - Repetitive Sequences, Nucleic Acid KW - Transcription Factors -- physiology KW - Human T-lymphotropic virus 1 -- genetics KW - HTLV-I Antigens -- physiology KW - Human T-lymphotropic virus 1 -- drug effects KW - Genes, Viral -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Gene Expression Regulation -- drug effects KW - Transcription Factors -- genetics KW - HTLV-I Antigens -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79017752?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-13 N1 - Date created - 1989-07-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Mol Cell Biol. 1987 Jul;7(7):2610-3 [3475568] Nature. 1987 Apr 16-22;326(6114):711-3 [3031512] Science. 1987 Sep 11;237(4820):1324-9 [2888190] Nature. 1987 Oct 15-21;329(6140):648-51 [2821407] Cell. 1987 Jun 19;49(6):729-39 [3034432] Cell. 1987 Jun 19;49(6):741-52 [3034433] J Virol. 1987 Jul;61(7):2175-81 [3035218] J Biol Chem. 1987 Jun 25;262(18):8743-7 [3036825] Nature. 1987 Jul 9-15;328(6126):175-8 [2885756] Proc Natl Acad Sci U S A. 1987 Oct;84(19):6845-9 [3498942] Mol Cell Biol. 1987 Oct;7(10):3759-66 [3500398] Science. 1987 Dec 11;238(4833):1575-8 [2825351] Proc Natl Acad Sci U S A. 1988 Mar;85(5):1457-61 [2830620] J Virol. 1988 Apr;62(4):1339-46 [2831395] Nature. 1988 Jun 9;333(6173):504 [2836736] Nature. 1988 Jun 23;333(6175):776-8 [2838755] Science. 1988 Jul 1;241(4861):89-92 [2838905] Cell. 1988 Aug 12;54(4):541-52 [3135940] Cell. 1988 Aug 12;54(4):553-60 [3135941] Nature. 1988 Aug 11;334(6182):494-8 [2900470] Cell. 1988 Sep 23;54(7):1033-42 [3416354] Science. 1988 Sep 23;241(4873):1652-5 [2843985] Science. 1988 Oct 28;242(4878):540-6 [3140380] J Virol. 1988 Dec;62(12):4499-509 [3263510] Proc Natl Acad Sci U S A. 1988 Nov;85(21):7922-6 [2847147] Proc Natl Acad Sci U S A. 1988 Nov;85(21):8291-5 [2847157] Genes Dev. 1988 Sep;2(9):1055-62 [2847958] Genes Dev. 1988 Oct;2(10):1216-26 [3144478] Nucleic Acids Res. 1978 Sep;5(9):3157-70 [212715] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] Nucleic Acids Res. 1981 Jul 10;9(13):3047-60 [6269071] Nucleic Acids Res. 1981 Dec 11;9(23):6505-25 [6275366] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Proc Natl Acad Sci U S A. 1982 Nov;79(22):6899-902 [6294664] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] Proc Natl Acad Sci U S A. 1983 Jun;80(12):3618-22 [6304725] J Virol. 1983 Oct;48(1):135-48 [6310141] Cell. 1983 Dec;35(3 Pt 2):603-10 [6606489] J Virol. 1984 Jan;49(1):183-9 [6690710] Nature. 1984 Apr 19-25;308(5961):693-8 [6232463] Science. 1984 Oct 5;226(4670):57-61 [6089350] Nature. 1984 Oct 4-10;311(5985):433-8 [6090941] Virology. 1984 Dec;139(2):340-5 [6097028] Cell. 1985 May;41(1):3-5 [2986847] J Biol Chem. 1985 Sep 25;260(21):11852-8 [3930485] Science. 1986 Jul 18;233(4761):305-12 [3014651] Proc Natl Acad Sci U S A. 1986 Sep;83(17):6558-62 [3018737] Proc Natl Acad Sci U S A. 1986 Sep;83(18):6682-6 [2875459] Nature. 1986 Oct 9-15;323(6088):555-8 [3020435] Proc Natl Acad Sci U S A. 1986 Oct;83(19):7192-6 [3020538] Virology. 1986 Oct 30;154(2):249-58 [3639669] Proc Natl Acad Sci U S A. 1986 Nov;83(21):8112-6 [3022280] EMBO J. 1986 Nov;5(11):2883-8 [3024966] Cell. 1987 Jan 30;48(2):251-60 [3026638] J Virol. 1987 Mar;61(3):708-13 [3027397] Cell. 1987 Apr 10;49(1):47-56 [3030566] Nature. 1987 Sep 3-9;329(6134):73-5 [2442617] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chemoimmunotoxin therapy against a human colon tumor (HT-29) xenografted into nude mice. AN - 79011914; 2499420 AB - The efficacy of intracavitary chemoimmunotoxin therapy for cancer treatment was evaluated using the human colon carcinoma (HT-29) which had been xenografted i.p. into nude mice. Mice bearing HT-29 were treated with an immunotoxin consisting of the monoclonal antibody OVB3 coupled to Pseudomonas exotoxin (OVB3-PE), with cyclophosphamide (Cy), or with both OVB3-PE plus Cy. Mice given injections i.p. of 3 x 10(6) HT-29 ascites cells developed a localized disease that presented as both malignant ascites and solid tumor confined to the peritoneal cavity. All mice died within 30 to 40 days. Mice that received either three or six injections of OVB3-PE at a dose of 0.5 micrograms every other day beginning 3 days post-tumor inoculation exhibited significantly increased median survival times (MSTs) (P = 0.002) of 62 and 68 days, respectively, as compared to a MST of 33 days for the controls. OVB3 alone or an irrelevant monoclonal antibody conjugated to PE exhibited no antitumor activity. The therapeutic effects of the immunotoxin could be blocked by giving a large amount of unconjugated OVB3 at the same time. Treatment of mice with Cy alone at the maximal tolerated dose (250 mg/kg) on Days 10 and 17 after tumor inoculation increased the MST from 33 days to 54 days. The maximum tolerated dose could be increased to 300 mg/kg per injection if the Cy treatment was preceded by 100 mg/kg of S-2-(3-aminopropylamino)ethyl phosphorothioic acid (WR-2721), a sulfhydryl compound that selectively protects normal tissue against the toxicity of radiation and alkylating agents. Cy plus WR-2721 treatment on Days 10 and 17 increased the MST from 35 to 61 days (P = 0.002). Interestingly, groups of mice that received either two, four, or seven treatments of OVB3-PE following Cy plus WR-2721 therapy exhibited a further increase (P less than 0.002) in MSTs to 81, 87, and 96 days, respectively. Thus, the combination of cytoreductive chemotherapy with the OVB3-PE was significantly more effective for the intracavitary treatment of established HT-29 colon cancer xenografts than either chemotherapy or immunotoxin therapy alone. JF - Cancer research AU - Pearson, J W AU - FitzGerald, D J AU - Willingham, M C AU - Wiltrout, R H AU - Pastan, I AU - Longo, D L AD - Laboratory of Experimental Immunology, NCI-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1989/07/01/ PY - 1989 DA - 1989 Jul 01 SP - 3562 EP - 3567 VL - 49 IS - 13 SN - 0008-5472, 0008-5472 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Neoplasm KW - Bacterial Toxins KW - Exotoxins KW - Immunotoxins KW - Virulence Factors KW - Cyclophosphamide KW - 8N3DW7272P 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 - Combined Modality Therapy KW - Humans KW - Drug Resistance KW - Mice KW - Mice, Nude KW - Antibodies, Monoclonal -- immunology KW - Neoplasm Transplantation KW - Cyclophosphamide -- therapeutic use KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - Ascites KW - In Vitro Techniques KW - Pseudomonas aeruginosa KW - Antigens, Neoplasm -- immunology KW - Exotoxins -- administration & dosage KW - Colonic Neoplasms -- therapy KW - Immunotoxins -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79011914?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-27 N1 - Date created - 1989-07-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of the c-H-ras proto-oncogene by retrovirus insertion and chromosomal rearrangement in a Moloney leukemia virus-induced T-cell leukemia. AN - 78992102; 2542606 AB - A rearrangement of the c-H-ras locus was detected in a T-cell line (DA-2) established from a Moloney leukemia virus-induced tumor. This rearrangement was associated with the high-level expression of H-ras RNA and the H-ras gene product, p21. DNA from DA-2 cells transformed fibroblasts in DNA transfection experiments, and the transformed fibroblasts contained the rearranged H-ras locus. The rearrangement involved one allele and was present in tissue from the primary tumor from which the cell line was isolated. Cloning and sequencing of the rearranged allele and comparison with the normal allele demonstrated that the rearrangement was complex and probably resulted from the integration of a retrovirus in the H-ras locus between a 5' noncoding exon and the first coding exon and a subsequent homologous recombination between this provirus and another newly acquired provirus also located on chromosome 7. These events resulted in the translocation of the coding exons of the H-ras locus away from the 5' noncoding exon region to a new genomic site on chromosome 7. Sequencing of the coding regions of the gene failed to detect mutations in the 12th, 13th, 59th, or 61st codons. The possible reasons for the complexity of the rearrangement and the significance of the activation of the H-ras locus to T-cell transformation are discussed. JF - Journal of virology AU - Ihle, J N AU - Smith-White, B AU - Sisson, B AU - Parker, D AU - Blair, D G AU - Schultz, A AU - Kozak, C AU - Lunsford, R D AU - Askew, D AU - Weinstein, Y AD - Molecular Mechanisms of Carcinogenesis Laboratory, National Cancer Institute-Frederick, Cancer Research Facility, Maryland 21701. Y1 - 1989/07// PY - 1989 DA - July 1989 SP - 2959 EP - 2966 VL - 63 IS - 7 SN - 0022-538X, 0022-538X KW - DNA Transposable Elements KW - 0 KW - Membrane Proteins KW - Proto-Oncogene Proteins KW - RNA, Viral KW - HRAS protein, human KW - EC 3.6.5.2 KW - Proto-Oncogene Proteins p21(ras) KW - Index Medicus KW - Animals KW - Immunoblotting KW - Humans KW - Gene Rearrangement KW - Mice KW - Nucleic Acid Hybridization KW - Cloning, Molecular KW - Alleles KW - Base Sequence KW - Transfection KW - Restriction Mapping KW - Molecular Sequence Data KW - RNA, Viral -- genetics KW - Cell Line KW - Cell Transformation, Neoplastic KW - Genes, ras KW - Leukemia, T-Cell -- genetics KW - Leukemia, T-Cell -- microbiology KW - Moloney murine leukemia virus -- genetics KW - Gene Expression Regulation KW - Membrane Proteins -- genetics KW - Proto-Oncogene Proteins -- genetics KW - Leukemia, Experimental -- microbiology KW - Leukemia, Experimental -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78992102?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-13 N1 - Date created - 1989-07-13 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M27193; GENBANK N1 - SuppNotes - Cited By: Exp Cell Res. 1977 Mar 1;105(1):109-17 [65290] Cell. 1988 Sep 9;54(6):831-40 [2842066] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Virology. 1978 Oct 1;90(1):23-35 [82294] Science. 1979 Apr 6;204(4388):69-71 [219475] J Virol. 1979 Apr;30(1):255-66 [480454] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] Science. 1985 Dec 20;230(4732):1378-81 [2999983] Proc Natl Acad Sci U S A. 1986 Mar;83(6):1651-5 [3513183] EMBO J. 1986 Feb;5(2):301-9 [3011401] Science. 1986 Jun 13;232(4756):1410-3 [3012774] Proc Natl Acad Sci U S A. 1986 Jul;83(14):5010-4 [3014527] Eur J Biochem. 1987 May 15;165(1):7-12 [3494605] J Virol. 1987 Jul;61(7):2339-43 [2884332] J Virol. 1987 Aug;61(8):2489-98 [3037111] Mol Cell Biol. 1987 Aug;7(8):2933-40 [3670300] Methods Enzymol. 1980;65(1):499-560 [6246368] J Virol. 1980 Nov;36(2):408-20 [6253666] Proc Natl Acad Sci U S A. 1980 Jul;77(7):3937-41 [6254003] Proc Natl Acad Sci U S A. 1980 Sep;77(9):5201-5 [6159641] Cell. 1981 Feb;23(2):311-22 [6258797] Proc Natl Acad Sci U S A. 1981 Jun;78(6):3328-32 [6267583] Proc Natl Acad Sci U S A. 1981 Jun;78(6):3418-22 [6267589] J Virol. 1981 Jul;39(1):1-10 [6268802] Nature. 1982 Jun 10;297(5866):479-83 [6283358] J Exp Med. 1982 Sep 1;156(3):873-87 [6286838] J Virol. 1982 Jul;43(1):294-304 [6287003] Nature. 1982 Nov 11;300(5888):143-9 [6290897] Nature. 1982 Nov 11;300(5888):149-52 [7133135] J Virol. 1982 Oct;44(1):19-31 [7143566] Science. 1982 Dec 10;218(4577):1122-5 [6293052] Nature. 1982 Dec 23;300(5894):762-5 [7177195] Nature. 1983 Mar 3;302(5903):33-7 [6298635] Science. 1983 Jul 8;221(4606):155-7 [6344220] J Virol. 1983 Jul;47(1):217-20 [6864883] Nature. 1983 Jun 30;303(5920):775-9 [6866079] Proc Natl Acad Sci U S A. 1984 Jan;81(1):202-5 [6582476] Proc Natl Acad Sci U S A. 1984 Jul;81(13):4008-12 [6330729] J Virol. 1985 Mar;53(3):984-7 [2983103] Annu Rev Genet. 1984;18:553-612 [6397126] Proc Natl Acad Sci U S A. 1985 Oct;82(19):6687-91 [2995979] J Mol Biol. 1975 Nov 5;98(3):503-17 [1195397] J Virol. 1988 Mar;62(3):788-94 [3276924] Somatic Cell Genet. 1975 Oct;1(4):371-82 [1235912] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - cDNA and deduced amino acid sequences of human P450 IIA3 (CYP2A3). AN - 79081280; 2748347 JF - Nucleic acids research AU - Yamano, S AU - Nagata, K AU - Yamazoe, Y AU - Kato, R AU - Gelboin, H V AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda 20892. Y1 - 1989/06/26/ PY - 1989 DA - 1989 Jun 26 SP - 4888 VL - 17 IS - 12 SN - 0305-1048, 0305-1048 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Rats KW - Animals KW - Base Sequence KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - DNA -- isolation & purification KW - Genes KW - Cytochrome P-450 Enzyme System -- genetics KW - Cytochrome P-450 Enzyme System -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79081280?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-25 N1 - Date created - 1989-08-25 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - X13929; GENBANK N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1985 Feb;82(4):983-7 [3856261] DNA. 1989 Jan-Feb;8(1):1-13 [2651058] J Biol Chem. 1988 Mar 25;263(9):4166-71 [3346244] J Biol Chem. 1987 Feb 25;262(6):2787-93 [3818621] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - T cell activation induces rapid tyrosine phosphorylation of a limited number of cellular substrates. AN - 79042294; 2786526 AB - Activation of murine T cells by antigen, antibodies binding the T cell antigen receptor, or stimulatory anti-Thy-1 antibodies results in rapid phosphorylation of the T cell receptor zeta chain on tyrosine residues. The T cell receptor is itself unlikely to be a tyrosine kinase; rather, it is probable that this receptor is coupled to a nonreceptor tyrosine kinase. To understand further this protein kinase pathway, additional targets of the tyrosine kinase have been sought by comparing anti-phosphotyrosine antibody immunoblots of cellular proteins from unactivated and activated T cell hybridomas. In addition to the T cell receptor zeta chain, two proteins of 53 and 62 kDa are phosphorylated on tyrosine residues after T cell activation. These phosphorylations require stimulatory anti-Thy-1 antibodies, antigen, or antireceptor antibody stimulation. The 53-kDa protein is preferentially phosphorylated by antigen or antireceptor antibody. Of interest is that variants of the murine T cell hybridoma lacking the T cell receptor zeta chain or lacking surface antigen receptor can nonetheless be stimulated by anti-Thy-1 antibodies to phosphorylate the 62-kDa substrate. In contrast to the tyrosine kinases of oncogenic viruses, the kinase coupled to the T cell antigen receptor appears to have a limited number of targets. These proteins are candidates for critical substrates in this protein tyrosine kinase pathway. JF - The Journal of biological chemistry AU - Hsi, E D AU - Siegel, J N AU - Minami, Y AU - Luong, E T AU - Klausner, R D AU - Samelson, L E AD - Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1989/06/25/ PY - 1989 DA - 1989 Jun 25 SP - 10836 EP - 10842 VL - 264 IS - 18 SN - 0021-9258, 0021-9258 KW - Antibodies, Monoclonal KW - 0 KW - Ethers KW - Macromolecular Substances KW - Receptors, Antigen, T-Cell KW - Ionomycin KW - 56092-81-0 KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Hybridomas -- metabolism KW - Animals KW - Phosphorylation KW - Ethers -- pharmacology KW - Electrophoresis, Polyacrylamide Gel KW - Kinetics KW - Electrophoresis, Gel, Two-Dimensional KW - Hybridomas -- immunology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - Substrate Specificity KW - Antibodies, Monoclonal -- immunology KW - Lymphocyte Activation KW - T-Lymphocytes -- metabolism KW - Receptors, Antigen, T-Cell -- metabolism KW - Protein-Tyrosine Kinases -- metabolism KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79042294?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-18 N1 - Date created - 1989-07-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytochrome P-450 hPCN3, a novel cytochrome P-450 IIIA gene product that is differentially expressed in adult human liver. cDNA and deduced amino acid sequence and distinct specificities of cDNA-expressed hPCN1 and hPCN3 for the metabolism of steroid hormones and cyclosporine. AN - 79039806; 2732228 AB - Immunoblotting analysis of human liver microsome preparations revealed that human cytochrome P-450 PCN1 (hPCN1, Mr approximately 52,000) was expressed in each of 40 individual specimens examined. In about 10-20% of the livers, an immunologically related protein having a lower electrophoretic mobility (Mr approximately 52,500) was also detected. A single liver was found that expressed only the lower mobility protein, designated hPCN3, and RNA isolated from this liver was used to construct a lambda gt11 library. The library was screened with an hPCN1 cDNA probe resulting in the isolation of a unique full-length cDNA that was sequenced and shown to encode hPCN3. The deduced amino acid sequence of this cDNA contained 502 residues, a calculated molecular mass of 57,115 daltons, and displayed 84% similarity with hPCN1. The deduced amino-terminal sequence of hPCN3 was identical to that of HFLa, a major cytochrome P-450 expressed in human fetal liver that is immunologically cross-reactive with several family III cytochrome P-450s. hPCN1 and hPCN3 cDNAs were expressed in Hep G2 cells using a vaccinia virus expression system and shown to encode active enzymes, both characterized by reduced CO-binding spectra with lambda max at 450 nm. Enzymatic analysis revealed that both cytochrome P-450s were similarly active in catalyzing oxidation of the calcium channel blocking drug nifedipine. Both enzymes also catalyzed 6 beta-hydroxylation of the steroid hormones testosterone, progesterone, and androstenedione, although hPCN1 exhibited several-fold higher expressed activity than hPCN3. Several minor oxidation products of these steroids (e.g. 15 beta-hydroxytestosterone), comprising up to approximately 20% of the total metabolites, were formed by hPCN1 but not hPCN3, indicating that hPCN3 is a more highly regiospecific monooxygenase catalyst with steroid substrates. Clear differences were also detected in their catalytic activities toward the immunosuppressive drug cyclosporine, with two hydroxylated metabolites (M1 and M17) and one demethylated metabolite (M21) formed by hPCN1 but only one metabolite (M1) formed by hPCN3. These studies establish that hPCN3 is a newly described cytochrome P-450 that is differentially expressed in the adult human population and that has overlapping substrate specificity compared to hPCN1 for metabolism of steroid and drug substrates. JF - The Journal of biological chemistry AU - Aoyama, T AU - Yamano, S AU - Waxman, D J AU - Lapenson, D P AU - Meyer, U A AU - Fischer, V AU - Tyndale, R AU - Inaba, T AU - Kalow, W AU - Gelboin, H V AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/06/25/ PY - 1989 DA - 1989 Jun 25 SP - 10388 EP - 10395 VL - 264 IS - 18 SN - 0021-9258, 0021-9258 KW - Cyclosporins KW - 0 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Mixed Function Oxygenases KW - EC 1.- KW - CYP3A4 protein, human KW - EC 1.14.13.67 KW - CYP3A protein, human KW - EC 1.14.14.1 KW - CYP3A5 protein, human KW - Cytochrome P-450 CYP3A KW - Index Medicus KW - Vaccinia virus -- genetics KW - Immunoblotting KW - Animals KW - Base Sequence KW - Cyclosporins -- metabolism KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Substrate Specificity KW - Species Specificity KW - Cloning, Molecular KW - Mixed Function Oxygenases -- metabolism KW - Genes KW - Cytochrome P-450 Enzyme System -- genetics KW - Microsomes, Liver -- enzymology KW - DNA -- genetics KW - Cytochrome P-450 Enzyme System -- metabolism KW - Mixed Function Oxygenases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79039806?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-18 N1 - Date created - 1989-07-18 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - J04813; GENBANK N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cellular processing of a ricin-antibody conjugate. A kinetic analysis of the rate-limiting step. AN - 79021579; 2786524 AB - Upon exposure to holoricin-antibody conjugates, target cells display a period of no measurable intoxication followed by a concentration-dependent exponential decline in protein synthesis. The rate of this decline is increased by conjugate structural variables such as addition of a second ricin to the antibody or introduction of a peptide spacer between the toxin and antibody. Additionally, the rate is enhanced by the addition of ammonia or monensin. The relationship between immunotoxin concentration and the rate of protein synthesis inhibition is shown to obey typical Michaelis-Menten kinetics. By displacing bound immunotoxin with native antibody, it was demonstrated that the rate-limiting saturable process is not due to antibody-surface antigen interaction. Although addition of a second ricin as well as addition of ammonia elevated the measured rate of protein synthesis inhibition, curve-fitting techniques indicated that they did not elevate the maximal rate; however, introduction of a peptide spacer into the conjugate or addition of monensin increased the maximal rate of this saturable process. Additionally, the kinetic examination of the potentiation effects of ammonia and monensin indicates that they operate on different cellular processes involved with the intracellular routing toward intoxication. An equational model is developed which helps interpret the known features of the conjugate intoxication process. JF - The Journal of biological chemistry AU - Marsh, J W AD - Laboratory of Molecular Biology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1989/06/25/ PY - 1989 DA - 1989 Jun 25 SP - 10405 EP - 10410 VL - 264 IS - 18 SN - 0021-9258, 0021-9258 KW - Immunotoxins KW - 0 KW - Protein Synthesis Inhibitors KW - Ammonia KW - 7664-41-7 KW - Ricin KW - 9009-86-3 KW - Leucine KW - GMW67QNF9C KW - Index Medicus KW - Ammonia -- pharmacology KW - Protein Biosynthesis KW - Kinetics KW - Leucine -- metabolism KW - Cell Line KW - Immunotoxins -- pharmacology KW - Ricin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79021579?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-18 N1 - Date created - 1989-07-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alteration of mouse cytochrome P450coh substrate specificity by mutation of a single amino-acid residue. AN - 79045853; 2733794 AB - As a family of structurally-related enzymes, cytochrome P450 (P450) monooxygenases exhibit paradoxical characteristics: although collectively the enzymes display a broad range of substrate specificities, individually they are characterized by a high degree of substrate and product selectivity. Mouse P45015 alpha and P450coh, for example, which are expressed in female liver and male kidney cells, catalyse 15 alpha-hydroxylation of delta 4 3-ketone steroids, such as testosterone and 7-hydroxylation of coumarin, respectively. In spite of their divergent catalytic activities, however, these enzymes differ by only 11 amino acids within their 494 residues. To determine the structural basis of the different substrate specificities of P45015 alpha and P450coh we therefore altered each of these 11 residues by site-directed mutagenesis, expressing the mutant cytochromes in COS-1 cells. We report that the activities of both cytochromes depend critically on the identities of the amino acids at positions 117, 209 and 365 and, moreover, that a single mutation in which Phe 209 is substituted by Leu is sufficient to convert the specificity of P450coh from coumarin to steroid hydroxylation. JF - Nature AU - Lindberg, R L AU - Negishi, M AD - Pharmacogenetics Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/06/22/ PY - 1989 DA - 1989 Jun 22 SP - 632 EP - 634 VL - 339 IS - 6226 SN - 0028-0836, 0028-0836 KW - Amino Acids KW - 0 KW - Coumarins KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - coumarin KW - A4VZ22K1WT KW - Steroid Hydroxylases KW - EC 1.14.- KW - Index Medicus KW - Animals KW - Coumarins -- metabolism KW - Amino Acids -- genetics KW - Molecular Sequence Data KW - Steroid Hydroxylases -- metabolism KW - Mice KW - Amino Acid Sequence KW - Mutation KW - Cell Line KW - Cytochrome P-450 Enzyme System -- genetics KW - Substrate Specificity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79045853?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-20 N1 - Date created - 1989-07-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Polyacrylamide-streptavidin: a novel reagent for simplified construction of soluble multivalent macromolecular conjugates. AN - 79077439; 2738413 AB - We have developed a soluble macromolecular conjugation reagent, polyacrylamide-streptavidin (PASA), for the simplified preparation of multivalent protein-protein conjugates. Soluble linear polyacrylamide, with a molecular weight of approximately 10(6), has carboxyl groups generated by limited alkaline hydrolysis. It is then activated with carbodiimide, separated from excess carbodiimide, and conjugated to streptavidin. The resulting conjugate, which has approximately 20 streptavidin residues per molecule, can bind biotinylated proteins to produce homo- or heteroconjugates of known composition. We have used this technique to prepare soluble multivalent heteroligating antibody conjugates that can bind either of two antigenically distinct cell lines, as well as reagents that specifically label murine tumor cells with different MHC class I antigens. The method is potentially useful for making multivalent arrays of epitopes for measuring low affinity interactions such as that between the T cell receptor and MHC molecules, as well as for making immunotoxins, tumor labelling conjugates, and complex immunogens. JF - Journal of immunological methods AU - Nardelli, B AU - McHugh, L AU - Mage, M AD - Division of Cancer Biology and Diagnosis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/06/21/ PY - 1989 DA - 1989 Jun 21 SP - 233 EP - 239 VL - 120 IS - 2 SN - 0022-1759, 0022-1759 KW - Acrylic Resins KW - 0 KW - Antibodies KW - Bacterial Proteins KW - Carbodiimides KW - H-2 Antigens KW - Ligands KW - Macromolecular Substances KW - Biotin KW - 6SO6U10H04 KW - polyacrylamide KW - 9003-05-8 KW - Streptavidin KW - 9013-20-1 KW - Index Medicus KW - Chemistry KW - Chemical Phenomena KW - H-2 Antigens -- immunology KW - Flow Cytometry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79077439?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-02 N1 - Date created - 1989-08-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tumorigenicity of human mesothelial cell line transfected with EJ-ras oncogene. AN - 79025989; 2733039 AB - We performed this study to determine whether human mesothelial cells are capable of undergoing neoplastic change in vitro and to observe their interaction with the activated c-Ha-ras (HRAS1) oncogene EJ-ras, which has a role in the development of many malignant human tumors. Mesothelial cells are presumed to be the progenitor cells of malignant mesothelioma, a cancer strongly correlated with asbestos exposure. Previously, we established a non-tumorigenic cell line, MeT-5A, from normal human mesothelial cells after transfection with a plasmid containing the simian virus 40 (SV40) early-region genes. In the present study, we performed transfection of a plasmid containing the EJ-ras gene and the neomycin-resistance gene into these cells and selected a population resistant to G418, a neomycin analogue. Cells from this cell line formed rapidly growing sc tumors in NIH Swiss athymic nude mice, but untransfected with the vector DNA and selected for G418 resistance formed no tumors. The tumors formed by EJ-ras-transfected cells were established in vitro, and cells from these tumor cell lines exhibited a characteristic altered morphology. The cells had the same isoenzyme phenotype as the parent cells, and they expressed the mutant EJ-ras p21 protein. This first demonstration of malignant transformation of human mesothelial cells in vitro may permit molecular analysis of mesothelial carcinogenesis. JF - Journal of the National Cancer Institute AU - Reddel, R R AU - Malan-Shibley, L AU - Gerwin, B I AU - Metcalf, R A AU - Harris, C C AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, MD. Y1 - 1989/06/21/ PY - 1989 DA - 1989 Jun 21 SP - 945 EP - 948 VL - 81 IS - 12 SN - 0027-8874, 0027-8874 KW - Gentamicins KW - 0 KW - antibiotic G 418 KW - A08F5XTI6G KW - Index Medicus KW - Neoplasm Transplantation KW - Animals KW - Drug Resistance -- genetics KW - Transfection KW - Humans KW - Mice, Nude KW - Mice KW - Cell Line, Transformed KW - Gentamicins -- pharmacology KW - Oncogenes KW - Mesothelioma -- genetics KW - Mesothelioma -- pathology KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79025989?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-18 N1 - Date created - 1989-07-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characteristics of 2,3,7,8-tetrachlorodibenzo-p-dioxin induced endotoxin hypersensitivity: association with hepatotoxicity. AN - 79030546; 2472021 AB - Hepatic clearance is a major route of endotoxin detoxification. In the present study, the potential relationship between TCDD-induced endotoxin hypersensitivity and hepatotoxicity was examined. Acute doses of 50, 100, or 200 micrograms TCDD/kg body weight induced an endotoxin hypersensitive state in B6C3F1 mice as demonstrated by increased mortality 24-48 h following i.v. injection of endotoxin. This hypersensitive state occurred when endotoxin was administered 7 days following TCDD exposure, but not 1 day post-TCDD exposure. TCDD did not affect endogenous serum endotoxin levels. However, clearance of injected endotoxin was significantly inhibited following exposure to TCDD. Six hours post endotoxin treatment serum triglycerides were significantly increased in TCDD/endotoxin-treated mice compared to either treatment alone. Methylprednisolone and uridine were both examined in this model due to their roles in inflammation and RNA synthesis, respectively. Both compounds significantly reversed the mortality associated with the combined exposure. [3H]Uridine incorporation into liver was decreased following TCDD treatment alone, further suggesting impaired RNA synthesis. Studies performed on congenic mice indicate that the observed effects segregate with the Ah locus. The ability of methylprednisolone and uridine to reverse the mortality associated with TCDD/endotoxin treatment is consistent with an inflammatory response and impaired hepatic detoxification mechanisms. Thus, changes in hepatic handling of endotoxin, caused by progressive TCDD-induced liver dysfunction, may be responsible for the endotoxin hypersensitivity. JF - Toxicology AU - Rosenthal, G J AU - Lebetkin, E AU - Thigpen, J E AU - Wilson, R AU - Tucker, A N AU - Luster, M I AD - National Institute of Environmental Health Sciences, Systemic Toxicology Branch, Research Triangle Park, NC 27709. Y1 - 1989/06/16/ PY - 1989 DA - 1989 Jun 16 SP - 239 EP - 251 VL - 56 IS - 3 SN - 0300-483X, 0300-483X KW - Blood Glucose KW - 0 KW - Dioxins KW - Endotoxins KW - Lipids KW - Polychlorinated Dibenzodioxins KW - Receptors, Aryl Hydrocarbon KW - Receptors, Drug KW - RNA KW - 63231-63-0 KW - Alanine Transaminase KW - EC 2.6.1.2 KW - Methylprednisolone KW - X4W7ZR7023 KW - Index Medicus KW - Lipids -- blood KW - Receptors, Drug -- genetics KW - Animals KW - Drug Interactions KW - Blood Glucose -- metabolism KW - Mice KW - Blood Urea Nitrogen KW - RNA -- biosynthesis KW - Liver Diseases -- metabolism KW - Mice, Inbred DBA KW - Alanine Transaminase -- blood KW - Methylprednisolone -- pharmacology KW - Mice, Inbred C57BL KW - Female KW - Endotoxins -- metabolism KW - Chemical and Drug Induced Liver Injury KW - Polychlorinated Dibenzodioxins -- toxicity KW - Dioxins -- toxicity KW - Endotoxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79030546?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-25 N1 - Date created - 1989-07-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - No evidence for a role of alcohol or other psychoactive drugs in accelerating immunodeficiency in HIV-1-positive individuals. A report from the Multicenter AIDS Cohort Study. AN - 78995953; 2524608 AB - In a multicenter cohort study of homosexual men, the proportion of seropositives at enrollment who developed the acquired immunodeficiency syndrome (AIDS) during the following 18 months ranged from 5.5% to 8.2% in 1597 alcohol drinkers vs 9.2% in 109 nondrinkers with no clear trend according to use, and from 6.3% to 9.6% for 1662 users vs 7.2% for 83 nonusers of psychoactive drugs prior to enrollment. Among seropositive men with low initial T helper lymphocyte counts, those who continued to use drugs showed no significantly higher 18-month risk of AIDS than nonusers (13% vs 10%); the corresponding risks were 13% and 15%, respectively, for continued heavier vs continued lighter consumption of alcohol. No other manifestations of immunodeficiency were positively associated with substance use prior to enrollment. Prior use was not associated with low mean T helper cell counts at enrollment, and continued drug or alcohol use after enrollment was not associated with greater subsequent decline in counts. As used in a large cohort of homosexual men, psychoactive substances did not enhance the progression of human immunodeficiency virus infection. JF - JAMA AU - Kaslow, R A AU - Blackwelder, W C AU - Ostrow, D G AU - Yerg, D AU - Palenicek, J AU - Coulson, A H AU - Valdiserri, R O AD - National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1989/06/16/ PY - 1989 DA - 1989 Jun 16 SP - 3424 EP - 3429 VL - 261 IS - 23 SN - 0098-7484, 0098-7484 KW - Psychotropic Drugs KW - 0 KW - Ethanol KW - 3K9958V90M KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Multicenter Studies as Topic KW - Risk Factors KW - Humans KW - Cohort Studies KW - Acquired Immunodeficiency Syndrome -- immunology KW - Homosexuality KW - Time Factors KW - T-Lymphocytes, Helper-Inducer -- immunology KW - Male KW - Leukocyte Count KW - Ethanol -- adverse effects KW - HIV-1 -- immunology KW - Psychotropic Drugs -- adverse effects KW - HIV Seropositivity -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78995953?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-29 N1 - Date created - 1989-06-29 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: JAMA. 1990 Jan 19;263(3):371-3 [2322330] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Methylene blue for neutralization of heparin. AN - 79212111; 2781510 AB - Patients with protamine allergy present a difficult dilemma when reversal of heparin is required for excessive bleeding. Premedication with steroids and antihistamines has not been shown to effectively prevent anaphylactic reactions in patients with hypersensitivity to protamine. Other heparin antagonists are either not available or are too toxic for human use. This report describes a patient in whom methylene blue was used effectively to neutralize heparin and decrease bleeding due to heparinization. In vitro testing was then done to further define the interaction of heparin and methylene blue. This testing demonstrated that methylene blue neutralized heparin levels of 1 u/ml as well as 10 u/ml. Methylene blue acted as an anticoagulant when present at levels of 3000 micrograms/ml. However, it acted as a coagulant when present in intermediate levels of 800 micrograms/ml and 1600 micrograms/ml. The plasma levels necessary for neutralization of heparin levels of 1 unit/ml (the levels achieved in patient therapeutically anticoagulated) are easily achieved using doses routinely used in treatment of methemoglobinemia. Although the toxicity of methylene blue has been well defined at the lower doses of 2-4 mg/Kg, work still needs to be done to determine safety of the drug at the higher doses necessary to neutralize heparin levels achieved in bypass patients. JF - Thrombosis research AU - Sloand, E M AU - Kessler, C M AU - McIntosh, C L AU - Klein, H G AD - National Institutes of Health, Department of Transfusion Medicine, Bethesda, MD. Y1 - 1989/06/15/ PY - 1989 DA - 1989 Jun 15 SP - 677 EP - 686 VL - 54 IS - 6 SN - 0049-3848, 0049-3848 KW - Heparin Antagonists KW - 0 KW - Methylene Blue KW - T42P99266K KW - Index Medicus KW - Humans KW - Adult KW - Prothrombin Time KW - Female KW - Partial Thromboplastin Time KW - Methylene Blue -- pharmacology KW - Heparin Antagonists -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79212111?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-26 N1 - Date created - 1989-10-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cellular alterations and enhanced induction of cleft palate after coadministration of retinoic acid and TCDD. AN - 79030445; 2734792 AB - 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and retinoic acid (RA) are both teratogenic in mice. TCDD is a highly toxic, stable environmental contaminant, while RA is a naturally occurring form of vitamin A. Exposure to TCDD induces hydronephrosis and cleft palate, and exposure to RA induces limb defects and cleft palate. Teratology studies previously have shown that the incidence of clefting is higher after exposure to RA + TCDD than would be observed for the same doses of either compound given alone. This study examines the cellular effects which result in cleft palate, after po administration on gestation Day (GD) 10 or 12 of RA + TCDD in corn oil (10 ml/kg total volume). Exposure on GD 10 to 6 micrograms TCDD + 40 mg RA/kg inhibited early growth of the shelves and clefting was due to a failure of shelves to meet and fuse. This effect on mesenchyme was observed in previous studies to occur after exposure on GD 10 to 40 mg/kg RA alone, but not after TCDD alone. After exposure on GD 12 to 6 micrograms TCDD + 80 mg RA/kg, clefting was due to a failure of shelves to fuse after making contact, because the medial cells differentiated into an oral-like epithelium. This response was observed in previous studies to occur after exposure to TCDD alone, but RA alone on GD 12 resulted in differentiation toward nasal-like cells. The interaction between TCDD and RA results in RA-like clefting after exposure on GD 10 and TCDD-like clefting after exposure on GD 12, and this clefting occurs at higher incidences than would occur after the same levels of either agent alone. After exposure on either GD 10 or 12 to RA + TCDD, the programmed cell death of the medial cells does not occur, and these cells continue to express EGF receptors and to bind 125I-EGF. The effects of RA and TCDD may involve modulation of the cells responses to embryonic growth and differentiation factors. JF - Toxicology and applied pharmacology AU - Abbott, B D AU - Birnbaum, L S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/06/15/ PY - 1989 DA - 1989 Jun 15 SP - 287 EP - 301 VL - 99 IS - 2 SN - 0041-008X, 0041-008X KW - Dioxins KW - 0 KW - Iodine Radioisotopes KW - Polychlorinated Dibenzodioxins KW - Tritium KW - 10028-17-8 KW - Tretinoin KW - 5688UTC01R KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Receptor, Epidermal Growth Factor -- drug effects KW - Administration, Oral KW - Animals KW - Mice, Inbred C57BL KW - Mice KW - Drug Synergism KW - Autoradiography KW - Female KW - Pregnancy KW - Cleft Palate -- chemically induced KW - Cleft Palate -- pathology KW - Tretinoin -- toxicity KW - Polychlorinated Dibenzodioxins -- toxicity KW - Dioxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79030445?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-25 N1 - Date created - 1989-07-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - TCDD alters medial epithelial cell differentiation during palatogenesis. AN - 79028635; 2734791 AB - 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widely distributed, persistent environmental contaminant that is teratogenic in mice, where it induces hydronephrosis and cleft palate. The incidence of clefting has been shown to be dose dependent after exposure on either gestation Day (GD) 10 or 12, although the embryo is more susceptible on GD 12. TCDD-exposed palatal shelves meet but do not fuse, and programmed cell death of the medial epithelial cells is inhibited. The mechanism of action through which TCDD alters the program of medial cell development has not been examined in earlier studies, and it is not known whether the mechanism is the same regardless of the dose or developmental stage of exposure. In this study, C57BL/6N mice, a strain sensitive to TCDD, were dosed orally on GD 10 or 12 with 0, 6, 12, 24, or 30 micrograms/kg body wt, in 10 ml corn oil/kg. Embryonic palatal shelves were examined on GD 14, 15, or 16. The degree of palatal closure, epithelial surface morphology, and cellular ultrastructure, the incorporation of [3H]TdR, the expression of EGF receptors, and the binding of 125I-EGF were assessed. After exposure on GD 10 or 12, TCDD altered the differentiation pathway of the medial epithelial cells. The palatal shelves were of normal size and overall morphology, but fusion of the medial epithelia of the opposing shelves did not occur. TCDD prevented programmed cell death of the medial peridermal cells. The expression of EGF receptors by medial cells continued through Day 16 and the receptors were able to bind ligand. The medial cells differentiated into a stratified, squamous, keratinizing epithelium. The shift in phenotype to an oral-like epithelium occurred after exposure on either GD 10 or 12. At the lower dose (6 micrograms/kg), fewer cleft palates were produced, but those shelves which did respond had a fully expressed shift in differentiation. Whether the exposure begins on GD 10 or 12 or whether the dosing level produces only a few cleft palates within a litter, TCDD produced cleft palate by altering the differentiation program of the medial cells. JF - Toxicology and applied pharmacology AU - Abbott, B D AU - Birnbaum, L S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/06/15/ PY - 1989 DA - 1989 Jun 15 SP - 276 EP - 286 VL - 99 IS - 2 SN - 0041-008X, 0041-008X KW - Dioxins KW - 0 KW - Iodine Radioisotopes KW - Polychlorinated Dibenzodioxins KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Thymidine KW - VC2W18DGKR KW - Index Medicus KW - Administration, Oral KW - Animals KW - Receptor, Epidermal Growth Factor -- immunology KW - Cell Division -- drug effects KW - Mice KW - Pregnancy KW - Thymidine -- metabolism KW - Phenotype KW - Receptor, Epidermal Growth Factor -- drug effects KW - Mice, Inbred C57BL KW - Cell Differentiation -- drug effects KW - Female KW - Palate -- drug effects KW - Polychlorinated Dibenzodioxins -- toxicity KW - Palate -- cytology KW - Dioxins -- toxicity KW - Palate -- embryology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79028635?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-25 N1 - Date created - 1989-07-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of a selenocysteyl-tRNA(Ser) in mammalian cells that recognizes the nonsense codon, UGA. AN - 78988689; 2498338 AB - The presence of a unique opal suppressor seryl-tRNA in higher vertebrates which is converted to phosphoseryl-tRNA has been known for several years, but its function has been uncertain (see Hatfield, D. (1985) Trends Biochem. Sci. 10, 201-204 for review). In the present study, we demonstrate that this tRNA species also occurs in vivo as selenocysteyl-tRNA(Ser) suggesting that it functions both as a carrier molecule upon which selenocysteine is synthesized and as a direct selenocysteine donor to a growing polypeptide chain in response to specific UGA codons. [75Se]Seleno[3H]cysteyl-tRNA(Ser) formed by administering 75Se and [3H]serine to rat mammary tumor cells (TMT-081-MS) in culture was isolated from the cell extract. The amino acid attached to the tRNA was identified as selenocysteine following its deacylation and reaction with iodoacetate and 3-bromopropionate. The resulting alkyl derivatives co-chromatographed on an amino acid analyzer with authentic carboxymethylselenocysteine and carboxyethylselenocysteine. Seryl-tRNA(Ser) and phosphoseryl-tRNA(Ser) (Hatfield, D., Diamond, A., and Dudock, B. (1982) Proc. Natl. Acad. Sci. U. S. A. 79, 6215-6219), which co-migrate on a reverse phase chromatographic column with selenocysteyl-tRNA(Ser), were also identified in extracts of TMT-018-MS cells. Hence, we propose that a metabolic pathway for selenocysteine synthesis in mammalian cells is the conversion of seryl-tRNA(Ser) via phosphoseryl-tRNA(Ser) to selenocysteyl-tRNA(Ser). In a ribosomal binding assay selenocysteyl-tRNA(Ser) recognizes UGA but not any of the serine codons. Selenocysteyl-tRNA(Ser) is deacylated more readily than seryl-tRNA(Ser) (i.e. 58% deacylation during 15 min at pH 8.0 and 37 degrees C as compared to 41%). JF - The Journal of biological chemistry AU - Lee, B J AU - Worland, P J AU - Davis, J N AU - Stadtman, T C AU - Hatfield, D L AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/06/15/ PY - 1989 DA - 1989 Jun 15 SP - 9724 EP - 9727 VL - 264 IS - 17 SN - 0021-9258, 0021-9258 KW - Codon KW - 0 KW - RNA, Messenger KW - RNA, Transfer, Amino Acyl KW - RNA, Transfer, Ser KW - Selenium Radioisotopes KW - selenocysteinyl-tRNA KW - Tritium KW - 10028-17-8 KW - Serine KW - 452VLY9402 KW - Selenious Acid KW - F6A27P4Q4R KW - Selenium KW - H6241UJ22B KW - Index Medicus KW - Rats KW - Selenium -- metabolism KW - Ribosomes -- metabolism KW - Animals KW - Base Sequence KW - RNA, Transfer, Ser -- metabolism KW - Mammary Neoplasms, Experimental -- metabolism KW - Serine -- metabolism KW - RNA, Transfer, Ser -- genetics KW - Cell Line KW - RNA, Transfer, Amino Acyl -- metabolism KW - RNA, Transfer, Amino Acyl -- genetics KW - RNA, Transfer, Amino Acyl -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78988689?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-13 N1 - Date created - 1989-07-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human tumor infiltrating lymphocytes. Analysis of lymphokine mRNA expression and relevance to cancer immunotherapy. AN - 78979760; 2723437 AB - Tumor infiltrating lymphocytes (TIL) isolated from 12 patients with metastatic malignant melanoma, renal cell carcinoma, or breast adenocarcinoma were expanded in rIL-2 for 22 to 45 days (median 33 days) and analyzed for lymphokine mRNA expression and patterns of TCR gene rearrangement. All TIL cultures were significantly enriched for T cells, with CD3+ CD8+ cells predominant in 8 of 10 cases tested, and demonstrated an oligoclonal (rather than polyclonal) pattern of TCR gene rearrangement. Nine of 12 cultures could effectively lyse the autologous targets in short term chromium release assays. IL-2 expanded-TIL expressed mRNA for TNF-alpha and TNF-beta (lymphotoxin) and, in 5 of 9 (41%) cases, granulocyte/macrophage-colony stimulating factor mRNA but not IL-1 beta or IL-2 transcripts. Cultured TIL deprived of rIL-2 for 4 days did not constitutively express mRNA for any of the lymphokines tested. One long term TIL line in culture was followed and periodically tested for lytic activity and TNF-mRNA expression. Loss of the specific cytolytic but not proliferative activity at day 85 was associated with disappearance of TNF mRNA. Profiles of lymphokine secretion may provide a useful marker for functionally characterizing different T cell subsets and may provide correlates of the in vivo anti-tumor effects of these cells when TIL are adoptively transferred into cancer-bearing patients. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Belldegrun, A AU - Kasid, A AU - Uppenkamp, M AU - Topalian, S L AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/06/15/ PY - 1989 DA - 1989 Jun 15 SP - 4520 EP - 4526 VL - 142 IS - 12 SN - 0022-1767, 0022-1767 KW - Lymphokines KW - 0 KW - RNA, Messenger KW - Abridged Index Medicus KW - Index Medicus KW - Melanoma -- analysis KW - Kidney Neoplasms -- pathology KW - Kidney Neoplasms -- therapy KW - Humans KW - Kidney Neoplasms -- analysis KW - Gene Rearrangement KW - Nucleic Acid Hybridization KW - Phenotype KW - Carcinoma -- therapy KW - Melanoma -- pathology KW - Tumor Cells, Cultured KW - Carcinoma -- pathology KW - Carcinoma -- analysis KW - Cytotoxicity Tests, Immunologic KW - Melanoma -- therapy KW - Lymphocytes -- pathology KW - Cell Movement KW - Lymphokines -- metabolism KW - RNA, Messenger -- metabolism KW - Immunotherapy KW - Lymphokines -- genetics KW - Lymphocytes -- classification KW - Lymphocytes -- analysis KW - Neoplasms -- therapy KW - RNA, Messenger -- isolation & purification KW - Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78979760?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-06 N1 - Date created - 1989-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanism of lysis by large granular lymphocyte granule cytolysin: generation of a stable cytolysin-RBC intermediate. AN - 78978040; 2723433 AB - The effect of ionic strength and pH on the hemolytic activity of large granular lymphocyte granule cytolysin was examined in detail. Cytolysin-mediated lysis of RBC was inhibited by either low ionic strength or low pH. Under these conditions a nonlytic cytolysin-RBC intermediate was formed as revealed by hemolysis when cytolysin pretreated cells were washed and resuspended at physiologic ionic strength and pH. Formation of the cytolysin-RBC intermediate at low ionic strength (250 mM sucrose), pH 7.3, required greater than 0.1 mM calcium. In contrast, formation of the intermediate at physiologic ionic strength (150 mM NaCl), pH 6.0, was calcium independent. Both types of intermediates were stable at 37 degrees C and required calcium to induce subsequent lysis. The degree of lysis of the intermediate generated at low ionic strength was similar to that measured under standard conditions with the use of either whole granule preparations or purified cytolysin. However, lysis of intermediates formed at pH 6.0 was much less efficient. Our data indicate that a stable cytolysin-RBC intermediate can be formed in which cytolysin is present in an unreactive state on the RBC surface; under conditions of physiologic ionic strength and calcium concentrations this intermediate rapidly lyses. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Kuta, A E AU - Reynolds, C R AU - Henkart, P A AD - Experimental Immunology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/06/15/ PY - 1989 DA - 1989 Jun 15 SP - 4378 EP - 4384 VL - 142 IS - 12 SN - 0022-1767, 0022-1767 KW - Cytotoxins KW - 0 KW - Killer Factors, Yeast KW - Proteins KW - Calcium KW - SY7Q814VUP KW - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Osmolar Concentration KW - Animals KW - Rats, Inbred F344 KW - Hydrogen-Ion Concentration KW - Calcium -- physiology KW - Cell Communication KW - Cytotoxins -- isolation & purification KW - Cytotoxicity, Immunologic KW - Cytotoxins -- physiology KW - Hemolysis KW - Cytoplasmic Granules -- physiology KW - Cytoplasmic Granules -- immunology KW - Erythrocytes -- physiology KW - Killer Cells, Natural -- physiology KW - Proteins -- physiology KW - Killer Cells, Natural -- immunology KW - Erythrocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78978040?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-06 N1 - Date created - 1989-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prognostic variables in recurrent limb melanoma treated with hyperthermic antiblastic perfusion. AN - 78969374; 2720604 AB - Between October 1969 and December 1986, 136 patients with recurrent limb melanoma were treated with hyperthermic antiblastic perfusion (HAP). This retrospective analysis is aimed at identifying tumor-related and treatment-related variables likely to influence tumor response, locoregional control, disease-free survival, and overall survival. Independent factors predicting a complete response (CR) were the number of lesions (P less than 0.0001) and the minimum tumor temperature (minT) (P = 0.03). Only a positive trend was observed for the drug dose (P = 0.08). However, the proportion of CR was significantly higher (57.7%; P = 0.02) in patients who had a minT of 41.5 degrees C or greater and who were given a dose equal to or greater than the standard dose than in patients treated with lower temperatures and/or lower drug doses. The occurrence of a CR significantly increased the rates of locoregional control (77%; P = 0.007), disease-free survival (55.6%; P = 0.006), and overall survival (68.6%; P = 0.03). Treatment optimization may provide further therapeutic improvements by increasing the incidence of CR. However, the overall survival rates also were influenced by the number of lesions (P = 0.0014), sex (P = 0.04), and the number of previous relapses (P = 0.01). Therefore, tumor aggressiveness also is crucial in determining the outcome of the disease, and only early treatment with HAP can reduce the risk of distant metastases. JF - Cancer AU - Di Filippo, F AU - Calabrò, A AU - Giannarelli, D AU - Carlini, S AU - Cavaliere, F AU - Moscarelli, F AU - Cavaliere, R AD - III Department of Surgery, Regina Elena National Cancer Institute, Rome, Italy. Y1 - 1989/06/15/ PY - 1989 DA - 1989 Jun 15 SP - 2551 EP - 2561 VL - 63 IS - 12 SN - 0008-543X, 0008-543X KW - Melphalan KW - Q41OR9510P KW - Abridged Index Medicus KW - Index Medicus KW - Neoplasm Staging KW - Lymphatic Metastasis KW - Humans KW - Retrospective Studies KW - Prognosis KW - Aged KW - Extremities KW - Prospective Studies KW - Aged, 80 and over KW - Adult KW - Melphalan -- therapeutic use KW - Middle Aged KW - Neoplasm Recurrence, Local KW - Female KW - Male KW - Remission Induction KW - Melanoma -- mortality KW - Melanoma -- secondary KW - Hyperthermia, Induced KW - Skin Neoplasms -- therapy KW - Melanoma -- therapy KW - Chemotherapy, Cancer, Regional Perfusion -- methods KW - Chemotherapy, Cancer, Regional Perfusion -- adverse effects KW - Skin Neoplasms -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78969374?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-06 N1 - Date created - 1989-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Case-control study of colorectal cancer and fecal mutagenicity. AN - 78953247; 2655896 AB - Fecal mutagenicity was measured in 68 patients with colorectal cancer and in 114 controls, using Salmonella tester strains TA98 and TA100 with and without S9 activation. Samples were also tested for fecapentaenes by high-performance liquid chromatography, to permit the separation of fecapentaene and non-fecapentaene mutagenicity. Overall, no significant case-control differences in fecal mutagenicity were observed. However, when samples containing high concentrations of fecapentaenes were excluded, non-fecapentaene TA98 mutagenicity was observed in eight cases (12%) and only four controls (4%), resulting in an estimated relative risk of 4.4 (95% confidence interval = 1.0-21.1). The association of colorectal cancer risk with non-fecapentaene TA98 mutagenicity could not be explained as an artifact of diagnostic workup or gastrointestinal bleeding among the cases. Smoking could also be excluded as a source of the TA98 mutagenicity seen, but possible dietary origins are still being explored. JF - Cancer research AU - Schiffman, M H AU - Andrews, A W AU - Van Tassell, R L AU - Smith, L AU - Daniel, J AU - Robinson, A AU - Hoover, R N AU - Rosenthal, J AU - Weil, R AU - Nair, P P AD - Epidemiology and Biostatistics Program, Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/06/15/ PY - 1989 DA - 1989 Jun 15 SP - 3420 EP - 3424 VL - 49 IS - 12 SN - 0008-5472, 0008-5472 KW - Mutagens KW - 0 KW - Index Medicus KW - Reference Values KW - Mutagenicity Tests KW - Humans KW - Salmonella typhimurium -- drug effects KW - Rectal Neoplasms -- physiopathology KW - Feces -- analysis KW - Adenocarcinoma -- physiopathology KW - Colonic Neoplasms -- physiopathology KW - Mutagens -- analysis KW - Mutagens -- isolation & purification KW - Mutagens -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78953247?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-06 N1 - Date created - 1989-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Forskolin stimulates pinealocyte cGMP accumulation. Dramatic potentiation by an alpha 1-adrenergic----[Ca2+]i mechanism involving protein kinase C. AN - 79049158; 2544448 AB - The effect of forskolin on cGMP regulation was investigated using dispersed rat pinealocytes. Forskolin stimulated cGMP accumulation in a concentration-dependent manner; this response was strongly potentiated by an alpha 1-adrenergic----[Ca2+]i mechanism involving protein kinase C. These findings provide further evidence that activation of two receptor-regulated signal transduction mechanisms may be commonly required for maximal stimulation of cGMP accumulation, and establish a new experimental approach to the study of cGMP regulation. JF - FEBS letters AU - Ho, A K AU - Chik, C L AU - Klein, D C AD - Section on Neuroendocrinology, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1989/06/05/ PY - 1989 DA - 1989 Jun 05 SP - 207 EP - 212 VL - 249 IS - 2 SN - 0014-5793, 0014-5793 KW - Cations, Divalent KW - 0 KW - Receptors, Adrenergic, alpha KW - Colforsin KW - 1F7A44V6OU KW - Phenylephrine KW - 1WS297W6MV KW - Calcimycin KW - 37H9VM9WZL KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinase C KW - EC 2.7.11.13 KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Cyclic GMP KW - H2D2X058MU KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Potassium KW - RWP5GA015D KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Dose-Response Relationship, Drug KW - Enzyme Activation KW - Adenylyl Cyclases -- metabolism KW - Calcimycin -- pharmacology KW - Rats KW - Rats, Inbred Strains KW - Cyclic AMP -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Potassium -- pharmacology KW - Female KW - Phenylephrine -- pharmacology KW - Protein Kinase C -- metabolism KW - Calcium -- metabolism KW - Pineal Gland -- metabolism KW - Cyclic GMP -- metabolism KW - Colforsin -- pharmacology KW - Pineal Gland -- cytology KW - Receptors, Adrenergic, alpha -- metabolism KW - Pineal Gland -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79049158?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-28 N1 - Date created - 1989-07-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Site-directed mutagenesis of beta-adrenergic receptors. Identification of conserved cysteine residues that independently affect ligand binding and receptor activation. AN - 78993608; 2542304 AB - Using site-directed mutagenesis of the human beta 2-adrenergic receptor and continuous expression in B-82 cells, the role of 3 conserved cysteines in transmembrane domains and 2 conserved cysteines in the third extracellular domain in receptor function was examined. Cysteine was replaced with serine in each mutant receptor as this amino acid is similar to cysteine in size but it cannot form disulfide linkages. Replacement of cysteine residues 77 and 327, in the second and seventh transmembrane-spanning domains, respectively, had no effect on ligand binding or the ability of the receptor to mediate isoproterenol stimulation of adenylate cyclase. Substitution of cysteine 285, in the sixth transmembrane domain of the receptor, produced a mutant receptor with normal ligand-binding properties but a significantly attenuated ability to mediate stimulation of adenylate cyclase. Mutation of cysteine residues 190 and 191, in the third extracellular loop of the beta 2 receptor, had qualitatively similar effects on ligand binding and isoproterenol-mediated stimulation of adenylate cyclase. Replacement of either of these residues with serine produced mutant receptors that displayed a marked loss in affinity for both beta-adrenergic agonists and antagonists. Replacement of both cysteine 190 and 191 with serine had an even greater effect on the ability of the receptor to bind ligands. Consistent with the loss of Ser190 and/or Ser191 mutant receptor affinity for agonists was a corresponding shift to the right in the dose-response curve for isoproterenol-induced increases in intracellular cyclic AMP concentrations in cells expressing the mutant receptors. These data implicate one of the conserved transmembrane cysteine residues in the human beta 2-adrenergic receptor in receptor activation by agonists and also suggest that conserved cysteine residues in an extracellular domain of the receptor may be involved in ligand binding. JF - The Journal of biological chemistry AU - Fraser, C M AD - Section of Receptor Biochemistry and Molecular Biology, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892. Y1 - 1989/06/05/ PY - 1989 DA - 1989 Jun 05 SP - 9266 EP - 9270 VL - 264 IS - 16 SN - 0021-9258, 0021-9258 KW - Membrane Proteins KW - 0 KW - Receptors, Adrenergic, beta KW - Serine KW - 452VLY9402 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Cysteine KW - K848JZ4886 KW - Index Medicus KW - Animals KW - L Cells (Cell Line) -- metabolism KW - Humans KW - L Cells (Cell Line) -- physiology KW - Amino Acid Sequence KW - GTP-Binding Proteins -- physiology KW - Mice KW - Membrane Proteins -- genetics KW - Serine -- genetics KW - Cloning, Molecular KW - Extracellular Space -- physiology KW - Extracellular Space -- metabolism KW - GTP-Binding Proteins -- metabolism KW - Molecular Sequence Data KW - Receptors, Adrenergic, beta -- genetics KW - Cysteine -- genetics KW - Receptors, Adrenergic, beta -- physiology KW - Mutation KW - Signal Transduction KW - Cysteine -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78993608?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-05 N1 - Date created - 1989-07-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transcription of Xenopus selenocysteine tRNA Ser (formerly designated opal suppressor phosphoserine tRNA) gene is directed by multiple 5'-extragenic regulatory elements. AN - 78987815; 2524488 AB - A tRNA gene whose product is aminoacylated with serine and the serine moiety is then phosphorylated to form phosphoseryl-tRNA (see Hatfield, D. (1985) Trends Biochem. Sci. 10, 201-204 for review) has now been shown to form selenocysteyl-tRNA; hence the corresponding gene is designated as selenocysteine tRNA Ser (B. J. Lee, P. J. Worland, J. N. Davis, T. C. Stadtman, and D. Hatfield (1989) J. Biol. Chem. 264, in press). In the present study, we show that the expression of this unique tRNA gene is governed by at least three upstream regulatory elements. In initial studies, the relative efficiencies of transcription of the human, rabbit, chicken, and Xenopus selenocysteine tRNA genes were compared in vivo in Xenopus oocytes and in vitro in HeLa cell extracts. The Xenopus gene was severalfold more actively expressed, both in vivo and in vitro, than the human and rabbit genes, whereas the chicken gene was poorly expressed. Exchange of the 5'-flanking regions of the Xenopus and chicken genes, which have identical gene sequences, reversed their levels of transcription, demonstrating that a regulatory site or sites exist upstream of these genes. Deletion-substitution mutants in the Xenopus gene and its 5'-flanking sequence show in in vitro assays that 1) the level of transcription is reduced substantially when a GC-rich stretch that is immediately upstream of a TATA box in the -30 region is removed; 2) the level of transcription is virtually abolished when the TATA box is removed; and 3) deletions up to and further upstream of the GC-rich region do not affect the level of transcription. The same deletions, when used in in vivo assays, demonstrate a step-down in expression with the deletion removing the GC-rich region, a further step-down in expression with the deletion removing the TATA box, but the most pronounced reduction in expression was observed with a deletion removing an AT-rich region between nucleotides -62 and -76. Thus, a regulatory site was identified in vivo which was not detected in vitro, and transcription of the selenocysteine tRNA Ser gene is determined by multiple upstream regulatory elements. JF - The Journal of biological chemistry AU - Lee, B J AU - Kang, S G AU - Hatfield, D AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/06/05/ PY - 1989 DA - 1989 Jun 05 SP - 9696 EP - 9702 VL - 264 IS - 16 SN - 0021-9258, 0021-9258 KW - RNA, Transfer, Amino Acid-Specific KW - 0 KW - RNA, Transfer, Ser KW - Selenocysteine KW - 0CH9049VIS KW - RNA Polymerase III KW - EC 2.7.7.6 KW - Selenium KW - H6241UJ22B KW - Cysteine KW - K848JZ4886 KW - Index Medicus KW - Animals KW - Chromosome Deletion KW - Chickens KW - Base Sequence KW - Genes KW - Humans KW - Molecular Sequence Data KW - Rabbits KW - Amino Acid Sequence KW - Mutation KW - Xenopus -- genetics KW - Selenium -- metabolism KW - Regulatory Sequences, Nucleic Acid KW - Cysteine -- metabolism KW - RNA, Transfer, Ser -- metabolism KW - RNA, Transfer, Amino Acid-Specific -- genetics KW - Transcription, Genetic KW - RNA, Transfer, Ser -- isolation & purification KW - RNA, Transfer, Ser -- genetics KW - Cysteine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78987815?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-05 N1 - Date created - 1989-07-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Results of a randomized trial comparing BCNU plus radiotherapy, streptozotocin plus radiotherapy, BCNU plus hyperfractionated radiotherapy, and BCNU following misonidazole plus radiotherapy in the postoperative treatment of malignant glioma. AN - 85285132; pmid-2542193 AB - In Brain Tumor Cooperative Group Study 77-02, eleven institutions randomized 603 adult patients with supratentorial malignant glioma to one of four treatment groups following surgery: conventional radiotherapy (6000 cGy in 30-35 fractions) + BCNU, conventional radiotherapy + streptozotocin, hyperfractionated (twice daily) radiotherapy (6600 cGy in 60 fractions) + BCNU, and conventional radiotherapy with misonidazole followed by BCNU. Data were analyzed for the total randomized population and for the 557 patients (86% with glioblastoma multiforme) who met protocol eligibility specifications (including confirmed histopathology on central review). Median survival was approximately 10 months following randomization. Overall there was no statistically significant difference in survival among the four groups. Among non-glioblastoma patients, the misonidazole group appeared to have poor survival. Peripheral neuropathy was a dose-limiting toxicity with misonidazole. It is concluded that neither the addition of misonidazole nor hyperfractionated radiotherapy as given in this protocol offered any advantage over conventional radiotherapy plus either BCNU or streptozotocin for treatment of malignant glioma. JF - International Journal of Radiation Oncology, Biology, Physics AU - Deutsch, M AU - Green, S B AU - Strike, T A AU - Burger, P C AU - Robertson, J T AU - Selker, R G AU - Shapiro, W R AU - Mealey, J AU - Ransohoff, J AU - Paoletti, P AD - Clinical and Diagnostic Trials Section, Biometry Branch, NCI, Bethesda, MD 20892. PY - 1989 SP - 1389 EP - 1396 VL - 16 IS - 6 SN - 0360-3016, 0360-3016 KW - Glioblastoma KW - Support, U.S. Gov't, P.H.S. KW - Astrocytoma KW - Random Allocation KW - Combined Modality Therapy KW - Human KW - Carmustine KW - Prognosis KW - Aged KW - Streptozocin KW - Supratentorial Neoplasms KW - Comparative Study KW - Radiotherapy Dosage KW - Adult KW - Multicenter Studies KW - Misonidazole KW - Middle Age KW - Glioma KW - Adolescent UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85285132?accountid=14244 LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Habituation and maternal encouragement of attention in infancy as predictors of toddler language, play, and representational competence. AN - 85164807; pmid-2737021 AB - In a longitudinal study, infants' habituation and mothers' encouragement of attention were assessed at 5 months, and toddlers' language comprehension, language production, and pretense play and mothers' encouragement of attention were assessed at 13 months. Structural equation modeling was used to examine the unique contributions of infant habituation and maternal stimulation to toddlers' cognitive abilities. Habituation predicted language comprehension, pretense play, and a latent variable of language and play after the influences of both 5- and 13-month maternal encouragement of attention were partialed. Likewise, early maternal encouragement of attention explained unique variance in toddlers' language comprehension and the language-and-play latent variable after infant habituation was controlled. These findings indicate that links between early habituation and later cognitive development are direct and not solely mediated by maternal stimulation, and that maternal stimulation of young infants influences the development of children's representational competence over and above infants' own information-processing abilities. JF - Child Development AU - Tamis-LeMonda, C S AU - Bornstein, M H AD - National Institute of Child Health and Human Development, Bethesda, MD 20892. PY - 1989 SP - 738 EP - 751 VL - 60 IS - 3 SN - 0009-3920, 0009-3920 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85164807?accountid=14244 LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Effects of sodium bromate on ionic concentrations and osmolalities of the cochlear fluids in guinea pigs. AN - 85142890; pmid-2753829 AB - Effects of sodium bromate on cochlear potentials and electrolyte composition of the cochlear fluids in guinea pigs were investigated following administration of sodium bromate into the cochlea, using perilymphatic perfusion. Cochlear microphonics and the whole nerve action potential of the auditory nerve were markedly suppressed. The K+ and Cl- activities in the endolymph as well as the endocochlear dc potential (EP) decreased significantly and irreversibly, in proportion to the concentration of sodium bromate. A negative EP never developed during the monitoring of 120 min. Microsamples of the endolymph showed substantial decreases of K+ and Cl- concentrations and an increase in the concentration of Na+. Osmolality of the endolymph was much lower than that of the perilymph. The severe edema of the stria vascularis and collapse of Reissner's membrane were histologically evident. These events suggest a breakdown of the endolymph-perilymph barrier, coincident with an inhibition of the strial active transport, as a result of the ototoxic action of sodium bromate. The possible ion and water movement across the endolymph-perilymph barrier in the presence of sodium bromate is discussed. JF - Hearing Research AU - Muratsuka, Y AU - Ueda, H AU - Konishi, T AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina. PY - 1989 SP - 241 EP - 249 VL - 39 IS - 3 SN - 0378-5955, 0378-5955 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85142890?accountid=14244 LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - The uniform carcinogenic action of alkylnitrosoureas in Syrian hamsters. AN - 79355237; 2590502 AB - The carcinogenic effects of a number of alkylnitrosoureas in Syrian golden hamsters have been compared by administering them by gavage as solutions in corn oil/ethyl acetate. The compounds were methyl-, ethyl-, 2-hydroxyethyl-, 2-oxopropyl-, and 2-phenylethylnitrosourea and the dialkylnitrosoureas dimethyl- and diethylnitrosourea, ethylnitrosohydroxyethylurea, ethylnitroso-2-oxopropylurea, 2-oxopropylnitrosochloroethylurea, and hydroxyethylnitrosoethylurea. All were given at approximately equimolar doses and, in most cases, to male and female hamsters. Most of the hamsters died with tumors associated with the treatments. Methylnitrosourea, ethylnitrosourea, and hydroxyethylnitrosourea, but not oxopropylnitrosourea, gave rise to a high incidence of tumors of the forestomach, while the dialkylnitrosoureas produced smaller numbers of forestomach tumors. All of the alkylnitrosoureas induced hemangiosarcomas of the spleen, which was the most common tumor produced by these carcinogens. Tumors of other types were uncommon, except that ethylnitrosourea and ethylnitrosohydroxyethylurea induced tumors of the cervix in about half of the animals and ethylnitrosooxopropylurea induced some nervous system tumors. The small number of common target organs of alkylnitrosoureas in hamsters contrasted sharply with the broad spectrum of tumors they induced in rats, depending on the nature of the alkyl groups, and with a quite different order of potency in the latter species. JF - Biomedical and environmental sciences : BES AU - Lijinsky, W AU - Kovatch, R M AD - BRI-Basic Research Program, NCI-Frederick Cancer Research Facility, Frederick 21701. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 167 EP - 173 VL - 2 IS - 2 SN - 0895-3988, 0895-3988 KW - Carcinogens KW - 0 KW - Nitrosourea Compounds KW - Index Medicus KW - Animals KW - Carcinogenicity Tests KW - Mesocricetus KW - Male KW - Female KW - Cricetinae KW - Nitrosourea Compounds -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79355237?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-25 N1 - Date created - 1990-01-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenesis by nitrosamines and azoxyalkanes by different routes of administration to rats. AN - 79353865; 2590501 AB - The effects of administering similar doses of some simple alkylating agents to rats by different regimens have been compared. Two of the compounds were methylating agents, nitrosodimethylamine and azoxymethane; two were ethylating agents, nitrosodiethylamine and azoxyethane; and nitrosomethylethylamine was both a methylating and an ethylating agent. The treatments gave rise to tumors in almost all treated rats. The results indicate the importance of pharmacokinetics in determining which organs are the targets of the alkylating carcinogens. JF - Biomedical and environmental sciences : BES AU - Lijinsky, W AU - Kovatch, R M AD - NCI-Frederick Cancer Research Facility, BRI-Basic Research Program, Maryland 21701. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 154 EP - 159 VL - 2 IS - 2 SN - 0895-3988, 0895-3988 KW - Alkylating Agents KW - 0 KW - Azo Compounds KW - Nitrosamines KW - Index Medicus KW - Rats KW - Administration, Oral KW - Animals KW - Rats, Inbred F344 KW - Sex Factors KW - Intubation, Gastrointestinal KW - Carcinogenicity Tests KW - Male KW - Female KW - Administration, Intravesical KW - Nitrosamines -- administration & dosage KW - Nitrosamines -- toxicity KW - Azo Compounds -- administration & dosage KW - Azo Compounds -- toxicity KW - Alkylating Agents -- toxicity KW - Alkylating Agents -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79353865?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-25 N1 - Date created - 1990-01-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of colloidal gold cytochemistry in the study of the basic cell biology of cancer. AN - 79200753; 2570523 AB - We are currently investigating the morphologic aspects of two areas of the basic cell biology of cancer: tumor-specific surface antigens as targets for immunotoxins, and the phenomenon of multidrug resistance in chemotherapy of human tumors. Colloidal gold cytochemistry has provided a useful method for the electron-microscopic cytochemical detection of materials endocytosed by cells in culture. This technique has been used to study the internalization pathway of ligands bound to the surface of cancer cells, particularly antibodies for use as immunologic targeting reagents for the construction of immunotoxins. These colloidal gold conjugates with monoclonal antibodies have demonstrated the internalization of these immunologic reagents through coated pits and receptosomes, which is a necessary step in the delivery of immunotoxins into the cell where they can mediate their cell-killing functions. Morphologic methods have been employed for the screening and selection of monoclonal antibodies reactive with the surface of human ovarian cancer cells for use as immunotoxins and have demonstrated the in vivo activity of immunotoxins made with these antibodies and Pseudomonas exotoxin in a nude mouse model system. In other studies, we have employed such reagents for the immunocytochemical detection of the surface expression of P170, the cell-surface efflux pump protein responsible for the phenotype of multidrug resistance in tumor cells, and to investigate the distribution of this protein by using immunocytochemistry in normal human tissues. These results have suggested a role for P170 in normal cell membrane transport of metabolites in various organ systems. JF - The American journal of anatomy AU - Willingham, M C AD - Ultrastructural Cytochemistry Section, National Cancer Institute, Bethesda, Maryland 20892. PY - 1989 SP - 109 EP - 127 VL - 185 IS - 2-3 SN - 0002-9106, 0002-9106 KW - Clathrin KW - 0 KW - Immunotoxins KW - Epidermal Growth Factor KW - 62229-50-9 KW - Gold KW - 7440-57-5 KW - Horseradish Peroxidase KW - EC 1.11.1.- KW - Index Medicus KW - Endosomes -- physiology KW - Horseradish Peroxidase -- pharmacokinetics KW - Endosomes -- ultrastructure KW - Endocytosis KW - Clathrin -- metabolism KW - Humans KW - Temperature KW - Drug Resistance KW - Microinjections KW - Immunotoxins -- metabolism KW - Endosomes -- metabolism KW - Epidermal Growth Factor -- pharmacokinetics KW - Neoplasms -- pathology KW - Neoplasms -- physiopathology KW - Immunohistochemistry -- methods KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79200753?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-26 N1 - Date created - 1989-09-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pharmacokinetics of subcutaneous azidothymidine in rhesus monkeys. AN - 79157708; 2764527 AB - The pharmacokinetics of subcutaneous bolus and continuous infusion azidothymidine (AZT) was studied in rhesus monkeys. Three animals received 100 mg/m2 as a bolus injection both intravenously and subcutaneously, with the order of administration randomly determined. Two animals received a continuous subcutaneous infusion of 25 mg/m2 per h for 12 or 24 h. AZT was measured in plasma by a reverse-phase high-pressure liquid chromatographic assay. Following intravenous bolus administration, AZT elimination was rapid, with a mean half-life of 1.2 h and a mean clearance of 318 ml/min per m2 (range, 200 to 441 ml/min per m2). The bolus subcutaneous dose was rapidly (time to peak concentration, 15 to 30 min) and nearly completely (fraction absorbed, 92%) absorbed without evidence of local tissue toxicity. With continuous subcutaneous infusion of AZT, the steady state was attained within 4 h and steady-state concentrations in plasma in the two animals exceeded 3.0 mumol/liter. No local tissue toxicity was observed at the infusion site. The subcutaneous route may be a practical alternative to intravenous administration of AZT and deserves further clinical study. JF - Antimicrobial agents and chemotherapy AU - Balis, F M AU - McCully, C AU - Gough, L AU - Pizzo, P A AU - Poplack, D G AD - Pediatric Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 810 EP - 812 VL - 33 IS - 6 SN - 0066-4804, 0066-4804 KW - Zidovudine KW - 4B9XT59T7S KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Injections, Intravenous KW - Injections, Subcutaneous KW - Macaca mulatta KW - Male KW - Biological Availability KW - Zidovudine -- pharmacokinetics KW - Zidovudine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79157708?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-21 N1 - Date created - 1989-09-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: N Engl J Med. 1987 Jul 23;317(4):185-91 [3299089] Cancer. 1988 Jul 15;62(2):407-11 [2454724] N Engl J Med. 1988 Oct 6;319(14):889-96 [3166511] J Clin Oncol. 1988 Dec;6(12):1882-6 [3199171] Clin Pharmacol Ther. 1987 Apr;41(4):407-12 [3549120] Lancet. 1976 Dec 11;2(7998):1278-80 [63749] J Pharm Sci. 1982 Mar;71(3):372-3 [7069605] Proc Natl Acad Sci U S A. 1985 Oct;82(20):7096-100 [2413459] Ann Intern Med. 1989 Feb 15;110(4):279-85 [2643914] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Regulation of mouse CYP1A1 gene expression by dioxin: requirement of two cis-acting elements during induction. AN - 79140276; 2548080 AB - The mouse cytochrome P1450 (CYP1A1) gene is responsible for the metabolism of numerous carcinogens and toxic chemicals. Induction by the environmental contaminant tetrachlorodibenzo-p-dioxin (TCDD) requires a functional aromatic hydrocarbon (Ah) receptor. We examined the 5'-flanking region of the CYP1A1 gene in mouse hepatoma Hepa-1 wild-type cells and a mutant line having a defect in chromatin binding of the TCDD-receptor complex. We identified two cis-acting elements (distal, -1071 to -901 region; proximal, -245 to -50 region) required for constitutive and TCDD-inducible CYP1A1 gene expression. Three classes of DNA-protein complexes binding to the distal element were identified: class I, found only in the presence of TCDD and a functional Ah receptor, that was heat labile and not competed against by simian virus 40 (SV40) early promoter DNA; class II, consisting of at least three constitutive complexes that were heat stable and bound to SV40 DNA; and class III, composed of at least three constitutive complexes that were thermolabile and were not competed against by SV40 DNA. Essential contacts for these proteins were centered at -993 to -990 for the class I complex, -987, -986, or both for the class II complexes, and -938 to -927 for the class III complexes. The proximal element was absolutely essential for both constitutive and TCDD-inducible CYP1A1 gene expression, and at least two constitutive complexes bound to this region. These data are consistent with the proximal element that binds proteins being necessary but not sufficient for inducible gene expression; interaction of these proteins with those at the distal element was found to be required for full CYP1A1 induction by TCDD. JF - Molecular and cellular biology AU - Neuhold, L A AU - Shirayoshi, Y AU - Ozato, K AU - Jones, J E AU - Nebert, D W AD - Laboratory of Developmental Pharmacology, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 2378 EP - 2386 VL - 9 IS - 6 SN - 0270-7306, 0270-7306 KW - DNA-Binding Proteins KW - 0 KW - Dioxins KW - Oligonucleotides KW - Polychlorinated Dibenzodioxins KW - Receptors, Drug KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - Animals KW - Chromosome Deletion KW - Simian virus 40 -- genetics KW - Mice KW - Plasmids KW - Oligonucleotides -- metabolism KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Hot Temperature KW - Receptors, Drug -- metabolism KW - Base Sequence KW - Transfection KW - Binding, Competitive KW - Molecular Sequence Data KW - Oligonucleotides -- chemical synthesis KW - Methylation KW - Cell Line KW - DNA-Binding Proteins -- metabolism KW - Regulatory Sequences, Nucleic Acid KW - Cytochrome P-450 Enzyme System -- genetics KW - Polychlorinated Dibenzodioxins -- pharmacology KW - Dioxins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79140276?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-21 N1 - Date created - 1989-09-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 1982 Dec;42(12):5030-7 [6291746] Cell. 1986 Dec 5;47(5):777-84 [3096578] DNA. 1986 Oct;5(5):403-11 [3023000] Mol Cell Biol. 1986 Jan;6(1):218-26 [3023824] Mol Cell Biol. 1986 Dec;6(12):4168-78 [3025641] Mol Cell Biol. 1986 Dec;6(12):4305-16 [3025651] Cell. 1987 Apr 10;49(1):19-27 [3030565] Nature. 1987 Jun 4-10;327(6121):369-70 [3587357] Nature. 1987 Jun 11-17;327(6122):464-6 [3295564] Nucleic Acids Res. 1987 May 26;15(10):4179-91 [3588289] Annu Rev Biochem. 1987;56:945-93 [3304150] Mol Cell Biol. 1987 Dec;7(12):4542-8 [3501825] Proc Natl Acad Sci U S A. 1988 Apr;85(8):2528-32 [2833743] Basic Life Sci. 1988;43:45-64 [2896496] Proc Natl Acad Sci U S A. 1988 Aug;85(16):5859-63 [3413062] Cell. 1988 Sep 23;54(7):1033-42 [3416354] Cell. 1988 Sep 23;54(7):1043-51 [3416355] Cell. 1988 Sep 23;54(7):931-42 [2843293] Cell. 1988 Sep 23;54(7):943-53 [2843294] J Biol Chem. 1988 Nov 25;263(33):17221-4 [2846558] Genes Dev. 1988 Jul;2(7):801-6 [3061875] DNA. 1989 Jan-Feb;8(1):1-13 [2651058] Int J Biochem. 1989;21(3):243-52 [2545475] J Virol. 1979 Aug;31(2):360-9 [225559] J Biol Chem. 1979 Nov 10;254(21):11015-23 [500620] Methods Enzymol. 1980;65(1):499-560 [6246368] Cell. 1980 Jun;20(2):269-81 [6248238] J Biol Chem. 1982 Jun 10;257(11):6402-7 [6896205] Annu Rev Pharmacol Toxicol. 1982;22:517-54 [6282188] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] J Biol Chem. 1984 May 10;259(9):5400-2 [6715350] Mol Pharmacol. 1984 Jul;26(1):117-21 [6749129] J Biol Chem. 1984 Oct 25;259(20):12357-63 [6490616] J Biol Chem. 1985 Feb 10;260(3):1790-5 [3968086] Nucleic Acids Res. 1985 Oct 25;13(20):7269-88 [2997746] Nucleic Acids Res. 1986 Feb 11;14(3):1465-77 [3456557] Proc Natl Acad Sci U S A. 1986 May;83(9):2802-6 [3010318] Cell. 1986 Aug 29;46(5):705-16 [3091258] Nature. 1986 Aug 21-27;322(6081):697-701 [3018583] Nature. 1986 Aug 21-27;322(6081):750-2 [3748156] Dev Biol. 1973 Nov;35(1):83-96 [4362668] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Occurrence and relevance of chemically induced benign neoplasms in long-term carcinogenicity studies. AN - 79130864; 2667783 AB - Recent carcinogenicity studies conducted and evaluated by the National Toxicology Program/National Institute of Environmental Health Sciences were examined to determine the frequency of chemically increased incidences of neoplasia. Many of the chemicals originally selected for study were chosen because of an a priori suggestion that they might be carcinogens. Of the 143 chemical studies evaluated, usually involving male and female rats and mice, 42 (29%) did not induce any neoplasms, 20 (14%) gave marginal or equivocal neoplastic responses, and 81 (57%) showed positive neoplastic responses in one or more of the 524 species-gender experiments. Of these 81 positive studies, 60 (74%) were considered positive based on malignant neoplasia, 16 (20%) were positive due primarily to benign neoplasia, but had supporting evidence of malignant neoplasia in the same organ/tissue, and 5 (6%) were positive based only on benign neoplasia. These five chemicals are a) allyl isothiocyanate (transitional cell papillomas of the urinary bladder in male rats), b) 2-amino-4-nitrophenol (tubular cell adenomas of the kidney in male rats), c) asbestos intermediate range chrysotile (adenomatous polyps of the large intestine in male rats), d) decabromodiphenyl oxide (neoplastic nodules of the liver in male and female rats), and e) nitrofurazone (fibroadenomas of the mammary gland in female rats and benign mixed tumors and granulosa cell tumors of the ovary in female mice). For all but one of these lesions (mammary gland), the occurrence in historic controls is low. Thus, only 5 of the 143 chemicals studied (3.5%) induced benign neoplasia alone, and those observed benign neoplasms are known to progress to malignancy. Accordingly, we consider chemically induced benign neoplasia to be an important indicator of a chemical's carcinogenic potential in rodents, and believe it should continue to be made an integral part of the overall weight-of-the-evidence evaluation process for identifying potential human health hazards. JF - Cancer metastasis reviews AU - Huff, J E AU - Eustis, S L AU - Haseman, J K AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 1 EP - 22 VL - 8 IS - 1 SN - 0167-7659, 0167-7659 KW - Carcinogens KW - 0 KW - Index Medicus KW - Rats KW - Animals KW - Mice KW - Male KW - Female KW - Carcinogens -- toxicity KW - Neoplasms, Experimental -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79130864?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-21 N1 - Date created - 1989-09-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Cancer Metastasis Rev 1989 Dec;8(3):281 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cyclosporine therapy of aplastic anaemia, congenital and acquired red cell aplasia. AN - 79127803; 2503027 AB - We treated 22 patients with severe aplastic anaemia refractory to antithymocyte globulin (ATG) with cyclosporine, alone or in combination with prednisone. Eight patients showed significant clinical improvement, all but one to transfusion-independence. Although cyclosporine alone was effective, the addition of prednisone resulted in prompter and fuller haematologic improvement. No patient with an absolute granulocyte count less than 0.2 x 10(9)/l responded to treatment. Haematologic remissions were sustained beyond the treatment period. Of nine patients with Diamond-Blackfan syndrome, one showed a complete response to two separate courses of cyclosporine and relapse with withdrawal of therapy, and a second achieved significant reduction in corticosteroid dose without relapse; however, seven cases failed to respond. Two of three adults with acquired pure red cell aplasia recovered. A combination of cyclosporine and corticosteroids may be effective therapy in patients with aplastic anaemia who have failed ATG treatment. Occasional cases of congenital and acquired pure red cell aplasia may also respond to cyclosporine. JF - British journal of haematology AU - Leonard, E M AU - Raefsky, E AU - Griffith, P AU - Kimball, J AU - Nienhuis, A W AU - Young, N S AD - Clinical Hematology Branch, National Heart, Lung and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 278 EP - 284 VL - 72 IS - 2 SN - 0007-1048, 0007-1048 KW - Cyclosporins KW - 0 KW - Prednisone KW - VB0R961HZT KW - Index Medicus KW - Drug Therapy, Combination KW - Prednisone -- therapeutic use KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Child KW - Adolescent KW - Male KW - Female KW - Blood Cell Count KW - Child, Preschool KW - Red-Cell Aplasia, Pure -- blood KW - Cyclosporins -- adverse effects KW - Red-Cell Aplasia, Pure -- drug therapy KW - Anemia, Aplastic -- drug therapy KW - Cyclosporins -- therapeutic use KW - Anemia, Aplastic -- blood KW - Red-Cell Aplasia, Pure -- congenital UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79127803?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-18 N1 - Date created - 1989-09-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Br J Haematol. 1989 Nov;73(3):432 [2513870] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The tobacco withdrawal syndrome: performance decrements assessed on a computerized test battery. AN - 79122780; 2752917 AB - The effects of tobacco abstinence and resumption of smoking on cognitive performance were studied in seven cigarette smokers. Subjects were trained on a computerized performance assessment battery (PAB) that included five different tests. Baseline data were obtained under conditions of minimally restricted cigarette smoking. This baseline smoking phase ended at 1000 h on the first day of tobacco deprivation and the PAB was then administered at intervals of 1, 4 and 8 h, and once at 1000 h on each of the next 9 days. Upon resumption of smoking (1000 h on day 11), testing was conducted at intervals of 1, 4, 8 and 24 h. The main findings were that tobacco deprivation resulted in significantly increased response latencies on all of the tests and decreased accuracy on two tests. Some performance impairments were observed within 4 h after the start of the smoke deprivation phase. Impairments peaked at 24-48 h and then begun to return toward baseline values; however, some measures remained significantly changed throughout the 10 days of abstinence. Performance decrements that were still evident throughout the deprivation phase were at least partially reversed after 1 h of resumption of smoking; all values returned to baseline levels within 24 h of resumption of smoking. JF - Drug and alcohol dependence AU - Snyder, F R AU - Davis, F C AU - Henningfield, J E AD - National Institute on Drug Abuse, Addiction Research Center, Baltimore, MD 21224. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 259 EP - 266 VL - 23 IS - 3 SN - 0376-8716, 0376-8716 KW - Nicotine KW - 6M3C89ZY6R KW - Index Medicus KW - Microcomputers KW - Humans KW - Adult KW - Psychological Tests -- instrumentation KW - Psychometrics KW - Male KW - Smoking -- therapy KW - Cognition -- drug effects KW - Nicotine -- adverse effects KW - Substance Withdrawal Syndrome -- psychology KW - Smoking -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79122780?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-30 N1 - Date created - 1989-08-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Acceleration of ethanol metabolism by past thiamine deficiency. AN - 79119526; 2665563 AB - Six months after severe thiamine deficiency, when their body and liver weights had normalized, male Sprague-Dawley rats were exposed to constant ethanol vapor concentrations for 6 days in an inhalation chamber and blood ethanol concentrations (BECs) were determined. Previously induced thiamine deficiency was associated with about a 50% reduction of BECs and a significant increase in liver alcohol dehydrogenase (ADH) activity suggesting a persistent acceleration of ethanol metabolism. No significant changes were found in liver aldehyde dehydrogenase activity, plasma levels of thyroxine, testosterone, or estradiol, or brain or liver histology. Plasma growth hormone concentrations were about 60% lower in the experimental group than in controls, but this effect of previous thiamine deprivation did not correlate with changes in ADH activity. Therefore, it remains to be elucidated how thiamine deficiency-induced central nervous system alterations may contribute to the development of metabolic tolerance to ethanol. JF - Alcoholism, clinical and experimental research AU - Martin, P R AU - Impeduglia, G AU - Giri, P R AU - Karanian, J AD - Laboratory of Clinical Studies, DICBR, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 457 EP - 460 VL - 13 IS - 3 SN - 0145-6008, 0145-6008 KW - Ethanol KW - 3K9958V90M KW - Alcohol Dehydrogenase KW - EC 1.1.1.1 KW - Aldehyde Dehydrogenase KW - EC 1.2.1.3 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Aldehyde Dehydrogenase -- blood KW - Animals KW - Liver -- enzymology KW - Alcohol Dehydrogenase -- blood KW - Male KW - Ethanol -- pharmacokinetics KW - Alcoholism -- enzymology KW - Thiamine Deficiency -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79119526?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-25 N1 - Date created - 1989-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression and phase variation of gonococcal P.II genes in Escherichia coli involves ribosomal frameshifting and slipped-strand mispairing. AN - 79099043; 2501632 AB - Expression and phase variation of Neisseria gonorrhoeae P.II genes in Escherichia coli were studied using TnphoA fusions. Fusions were created in the P.IIc gene of N. gonorrhoeae JS3 using lambda TnphoA-1 and were characterized by restriction digestion and dideoxy sequencing. Three fusions were chosen for further study; Tnp7 (fusion junction at mature amino acid 7), Tnp57 (amino acid 57), Tnp66 (amino acid 66). All fusions were in frame with the P.IIc coding sequence but were out of frame with the purported initiation codon. All fusion constructions were shown to phase vary in E. coli in an analogous fashion to that seen in N. gonorrhoeae, i.e. phase changes (in a recA background) at a frequency of c. 10(-3) accompanied by an alteration at the DNA level of the number of coding repeats (CRs). In vitro mutagenesis of the fusion constructions indicated that expression of out of frame P.II genes in E. coli was probably the result of ribosomal frameshifting within the run of 'A' residues immediately preceding the CR region and not due to low-level false initiation at codons other than the ATG initiation codon (as had previously been suggested). The mechanism for P.IIc::phoA phase variation appears to be related to the 'slipped-strand mispairing' mechanism responsible for frameshift mutations in a number of other bacterial genes containing short, direct, tandem repeats. JF - Molecular microbiology AU - Belland, R J AU - Morrison, S G AU - van der Ley, P AU - Swanson, J AD - Laboratory of Microbial Structure and Function, Rocky Mountain Laboratories, NIAID, Hamilton, Montana 59840. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 777 EP - 786 VL - 3 IS - 6 SN - 0950-382X, 0950-382X KW - Antigens, Bacterial KW - 0 KW - DNA, Ribosomal KW - Recombinant Fusion Proteins KW - opacity proteins KW - Alkaline Phosphatase KW - EC 3.1.3.1 KW - Index Medicus KW - Phenotype KW - Base Sequence KW - DNA Repair KW - Restriction Mapping KW - Recombinant Fusion Proteins -- genetics KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Alkaline Phosphatase -- metabolism KW - Alkaline Phosphatase -- genetics KW - Mutation KW - Cloning, Molecular KW - Genes, Bacterial KW - Antigens, Bacterial -- biosynthesis KW - Neisseria gonorrhoeae -- genetics KW - Escherichia coli -- genetics KW - Gene Expression Regulation KW - DNA, Ribosomal -- genetics KW - Antigens, Bacterial -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79099043?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-25 N1 - Date created - 1989-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Persistence of hepatic fibrosis and tissue eggs following treatment of Schistosoma japonicum infected mice. AN - 79057480; 2500856 AB - The persistence of hepatic fibrosis and of Schistosoma japonicum eggs in the tissues of mice was examined after chemotherapy. C57BL/6 mice infected with a Philippine strain of S. japonicum were treated with praziquantel or amoscanate 7 or 8 weeks after infection. Groups of mice were killed at the time of treatment and 3, 8, 26, and 52 weeks later. The number of eggs per worm pair in the tissues did not change during the year after treatment. However, S. japonicum eggs injected into the tail vein were gradually destroyed in the lungs. Hepatic fibrosis increased in the 1st few weeks after treatment and did not change significantly thereafter. Praziquantel, but not amoscanate, had an immediate toxic effect on the most mature eggs in the tissues which was accompanied by a marked but transient decrease in eggs passed in the feces. Less mature eggs appeared unaffected by the drug and the passage of eggs in the feces resumed as these matured. Egg passage then ceased as the supply of viable eggs was exhausted. JF - The American journal of tropical medicine and hygiene AU - Cheever, A W AU - Deb, S AD - National Institutes of Health, Bethesda, Maryland. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 620 EP - 628 VL - 40 IS - 6 SN - 0002-9637, 0002-9637 KW - Isothiocyanates KW - 0 KW - Thiocyanates KW - Praziquantel KW - 6490C9U457 KW - Diphenylamine KW - 9N3CBB0BIQ KW - amoscanate KW - X0MK46CVRB KW - Abridged Index Medicus KW - Index Medicus KW - Thiocyanates -- pharmacology KW - Lung -- parasitology KW - Diphenylamine -- pharmacology KW - Animals KW - Feces -- parasitology KW - Liver -- parasitology KW - Mice KW - Parasite Egg Count KW - Diphenylamine -- analogs & derivatives KW - Time Factors KW - Schistosomiasis japonica -- drug therapy KW - Praziquantel -- pharmacology KW - Liver Cirrhosis, Experimental -- chemically induced KW - Schistosoma japonicum -- growth & development KW - Liver Cirrhosis, Experimental -- parasitology KW - Schistosoma japonicum -- drug effects KW - Ovum -- drug effects KW - Liver Cirrhosis, Experimental -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79057480?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-02 N1 - Date created - 1989-08-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reversal of the toxic effects of cachectin by concurrent insulin administration. AN - 79052995; 2660586 AB - Rats treated with recombinant human tumor necrosis factor-cachectin, 100 micrograms/kg ip twice daily for 5 consecutive days, had a 56% decrease in food intake, a 54% decrease in nitrogen balance, and a 23-g decrease in body weight gain vs. saline-treated controls. Concurrent neutral protamine hagedorn insulin administration of 2 U/100 g sc twice daily reversed all of these changes to control levels without causing any treatment deaths. The improvement seen with insulin was dose independent. Five days of cachectin treatment caused a severe interstitial pneumonitis, periportal inflammation in the liver, and an increase in wet organ weight in the heart, lungs, kidney, and spleen. Concurrent insulin treatment led to near total reversal of these histopathologic changes. Cachectin treatment did not significantly change blood glucose levels from control values of 130-140 mg/dl, but insulin plus cachectin caused a significant decrease in blood glucose from 1 through 12 h after injection. Administration of high-dose insulin can near totally reverse the nutritional and histopathologic toxicity of sublethal doses of cachectin in rats. JF - The American journal of physiology AU - Fraker, D L AU - Merino, M J AU - Norton, J A AD - Surgical Metabolism Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - E725 EP - E731 VL - 256 IS - 6 Pt 1 SN - 0002-9513, 0002-9513 KW - Blood Glucose KW - 0 KW - Insulin KW - Recombinant Proteins KW - Tumor Necrosis Factor-alpha KW - Nitrogen KW - N762921K75 KW - Index Medicus KW - Animals KW - Reference Values KW - Liver -- pathology KW - Blood Glucose -- metabolism KW - Lung -- pathology KW - Nitrogen -- metabolism KW - Recombinant Proteins -- toxicity KW - Rats KW - Rats, Inbred F344 KW - Liver -- drug effects KW - Body Weight -- drug effects KW - Lung -- drug effects KW - Recombinant Proteins -- antagonists & inhibitors KW - Recombinant Proteins -- administration & dosage KW - Male KW - Organ Size -- drug effects KW - Tumor Necrosis Factor-alpha -- toxicity KW - Tumor Necrosis Factor-alpha -- administration & dosage KW - Tumor Necrosis Factor-alpha -- antagonists & inhibitors KW - Insulin -- pharmacology KW - Insulin -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79052995?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-18 N1 - Date created - 1989-07-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment of postoperative pain: comparison between administration at fixed hours and 'on demand' with intramuscular analgesics. AN - 79049478; 2737311 AB - From the data in the literature it can be seen that 40% of the surgical population has insufficient postoperative analgesia. Many reasons have been given for this: pain control delegated to the doctor on duty and/or the nursing staff; administration of drugs 'on demand', if the patient asks for them, or the nurses feel it to be necessary; fear of causing side effects such as respiratory insufficiency; or provoking addiction by giving narcotics. The aim of this paper is to evaluate the intensity of pain, the side effects, the degree of activity, anxiety, feeling of weakness and the mood of patients surgically treated for oncological diseases of the thorax and upper abdomen, comparing two different antalgic approaches. Thirty-five patients were studied. Pain was treated on demand with a narcotic, or an anti-inflammatory drug, or not treated at all; 20 patients were treated with analgesics given at predetermined hours, following the regime: methadone 10 mg intramuscularly (i.m.) every 12 h from the first to the third day following surgery and sodium diclofenac 75 mg (i.m.) every 12 h from the fourth to the seventh day. Results showed that patients treated with analgesics given intramuscularly at fixed hours have a significantly better pain control during the whole week of treatment (P less than 0.001), on average sleep more (P less than 0.001), spend more time standing or sitting and fewer hours lying down (P less than 0.001), have a higher performance status and feel less weak (P less than 0.05) than the group of patients treated with drugs 'on demand', or not treated at all. JF - European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology AU - De Conno, F AU - Ripamonti, C AU - Gamba, A AU - Prada, A AU - Ventafridda, V AD - Pain Therapy Division, National Cancer Institute, Milan, Italy. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 242 EP - 246 VL - 15 IS - 3 SN - 0748-7983, 0748-7983 KW - Diclofenac KW - 144O8QL0L1 KW - Methadone KW - UC6VBE7V1Z KW - Index Medicus KW - Drug Administration Schedule KW - Humans KW - Thoracic Neoplasms -- surgery KW - Injections, Intramuscular KW - Middle Aged KW - Abdominal Neoplasms -- surgery KW - Male KW - Female KW - Methadone -- adverse effects KW - Pain, Postoperative -- drug therapy KW - Diclofenac -- adverse effects KW - Pain, Postoperative -- psychology KW - Methadone -- administration & dosage KW - Diclofenac -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79049478?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-03 N1 - Date created - 1989-08-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 3,4-Methylenedioxymethamphetamine ("ecstasy") selectively destroys brain serotonin terminals in rhesus monkeys. AN - 79039023; 2471824 AB - 3,4-Methylenedioxymethamphetamine (MDMA, "Ecstasy"), an amphetamine analog, is a "designer drug" which is being increasingly abused. The potential neurotoxic hazard of MDMA in humans was assessed by examining the effects of repeated systemic administration of MDMA on selected neurochemical and behavioral measures in rhesus monkeys. In the first study, MDMA (2.5 or 10 mg/kg twice daily for 4 days) produced selective and significant neurochemical decreases in cerebrospinal fluid (CSF) concentrations of 5-hydroxyindoleacetic acid (5-HIAA) and brain concentrations of serotonin and 5-HIAA. At the high dose of MDMA, a selective decrease in serotonin uptake sites (reflecting destruction of brain serotonin terminals) was observed. To determine if these changes after high dose MDMA were pharmacologic or truly neurotoxic, in a subsequent study monkeys were treated with MDMA (10 mg/kg twice daily for 4 days) and then monitored for 14 weeks. Throughout this period, CSF 5-HIAA was decreased in MDMA-treated animals but not in saline-injected controls. At the end of this period, significant decreases in the concentration of serotonin, 5-HIAA and serotonin uptake sites were observed in cerebral cortex and striatum but not in hypothalamus or spinal cord. In contrast to these widespread alterations in serotonin markers, comparable noradrenergic and dopaminergic measures in CSF and brain appeared generally unaffected. These data demonstrating potent and selective effects of MDMA on various brain serotonin parameters in rhesus monkeys suggest that the drug may produce similar effects in humans. JF - The Journal of pharmacology and experimental therapeutics AU - Insel, T R AU - Battaglia, G AU - Johannessen, J N AU - Marra, S AU - De Souza, E B AD - Laboratory of Clinical Science, National Institute of Mental Health, Poolesville, Maryland. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 713 EP - 720 VL - 249 IS - 3 SN - 0022-3565, 0022-3565 KW - Amphetamines KW - 0 KW - Serotonin KW - 333DO1RDJY KW - 3,4-Methylenedioxyamphetamine KW - 4764-17-4 KW - Hydroxyindoleacetic Acid KW - 54-16-0 KW - N-Methyl-3,4-methylenedioxyamphetamine KW - KE1SEN21RM KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Homovanillic Acid KW - X77S6GMS36 KW - Index Medicus KW - Behavior, Animal -- drug effects KW - Animals KW - Norepinephrine -- metabolism KW - Body Weight -- drug effects KW - Hydroxyindoleacetic Acid -- cerebrospinal fluid KW - Dopamine -- metabolism KW - Macaca mulatta KW - Homovanillic Acid -- metabolism KW - Male KW - Nerve Endings -- drug effects KW - Brain Chemistry -- drug effects KW - 3,4-Methylenedioxyamphetamine -- analogs & derivatives KW - Serotonin -- metabolism KW - 3,4-Methylenedioxyamphetamine -- toxicity KW - Amphetamines -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79039023?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-21 N1 - Date created - 1989-07-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Microsomal metabolism of the Z and E isomers of N-nitroso-N-methyl-N-n-pentylamine. AN - 79031499; 2731161 AB - N-Nitrosomethyl-N-n-pentylamine was separated into its E and Z isomers by HPLC. When the metabolism was examined using microsomes isolated from uninduced Fischer 344 rats, it was found that, at a constant final concentration of 0.5 mM, the yield of formaldehyde produced increased as the proportion of the Z isomer rose. The yield of valeraldehyde, on the other hand, decreased with an increasing proportion of the Z isomer. Kinetic constants were determined for the metabolism of the two isomers. During the metabolism of the Z isomer, the Vmax was 2.2-fold higher for the formation of formaldehyde than that for the E. The Vmax for valeraldehyde was 2.0-fold lower during the metabolism of the Z isomer. The results indicate that the relative position of the nitroso group can have a profound effect on the metabolism of each side of this type of molecule. JF - Cancer letters AU - He, C AU - Farrelly, J G AD - NCI-Frederick Cancer Research Facility, BRI-Basic Research Program, MD 21701. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 189 EP - 194 VL - 45 IS - 3 SN - 0304-3835, 0304-3835 KW - Aldehydes KW - 0 KW - Nitrosamines KW - N-amyl-N-methylnitrosamine KW - 13256-07-0 KW - Formaldehyde KW - 1HG84L3525 KW - pentanal KW - B975S3014W KW - Index Medicus KW - Rats KW - Esophageal Neoplasms -- chemically induced KW - Animals KW - Rats, Inbred F344 KW - Formaldehyde -- metabolism KW - Isomerism KW - Aldehydes -- metabolism KW - Male KW - Chromatography, High Pressure Liquid KW - Nitrosamines -- toxicity KW - Microsomes, Liver -- metabolism KW - Nitrosamines -- pharmacokinetics KW - Nitrosamines -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79031499?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-21 N1 - Date created - 1989-07-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fenfluramine selectively and differentially decreases the density of serotonergic nerve terminals in rat brain: evidence from immunocytochemical studies. AN - 79025873; 2732954 AB - Fenfluramine is an amphetamine derivative which is used primarily as an anorectic agent in the treatment of obesity. High doses of fenfluramine have been reported to cause long-term decreases in brain serotonin (5-HT) levels and density of high-affinity 5-HT uptake sites, actions characteristic of a "neurotoxic" effect of the drug. In view of these neurochemical changes, we used immunocytochemistry to assess, in detail, the effects of fenfluramine treatment on the morphology and density of 5-HT-like immunoreactive neurons in rat brain. Twelve to 18 hr after high dose dl-fenfluramine HCl treatment (24 mg/kg s.c., twice daily for 4 days), there was a profound regional decrease in density of fine-caliber 5-HT-like immunoreactive fibers and terminals in brain. This effect was especially apparent in cerebral cortex, hippocampus, cerebellum and striatum and less striking decreases were noted in septum, locus ceruleus and hypothalamus. On the other hand, 5-HT-like immunoreactive somata in midbrain nuclei and fibers and terminals in spinal cord appeared unaffected after fenfluramine treatment. Remaining 5-HT-like immunoreactive fibers and terminals displayed morphology characteristic of degenerating axons (thickening, swollen varicosities and fragmentation). Two weeks after the 4-day treatment regimen, patterns of 5-HT-like immunostaining appeared similar to those noted immediately (i.e., 18 hr) after drug treatment; however, the presence of grossly deformed fibers and terminals seen shortly after drug treatment was lacking. Tyrosine hydroxylase-like immunoreactivity, used to assess changes in catecholamine-containing neurons, appeared unaffected by drug treatment. These data suggest that, in rats, high s.c. doses of fenfluramine may be neurotoxic to some 5-HT-like immunoreactive axons and terminals. The relevance of these observations to the continued therapeutic use in humans of smaller p.o. doses of fenfluramine remains to be determined. JF - The Journal of pharmacology and experimental therapeutics AU - Appel, N M AU - Contrera, J F AU - De Souza, E B AD - Laboratory of Neurobiology, National Institute on Drug Abuse Addiction Research Center, Baltimore, Maryland. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 928 EP - 943 VL - 249 IS - 3 SN - 0022-3565, 0022-3565 KW - Fenfluramine KW - 2DS058H2CF KW - Serotonin KW - 333DO1RDJY KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Brain Chemistry -- drug effects KW - Serotonin -- metabolism KW - Immunohistochemistry KW - Male KW - Fenfluramine -- toxicity KW - Brain -- drug effects KW - Nerve Endings -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79025873?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-21 N1 - Date created - 1989-07-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Anticonvulsant activities of 1-phenylcyclohexylamine and its conformationally restricted analog 1,1-pentamethylenetetrahydroisoquinoline. AN - 79025549; 2659775 AB - 1-Phenylcyclohexylamine (PCA), an analog of phenyclidine (PCP) in which the piperidine ring is replaced by a primary amino group, and its conformationally restricted analog 1,1-pentamethylenetetrahydroisoquinoline (PM-THIQ) were potent anticonvulsants in the mouse maximal electroshock (MES) seizure test (ED50 values, 7.0 and 14.3 mg/kg, respectively). At higher doses, the drugs caused motor impairment (TD50 values, 16.3 and 43.0 mg/kg) and blocked the behavioral effects and lethality of i.p. injected N-methyl-D-aspartate (NMDA) (ED50 values, 36.3 and 127 mg/kg). The separation in potencies in the MES seizure and motor toxicity tests of PCA and PM-THIQ contrasts with PCP which was equally potent in both tests. Several compounds that were structurally related to PM-THIQ (N-ethyl-PCA, 2-methyl-PCA, N-methyl-PM-THIQ, tetrahydroisoquinoline and benzylamine) also blocked MES seizures and caused motor impairment, but failed to show as great a separation between MES anticonvulsant activity and motor toxicity. None of the compounds protected against seizures induced by the chemoconvulsant pentylenetetrazol at doses that lacked motor toxicity. The drugs were also evaluated for their ability to displace [3H]-1-[1-(2-thienyl)-cyclohexyl]piperidine from binding to high affinity acceptor sites (presumably on NMDA receptor-coupled channels) in rat brain homogenates. The rank order of potencies in the binding assay was similar to that in the behavioral tests, except for 2-methyl-PCA which was behaviorally more potent than expected.(ABSTRACT TRUNCATED AT 250 WORDS) JF - The Journal of pharmacology and experimental therapeutics AU - Rogawski, M A AU - Thurkauf, A AU - Yamaguchi, S AU - Rice, K C AU - Jacobson, A E AU - Mattson, M V AD - Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 708 EP - 712 VL - 249 IS - 3 SN - 0022-3565, 0022-3565 KW - Anticonvulsants KW - 0 KW - Cyclohexylamines KW - Isoquinolines KW - Tetrahydroisoquinolines KW - Aspartic Acid KW - 30KYC7MIAI KW - N-Methylaspartate KW - 6384-92-5 KW - 1,1-pentamethylenetetrahydroisoquinoline KW - 89248-68-0 KW - 1-phenylcyclohexylamine KW - HBO2D49I2S KW - Phencyclidine KW - J1DOI7UV76 KW - Index Medicus KW - Seizures -- chemically induced KW - Animals KW - Aspartic Acid -- analogs & derivatives KW - Phencyclidine -- metabolism KW - Brain -- drug effects KW - Motor Activity -- drug effects KW - Mice KW - Brain -- metabolism KW - Seizures -- prevention & control KW - Male KW - Isoquinolines -- pharmacology KW - Cyclohexylamines -- toxicity KW - Anticonvulsants -- toxicity KW - Cyclohexylamines -- pharmacology KW - Isoquinolines -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79025549?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-21 N1 - Date created - 1989-07-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Repeated swim stress alters brain benzodiazepine receptors measured in vivo. AN - 79025494; 2543808 AB - The effects of repeated swim stress on brain benzodiazepine receptors were examined in the mouse using both an in vivo and in vitro binding method. Specific in vivo binding of [3H]Ro15-1788 to benzodiazepine receptors was decreased in the hippocampus, cerebral cortex, hypothalamus, midbrain and striatum after repeated swim stress (7 consecutive days of daily swim stress) when compared to nonstressed mice. In vivo benzodiazepine receptor binding was unaltered after repeated swim stress in the cerebellum and pons medulla. The stress-induced reduction in in vivo benzodiazepine receptor binding did not appear to be due to altered cerebral blood flow or to an alteration in benzodiazepine metabolism or biodistribution because there was no difference in [14C]iodoantipyrine distribution or whole brain concentrations of clonazepam after repeated swim stress. Saturation binding experiments revealed a change in both apparent maximal binding capacity and affinity after repeated swim stress. Moreover, a reduction in clonazepam's anticonvulsant potency was also observed after repeated swim stress [an increase in the ED50 dose for protection against pentylenetetrazol-induced seizures], although there was no difference in pentylenetetrazol-induced seizure threshold between the two groups. In contrast to the results obtained in vivo, no change in benzodiazepine receptor binding kinetics was observed using the in vitro binding method. These data suggest that environmental stress can alter the binding parameters of the benzodiazepine receptor and that the in vivo and in vitro binding methods can yield substantially different results. JF - The Journal of pharmacology and experimental therapeutics AU - Weizman, R AU - Weizman, A AU - Kook, K A AU - Vocci, F AU - Deutsch, S I AU - Paul, S M AD - Section on Molecular Pharmacology, National Institute of Mental Health, Bethesda, Maryland. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 701 EP - 707 VL - 249 IS - 3 SN - 0022-3565, 0022-3565 KW - Receptors, GABA-A KW - 0 KW - Tritium KW - 10028-17-8 KW - Flumazenil KW - 40P7XK9392 KW - Clonazepam KW - 5PE9FDE8GB KW - Pentylenetetrazole KW - WM5Z385K7T KW - Index Medicus KW - Seizures -- chemically induced KW - Animals KW - Swimming KW - Mice KW - Seizures -- prevention & control KW - Cerebrovascular Circulation KW - Clonazepam -- therapeutic use KW - Male KW - Stress, Physiological -- metabolism KW - Receptors, GABA-A -- metabolism KW - Brain -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79025494?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-21 N1 - Date created - 1989-07-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Analysis of gag proteins from mouse mammary tumor virus. AN - 79024968; 2542570 AB - Structural proteins designated p10gag, p21gag, p8gag, p3gag, p27gag, and p14gag from the C3H strain of mouse mammary tumor virus (MMTV) were purified by reversed-phase high-pressure liquid chromatography. The N- and C-terminal amino acid sequences and amino acid composition of each protein were determined and compared with the amino acids encoded by the proviral DNA sequences for the MMTV gag gene. The results show that each of the purified proteins is a proteolytic cleavage product derived from the predicted primary translational product of the gag gene (Pr77gag) and that their order in Pr77gag is p10-pp21-p8-p3-n-p27-p14 (where n represents 17 predicted residues that were not identified among the purified proteins). Purified p10gag lacks the initiator methionine and has a myristoyl group attached in amide linkage to the N-terminal glycine residue predicted by the second codon of the gag gene. The cleavage products are contiguous in the sequence of Pr77gag, and the C-terminal residue of p14gag is encoded by the last codon of the gag gene. By analogy with other retrovirus, p14gag is the viral nucleocapsid protein, p10gag is the matrix protein, and p27gag is the capsid protein of mature MMTV. Proteolytic cleavage sites in MMTV Pr77gag bear a striking resemblance to cleavage sites in the gag precursors of D-type retroviruses, suggesting that these viral proteases have similar specificities. JF - Journal of virology AU - Hizi, A AU - Henderson, L E AU - Copeland, T D AU - Sowder, R C AU - Krutzsch, H C AU - Oroszlan, S AD - Laboratory of Molecular Virology and Carcinogenesis, National Cancer Institute-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 2543 EP - 2549 VL - 63 IS - 6 SN - 0022-538X, 0022-538X KW - DNA, Viral KW - 0 KW - Gene Products, gag KW - Retroviridae Proteins KW - Index Medicus KW - Animals KW - Base Sequence KW - Electrophoresis, Polyacrylamide Gel KW - Molecular Sequence Data KW - Genes, Viral KW - Amino Acid Sequence KW - DNA, Viral -- genetics KW - Chromatography, High Pressure Liquid KW - Retroviridae Proteins -- analysis KW - Mammary Tumor Virus, Mouse -- analysis KW - Retroviridae Proteins -- isolation & purification KW - Mammary Tumor Virus, Mouse -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79024968?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-27 N1 - Date created - 1989-06-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Virol. 1984 Nov;52(2):492-500 [6333515] Curr Top Microbiol Immunol. 1983;106:57-78 [6315307] J Virol. 1985 Sep;55(3):778-87 [3927012] Science. 1986 Apr 25;232(4749):485-7 [2421409] Cell. 1986 May 9;45(3):375-85 [2421920] Proc Natl Acad Sci U S A. 1986 Oct;83(19):7246-50 [3489936] J Virol. 1986 Nov;60(2):450-9 [2430109] J Virol. 1987 Feb;61(2):480-90 [3027377] J Virol. 1987 Apr;61(4):1045-53 [3493352] J Biol Chem. 1987 Apr 15;262(11):4961-7 [2435721] Proc Natl Acad Sci U S A. 1987 Jun;84(12):4298-302 [3035577] Proc Natl Acad Sci U S A. 1987 Oct;84(20):7041-5 [2823251] J Virol. 1988 May;62(5):1808-9 [3357211] J Virol. 1988 Aug;62(8):2587-95 [3292789] J Virol. 1988 Sep;62(9):3328-33 [2841485] Proc Natl Acad Sci U S A. 1988 Nov;85(22):8420-4 [3141927] Annu Rev Cell Biol. 1988;4:611-47 [3058168] Nature. 1970 Aug 15;227(5259):680-5 [5432063] Virology. 1978 Mar;85(1):168-74 [206000] Proc Natl Acad Sci U S A. 1978 Mar;75(3):1404-8 [206897] Virology. 1978 Nov;91(1):106-15 [214954] Virology. 1978 Dec;91(2):407-22 [217155] Virology. 1979 Jul 15;96(1):249-57 [223301] Adv Cancer Res. 1979;29:347-418 [89801] Cell. 1979 Aug;17(4):1003-12 [226264] Virology. 1979 Dec;99(2):358-71 [229627] J Virol. 1980 Aug;35(2):340-8 [6255175] Biochemistry. 1980 Nov 11;19(23):5290-6 [6255989] J Biol Chem. 1981 Aug 25;256(16):8400-6 [6267042] J Virol. 1982 Feb;41(2):414-22 [6281457] Proc Natl Acad Sci U S A. 1983 Jan;80(2):339-43 [6340098] J Virol. 1983 May;46(2):355-61 [6302307] J Virol. 1983 Oct;48(1):314-9 [6310154] Nucleic Acids Res. 1983 Oct 25;11(20):6943-55 [6314267] Curr Top Microbiol Immunol. 1983;106:1-34 [6196157] Curr Top Microbiol Immunol. 1985;115:221-33 [2983943] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tracheoesophageal fistula in the patient with lymphoma: case report and review of the literature. AN - 79024446; 2471284 AB - Tracheoesophageal fistula (TEF) occurs only rarely in the patient with lymphoma. Two cases are presented to illustrate the challenges in managing TEF in this patient population. Most of the 38 previously reported cases have occurred in patients who have undergone radiation therapy, although several patients have had TEF as an initial manifestation of lymphoma. TEF is usually, but not universally, associated with the presence of active lymphoma. The surgical approach should be individualized, based on the patient's overall condition, the site and size of the fistula, and sites of disease. Often a conservative surgical approach is warranted with the expectation that many of these fistulas will close after radiation therapy or chemotherapy. Patients with lymphoma-related TEF have a better prognosis than do those with TEF caused by carcinoma of the lung or esophagus. JF - Surgery AU - Perry, R R AU - Rosenberg, R K AU - Pass, H I AD - Thoracic Oncology Section, National Cancer Institute, Bethesda, Md. 20892. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 770 EP - 777 VL - 105 IS - 6 SN - 0039-6060, 0039-6060 KW - Cytarabine KW - 04079A1RDZ KW - Bleomycin KW - 11056-06-7 KW - Vincristine KW - 5J49Q6B70F KW - Etoposide KW - 6PLQ3CP4P3 KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Prednisone KW - VB0R961HZT KW - Methotrexate KW - YL5FZ2Y5U1 KW - Abridged Index Medicus KW - Index Medicus KW - Combined Modality Therapy KW - Prednisone -- therapeutic use KW - Humans KW - Etoposide -- therapeutic use KW - Prognosis KW - Reoperation KW - Cytarabine -- therapeutic use KW - Cyclophosphamide -- therapeutic use KW - Vincristine -- therapeutic use KW - Adult KW - Methotrexate -- therapeutic use KW - Doxorubicin -- therapeutic use KW - Follow-Up Studies KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Bleomycin -- therapeutic use KW - Female KW - Tracheoesophageal Fistula -- diagnosis KW - Skin Neoplasms -- drug therapy KW - Tracheoesophageal Fistula -- surgery KW - Lymphomatoid Granulomatosis -- complications KW - Tracheoesophageal Fistula -- etiology KW - Hodgkin Disease -- drug therapy KW - Skin Neoplasms -- complications KW - Hodgkin Disease -- complications KW - Lymphomatoid Granulomatosis -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79024446?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-28 N1 - Date created - 1989-06-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Allergic reactions to amyl nitrite inhalation. AN - 79023846; 2567119 JF - The American journal of medicine AU - Dax, E M AU - Lange, W R AU - Jaffe, J H AD - National Institute on Drug Abuse Addiction Research Center, Baltimore, Maryland 21224. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 732 VL - 86 IS - 6 Pt 1 SN - 0002-9343, 0002-9343 KW - Amyl Nitrite KW - 8017-89-8 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Adult KW - Pruritus -- chemically induced KW - Administration, Inhalation KW - Time Factors KW - Male KW - Amyl Nitrite -- administration & dosage KW - Amyl Nitrite -- adverse effects KW - Drug Hypersensitivity -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79023846?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-06 N1 - Date created - 1989-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Protective, restorative, and therapeutic properties of recombinant colony-stimulating factors. AN - 79018492; 2471557 AB - Pretreatment of mice with recombinant murine (rM) colony-stimulating factor-granulocyte-macrophage (CSF-gm) or recombinant human (rH) CSF-g provides partial protection from the lethal effects of ionizing radiation or the alkylating agent cyclophosphamide (CTX). In addition, these agents can significantly prolong survival if administered following lethal doses of irradiation or CTX. To induce protective activity, cytokines were injected 20 hours before lethal irradiation or CTX administration. To accelerate recovery from lethal irradiation, the cytokines must be administered shortly following irradiation, and the induction of maximal levels of activity is dependent on chronic administration. In contrast, because of their longer half-lives, accelerated recovery from alkylating agents requires a delay of at least 24 to 48 hours to allow complete clearance of CTX before administration of a CSF. Studies quantitating peripheral blood leukocytes and bone marrow cellularity as well as colony-forming units per culture (CFU-C) frequency and CFU-C per femur revealed a significant correlation between these parameters and the ability to survive lethal irradiation. This is a US government work. There are no restrictions on its use. JF - Blood AU - Talmadge, J E AU - Tribble, H AU - Pennington, R AU - Bowersox, O AU - Schneider, M A AU - Castelli, P AU - Black, P L AU - Abe, F AD - Program Resources, Inc, National Cancer Institute-Frederick Cancer Research Facility, MD. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 2093 EP - 2103 VL - 73 IS - 8 SN - 0006-4971, 0006-4971 KW - Colony-Stimulating Factors KW - 0 KW - Growth Substances KW - Recombinant Proteins 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 - Injections, Intraperitoneal KW - Animals KW - Bone Marrow -- pathology KW - Drug Administration Schedule KW - Leukopenia -- pathology KW - Recombinant Proteins -- pharmacokinetics KW - Mice, Nude KW - Mice KW - Cyclophosphamide -- toxicity KW - Mice, Inbred BALB C KW - Leukopenia -- chemically induced KW - Hematopoiesis -- drug effects KW - Kinetics KW - Mice, Inbred C57BL KW - Colony-Forming Units Assay KW - Bone Marrow -- drug effects KW - Recombinant Proteins -- therapeutic use KW - Recombinant Proteins -- administration & dosage KW - Radiation Chimera KW - Bone Marrow Transplantation KW - Female KW - Colony-Stimulating Factors -- therapeutic use KW - Growth Substances -- therapeutic use KW - Colony-Stimulating Factors -- pharmacokinetics KW - Growth Substances -- administration & dosage KW - Colony-Stimulating Factors -- administration & dosage KW - Growth Substances -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79018492?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-14 N1 - Date created - 1989-07-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Benzodiazepine withdrawal delirium with catatonic features. Occurrence in patients with partial seizure disorders. AN - 79012707; 2730383 AB - We report the cases of 3 patients with medically intractable seizures in whom withdrawal of treatment with a long-acting benzodiazepine (clorazepate dipotassium, 2 patients; clonazepam, 1 patient) was followed by delirium with catatoniclike features. While an increase in seizure frequency occurred during withdrawal and prior to the onset of behavioral changes, electroencephalograms did not show epileptiform activity during the delirium. We compared these 3 patients with 10 others with intractable seizures in whom antiepileptic therapy was withdrawn without subsequent behavior changes. High-dose benzodiazepine therapy and a history of viral encephalitis may be risk factors for withdrawal delirium. JF - Archives of neurology AU - Hauser, P AU - Devinsky, O AU - De Bellis, M AU - Theodore, W H AU - Post, R M AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 696 EP - 699 VL - 46 IS - 6 SN - 0003-9942, 0003-9942 KW - Benzodiazepines KW - 12794-10-4 KW - Clonazepam KW - 5PE9FDE8GB KW - Clorazepate Dipotassium KW - 63FN7G03XY KW - Abridged Index Medicus KW - Index Medicus KW - Virus Diseases KW - Clonazepam -- adverse effects KW - Humans KW - Encephalitis -- etiology KW - Adult KW - Encephalitis -- complications KW - Male KW - Female KW - Clorazepate Dipotassium -- adverse effects KW - Catatonia -- chemically induced KW - Benzodiazepines -- therapeutic use KW - Substance Withdrawal Syndrome KW - Delirium -- chemically induced KW - Benzodiazepines -- adverse effects KW - Seizures -- etiology KW - Seizures -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79012707?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-07 N1 - Date created - 1989-07-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Suppression of UAA and UGA termination codons in mutant murine leukemia viruses. AN - 78991985; 2542597 AB - Genomes of mammalian type C retroviruses contain a UAG termination codon between the gag and pol coding regions. The pol region is expressed in the form of a gag-pol fusion protein following readthrough suppression of the UAG codon. We have used oligonucleotide-directed mutagenesis to change the UAG in Moloney murine leukemia virus to UAA or UGA. These alternate termination codons were also suppressed, both in infected cells and in reticulocyte lysates. Thus, the signal or context inducing suppression of UAG in wild-type Moloney murine leukemia virus is also effective with UAA and UGA. Further, mammalian cells and cell extracts contain tRNAs capable of translating UAA and UGA as amino acids. To our knowledge, this is the first example of natural suppression of UAA in higher eucaryotes. JF - Journal of virology AU - Feng, Y X AU - Levin, J G AU - Hatfield, D L AU - Schaefer, T S AU - Gorelick, R J AU - Rein, A AD - Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 2870 EP - 2873 VL - 63 IS - 6 SN - 0022-538X, 0022-538X KW - Codon KW - 0 KW - RNA, Messenger KW - Index Medicus KW - Protein Biosynthesis KW - Animals KW - Transfection KW - Electrophoresis, Polyacrylamide Gel KW - Precipitin Tests KW - Mutation KW - Leukemia Virus, Murine -- genetics KW - Codon -- genetics KW - Suppression, Genetic KW - RNA, Messenger -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78991985?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-27 N1 - Date created - 1989-06-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Virology. 1976 Jul 15;72(2):523-6 [181914] J Virol. 1989 May;63(5):2405-10 [2784837] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Nature. 1980 Jan 3;283(5742):41-6 [7350525] J Virol. 1980 Mar;33(3):983-92 [6154154] J Virol. 1980 May;34(2):464-73 [7373716] Cell. 1981 Aug;25(2):497-506 [6912798] Nature. 1981 Oct 15-21;293(5833):543-8 [6169994] Proc Natl Acad Sci U S A. 1982 Oct;79(20):6215-9 [6815648] DNA. 1984 Dec;3(6):479-88 [6096101] Proc Natl Acad Sci U S A. 1985 Mar;82(6):1618-22 [3885215] Gene. 1985;33(1):103-19 [2985470] J Mol Biol. 1985 May 5;183(1):31-42 [2989539] J Virol. 1986 Oct;60(1):267-74 [2427747] Proc Natl Acad Sci U S A. 1986 Oct;83(19):7246-50 [3489936] Gene. 1986;49(3):383-8 [3552889] Nature. 1971 Feb 19;229(5286):564-6 [4925356] Proc Natl Acad Sci U S A. 1987 May;84(9):2668-72 [3472229] J Mol Biol. 1986 Dec 20;192(4):725-35 [3295253] FEBS Lett. 1988 Aug 1;235(1-2):1-15 [3042454] J Virol. 1988 Oct;62(10):3574-80 [2843660] J Virol. 1988 Nov;62(11):4376-80 [2459414] Proc Natl Acad Sci U S A. 1988 Nov;85(22):8420-4 [3141927] J Virol. 1989 Mar;63(3):1326-37 [2521676] Cell. 1978 Jan;13(1):189-99 [202399] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A recombinant immunotoxin consisting of two antibody variable domains fused to Pseudomonas exotoxin. AN - 78984808; 2498664 AB - Antibodies and growth factors have been chemically coupled to different toxins to produce cytotoxic molecules that selectively kill cells bearing appropriate antigens or receptors. Antibody-toxin conjugates (immunotoxins) produced using conventional chemical coupling techniques have several undesirable characteristics. The smallest binding unit of an antibody is an Fv fragment which consists of a light and heavy chain variable domain. Recently, active single chain Fv fragments of antibodies have been produced in Escherichia coli by attaching the light and heavy chain variable domains together with a peptide linker. Here we describe the construction and expression in E. coli of a single chain antibody toxin fusion protein, anti-Tac(Fv)-PE40, in which the variable regions of anti-Tac, a monoclonal antibody to the p55 subunit of the human interleukin-2 receptor, are joined in peptide linkage to PE40, a modified form of Pseudomonas exotoxin lacking its binding domain. Anti-Tac(Fv)-PE40 was very cytotoxic to two interleukin-2 receptor-bearing human cell lines but was not cytotoxic to receptor-negative cells. JF - Nature AU - Chaudhary, V K AU - Queen, C AU - Junghans, R P AU - Waldmann, T A AU - FitzGerald, D J AU - Pastan, I AD - Laboratory of Molecular Biology, DCBD, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/06/01/ PY - 1989 DA - 1989 Jun 01 SP - 394 EP - 397 VL - 339 IS - 6223 SN - 0028-0836, 0028-0836 KW - Antibodies, Monoclonal KW - 0 KW - Exotoxins KW - Immunoglobulin Heavy Chains KW - Immunoglobulin Variable Region KW - Immunotoxins KW - Macromolecular Substances KW - Receptors, Interleukin-2 KW - Recombinant Fusion Proteins KW - Index Medicus KW - Humans KW - Recombinant Fusion Proteins -- isolation & purification KW - Escherichia coli -- genetics KW - Amino Acid Sequence KW - Plasmids KW - Immunoglobulin Heavy Chains -- genetics KW - Receptors, Interleukin-2 -- immunology KW - Base Sequence KW - Molecular Sequence Data KW - Recombinant Fusion Proteins -- pharmacology KW - Cell Line KW - Pseudomonas -- genetics KW - Immunoglobulin Variable Region -- genetics KW - Exotoxins -- genetics KW - Immunotoxins -- isolation & purification KW - Immunotoxins -- pharmacology KW - Immunoglobulin Variable Region -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78984808?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-06 N1 - Date created - 1989-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA adduct formation and removal in specific liver cell populations during chronic dietary administration of 2-acetylaminofluorene. AN - 78979296; 2720908 AB - The concentration of DNA adducts in specific hepatic cell types has been determined in F344 rats fed 0.02% 2-acetylaminofluorene (AAF) for 28 days followed by control diet for an additional 28 days. In animals killed at 28 days of AAF feeding, the major DNA adduct, N-(deoxyguanosin-8-yl)-2-aminofluorene, was present in each cell type in the order: hepatocytes (282 +/- 28 fmol/micrograms DNA) greater than whole liver (232 +/- 33 fmol/micrograms DNA) greater than nonparenchymal cells (128 +/- 30 fmol/micrograms DNA) greater than bile duct fraction (60 +/- 12 fmol/micrograms DNA). After an additional 28 days on control diet, the adduct level in each cell fraction was 30-40 fmol/micrograms DNA. Adduct removal was biphasic in whole liver, hepatocytes and nonparenchymal cells, with a fast phase apparent until the adduct concentration reached approximately 60 fmol/micrograms DNA. In whole liver and hepatocytes this level was obtained in approximately seven days, and in nonparenchymal cells the fast phase was complete in about two days. Adduct removal in the bile duct fraction exhibited only a single slow phase. At the end of the AAF feeding, hepatocytes accounted for 86% of the total liver DNA adducts. After an additional 28 days on control diet, hepatocyte adducts still contributed a major fraction (67%) of the total persistent adduct population. Thus, hepatocytes, the target cell for AAF-induced hepatic tumors, dominate the adduct formation and removal profile observed in whole liver. JF - Carcinogenesis AU - Poirier, M C AU - Beland, F A AU - Deal, F H AU - Swenberg, J A AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 1143 EP - 1145 VL - 10 IS - 6 SN - 0143-3334, 0143-3334 KW - DNA KW - 9007-49-2 KW - 2-Acetylaminofluorene KW - 9M98QLJ2DL KW - Index Medicus KW - Rats KW - Administration, Oral KW - Animals KW - Rats, Inbred F344 KW - Liver Neoplasms, Experimental -- pathology KW - Diet KW - Bile Ducts -- metabolism KW - Male KW - 2-Acetylaminofluorene -- administration & dosage KW - Liver -- pathology KW - 2-Acetylaminofluorene -- toxicity KW - 2-Acetylaminofluorene -- metabolism KW - Liver -- drug effects KW - DNA -- metabolism KW - Liver -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78979296?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-12 N1 - Date created - 1989-07-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Biochemical characterization of the inhibitory effect of CsA on cytolytic T lymphocyte effector functions. AN - 78974926; 2541201 AB - We have examined the effects of cyclosporine A (CsA) on a number of CTL effector functions. CsA partially inhibited the CTL-mediated lysis of Ag-bearing target cells. Both target cell- and anti-TCR mAb-induced granule exocytosis were markedly inhibited by CsA. In addition, marked inhibition of PMA and calcium ionophore (A23187) induced granule exocytosis was produced by CsA suggesting that the inhibitory effects of CsA on granule exocytosis involve biochemical events after protein kinase C activation and increases in intracellular free Ca2+. CsA had no inhibitory effects on TCR-mediated phosphatidylinositol metabolism. The inhibitory effects of CsA were not mediated by the cAMP-dependent protein kinase inhibitory pathway and no effect of CsA on the Ca2+-induced binding of calmodulin to calmodulin-binding proteins could be demonstrated. CsA was also a potent inhibitor of IgE receptor-mediated exocytosis in rat basophil leukemia cells. CsA had no effect on receptor-mediated phosphatidylinositol hydrolysis; 400 ng/ml CsA resulted in a 90% inhibition of serotonin release but had no effect on phosphatidylinositol hydrolysis. These results indicate that CsA may inhibit some common event in Ca2+-dependent secretory cells. Taken together, these results suggest that CsA does not inhibit signal transduction but rather interferes with the biochemical events in the later stages of Ca2+-dependent reactions that follow the binding of calmodulin to cytoskeletal or cytoplasmic calmodulin binding proteins. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Trenn, G AU - Taffs, R AU - Hohman, R AU - Kincaid, R AU - Shevach, E M AU - Sitkovsky, M AD - Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20912. Y1 - 1989/06/01/ PY - 1989 DA - 1989 Jun 01 SP - 3796 EP - 3802 VL - 142 IS - 11 SN - 0022-1767, 0022-1767 KW - Calmodulin-Binding Proteins KW - 0 KW - Cyclosporins KW - Phosphatidylinositol 4,5-Diphosphate KW - Phosphatidylinositols KW - Receptors, Antigen, T-Cell KW - Calcimycin KW - 37H9VM9WZL KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Exocytosis -- drug effects KW - Animals KW - Phosphatidylinositols -- metabolism KW - Cytoplasmic Granules -- physiology KW - Calmodulin-Binding Proteins -- metabolism KW - Mice KW - Receptors, Antigen, T-Cell -- physiology KW - Mast Cells -- drug effects KW - Mast Cells -- physiology KW - Cytoplasmic Granules -- drug effects KW - Receptors, Antigen, T-Cell -- drug effects KW - T-Lymphocytes, Cytotoxic -- immunology KW - Cytotoxicity, Immunologic -- drug effects KW - Cyclosporins -- pharmacology KW - T-Lymphocytes, Cytotoxic -- metabolism KW - T-Lymphocytes, Cytotoxic -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78974926?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-22 N1 - Date created - 1989-06-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transformation of human neonatal prostate epithelial cells by strontium phosphate transfection with a plasmid containing SV40 early region genes. AN - 78956716; 2541897 AB - Neonatal human prostatic epithelial cells (NP-2s) were transfected by strontium phosphate coprecipitation with a plasmid (pRSV-T) containing the SV40 early region genes. The cells transfected with pRSV-T, but not the sham-transfected controls, formed rapidly growing, multilayered colonies within 2 weeks at a frequency of 1 x 10(-4) in a serum-free medium (P4-8F). In all, 28 colonies of transformed cells were isolated. Three of these have been cultured for a sufficient length of time to show that their growth potentials are well beyond that of the normal progenitor cells (NP-2s). There is also little or no indication of the culture "crisis" commonly seen in SV40-transformed cells in these transfected lines. All contain cytokeratins and SV40 T-antigen as revealed by immunofluorescence, have ultrastructural features of epithelial cells, and are pseudodiploid. None have produced tumors within 1 year after s.c. injection into nude mice. The transformed as well as the parental NP-2s cells require bovine pituitary extract for growth in serum-free medium and are stimulated by transforming growth factor beta 1 (TGF-beta 1) and epidermal growth factor in clonal growth assays. In contrast, a prostatic carcinoma cell line (PC-3) is inhibited by TGF-beta 1. This serum-free system and immortalized transfected clones will be useful for studying the action of putative prostatic carcinogens and tumor-promoting agents. JF - Cancer research AU - Kaighn, M E AU - Reddel, R R AU - Lechner, J F AU - Peehl, D M AU - Camalier, R F AU - Brash, D E AU - Saffiotti, U AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/06/01/ PY - 1989 DA - 1989 Jun 01 SP - 3050 EP - 3056 VL - 49 IS - 11 SN - 0008-5472, 0008-5472 KW - Phosphates KW - 0 KW - Protein Precursors KW - Proteins KW - Transforming Growth Factor beta KW - strontium phosphate KW - 14414-90-5 KW - Strontium KW - YZS2RPE8LE KW - Index Medicus KW - Proteins -- pharmacology KW - Humans KW - Simian virus 40 KW - Infant, Newborn KW - Chromosome Aberrations KW - Cell Division -- drug effects KW - Male KW - Cell Line KW - Cell Survival KW - Karyotyping KW - Transfection KW - Phosphates -- pharmacology KW - Prostate -- pathology KW - Prostate -- ultrastructure KW - Strontium -- pharmacology KW - Cell Transformation, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78956716?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-23 N1 - Date created - 1989-06-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Parenteral antisecretory drug therapy in patients with Zollinger-Ellison syndrome. AN - 78937552; 2565842 AB - Forty-six patients with Zollinger-Ellison syndrome were studied prospectively to determine a safe and effective method and criterion for controlling gastric acid hypersecretion during periods when oral antisecretory agents could not be used. In each patient it was possible to reduce acid secretion to less than or equal to 10 mEq/h after an i.v. bolus of 150 or 300 mg of cimetidine and a stepwise titration of cimetidine given by continuous infusion. The mean dose given by i.v. infusion was 2.9 mg/kg body wt.h but there was a wide range (0.5-7.0 mg/kg body wt.h) and the minimal dose had to be determined individually for each patient. The minimal i.v. cimetidine dose did not correlate with basal or maximal acid output or fasting gastrin concentration, but correlated closely with either the previous oral dose of cimetidine (r = 0.96, p less than 0.001) or the previous oral dose of ranitidine or famotidine (r = 0.95, p less than 0.001). To study the efficacy and safety of an i.v. infusion of cimetidine, 34 patients undergoing surgery were maintained on i.v. cimetidine for a mean of 12 days (range 1-83 days). One-half of the patients did not require dose adjustment, whereas the remainder required an average of 2 adjustments, usually in the first 3 postoperative days. No patient developed complications attributable to gastric acid hypersecretion in the postoperative period, and there was no detectable neurologic, hematologic, or hepatic toxicity. This study demonstrates that a continuous i.v. infusion of cimetidine adequately inhibits gastric acid hypersecretion in patients with Zollinger-Ellison syndrome. However, high doses were frequently required, the dose had to be determined in a stepwise fashion individually for each patient, and the i.v. dose correlated with the previous oral dose. Reducing acid secretion to less than or equal to 10 mEq/h was a safe criterion during surgery and continuous i.v. cimetidine was safe and effective in achieving this degree of control for up to 83 days. JF - Gastroenterology AU - Saeed, Z A AU - Norton, J A AU - Frank, W O AU - Young, M D AU - Maton, P N AU - Gardner, J D AU - Jensen, R T AD - Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland. Y1 - 1989/06// PY - 1989 DA - June 1989 SP - 1393 EP - 1402 VL - 96 IS - 6 SN - 0016-5085, 0016-5085 KW - Histamine H2 Antagonists KW - 0 KW - Cimetidine KW - 80061L1WGD KW - Aspartate Aminotransferases KW - EC 2.6.1.1 KW - Alanine Transaminase KW - EC 2.6.1.2 KW - Abridged Index Medicus KW - Index Medicus KW - Administration, Oral KW - Drug Administration Schedule KW - Infusions, Intravenous KW - Dose-Response Relationship, Drug KW - Humans KW - Aged KW - Histamine H2 Antagonists -- administration & dosage KW - Aspartate Aminotransferases -- blood KW - Alanine Transaminase -- blood KW - Prospective Studies KW - Postoperative Complications -- blood KW - Adult KW - Middle Aged KW - Female KW - Male KW - Zollinger-Ellison Syndrome -- surgery KW - Zollinger-Ellison Syndrome -- drug therapy KW - Cimetidine -- administration & dosage KW - Gastric Acid -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78937552?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-15 N1 - Date created - 1989-06-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Protein kinase C activity can desensitize the gonadotropin-responsive adenylate cyclase in Leydig tumor cells. But hCG-induced desensitization does not involve protein kinase C activation. AN - 79002971; 2722787 AB - The murine Leydig tumor cell line, MLTC-1, contains a gonadotropin receptor-coupled adenylate cyclase. Although the binding of human choriogonadotropin (hCG) initially causes cells to accumulate cAMP, in time, the response to hCG is attenuated by desensitization. Treating intact cells with the tumor promoter, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), or with diacylglycerol also causes desensitization of the hCG response. These compounds are activators of calcium/phospholipid-dependent protein kinase (PKC). Treating MLTC-1 cells with TPA or dioctanoylglycerol increased the portion of PKC in the cell membrane fraction. This phenomenon is associated with activation of PKC. Treating isolated membranes with purified PKC desensitize the hCG response. Thus, desensitization caused by TPA or dioctanoylglycerol is probably mediated by PKC. PKC is normally activated when phosphoinositides are metabolized to diacylglycerol and inositol phosphates. There was no significant accumulation of inositol phosphates when cells were treated with hCG. hCG did not increase the portion of PKC in the cell membrane fraction. However, hCG could desensitize isolated membranes, but TPA could not. We conclude that although protein kinase C activity can desensitize the gonadotropin response, hCG does not cause desensitization by activating PKC. The implications of this observation are discussed. JF - The Journal of biological chemistry AU - Inoue, Y AU - Rebois, R V AD - Laboratory of Molecular and Cellular Neurobiology, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892. Y1 - 1989/05/25/ PY - 1989 DA - 1989 May 25 SP - 8504 EP - 8508 VL - 264 IS - 15 SN - 0021-9258, 0021-9258 KW - Chorionic Gonadotropin KW - 0 KW - Diglycerides KW - 1,2-dioctanoylglycerol KW - 1069-87-0 KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Inositol KW - 4L6452S749 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Diglycerides -- pharmacology KW - Phorbol 12,13-Dibutyrate -- metabolism KW - Enzyme Activation KW - Kinetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Inositol -- metabolism KW - Cell Line KW - Binding Sites KW - Protein Kinase C -- metabolism KW - Leydig Cell Tumor -- enzymology KW - Chorionic Gonadotropin -- pharmacology KW - Adenylyl Cyclases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79002971?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-29 N1 - Date created - 1989-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Structure of the human thyroid peroxidase gene: comparison and relationship to the human myeloperoxidase gene. AN - 79159423; 2548579 AB - All exons of the human thyroid peroxidase gene were cloned from phage and cosmid libraries and sequenced, including 2599 base pairs of upstream DNA. The gene contains 17 exons and covers at least 150 kilobase pairs of chromosome 2. The transcription start site was identified by both S1 mapping and primer extension; a typical TATA box was found 25 bases upstream of the putative start site. A comparison of the gene structures of thyroid peroxidase and a granulocyte protein, myeloperoxidase, revealed that the positions of the 3rd through 11th exon-intron junctions in thyroid peroxidase coincide exactly with those of the 2nd through 11th exon-intron junctions in myeloperoxidase except the 7th myeloperoxidase junction, that does not have any counterpart in thyroid peroxidase. The amino acid codon separation pattern in each junction is well conserved between both enzymes. Four exons, unique to thyroid peroxidase, are located at the 3' end of the gene (exons 13-16), each of which encompasses a different protein module. Three of these modules, representing exons 13, 14, and 15, bear significant similarities to C4b-beta 2 glycoprotein, the EGF-LDL receptor, and a typical transmembrane domain, respectively. The genes coding for these modules were probably fused to an ancestral peroxidase gene to generate the present thyroid peroxidase gene. The data suggest that intron loss, and/or insertion, and exon shuffling have played important roles in the evolution of the thyroid peroxidase gene. JF - Biochemistry AU - Kimura, S AU - Hong, Y S AU - Kotani, T AU - Ohtaki, S AU - Kikkawa, F AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/05/16/ PY - 1989 DA - 1989 May 16 SP - 4481 EP - 4489 VL - 28 IS - 10 SN - 0006-2960, 0006-2960 KW - DNA KW - 9007-49-2 KW - Peroxidase KW - EC 1.11.1.7 KW - Iodide Peroxidase KW - EC 1.11.1.8 KW - Index Medicus KW - Base Sequence KW - Sequence Homology, Nucleic Acid KW - Exons KW - Biological Evolution KW - Multigene Family KW - Humans KW - DNA -- genetics KW - Molecular Sequence Data KW - Introns KW - Transcription, Genetic KW - Amino Acid Sequence KW - Cloning, Molecular KW - Peroxidase -- genetics KW - Iodide Peroxidase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79159423?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-28 N1 - Date created - 1989-09-28 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M25710; GENBANK; M25711; M25703; M25704; M25701; M25702; J02856; M25707; M25712; M25713; M25708; M25714; M25705; M25715; M25706; M25709 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Metabolic and cellular basis of 2-butoxyethanol-induced hemolytic anemia in rats and assessment of human risk in vitro. AN - 79019379; 2730682 AB - Recent work in this laboratory indicated that 2-butoxyethanol (BE) causes acute hemolytic anemia in rats, and activation of BE to butoxyacetic acid (BAA), presumably through the intermediate 2-butoxyacetaldehyde (BAL), is a prerequisite for development of hematotoxicity. In the present studies, the effects of BE and its metabolites, BAL and BAA, on erythrocytes from rats and humans were investigated in vitro. Incubation of BE (up to 10 mM) with blood from male F344 rats caused no hemolysis and resulted in no metabolic alteration of BE. Further, addition of alcohol and aldehyde dehydrogenases, with their co-factors, to the incubation mixture failed to alter BE or its effect. At 20 mM, BE caused significant (P less than or equal to 0.05) hemolysis of rat erythrocytes accompanied by a significant (P less than or equal to 0.05) decrease in hematocrit (HCT). In contrast, incubation of BAL or BAA with rat blood caused time- and concentration-dependent swelling of red blood cells followed by hemolysis; however, BAA was significantly more efficacious than BAL. Addition of aldehyde dehydrogenase and its co-factors significantly (P less than or equal to 0.05) potentiated the effect of BAL on rat erythrocytes. Further in vitro investigation of the cellular mechanisms involved in the hemolytic effect revealed that incubation of rat blood with BAA or BAL caused a time- and concentration-dependent decrease in blood ATP concentration. As observed with the hemolytic effects, the decrease in blood ATP was significantly (P less than or equal to 0.05) greater with BAA than with BAl and was not induced by BE. Further, BAA caused no significant changes in the concentration of reduced glutathione and glucose-6-phosphate dehydrogenase in rat erythrocytes. Assessment of human sensitivity by incubation of human blood with BAA showed minimal swelling or hemolysis of erythrocytes with minimal decline in blood ATP levels at BAA concentrations several-fold higher than required to cause complete hemolysis of rat erythrocytes. In summary, the current studies confirm that the hemolytic effect of BE can be attributed primarily to its metabolite BAA, that hemolysis of rat erythrocytes by BAA or BAL is preceded by swelling and ATP depletion, suggesting that the erythrocyte membrane is the most likely target, and, finally, that human erythrocytes are comparatively insensitive to the hemolytic effects of BAA in vitro. JF - Biochemical pharmacology AU - Ghanayem, B I AD - National Institute of Environmental Health Sciences, National Toxicology Program/Systemic Toxicology Branch, Research Triangle Park, NC 27709. Y1 - 1989/05/15/ PY - 1989 DA - 1989 May 15 SP - 1679 EP - 1684 VL - 38 IS - 10 SN - 0006-2952, 0006-2952 KW - Acetates KW - 0 KW - Ethylene Glycols KW - Glycolates KW - n-butoxyacetic acid KW - 2516-93-0 KW - n-butoxyacetaldehyde KW - 29043-89-8 KW - Ethanol KW - 3K9958V90M KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Aldehyde Dehydrogenase KW - EC 1.2.1.3 KW - Acetaldehyde KW - GO1N1ZPR3B KW - n-butoxyethanol KW - I0P9XEZ9WV KW - Index Medicus KW - Acetaldehyde -- analogs & derivatives KW - Animals KW - Erythrocytes -- drug effects KW - Ethanol -- pharmacology KW - Humans KW - Adenosine Triphosphate -- blood KW - Erythrocytes -- metabolism KW - Rats KW - Risk KW - Rats, Inbred F344 KW - Aldehyde Dehydrogenase -- pharmacology KW - In Vitro Techniques KW - Acetaldehyde -- toxicity KW - Acetates -- toxicity KW - Male KW - Anemia, Hemolytic -- chemically induced KW - Ethylene Glycols -- toxicity KW - Ethylene Glycols -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79019379?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-26 N1 - Date created - 1989-06-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - IL-4 regulates IL-2 induction of lymphokine-activated killer activity from human lymphocytes. AN - 78987571; 2654291 AB - IL-4 is a pluripotent lymphokine acting on various cell types. We investigated the role of human IL-4 on the generation of lymphokine-activated killer (LAK) activity. Human IL-4 alone did not induce LAK activity and inhibited IL-2 induction of LAK activity from unstimulated PBMC, peripheral blood null cells, spleen cells, and lymph node cells in a dose-dependent manner. IL-4 also inhibited several phenomena induced by IL-2 such as cell proliferation, augmentation of NK activity, increase of Leu-19+ cells, and expression of IL-2R(p55) on either CD3+ or Leu-19+ cells. IL-4, however, augmented cell proliferation with other T cell mitogens including PHA, Con A, PMA, or allo-MHC Ag with or without IL-2. In contrast to unstimulated cells, IL-4 alone induced marked cell proliferation and LAK activity as well as Leu-19+ cells from in vitro IL-2 preactivated PBMC or null cells, and did not inhibit IL-2 induced cell proliferation, LAK activity, Leu-19+ cells and IL-2R(p55) expression, but rather augmented them with low doses of IL-2. Although IL-4 alone induced LAK activity from peripheral blood of some patients previously given IL-2, IL-4 inhibited in vitro LAK generation with IL-2 from these cells in most cases. Therefore, IL-4 appears to directly inhibit the IL-2 activation pathway via IL-2R(p70) and prevent resting LAK precursors from proliferating and differentiating into final effector cells. However, once cells were sufficiently preactivated by IL-2, IL-4 induced LAK activity and did not inhibit IL-2 activation of these cells. These data suggest an immunoregulatory role of IL-4 on human null cells and T cells. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Kawakami, Y AU - Custer, M C AU - Rosenberg, S A AU - Lotze, M T AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/05/15/ PY - 1989 DA - 1989 May 15 SP - 3452 EP - 3461 VL - 142 IS - 10 SN - 0022-1767, 0022-1767 KW - Adjuvants, Immunologic KW - 0 KW - Biological Factors KW - Cytokines KW - Growth Inhibitors KW - Interleukin-2 KW - Interleukins KW - Interleukin-4 KW - 207137-56-2 KW - Abridged Index Medicus KW - Index Medicus KW - Phenotype KW - Kinetics KW - Humans KW - Growth Inhibitors -- pharmacology KW - Lymphoid Tissue -- immunology KW - Biological Factors -- pharmacology KW - Drug Synergism KW - Killer Cells, Natural -- immunology KW - Lymphocyte Activation -- drug effects KW - Interleukin-2 -- pharmacology KW - Lymphocytes -- immunology KW - Interleukins -- pharmacology KW - Interleukin-2 -- therapeutic use KW - Lymphocytes -- classification KW - Cytotoxicity, Immunologic -- drug effects KW - Adjuvants, Immunologic -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78987571?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-19 N1 - Date created - 1989-06-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of MHC cDNA clones in the domestic cat. Diversity and evolution of class I genes. AN - 78984831; 2715636 AB - The abundant functional polymorphism and evolutionary divergence of mammalian MHC class I genes has been affirmed recently by sequence analysis of more than 40 mouse H-2 and human HLA transcripts. In a comparative approach to the evolution of the MHC, we isolated eight molecular clones of feline MHC (termed FLA for feline leukocyte antigen) class I genes from a cDNA library of a cat T cell lymphoma line. DNA sequence analysis of eight clones revealed that they all fell into one of two internally identical allelic groups which differed by 9% of their nucleotide sequences. The occurrence of only two allelic cDNA clones is consistent with the expression of a single heterozygous functional class I gene in the studied cell line despite the occurrence of more than 20 class I copies estimated to be present in the cat genome. Comparison of the FLA class I coding sequence with other class I genes from other species revealed that the domestic cat genes display 81 to 82% sequence identity with human, and 73 to 79% sequence identity with mouse class I genes. Feline and human class I genes have similar sequences and protein structures, with three (alpha) extracellular domains, one transmembrane domain, and one cytoplasmic domain. Variable codons detected in FLA class I alleles were, in most cases, in positions which were also variable in humans and mice, whereas invariant positions with defined functional constraints were generally conserved and invariant between the three species as well. Southern analysis of DNA from diverse species of Felidae revealed a similar numerosity and restriction pattern indicating conservation of the organization of class I genes during the Felidae radiation. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Yuhki, N AU - Heidecker, G F AU - O'Brien, S J AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, MD 21701-1013. Y1 - 1989/05/15/ PY - 1989 DA - 1989 May 15 SP - 3676 EP - 3682 VL - 142 IS - 10 SN - 0022-1767, 0022-1767 KW - Histocompatibility Antigens Class I KW - 0 KW - feline leukocyte antigen KW - DNA KW - 9007-49-2 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Base Sequence KW - Alleles KW - Sequence Homology, Nucleic Acid KW - Humans KW - Molecular Sequence Data KW - Rabbits KW - Mice KW - Amino Acid Sequence KW - Species Specificity KW - Cloning, Molecular KW - DNA -- isolation & purification KW - Cats -- genetics KW - Biological Evolution KW - Cats -- immunology KW - Histocompatibility Antigens Class I -- isolation & purification KW - Histocompatibility Antigens Class I -- genetics KW - Genes, MHC Class I UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78984831?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-19 N1 - Date created - 1989-06-19 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M26319; GENBANK; M26318 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 2,3,7,8-Tetrachlorodibenzo-p-dioxin enhancement of N-methyl-N'-nitro-N-nitrosoguanidine-induced transformation of rat tracheal epithelial cells in culture. AN - 78963308; 2713855 AB - The abilities of various dioxins to induce toxicity or transformation of rat tracheal epithelial cells in culture were examined. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) was not cytotoxic and did not induce transformation as measured by the induction of growth-altered, preneoplastic cells (termed enhanced growth variants). However, TCDD enhanced the transformation of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-initiated rat tracheal epithelial cells. Other dioxin congeners with 0 to 3 chloro substitutions were inactive in enhancing MNNG transformation. TCDD was most effective at a concentration of 0.3 nM and when treatment was administered immediately after MNNG exposure. The dose-response curves for enhancement of MNNG-induced transformation and induction of aryl hydrocarbon hydroxylase activity by TCDD were similar. These results are consistent with the hypothesis that the enhancement of cell transformation by TCDD is mediated through the TCDD receptor. TCDD also enhanced transformation when the cells were treated before MNNG treatment. The ability of 12-O-tetradecanoylphorbol-13-acetate (TPA) to enhance MNNG-induced rat tracheal epithelial transformation was also examined. In contrast to the findings with TCDD, the number of transformed colonies was increased only by pretreatment with TPA followed by MNNG. TPA-pretreatment enhanced equally the number of normal cells forming colonies and the total number of transformed colonies after selection; therefore, the transformation frequency (transformants per total surviving colonies) was unchanged by TPA. In contrast, TCDD treatment enhanced the transformation frequency in MNNG-exposed cultures since the number of transformed colonies increased while the number of total colonies remained constant. Thus, TCDD appears to act by a different mechanism than TPA. TCDD enhancement of MNNG-induced transformation may be attributed to a promotional effect, a comutagenic action, or a modulation of cell proliferation and/or differentiation mediated through the TCDD receptor. JF - Cancer research AU - Tanaka, N AU - Nettesheim, P AU - Gray, T AU - Nelson, K AU - Barrett, J C AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/05/15/ PY - 1989 DA - 1989 May 15 SP - 2703 EP - 2708 VL - 49 IS - 10 SN - 0008-5472, 0008-5472 KW - Dioxins KW - 0 KW - Polychlorinated Dibenzodioxins KW - Methylnitronitrosoguanidine KW - 12H3O2UGSF KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - Epithelium -- pathology KW - Male KW - Epithelium -- drug effects KW - Trachea -- pathology KW - Polychlorinated Dibenzodioxins -- toxicity KW - Cell Transformation, Neoplastic -- drug effects KW - Trachea -- drug effects KW - Dioxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78963308?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-12 N1 - Date created - 1989-06-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Infective endocarditis in opiate addicts: analysis of 80 cases studied at necropsy. AN - 78954197; 2711995 AB - Eighty opiate addicts were studied at necropsy. Fifty-nine patients had anatomic evidence of active infective endocarditis (IE); 11 had healed IE; and 10 had both. Of the 80 patients, the first episode of IE involved a single right-sided cardiac valve in 24 patients (30%); both a right- and a left-sided valve in 13 patients (16%); a single left-sided valve in 33 patients (41%); and both left-sided valves in 10 patients (13%). Of the 320 cardiac valves in the 80 patients, 103 were sites of vegetations, an average of 1.3 of the 4 valves. Of the 80 patients, the tricuspid valve was infected in 35 (44%), mitral in 34 (43%), aortic in 32 (40%) and pulmonic in 2 (3%). Of the 103 infected cardiac valves, the infection caused sufficient damage to cause dysfunction in 70 (68%): in 28 (88%) of 32 infected aortic valves; in 22 (63%) of 35 infected tricuspid valves; in 19 (56%) of the 34 infected mitral valves; and in 1 of the 2 infected pulmonic valves. Of the 80 patients, 57 (71%) had sufficient valvular damage to cause valvular dysfunction. Of the 80 patients, gross examination of the valves at necropsy indicated that the infected valve almost certainly had been anatomically normal in 65 patients (81%) and abnormal in 15 patients (19%) before the onset of IE. Of the 65 patients with previously anatomically normal valves, 86 (33%) of their 260 cardiac valves were sites of infection (average 1.3 valves/patient); of the 15 patients with infection superimposed on a previously abnormal valve, the infection in each involved previously abnormal valves (21 in the 15 patients) or 17 (28%) of their 60 cardiac valves were sites of infection (average 1.1 valve/patient). Of the 15 patients with abnormal cardiac valves before the infection, 7 had congenitally bicuspid aortic valves and 8 had diffuse fibrous thickening of the mitral valve typical of rheumatic heart disease with (6 patients) or without (2 patients) diffuse fibrous thickening of tricuspid aortic valves. Of the 80 patients, 42 (53%) died during their first episode of active IE, 17 (21%) underwent operative excision with or without valve replacement during the active IE, and in 21 patients (26%) the first episode of active IE healed. In 10 of the latter 21 patients, active IE recurred and was fatal. A total of 19 patients had cardiac valve excision with or without replacement, 17 during active IE and 2 after healing.(ABSTRACT TRUNCATED AT 250 WORDS) JF - The American journal of cardiology AU - Dressler, F A AU - Roberts, W C AD - Pathology Branch, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989/05/15/ PY - 1989 DA - 1989 May 15 SP - 1240 EP - 1257 VL - 63 IS - 17 SN - 0002-9149, 0002-9149 KW - Abridged Index Medicus KW - Index Medicus KW - Heart Valves -- surgery KW - Myocardium -- pathology KW - Humans KW - Adult KW - Postoperative Complications -- mortality KW - Heart Valves -- pathology KW - Middle Aged KW - Recurrence KW - Male KW - Female KW - Opioid-Related Disorders -- mortality KW - Endocarditis, Bacterial -- etiology KW - Endocarditis, Bacterial -- mortality KW - Endocarditis, Bacterial -- pathology KW - Opioid-Related Disorders -- complications KW - Opioid-Related Disorders -- pathology KW - Endocarditis, Bacterial -- surgery UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78954197?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-07 N1 - Date created - 1989-06-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine inhibits proton motive force in energized liver mitochondria. AN - 78927482; 2540715 AB - It is known that 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which induces Parkinson's-like disease in primates and humans, depletes hepatocytes of ATP and subsequently causes cell death. Incubation of rat liver mitochondria with MPTP and 1-methyl-4-phenyl pyridinium ion (MPP+) significantly inhibited incorporation of 32Pi into ATP.MPTP and MPP+ inhibited the development of membrane potential and pH gradient in energized rat liver mitochondria, suggesting that reduction of the proton motive force may have reduced ATP synthesis. Since deprenyl, an inhibitor of monoamine oxidase, prevented the formation of MPP+ and inhibited the decrease in membrane potential caused by MPTP, but not that caused by MPP+, these effects of MPTP, as well as cell death, probably were mediated by MPP+. This mechanism may play a role in the specific loss of dopaminergic neurons resulting in MPTP-induced Parkinson's disease. JF - Archives of biochemistry and biophysics AU - Singh, Y AU - Bhatnagar, R AU - Sidhu, G S AU - Batra, J K AU - Krishna, G AD - Section on Drug Tissue Interaction, National Heart, Lung and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989/05/15/ PY - 1989 DA - 1989 May 15 SP - 217 EP - 222 VL - 271 IS - 1 SN - 0003-9861, 0003-9861 KW - Neurotoxins KW - 0 KW - Protons KW - Pyridines KW - Pyridinium Compounds KW - Selegiline KW - 2K1V7GP655 KW - Adenosine Triphosphate KW - 8L70Q75FXE 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 - Dose-Response Relationship, Drug KW - Hydrogen-Ion Concentration KW - Action Potentials -- drug effects KW - Rats KW - Rats, Inbred Strains KW - Selegiline -- pharmacology KW - Energy Metabolism -- drug effects KW - Membrane Potentials -- drug effects KW - Male KW - Pyridinium Compounds -- antagonists & inhibitors KW - Mitochondria, Liver -- metabolism KW - Pyridinium Compounds -- pharmacology KW - Neurotoxins -- pharmacology KW - Pyridines -- antagonists & inhibitors KW - Mitochondria, Liver -- drug effects KW - Pyridines -- pharmacology KW - Adenosine Triphosphate -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78927482?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-07 N1 - Date created - 1989-06-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Analgesic use and chronic renal disease. AN - 78916020; 2651928 AB - To examine the use of analgesics as a cause of chronic renal disease, we performed a multicenter case-control study of 554 adults with newly diagnosed kidney disease (serum creatinine, greater than or equal to 130 mumol per liter [1.5 mg per deciliter]) and 516 matched control subjects selected randomly from the same area of North Carolina. Histories of use of analgesics (phenacetin, acetaminophen, and aspirin) were obtained by telephone interview with the patients or their proxies. Daily users of analgesics had significantly more renal disease than infrequent users (odds ratio, 2.79; 95 percent confidence interval, 1.85 to 4.21). The risk of renal disease was highest in daily users of phenacetin (odds ratio, 5.11; confidence interval, 1.76 to 14.9, after adjustment for the effects of other analgesics). The risk of renal disease was also increased in daily users of acetaminophen; after adjustment for the use of aspirin and phenacetin, the odds ratio was 3.21 (confidence interval, 1.05 to 9.80). There was no increased risk in daily aspirin users (adjusted odds ratio, 1.32; confidence interval, 0.69 to 2.51). The risks with daily use of either phenacetin or acetaminophen changed little after adjustment for diabetes, hypertension, and the indication for analgesic use. We conclude that the long-term, regular use of phenacetin may increase the risk of chronic renal disease. The long-term, daily use of acetaminophen, the major metabolite of phenacetin, is associated independently with an increased risk of chronic renal disease. We could find no increased risk in daily users of aspirin. JF - The New England journal of medicine AU - Sandler, D P AU - Smith, J C AU - Weinberg, C R AU - Buckalew, V M AU - Dennis, V W AU - Blythe, W B AU - Burgess, W P AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/05/11/ PY - 1989 DA - 1989 May 11 SP - 1238 EP - 1243 VL - 320 IS - 19 SN - 0028-4793, 0028-4793 KW - Analgesics KW - 0 KW - Acetaminophen KW - 362O9ITL9D KW - Phenacetin KW - ER0CTH01H9 KW - Aspirin KW - R16CO5Y76E KW - Abridged Index Medicus KW - Index Medicus KW - Multicenter Studies as Topic KW - Phenacetin -- adverse effects KW - Dose-Response Relationship, Drug KW - Humans KW - Acetaminophen -- adverse effects KW - Retrospective Studies KW - Aged KW - Aspirin -- adverse effects KW - Risk Factors KW - Adult KW - Headache -- drug therapy KW - Chronic Disease KW - Middle Aged KW - Arthritis -- drug therapy KW - Analgesics -- administration & dosage KW - Analgesics -- adverse effects KW - Kidney Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78916020?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-30 N1 - Date created - 1989-05-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: N Engl J Med. 1989 Oct 19;321(16):1125-7 [2797072] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of a novel site specific endonuclease produced by Mycoplasma fermentans: discovery while characterizing DNA binding proteins in T lymphocyte cell lines. AN - 19624575; 8739163 AB - We have discovered a new restriction endonuclease, MfeI, in nuclear extracts from T cells contaminated with Mycoplasma fermentans. This endonuclease was identified while studying proteins binding to the interleukin-2 receptor alpha chain gene promoter. MfeI cuts at the recognition sequence C'AATTG generating EcoRI compatible cohesive ends. Potential applications are discussed. Images JF - Nucleic Acids Research AU - Halden, N F AU - Wolf, J B AU - Leonard, W J AD - Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1989/05/11/ PY - 1989 DA - 1989 May 11 SP - 3491 EP - 3499 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 17 IS - 9 SN - 0305-1048, 0305-1048 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology; Biotechnology and Bioengineering Abstracts; Immunology Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - Promoters KW - Mycoplasma fermentans KW - Interleukin 2 KW - DNA-binding protein KW - Lymphocytes T KW - Endonuclease KW - J 02310:Genetics & Taxonomy KW - A 01310:Products of Microorganisms KW - N 14835:Protein-Nucleic Acids Association KW - F 06910:Microorganisms & Parasites KW - W 30945:Fermentation & Cell Culture UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19624575?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2008-12-01 N1 - Last updated - 2015-03-27 N1 - SubjectsTermNotLitGenreText - Promoters; Interleukin 2; DNA-binding protein; Lymphocytes T; Endonuclease; Mycoplasma fermentans ER - TY - JOUR T1 - Interferon-alpha but not AZT suppresses HIV expression in chronically infected cell lines. AN - 78962542; 2470148 AB - Promonocytic (U1) and T lymphocytic (ACH-2) cell lines chronically infected with human immunodeficiency virus type 1 (HIV-1) constitutively express low levels of virus, but expression can be induced by phorbol esters and cytokines. Whereas ACH-2 cells produce infectious virions, U1 cells produce defective, noninfectious particles. Although 3'-azido-3'-deoxythimidine (AZT) prevented acute HIV infection of susceptible cells, it did not prevent the induction of HIV expression in the infected cell lines. In contrast, interferon alpha (IFN-alpha) inhibited the release of reverse transcriptase and viral antigens into the culture supernatant after phorbol ester stimulation of both cell lines. Further, IFN-alpha suppressed the production or release (or both) of whole HIV virions, but had no effect on the amount of cell-associated viral proteins. Also, after phorbol ester stimulation of ACH-2 cells, IFN-alpha reduced the number of infectious viral particles secreted into the culture supernatant, but had no effect on the infectivity of cell-associated virus. These findings lend support to the combined use of antiviral agents that have action at both the early (AZT) and the late (IFN-alpha) stages of HIV replication. JF - Science (New York, N.Y.) AU - Poli, G AU - Orenstein, J M AU - Kinter, A AU - Folks, T M AU - Fauci, A S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1989/05/05/ PY - 1989 DA - 1989 May 05 SP - 575 EP - 577 VL - 244 IS - 4904 SN - 0036-8075, 0036-8075 KW - Interferon Type I KW - 0 KW - Recombinant Proteins KW - Zidovudine KW - 4B9XT59T7S KW - RNA-Directed DNA Polymerase KW - EC 2.7.7.49 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - AIDS/HIV KW - Acquired Immunodeficiency Syndrome -- therapy KW - Immunoblotting KW - Transcription, Genetic KW - Monocytes -- microbiology KW - Virion -- physiology KW - Vacuoles -- microbiology KW - RNA-Directed DNA Polymerase -- metabolism KW - Virion -- drug effects KW - Drug Therapy, Combination KW - Virion -- ultrastructure KW - T-Lymphocytes -- microbiology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Gene Expression Regulation KW - Microscopy, Electron KW - Cell Membrane -- microbiology KW - Cell Line KW - Interferon Type I -- administration & dosage KW - Virus Replication -- drug effects KW - Interferon Type I -- pharmacology KW - Zidovudine -- pharmacology KW - Zidovudine -- administration & dosage KW - HIV-1 -- physiology KW - HIV-1 -- drug effects KW - HIV-1 -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78962542?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-20 N1 - Date created - 1989-06-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Analysis of the glycosylation and phosphorylation of the lysosomal enzyme, beta-hexosaminidase B, by site-directed mutagenesis. AN - 78956359; 2708385 AB - Lysosomal enzymes require a mannose 6-phosphate recognition marker, constructed on asparagine-linked oligosaccharide chains, for targeting to lysosomes. We have identified the glycosylation sites of human beta-hexosaminidase B and have determined the influence of individual oligosaccharides on the phosphorylation, lysosomal targeting, and catalytic activity of the enzyme. The five potential glycosylation sites of the hexosaminidase beta-chain were modified individually by site-directed mutagenesis, and the constructs were expressed in COS 1 cells. By this analysis, we determined that four of the five potential sites were glycosylated. Two of the four oligosaccharides were preferentially phosphorylated. The absence of these two preferentially phosphorylated oligosaccharides resulted in greatly reduced amounts of the lysosomal form of the enzyme with increased secretion into the medium. The catalytic activity of beta-hexosaminidase B was not significantly altered by the absence of individual oligosaccharides suggesting the folding and assembly of the enzyme was not disrupted. JF - The Journal of biological chemistry AU - Sonderfeld-Fresko, S AU - Proia, R L AD - Genetics and Biochemistry Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1989/05/05/ PY - 1989 DA - 1989 May 05 SP - 7692 EP - 7697 VL - 264 IS - 13 SN - 0021-9258, 0021-9258 KW - Glycoproteins KW - 0 KW - Membrane Glycoproteins KW - mannoproteins KW - Hexosaminidases KW - EC 3.2.1.- KW - Index Medicus KW - Animals KW - Phosphorylation KW - Transfection KW - Humans KW - DNA Mutational Analysis KW - Protein Processing, Post-Translational KW - Cercopithecus aethiops KW - Biological Transport KW - Lysosomes -- enzymology KW - Glycosylation KW - Molecular Weight KW - Structure-Activity Relationship KW - Membrane Glycoproteins -- metabolism KW - Hexosaminidases -- genetics KW - Hexosaminidases -- metabolism KW - Glycoproteins -- metabolism KW - Glycoproteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78956359?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-02 N1 - Date created - 1989-06-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of a novel P450 expressed in rat lung: cDNA cloning and sequence, chromosome mapping, and induction by 3-methylcholanthrene. AN - 79098514; 2751996 AB - A novel P450 cDNA was isolated from a rat lung lambda gt11 library by hybridization with the rat P450 IIB1 cDNA probe. The cDNA-deduced amino acid sequence of this clone was 71% and 73% similar to rat IIA1 and IIA2 P450s; it was, therefore, designated IIA3 as the third member of the rat IIA subfamily. IIA3 demonstrates only 55% amino acid similarity with IIB1. Interestingly, this P450 also shared 85% and 94% amino acid similarities with human IIA3 and a mouse testosterone 15 alpha-hydroxylase P450, respectively, indicating that these P450s are orthologous counterparts to rat IIA3. Chromosome mapping, using mouse-hamster somatic cell hybrids, revealed that the IIA3 gene is localized on mouse chromosome 7. The IIA3 mRNA was detected in rat lung, and its level was induced 3-fold by treatment of rats with 3-methylcholanthrene. No IIA3 mRNA was seen in the liver, kidney, or intestine, even after long exposure of Northern blot filters to X-ray film. In contrast, the orthologous mouse and human IIA3 genes are expressed in liver. JF - Biochemistry AU - Kimura, S AU - Kozak, C A AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/05/02/ PY - 1989 DA - 1989 May 02 SP - 3798 EP - 3803 VL - 28 IS - 9 SN - 0006-2960, 0006-2960 KW - Methylcholanthrene KW - 56-49-5 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Rats KW - Animals KW - Base Sequence KW - Blotting, Northern KW - DNA -- genetics KW - Molecular Sequence Data KW - Enzyme Induction KW - Amino Acid Sequence KW - Female KW - Genes KW - Methylcholanthrene -- pharmacology KW - Cytochrome P-450 Enzyme System -- genetics KW - Lung -- drug effects KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Lung -- enzymology KW - Chromosome Mapping KW - Cloning, Molecular UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79098514?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-29 N1 - Date created - 1989-08-29 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - J02852; GENBANK N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prosthetics, orthotics, and assistive devices. 4. Orthotic management of selected disorders. AN - 85224450; pmid-2655561 AB - This self-directed learning module presents core information and new advances in the orthotic management of problems of the runner and of patients with neurovascular foot ulcers or arthritis. Additional topics covered include a comprehensive approach to positioning and splinting for burns and tone-reducing orthoses for spasticity management. It is part of the chapter on prosthetics, orthotics, and assistive devices for the Self-Directed Medical Knowledge Program Study Guide for practitioners and trainees in physical medicine and rehabilitation. JF - Archives of Physical Medicine and Rehabilitation AU - Hicks, J E AU - Leonard, J A AU - Nelson, V S AU - Fisher, S V AU - Esquenazi, A AD - National Institutes of Health, Bethesda, MD 20892. PY - 1989 SP - S210 EP - S217 VL - 70 IS - 5-S SN - 0003-9993, 0003-9993 KW - Burns KW - Muscle Spasticity KW - Arthritis KW - Human KW - Adult KW - Prosthesis Design KW - Child KW - Foot Diseases KW - Orthotic Devices UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85224450?accountid=14244 LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Decomposition and quality control considerations in biological work with fecapentaene preparations. AN - 79588896; 2519720 AB - Solutions of synthetic fecapentaene 12 (FP-12) intended for carcinogenicity studies were found to decompose extremely rapidly during customary dosage procedures. Apparent half-lives as short as 15 min were observed. While rates and even the qualitative course of decomposition were surprisingly variable in replicate experiments, high concentration and exposure to air were confirmed to be especially important destabilizing influences. The results suggested a primary role for a radical decomposition mechanism in the presence of atmospheric oxygen. Consistent with this hypothesis, FP-12 solutions were significantly stabilized by the radical chain-breaking antioxidant vitamin E. On the other hand, dithiothreitol greatly destabilized FP-12, presumably because of its nucleophilicity. The diacetyl diester of FP-12 was more soluble than the parent diol, but its decomposition rates in the presence and absence of vitamin E were similar to those of unesterified FP-12. Ultraviolet irradiation of an all-trans-FP-12 solution decreased its concentration by 70% in 0.5 min. The mutagenicities of the decomposition/isomerization products of FP-12, as studied in Salmonella typhimurium tester strain TA 100, ranged from negligible to comparable with all-trans-FP-12 itself. It is concluded that unchecked decomposition of fecapentaene preparations can profoundly affect biological tests therewith. While this can be largely controlled through the use of rigorous precautions, including protection from air, light, nucleophiles, and acids as well as selection of the lowest concentration compatible with the application at hand, the data argue strongly for inclusion of appropriate quality control measures in all future dosing operations to prove that the biological activity reported is that of the fecapentaene itself rather than that of a decomposed dosing solution. JF - Chemical research in toxicology AU - Streeter, A J AU - Donovan, P J AU - Anjo, T AU - Ohannesian, L AU - Sheffels, P R AU - Wu, P P AU - Keefer, L K AU - Andrews, A W AU - Bradford, W W AU - Reist, E J AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research Facility, Maryland 21701. PY - 1989 SP - 162 EP - 168 VL - 2 IS - 3 SN - 0893-228X, 0893-228X KW - Esters KW - 0 KW - Mutagens KW - Polyenes KW - diacetylfecapentaene-12 KW - 120789-74-4 KW - Vitamin E KW - 1406-18-4 KW - 1-(1-glycero)dodeca-1,3,5,7,9-pentaene KW - 84000-59-9 KW - Dithiothreitol KW - T8ID5YZU6Y KW - Index Medicus KW - Esters -- chemistry KW - Mutagenicity Tests KW - Solubility KW - Vitamin E -- chemistry KW - Esters -- chemical synthesis KW - Spectrophotometry, Ultraviolet KW - Quality Control KW - Chromatography, High Pressure Liquid KW - Dithiothreitol -- chemistry KW - Polyenes -- chemical synthesis KW - Polyenes -- toxicity KW - Mutagens -- toxicity KW - Mutagens -- chemical synthesis KW - Polyenes -- chemistry KW - Mutagens -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79588896?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-24 N1 - Date created - 1992-02-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Covalent bonding of the prosthetic heme to protein: a potential mechanism for the suicide inactivation or activation of hemoproteins. AN - 79588609; 2519716 AB - In this perspective we have described a newly characterized pathway for the metabolism of the prosthetic heme of cytochrome P-450, which results in the formation of protein-bound adducts. This reaction occurs when the cytochrome P-450 metabolizes a variety of xenobiotics as well as endogenous compounds such as hydrogen peroxide and lipid hydroperoxides. It also takes place during the reactions catalyzed by other hemoproteins, such as myoglobin and hemoglobin. In the case of the reaction of ferrous myoglobin with BrCCl3, under single-turnover conditions, an intact heme moiety becomes covalently bound to an active-site amino acid. This covalently altered protein has significantly enhanced reductive activity compared to that of native myoglobin, as demonstrated by its rapid reduction of molecular oxygen and CCl4. It also is more rapidly proteolyzed than myoglobin. These findings may have relevance to the P-450 cytochromes in which suicide inactivation, destruction of the heme prosthetic group, and loss of the protein is observed. The activation of hemoproteins to heme-protein adducts may also have toxicological significance, perhaps in oxygen reperfusion injury in the myocardium as well as other tissues by enhancing the production of oxygen-derived radicals from molecular oxygen and lipid hydroperoxides. Clearly, further research in the characterization of heme-protein adducts is necessary before their importance in protein turnover and oxygen-induced injury can be determined. JF - Chemical research in toxicology AU - Osawa, Y AU - Pohl, L R AD - Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. PY - 1989 SP - 131 EP - 141 VL - 2 IS - 3 SN - 0893-228X, 0893-228X KW - Hemeproteins KW - 0 KW - Heme KW - 42VZT0U6YR KW - Index Medicus KW - Animals KW - Biotransformation KW - Humans KW - Protein Binding KW - Hemeproteins -- metabolism KW - Heme -- metabolism KW - Hemeproteins -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79588609?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-24 N1 - Date created - 1992-02-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Recall memory deficit in schizophrenia. A possible manifestation of prefrontal dysfunction. AN - 79567186; 2487166 AB - Patients with schizophrenia have memory deficits when compared to other neuropsychiatric and normal samples, but the mechanism by which the deficits arise is obscure. In the present study, 13 older, less educated normal subjects, and 31 inpatients with schizophrenia were administered the Selective Reminding test. In addition, the schizophrenic patients received the Mini Mental State Exam and the Brief Psychiatric Rating Scale. While normal subjects performed at a higher level on various measures of recall, a significant effect of repeated trials was present for each group for each measure, indicating that both groups learned. Normal subjects also outperformed the patients on a test of recognition memory. However, the patients exhibited a significantly greater disparity between recognition and recall than did the normal subjects, suggesting they were better able to acquire new information than to retrieve it ('forgetting to remember'). Moreover, anergia, a factor measure on the Brief Psychiatric Rating Scale, correlated significantly with recall, but not recognition memory, in the patient group. The data are suggestive of prefrontal-type cognitive and behavioral deficits in schizophrenia. JF - Schizophrenia research AU - Goldberg, T E AU - Weinberger, D R AU - Pliskin, N H AU - Berman, K F AU - Podd, M H AD - Clinical Brain Disorders Branch, National Institute of Mental Health, Neurosciences Research Hospital, Washington, DC 20032. PY - 1989 SP - 251 EP - 257 VL - 2 IS - 3 SN - 0920-9964, 0920-9964 KW - Benztropine KW - 1NHL2J4X8K KW - Index Medicus KW - Benztropine -- adverse effects KW - Humans KW - Verbal Learning -- drug effects KW - Verbal Learning -- physiology KW - Memory, Short-Term -- physiology KW - Memory, Short-Term -- drug effects KW - Retention (Psychology) -- physiology KW - Benztropine -- administration & dosage KW - Psychiatric Status Rating Scales KW - Adult KW - Retention (Psychology) -- drug effects KW - Middle Aged KW - Neuropsychological Tests KW - Female KW - Male KW - Frontal Lobe -- physiopathology KW - Mental Recall -- physiology KW - Frontal Lobe -- drug effects KW - Schizophrenic Psychology KW - Schizophrenia -- drug therapy KW - Mental Recall -- drug effects KW - Schizophrenia -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79567186?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-08 N1 - Date created - 1991-03-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interactions between pentazocine and tripelennamine on autonomic and nociceptive measures in the dog. AN - 79205400; 2780781 AB - Pentazocine and tripelennamine, which have been abused in combination by humans, were evaluated for pharmacologic interactions on autonomic, behavioral, and antinociceptive measures in chronic spinal dogs. Pentazocine (0.31-5 mg/kg, IV) produced miosis, hypothermia and antinociception which was mediated by spinal and supraspinal reflexes; these effects were antagonized by naltrexone. Tripelennamine (0.63-2.5 mg/kg, IV) elicited mydriasis, hyperthermia and antinociception; these effects were not blocked by naltrexone. Tripelennamine produced antinociception only on the supraspinally-mediated skin twitch reflex. Interactions between pentazocine and tripelennamine varied depending on the response measured. Effects of both drugs on pupils were additive. Temperature effects were infra-additive, with the hyperthermic effects of tripelennamine predominating over the pentazocine hypothermia, resulting in a complete physiologic antagonism of pentazocine hypothermia. Antinociception, measured by flexor reflex depression, represented only the effect of pentazocine, whereas skin twitch reflex antinociception reflected either infra-additive or additive properties. The coadministration of nonconvulsive doses of pentazocine and tripelennamine produced seizures indicating a potentiated adverse interaction. In summary, the patterns of the pentazocine-triplennamine interactions were complex and the effects of tripelennamine could not be attributed to opioid activity. JF - Pharmacology, biochemistry, and behavior AU - Vaupel, D B AD - Neuropharmacology Laboratory, National Institute on Drug Abuse Addiction Research Center, Baltimore, MD 21224. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 245 EP - 251 VL - 33 IS - 1 SN - 0091-3057, 0091-3057 KW - Tripelennamine KW - 3C5ORO99TY KW - Naltrexone KW - 5S6W795CQM KW - Pentazocine KW - RP4A60D26L KW - Index Medicus KW - Behavior, Animal -- drug effects KW - Animals KW - Drug Interactions KW - Pupil -- drug effects KW - Body Temperature -- drug effects KW - Reflex -- drug effects KW - Dose-Response Relationship, Drug KW - Naltrexone -- pharmacology KW - Dogs KW - Time Factors KW - Female KW - Tripelennamine -- pharmacology KW - Pentazocine -- pharmacology KW - Autonomic Nervous System -- drug effects KW - Pentazocine -- antagonists & inhibitors KW - Tripelennamine -- antagonists & inhibitors KW - Nociceptors -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79205400?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-26 N1 - Date created - 1989-10-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Joining of linear plasmid DNA is reduced and error-prone in Bloom's syndrome cells. AN - 79172006; 2767047 AB - A linearized, replicating, shuttle vector plasmid, pZ189, was used to measure in vivo DNA joining ability of cells from patients with the cancer-prone, immunodeficient, chromosome breakage disorder, Bloom's syndrome (BS). The BS cell lines we studied were reported to contain reduced in vitro activity of DNA ligase I. We assessed in vivo joining ability by transfecting linear plasmids with overlapping or blunt ends (produced by EcoRI or StuI) into BS and normal fibroblast or lymphoblast host cells and measuring the amount of re-joined, replicated plasmids by their ability to transform bacteria. With plasmids having either overlapping or blunt ends we found a 1.3- to 3-fold lower (P less than 0.05) joining efficiency in BS cells than in the normal cells. The mutation frequency of the recovered plasmids was measured by screening for function of the suppressor tRNA contained in pZ189, for plasmid size, for presence of restriction sites, or by DNA sequencing. The spontaneous mutation frequency with the circular plasmid was 0.05-0.08% with both BS cell lines, values 2- to 21-fold higher (P less than 0.03) than with the normal cell lines. The mutation frequency with the linear plasmid passaged through both BS cell lines was 21-52%, values 1.4- to 5.4-fold higher (P less than 0.001) than with the normal lines. Detailed analysis of 210 recovered plasmids revealed an increase (P less than or equal to 0.001) in deletions, insertions or complex mutations at the joining sites, and in point mutations with the EcoRI cut plasmid with the BS cells in comparison to the normal cells.(ABSTRACT TRUNCATED AT 250 WORDS) JF - The EMBO journal AU - Rünger, T M AU - Kraemer, K H AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 1419 EP - 1425 VL - 8 IS - 5 SN - 0261-4189, 0261-4189 KW - DNA KW - 9007-49-2 KW - DNA Ligases KW - EC 6.5.1.- KW - Index Medicus KW - Transfection KW - DNA Damage KW - Humans KW - Mutation KW - DNA Ligases -- deficiency KW - DNA -- genetics KW - Bloom Syndrome -- genetics KW - Plasmids KW - Bloom Syndrome -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79172006?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-22 N1 - Date created - 1989-09-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Clin Invest. 1975 Jul;56(1):1-7 [124745] Proc Natl Acad Sci U S A. 1987 Jul;84(14):4944-8 [3474635] J Clin Invest. 1987 Dec;80(6):1613-7 [3680516] Proc Natl Acad Sci U S A. 1987 Nov;84(22):8016-20 [3479778] Genes Dev. 1987 Oct;1(8):751-61 [3428598] Proc Natl Acad Sci U S A. 1989 Jan;86(2):670-4 [2911598] FEBS Lett. 1976 Aug 1;67(1):1-8 [782919] Clin Immunol Immunopathol. 1979 Jan;12(1):12-9 [421370] Nucleic Acids Res. 1979 Nov 24;7(6):1513-23 [388356] Virology. 1981 Mar;109(2):353-65 [6259817] Proc Natl Acad Sci U S A. 1981 May;78(5):3133-7 [6942420] Clin Immunol Immunopathol. 1982 Feb;22(2):247-58 [6980748] Mol Cell Biol. 1982 Oct;2(10):1258-69 [6294502] Proc Natl Acad Sci U S A. 1983 May;80(10):3015-9 [6574469] Science. 1983 Aug 26;221(4613):851-3 [6879180] Clin Genet. 1984 Feb;25(2):166-74 [6705251] Mol Cell Biol. 1984 Mar;4(3):387-98 [6325874] Mol Cell Biol. 1984 Mar;4(3):435-41 [6325877] Proc Natl Acad Sci U S A. 1985 Oct;82(19):6622-6 [2995975] Gene. 1985;38(1-3):233-7 [2998945] Clin Immunol Immunopathol. 1985 May;35(2):226-33 [3878246] Proc Natl Acad Sci U S A. 1986 Nov;83(21):8273-7 [3464953] Somat Cell Mol Genet. 1987 Mar;13(2):111-7 [3031825] Cell. 1987 Jun 19;49(6):775-83 [3495343] J Am Acad Dermatol. 1987 Sep;17(3):479-88 [3655026] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Multiple mechanisms for the carcinogenic effects of asbestos and other mineral fibers. AN - 79128794; 2667990 AB - Asbestos and other mineral fibers are carcinogenic to humans and animals but differ from many carcinogens in that they do not induce gene mutations. An understanding of these interesting human carcinogens, therefore, is an important problem in cancer research. Asbestos and other fibers induce predominantly two types of cancers: mesotheliomas and bronchogenic carcinomas. Fiber size is an important factor in the carcinogenic activity of these substances as has been shown for mesothelioma induction. For bronchogenic carcinomas, but not for mesotheliomas, a synergistic effect of asbestos exposure and cigarette smoke has been observed in humans. The mechanisms by which fibers alone versus fibers in concert with other carcinogens induce cancers are probably distinct. In addition to fiber dimensions, fiber durability and surface properties of fibers are important properties affecting carcinogenicity. Evidence exists that asbestos is a complete carcinogen, an initiator and a promoter. Multiple mechanisms must be operative to explain the diverse effects of mineral fibers. Although asbestos is inactive as a gene mutagen, there is now clear evidence that it induces chromosomal mutations (aneuploidy and aberrations) in a wide variety of mammalian cells including mesothelial cells. Asbestos also induces transformation of cells in culture including mesothelial cells and fibroblasts. A mechanism for cell transformation, which is dependent on fiber dimension, has been proposed. The fibers are phagocytized by the cells and accumulate in the perinuclear region of the cells. When the cell undergoes mitosis, the physical presence of the fibers interferes with chromosome segregation and results in anaphase abnormalities. The transformed cells show aneuploidy and other chromosome abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Environmental health perspectives AU - Barrett, J C AU - Lamb, P W AU - Wiseman, R W AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 81 EP - 89 VL - 81 SN - 0091-6765, 0091-6765 KW - Carcinogens KW - 0 KW - Asbestos KW - 1332-21-4 KW - Index Medicus KW - Carcinoma, Bronchogenic -- etiology KW - Animals KW - Lung Neoplasms -- etiology KW - Cocarcinogenesis KW - Cell Transformation, Neoplastic -- etiology KW - Particle Size KW - Humans KW - Mesothelioma -- etiology KW - Mesothelioma -- genetics KW - Lung Neoplasms -- genetics KW - Cell Transformation, Neoplastic -- genetics KW - Asbestos -- adverse effects KW - Asbestos -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79128794?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-20 N1 - Date created - 1989-09-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Ann N Y Acad Sci. 1979;330:473-90 [294198] Drug Chem Toxicol. 1987;10(1-2):157-80 [2824166] Nature. 1987 Dec 10-16;330(6148):578-81 [2825033] Science. 1987 Dec 11;238(4833):1539-45 [3317834] Cancer Res. 1988 Jan 1;48(1):142-7 [3334988] Symp Fundam Cancer Res. 1986;39:45-56 [3321309] IARC Sci Publ. 1980;(30):485-9 [7053096] J Natl Cancer Inst. 1981 Nov;67(5):965-75 [6946253] J Natl Cancer Inst. 1981 Nov;67(5):977-89 [7029102] Science. 1982 Jan 8;215(4529):181-2 [6274023] Br J Cancer. 1982 Jan;45(1):124-35 [7059455] Cancer Lett. 1983 Mar;18(2):221-7 [6299520] Annu Rev Pharmacol Toxicol. 1983;23:595-615 [6347054] Sci Total Environ. 1983 Sep;30:147-66 [6316498] Cancer Res. 1984 May;44(5):2170-80 [6324999] Environ Res. 1984 Oct;35(1):277-92 [6092048] Carcinogenesis. 1985 Mar;6(3):473-5 [3978760] Carcinogenesis. 1985 Apr;6(4):523-9 [2985292] Br J Cancer. 1985 May;51(5):727-30 [2986668] Proc Natl Acad Sci U S A. 1985 Jun;82(11):3884-8 [2987952] Cancer Genet Cytogenet. 1986 Feb 15;20(3-4):191-201 [3943062] Mutat Res. 1986 Mar;169(3):141-8 [3005853] Cancer Genet Cytogenet. 1986 Jul;22(3):225-37 [3708554] JAMA. 1968 Apr 8;204(2):101-5 [5694531] Br J Cancer. 1974 Mar;29(3):252-69 [4364384] Adv Pharmacol Chemother. 1975;12(0):291-402 [1098431] Nature. 1975 Sep 4;257(5521):56-8 [1161005] Environ Res. 1975 Oct;10(2):165-73 [811459] Mutat Res. 1977 May;43(2):159-64 [194149] Br J Exp Pathol. 1977 Oct;58(5):465-73 [588440] Science. 1980 Jan 18;207(4428):311-3 [7350661] Proc Natl Acad Sci U S A. 1986 Aug;83(16):5992-6 [3461473] Cancer Res. 1986 Nov;46(11):5795-802 [3756923] Environ Res. 1980 Apr;21(2):416-22 [7408813] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Perturbations of the immune system by xenobiotics. AN - 79128745; 2667976 AB - Classically, immunotoxicology has been defined as the study of adverse effect on the immune system associated with exposure to environmental chemicals, pharmacologic agents, and biologicals. Although a multitude of immune system defects may occur, these can be generally categorized as immunomodulation (immune suppression or potentiation), hypersensitivity (i.e., allergy), and autoimmunity. We present here a brief synopsis of the ontogeny of immunotoxicology as a discipline including methodology currently used in our laboratory, as well as in others, for investigating the immunomodulatory potential of chemicals at the cellular and biochemical level. Additionally, we summarize some studies related to the immunosuppressive effects of one particular compound, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Last we discuss potential future directions and challenges in the field of immunotoxicology. JF - Environmental health perspectives AU - Luster, M I AU - Ackermann, M F AU - Germolec, D R AU - Rosenthal, G J AD - Division of Toxicology Research and Testing, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 157 EP - 162 VL - 81 SN - 0091-6765, 0091-6765 KW - Xenobiotics KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Toxicology -- methods KW - Immune System -- drug effects KW - Immune System -- physiopathology KW - Xenobiotics -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79128745?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-20 N1 - Date created - 1989-09-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: CRC Crit Rev Toxicol. 1977 May;5(1):67-101 [17515] Science. 1978 Mar 17;199(4334):1207-9 [204005] Arch Toxicol Suppl. 1980;4:95-108 [7002113] Annu Rev Pharmacol Toxicol. 1982;22:517-54 [6282188] Fundam Appl Toxicol. 1982 Nov-Dec;2(6):327-30 [6136448] Fundam Appl Toxicol. 1988 Jan;10(1):2-19 [3280374] Lancet. 1984 May 26;1(8387):1174-5 [6144890] Fundam Appl Toxicol. 1984 Oct;4(5):692-9 [6510600] Annu Rev Pharmacol Toxicol. 1987;27:23-49 [3555316] J Immunol. 1988 Feb 1;140(3):928-35 [3257509] Immunopharmacology. 1983 Aug;6(2):143-53 [6309701] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mortality among United States Coast Guard marine inspectors. AN - 79114624; 2751350 AB - Work history records and fitness reports were obtained for 1,767 marine inspectors of the U.S. Coast Guard between 1942 and 1970 and for a comparison group of 1,914 officers who had never been marine inspectors. Potential exposure to chemicals was assessed by one of the authors (RP), who is knowledgeable about marine inspection duties. Marine inspectors and noninspectors had a deficit in overall mortality compared to that expected from the general U.S. population (standardized mortality ratios [SMRs = 79 and 63, respectively]). Deficits occurred for most major causes of death, including infectious and parasitic diseases, digestive and urinary systems, and accidents. Marine inspectors had excesses of cirrhosis of the liver (SMR = 136) and motor vehicle accidents (SMR = 107), and cancers of the lymphatic and hematopoietic system (SMR = 157), whereas noninspectors had deficits for these causes of death. Comparison of mortality rates directly adjusted to the age distribution of the inspectors and noninspectors combined also demonstrated that mortality for these causes of death was greater among inspectors than noninspectors (directly adjusted ratio ratios of 190, 145, and 198) for cirrhosis of the liver, motor vehicle accidents, and lymphatic and hematopoietic system cancer, respectively. The SMRs rose with increasing probability of exposure to chemicals for motor vehicle accidents, cirrhosis of the liver, liver cancer, and leukemia, which suggests that contact with chemicals during inspection of merchant vessels may be involved in the development of these diseases among marine inspectors. JF - Archives of environmental health AU - Blair, A AU - Haas, T AU - Prosser, R AU - Morrissette, M AU - Blackman, K AU - Grauman, D AU - van Dusen, P AU - Moran, F AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, Maryland. PY - 1989 SP - 150 EP - 156 VL - 44 IS - 3 SN - 0003-9896, 0003-9896 KW - Abridged Index Medicus KW - Index Medicus KW - Ships KW - Myeloproliferative Disorders -- mortality KW - Accidents, Traffic -- mortality KW - Humans KW - Liver Neoplasms -- mortality KW - Adult KW - Middle Aged KW - Liver Cirrhosis -- mortality KW - Male KW - Mortality KW - Environmental Exposure KW - Cause of Death UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79114624?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-23 N1 - Date created - 1989-08-23 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - Testing for increased carcinogenicity using a survival-adjusted quantal response test. AN - 79095343; 2744275 AB - The linear trend test in proportions is frequently used to analyze the results of animal carcinogenicity experiments. This test has two major advantages over other frequently used tests; it is easily understood and it is simple to calculate. This test, however, fails to correct for treatment-related differences in survival across the experimental groups. A test which is a simple modification of the linear trend test in proportions and which has the same advantages is proposed to correct for differences in survival. The results of this modified test are compared to those of the linear trend test in proportions, the incidental tumor test, the logistic regression score test, the life table test, and the truncated trend test using information on the incidence of combined alveolar/bronchiolar adenomas or carcinomas in female B6C3F1 mice exposed to vinylcyclohexene diepoxide. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Portier, C J AU - Bailer, A J AD - Statistics and Biomathematics Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 731 EP - 737 VL - 12 IS - 4 SN - 0272-0590, 0272-0590 KW - Cyclohexanes KW - 0 KW - Cyclohexenes KW - Vinyl Compounds KW - 4-vinyl-1-cyclohexene dioxide KW - 596C064IG4 KW - Index Medicus KW - Vinyl Compounds -- toxicity KW - Animals KW - Adenoma -- chemically induced KW - Mice KW - Cyclohexanes -- toxicity KW - Female KW - Bronchial Neoplasms -- chemically induced KW - Mathematics KW - Carcinoma -- chemically induced KW - Carcinogenicity Tests UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79095343?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-25 N1 - Date created - 1989-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The histamine content of oriental foods. AN - 79086397; 2744659 AB - Several of the symptoms of scombroid poisoning (i.e. histamine toxicity) resemble those observed in people suffering from Chinese restaurant syndrome. Therefore, the histamine content of representative Chinese cuisine, which included 31 common dishes, 12 condiments and 12 basic ingredients from several sources, was measured using a sensitive and specific radioenzymatic assay. A further enzymatic procedure involving diamine oxidase was used to verify that the substance measured was histamine. A total of 184 assays were performed on 57 samples in the study. High levels of histamine were found in the cheeses, which were used as positive controls (863.6 micrograms histamine/g blue cheese and 107.4 micrograms histamine/g Parmesan cheese), and in some common condiments, including tamari (2392.2 micrograms histamine/g sample) and one brand of soy sauce (220.4 micrograms histamine/g sample). The histamine content of four condiments and three common dishes was over 10 micrograms histamine/g sample, while four condiments and 16 common dishes contained less than 1 microgram histamine/g sample. Calculations involving representative amounts of food that can be consumed at a typical oriental meal suggest that, in some cases, histamine intake may approach toxic levels. The results are discussed with regard to the possible role of histamine in reactions associated with restaurant meals. JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association AU - Chin, K W AU - Garriga, M M AU - Metcalfe, D D AD - Mast Cell Physiology Section, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 283 EP - 287 VL - 27 IS - 5 SN - 0278-6915, 0278-6915 KW - Histamine KW - 820484N8I3 KW - Index Medicus KW - Animals KW - Condiments -- analysis KW - Wine -- analysis KW - Decapoda (Crustacea) KW - Meat -- analysis KW - Cheese -- analysis KW - Food Analysis KW - Histamine -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79086397?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-18 N1 - Date created - 1989-08-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antidepressants. A comparative review of the clinical pharmacology and therapeutic use of the 'newer' versus the 'older' drugs. AN - 79082041; 2663417 AB - Supplementing but not supplanting the original series of tricyclic and monoamine oxidase (MAO) inhibitor compounds, a new generation of antidepressant medications has been developed and marketed throughout the past decade. Constituting a more diverse group of drugs than the standard agents, the newer drugs in general have more selective acute biochemical actions (reuptake blockade of a single neurotransmitter, inhibition of 1 subtype of MAO), enabling more precise targeting of symptoms and avoiding common antidepressant-associated side effects, especially anticholinergic and cardiovascular effects. Moreover, a number of recent additions to this group, such as bupropion and ademetionine (S-adenosyl-methionine), incorporate novel mechanisms of action, challenging previous concepts of how antidepressants work, and offering opportunities for research into the pathophysiology of mood disorders. Caution in prescribing the newer antidepressants must be applied, however, as recent experience, e.g. with nomifensine, suggests that unforeseen toxicities may not appear until a medication has been in use for several years. JF - Drugs AU - Rudorfer, M V AU - Potter, W Z AD - Section on Clinical Pharmacology, National Institute of Mental Health, Bethesda, Maryland. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 713 EP - 738 VL - 37 IS - 5 SN - 0012-6667, 0012-6667 KW - Antidepressive Agents KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Antidepressive Agents -- pharmacology KW - Depressive Disorder -- drug therapy KW - Antidepressive Agents -- therapeutic use KW - Antidepressive Agents -- classification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79082041?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-21 N1 - Date created - 1989-08-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cancer knowledge and related practices: results from the National Adolescent Student Health Survey. AN - 79080673; 2739365 AB - The National Adolescent Student Health Survey (NASHS) provides information on student knowledge, attitudes, and self-reported practices of eighth and 10th grade students in eight health areas. Data from the NASHS were reviewed relative to cancer risk factors, specifically, smoking, smokeless tobacco use, and nutrition. About 21% of 10th grade students reported smoking and a large percentage of both eighth and 10th grade students reported eating foods high in fat. The data indicate youth may be at increased risk for cancer and that much of that risk can be reduced by eliminating smoking and lowering dietary fat. JF - The Journal of school health AU - Portnoy, B AU - Christenson, G M AD - Division of Cancer Prevention and Control, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 218 EP - 224 VL - 59 IS - 5 SN - 0022-4391, 0022-4391 KW - Index Medicus KW - Nursing KW - United States KW - Plants, Toxic KW - Attitude to Health KW - Humans KW - Smoking -- adverse effects KW - Data Collection KW - Adolescent KW - National Health Programs KW - Male KW - Female KW - Tobacco, Smokeless KW - Nutritional Sciences -- education KW - Health Behavior KW - Neoplasms -- prevention & control KW - Health Education UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79080673?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-01 N1 - Date created - 1989-08-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Smokeless tobacco use by youth in the U.S. AN - 79076443; 2739361 AB - Oral snuff and chewing tobacco, commonly referred to as smokeless tobacco, are being used by many adolescent and young adult males, and no indication exists that use by this group is declining. Users are at risk for oral cancer, noncancerous oral pathology such as leukoplakias, and addiction. Information about patterns of smokeless tobacco use and motivations of users may help planners develop and implement interventions. Variables include the importance of peer and family influences, social image, knowledge of harmful effects, regional differences, use of other substances, and addiction. Due to the addictive nature of smokeless tobacco, older youth may need cessation programs. Health educators are encouraged to include smokeless tobacco in their tobacco use prevention programs and to develop and implement comprehensive tobacco interventions appropriate for their youth population. JF - The Journal of school health AU - Boyd, G M AU - Glover, E D AD - Smoking, Tobacco, and Cancer Program, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 189 EP - 194 VL - 59 IS - 5 SN - 0022-4391, 0022-4391 KW - Index Medicus KW - Nursing KW - United States KW - Motivation KW - Humans KW - Program Evaluation KW - Health Education KW - Adolescent KW - Male KW - School Health Services -- organization & administration KW - Plants, Toxic KW - Tobacco Use Disorder -- epidemiology KW - Tobacco KW - Tobacco Use Disorder -- psychology KW - Tobacco Use Disorder -- prevention & control KW - Tobacco, Smokeless UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79076443?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-01 N1 - Date created - 1989-08-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Essential elements of school-based smoking prevention programs. AN - 79068014; 2739360 AB - The current status of adolescent tobacco use in the United States is discussed in the context of the identification of those elements considered necessary for successful school-based smoking prevention programs. Also described are the conclusions of a National Cancer Institute-convened expert advisory panel charged with the task of addressing: What are the essential elements of a school-based smoking prevention program? The panel focused on nine areas in which sufficient data and experience existed to reach a preliminary conclusion or make a recommendation. The nine areas are: program impact, focus, context, and length; ideal age at intervention; need for peer and parental involvement; teacher training; and program implementation. The panel concluded U.S. school-based smoking prevention programs have had consistently positive effects, though these effects have been modest and often limited to delaying the onset of tobacco use. Though the panel felt many programs are suitable for dissemination, several research recommendations also are described. JF - The Journal of school health AU - Glynn, T J AD - Smoking, Tobacco, and Cancer Program, National Cancer Institute, Bethesda, MD 20892-4200. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 181 EP - 188 VL - 59 IS - 5 SN - 0022-4391, 0022-4391 KW - Index Medicus KW - Nursing KW - United States KW - Teaching KW - Tobacco Use Disorder -- epidemiology KW - Humans KW - Curriculum KW - Tobacco Use Disorder -- prevention & control KW - Peer Group KW - Parents KW - Health Education KW - Adolescent KW - Program Evaluation KW - Smoking -- prevention & control KW - School Health Services -- organization & administration UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79068014?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-01 N1 - Date created - 1989-08-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Metabolic processes in isolated rat small intestine villus cells: effects of cis-diamminedichloroplatinum (II). AN - 79060922; 2662287 AB - Intestinal cells were isolated from male Fischer 344 rats by the collagenase portal vein perfusion procedure and evaluated for direct effects of cis-diamminedichloroplatinum (CDDP) and ethylacrylate (EtAc) on metabolic activities. Specific activities of marker enzymes of intestinal crypt and villus cells indicated that the preparations contained predominantly villus cells. Cell viability was generally greater than 90%, and was maintained longest when the cells were suspended in M-199 medium supplemented with 1% BSA. EtAc, an industrial intermediate which is toxic to tissues which are directly exposed to this chemical, had no apparent effect on rates of glucose metabolism or protein synthesis in suspensions of the isolated intestinal cells. These metabolic processes, however, were inhibited by the anticancer agent, CDDP; the mechanism of cytotoxicity of CDDP may therefore be due to interference with intermediary metabolism. The present studies indicate that isolated intestinal cell suspensions may be useful in examining direct and immediate effects of chemicals which are toxic to the intestinal epithelium, and in evaluating potential cytotoxic effects of CDDP analogs which have been developed. JF - Research communications in chemical pathology and pharmacology AU - Kralovánszky, J AU - Jenkins, W L AU - Greenwell, A AU - Melnick, R L AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 299 EP - 316 VL - 64 IS - 2 SN - 0034-5164, 0034-5164 KW - Acrylates KW - 0 KW - Mutagens KW - ethyl acrylate KW - 71E6178C9T KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - Thymidine Kinase KW - EC 2.7.1.21 KW - alpha-Glucosidases KW - EC 3.2.1.20 KW - Sucrase KW - EC 3.2.1.48 KW - Glucose KW - IY9XDZ35W2 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Protein Biosynthesis KW - Animals KW - Cytosol -- metabolism KW - Cytosol -- drug effects KW - Glucose -- metabolism KW - Intestine, Small -- cytology KW - Intestine, Small -- metabolism KW - Thymidine Kinase -- metabolism KW - Mutagens -- pharmacology KW - Rats KW - Rats, Inbred F344 KW - Sucrase -- metabolism KW - Acrylates -- pharmacology KW - alpha-Glucosidases -- metabolism KW - In Vitro Techniques KW - Intestine, Small -- drug effects KW - L-Lactate Dehydrogenase -- metabolism KW - Male KW - Intestinal Mucosa -- cytology KW - Cisplatin -- pharmacology KW - Intestinal Mucosa -- metabolism KW - Intestinal Mucosa -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79060922?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-04 N1 - Date created - 1989-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Bronchoscopic phototherapy at comparable dose rates: early results. AN - 79036969; 2525011 AB - Photodynamic therapy is a recently introduced treatment for surface malignancies. Since January 1987, 10 patients with endobronchial neoplasms have had bronchoscopic photodynamic therapy at similar dose rates (400 mW/cm) for total atelectasis (2), carinal narrowing with respiratory insufficiency (2), or partial obstruction without collapse (4). Two patients underwent photodynamic therapy as a preliminary to immunotherapy. Histologies included endobronchial metastases (colon, ovary, melanoma, and sarcoma, 1 each; and renal cell, 3) and primary lung cancer (3). The 2 patients with total atelectasis had complete reexpansion after photodynamic therapy, which permitted eventual sleeve lobectomy in 1. Carinal narrowing was ameliorated in the 2 patients seen with inspiratory stridor, thereby permitting hospital discharge. Endoscopically resected fragments after photodynamic therapy exhibited avascular necrosis. These data support further controlled studies of photodynamic therapy by thoracic surgical oncologists to define its limitations as well as to improve and expand its efficacy as a palliative or surgical adjuvant. JF - The Annals of thoracic surgery AU - Pass, H I AU - Delaney, T AU - Smith, P D AU - Bonner, R AU - Russo, A AD - Thoracic Oncology Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 693 EP - 699 VL - 47 IS - 5 SN - 0003-4975, 0003-4975 KW - Hematoporphyrins KW - 0 KW - Dihematoporphyrin Ether KW - 97067-70-4 KW - Abridged Index Medicus KW - Index Medicus KW - Radiation Dosage KW - Humans KW - Adult KW - Hematoporphyrins -- therapeutic use KW - Middle Aged KW - Laser Therapy KW - Dose-Response Relationship, Radiation KW - Male KW - Female KW - Bronchoscopy KW - Photochemotherapy -- adverse effects KW - Bronchial Neoplasms -- drug therapy KW - Bronchial Neoplasms -- mortality KW - Photochemotherapy -- methods KW - Bronchial Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79036969?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-27 N1 - Date created - 1989-06-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dipyridamole potentiates the inhibition by 3'-azido-3'-deoxythymidine and other dideoxynucleosides of human immunodeficiency virus replication in monocyte-macrophages. AN - 79036284; 2542948 AB - Dipyridamole (DPM) is commonly used as a coronary vasodilator and inhibitor of platelet aggregation in the treatment of cardiovascular diseases. We report here that DPM potentiates the inhibitory effects of 3'-azido-3'-deoxythymidine (AZT) and 2',3'-dideoxycytidine against human immunodeficiency virus type 1 (HIV-1) in human monocyte-macrophages. At the same concentrations, DPM does not potentiate the toxic effects of AZT on these cells or on human bone marrow (granulocyte-monocyte) progenitor cells. Since monocyte-macrophage lineage cells appear to be the major reservoir for HIV-1 in vivo, these findings suggest the possibility of using DPM or its analogues in combination chemotherapy of HIV infections. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Szebeni, J AU - Wahl, S M AU - Popovic, M AU - Wahl, L M AU - Gartner, S AU - Fine, R L AU - Skaleric, U AU - Friedmann, R M AU - Weinstein, J N AD - Theoretical Immunology Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 3842 EP - 3846 VL - 86 IS - 10 SN - 0027-8424, 0027-8424 KW - Antiviral Agents KW - 0 KW - Dideoxynucleosides KW - Interferon Type I KW - Zidovudine KW - 4B9XT59T7S KW - Dipyridamole KW - 64ALC7F90C KW - Zalcitabine KW - 6L3XT8CB3I KW - Index Medicus KW - AIDS/HIV KW - Bone Marrow Cells KW - Dideoxynucleosides -- metabolism KW - Cell Survival -- drug effects KW - Interferon Type I -- biosynthesis KW - Humans KW - In Vitro Techniques KW - Biological Transport KW - Monocytes -- drug effects KW - Macrophages -- drug effects KW - Drug Synergism KW - Bone Marrow -- drug effects KW - HIV -- growth & development KW - HIV -- drug effects KW - Dipyridamole -- administration & dosage KW - Virus Replication -- drug effects KW - Zidovudine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79036284?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-28 N1 - Date created - 1989-06-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: N Engl J Med. 1987 Jul 23;317(4):185-91 [3299089] Blood. 1987 Feb;69(2):660-7 [3801675] J Clin Oncol. 1987 Mar;5(3):489-95 [3819811] Biochem J. 1986 Dec 15;240(3):879-83 [3827876] Proc Natl Acad Sci U S A. 1987 Apr;84(8):2469-73 [3470806] Antimicrob Agents Chemother. 1987 Feb;31(2):168-72 [3471180] J Biol Chem. 1987 Apr 25;262(12):5748-54 [3471758] N Engl J Med. 1987 May 14;316(20):1247-57 [3553945] N Engl J Med. 1987 Jul 23;317(4):192-7 [3299090] J Immunol. 1987 Aug 15;139(4):1342-7 [3039002] J Membr Biol. 1987;98(1):89-100 [3669065] J Leukoc Biol. 1988 Jan;43(1):91-7 [3275735] Lancet. 1988 Jan 16;1(8577):76-81 [2891981] Anticancer Res. 1987 Sep-Oct;7(5B):1023-38 [3324934] Acta Biochim Biophys Hung. 1988;23(1):75-82 [3137757] Cancer Res. 1988 Oct 1;48(19):5585-90 [3416311] J Exp Med. 1988 Sep 1;168(3):1111-25 [2844951] AIDS. 1988;2 Suppl 1:S137-42 [2852501] Cancer Chemother Pharmacol. 1987;19(1):80-3 [3815730] J Cell Physiol. 1970 Aug;76(1):77-84 [5471041] Cancer Res. 1976 Jun;36(6):1853-82 [773531] Exp Hematol. 1980 Mar;8(3):339-44 [7461045] J Clin Microbiol. 1982 Aug;16(2):413-5 [6181091] J Infect Dis. 1982 Oct;146(4):451-9 [7119475] Acta Virol. 1982 May;26(3):125-9 [6127012] Acta Virol. 1982 May;26(3):137-47 [6181668] Cell Biol Int Rep. 1983 Apr;7(4):263-70 [6850858] Cancer Res. 1983 Aug;43(8):3466-92 [6305486] Br J Clin Pharmacol. 1983 Oct;16(4):423-5 [6626435] Cell Immunol. 1984 May;85(2):373-83 [6232002] Cell Immunol. 1984 May;85(2):384-95 [6232003] Adv Enzyme Regul. 1984;22:27-55 [6382953] J Clin Invest. 1985 Aug;76(2):875-7 [2993366] Proc Natl Acad Sci U S A. 1985 Oct;82(20):7096-100 [2413459] Lancet. 1986 Mar 15;1(8481):575-80 [2869302] Science. 1986 Jul 11;233(4760):215-9 [3014648] Cancer Res. 1986 Dec;46(12 Pt 1):6191-9 [2946402] Erratum In: Proc Natl Acad Sci U S A 1989 Aug;86(15):5968 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - S-phase induction and transformation of quiescent NIH 3T3 cells by microinjection of phospholipase C. AN - 79036099; 2726744 AB - Two inositol phospholipid-specific phospholipase C (PLC) isozymes (PLC-I and -II) have been purified from bovine brain. When PLC-I or PLC-II was microinjected (100-700 micrograms/ml) into quiescent NIH 3T3 cells, a time- and dose-dependent induction of DNA synthesis occurred, as demonstrated by [3H]thymidine incorporation into nuclear DNA. In addition, approximately to 8 hr after PLC injection, NIH 3T3 fibroblasts appeared spindle-shaped, refractile, and highly vacuolated, displaying a morphology similar to transformed cells. The morphologic transformation was apparent for 26-30 hr after which the injected cells reverted back to a normal phenotype. Microinjected PLC at a high concentration (1 mg/ml) was cytotoxic, dissolving the cytoplasmic membrane and leaving behind cellular ghosts. PLC is a key regulatory enzyme involved in cellular membrane signal transduction. Introduction of exogenous PLC into NIH 3T3 cells by microinjection induced a growth and oncogenic potential, as demonstrated by the ability of microinjected PLC (approximately 10,000 molecules per cell) to override the cellular G0 block, inducing DNA synthesis and morphologic transformation of growth-arrested fibroblast cells. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Smith, M R AU - Ryu, S H AU - Suh, P G AU - Rhee, S G AU - Kung, H F AD - Biological Carcinogenesis and Development Program, National Cancer Institute-Frederick Cancer Research Facility, MD 21701. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 3659 EP - 3663 VL - 86 IS - 10 SN - 0027-8424, 0027-8424 KW - Isoenzymes KW - 0 KW - DNA KW - 9007-49-2 KW - Type C Phospholipases KW - EC 3.1.4.- KW - Index Medicus KW - Animals KW - Cattle KW - Isoenzymes -- physiology KW - Isoenzymes -- administration & dosage KW - In Vitro Techniques KW - Interphase KW - Mice KW - Microinjections KW - DNA -- biosynthesis KW - Cell Line KW - Type C Phospholipases -- physiology KW - Type C Phospholipases -- administration & dosage KW - Cell Cycle KW - Cell Transformation, Neoplastic -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79036099?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-28 N1 - Date created - 1989-06-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1984 Apr 19-25;308(5961):693-8 [6232463] Nature. 1988 Nov 3;336(6194):83-6 [2847055] Cell. 1984 Aug;38(1):109-17 [6380758] Nature. 1984 Nov 22-28;312(5992):315-21 [6095092] Nature. 1985 Jan 17-23;313(5999):241-3 [3918269] Science. 1985 Jun 14;228(4705):1313-5 [4001943] Nature. 1986 Apr 10-16;320(6062):540-3 [2938016] Cell. 1986 Jun 6;45(5):631-2 [3708690] Science. 1986 Jul 18;233(4761):305-12 [3014651] Life Sci. 1986 Jul 21;39(3):187-94 [3016436] Nature. 1986 Sep 11-17;323(6084):173-6 [3018591] Science. 1986 Dec 19;234(4783):1519-26 [3024320] Biochem Biophys Res Commun. 1986 Nov 26;141(1):137-44 [3541924] Annu Rev Biochem. 1987;56:159-93 [3304132] J Biol Chem. 1987 Sep 15;262(26):12511-8 [3040753] Proc Natl Acad Sci U S A. 1987 Oct;84(19):6649-53 [3477795] Science. 1988 Feb 5;239(4840):640-3 [2829356] J Biol Chem. 1988 Feb 25;263(6):2577-80 [2830256] Nature. 1988 Mar 17;332(6161):269-72 [2831461] Nature. 1988 Mar 17;332(6161):272-5 [2450282] Nature. 1988 May 12;333(6169):129-34 [3130578] FASEB J. 1988 Jul;2(10):2569-74 [2838362] Cell. 1988 Jul 15;54(2):161-9 [3390863] Nature. 1988 Jul 21;334(6179):268-70 [3398923] Proc Natl Acad Sci U S A. 1988 Aug;85(15):5419-23 [2840660] Proc Natl Acad Sci U S A. 1988 Aug;85(16):5799-803 [2842749] Nature. 1984 Aug 9-15;310(5977):508-11 [6611509] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of oligonucleotide transport into living cells. AN - 79020026; 2726730 AB - Addition of antisense oligonucleotides to cell cultures has been used to specifically inhibit gene expression. We have investigated the mechanism by which oligonucleotides enter living cells. These compounds are taken up by cells in a saturable, size-dependent manner compatible with receptor-mediated endocytosis. Polynucleotides of any length are competitive inhibitors of oligomer transport, providing they possess a 5'-phosphate moiety. Using oligo(dT)-cellulose for affinity purification, we have identified an 80-kDa surface protein that may mediate transport. Knowledge of the oligonucleotide transport mechanism should facilitate the design of more effective synthetic antisense oligomers as potential clinical agents. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Loke, S L AU - Stein, C A AU - Zhang, X H AU - Mori, K AU - Nakanishi, M AU - Subasinghe, C AU - Cohen, J S AU - Neckers, L M AD - Laboratory of Pathology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 3474 EP - 3478 VL - 86 IS - 10 SN - 0027-8424, 0027-8424 KW - Membrane Proteins KW - 0 KW - Oligonucleotides KW - Chloroquine KW - 886U3H6UFF KW - Acridine Orange KW - F30N4O6XVV KW - Index Medicus KW - Microscopy, Fluorescence KW - Tumor Cells, Cultured KW - Chloroquine -- pharmacology KW - Membrane Proteins -- metabolism KW - Kinetics KW - Humans KW - In Vitro Techniques KW - Endocytosis -- drug effects KW - Cell Membrane -- metabolism KW - Biological Transport -- drug effects KW - Oligonucleotides -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79020026?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-28 N1 - Date created - 1989-06-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Annu Rev Biochem. 1977;46:669-722 [332066] Gene. 1988 Dec 10;72(1-2):333-41 [2854090] Eur J Biochem. 1978 Jul 3;87(3):459-65 [28225] Cell. 1980 Aug;21(1):67-77 [6157480] Biochemistry. 1981 Mar 31;20(7):1874-80 [7013804] Science. 1981 Oct 30;214(4520):504-9 [6170111] Proc Natl Acad Sci U S A. 1982 Oct;79(20):6186-90 [6292894] Proc Natl Acad Sci U S A. 1983 Apr;80(8):2258-62 [6300903] Proc Natl Acad Sci U S A. 1984 Jan;81(1):175-9 [6141558] EMBO J. 1984 Apr;3(4):795-800 [6723628] Annu Rev Biochem. 1985;54:367-402 [2411211] J Immunol. 1985 Nov;135(5):3403-10 [2413120] J Clin Invest. 1985 Dec;76(6):2182-90 [3001145] Proc Natl Acad Sci U S A. 1986 May;83(9):2787-91 [3010316] Proc Natl Acad Sci U S A. 1986 Jun;83(12):4143-6 [3012555] J Immunol. 1987 Mar 1;138(5):1502-9 [3492555] Proc Natl Acad Sci U S A. 1987 Feb;84(3):648-52 [3027696] J Exp Med. 1987 Apr 1;165(4):1141-59 [3104527] Biochem Pharmacol. 1987 May 15;36(10):1567-76 [3297064] Nature. 1987 Jul 30-Aug 5;328(6129):445-9 [3302722] Proc Natl Acad Sci U S A. 1988 Feb;85(4):1028-32 [3277186] J Immunol. 1988 Apr 1;140(7):2431-5 [2450923] Mol Cell Biol. 1988 Feb;8(2):963-73 [3280975] Curr Top Microbiol Immunol. 1988;141:282-9 [3063445] Cell. 1977 Nov;12(3):609-17 [72612] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retinoic acid and 2,3,7,8-tetrachlorodibenzo-p-dioxin selectively enhance teratogenesis in C57BL/6N mice. AN - 78995896; 2718176 AB - TCDD is one of the most toxic man-made compounds and an extremely potent teratogen in mice. Many of its toxic symptoms resemble those seen during vitamin A deficiency. Vitamin A and its derivatives, such as alltrans-retinoic acid (RA), are also teratogenic in mice, as well as many other species. Both TCDD and RA produce cleft palate in susceptible strains of mice. However, while TCDD produces hydronephrosis, RA does not, and TCDD does not produce limb bud defects while RA does. To determine whether TCDD and RA would enhance or antagonize the teratogenic effects of the other compound, C57BL/6N dams were treated po on Gestation Day (gd) 10 or 12 with 10 ml corn oil/kg containing TCDD (0-18 micrograms/kg), RA (0-200 mg/kg), or combinations of the two chemicals. Dams were killed on gd 18 and toxicity and teratogenicity assessed. Coadministration of TCDD and RA had no effect on maternal or fetal toxicity beyond what would be expected by either compound alone. Cleft palate was induced by RA at lower doses on gd 10 than on gd 12, but by TCDD at lower doses on gd 12 than on gd 10. Sensitivity to TCDD-induced hydronephrosis was similar on both gd 10 and 12. The limb bud defects were only observed when RA was administered on gd 10, not when given on gd 12. No other soft tissue or skeletal malformations were related to administration of TCDD or RA. No effect of TCDD was observed on the incidence or severity of limb bud defects induced by RA, nor did RA influence the incidence or severity of hydronephrosis induced by TCDD. However, the incidence of cleft palate was dramatically enhanced by coadministration of the xenobiotic and vitamin. On both gd 10 and 12, the dose-response curves for cleft palate induction were parallel, suggesting some similarities in mechanism between the two compounds. However, combination treatment resulted in a synergistic response that varied with the stage of development and was tissue specific. JF - Toxicology and applied pharmacology AU - Birnbaum, L S AU - Harris, M W AU - Stocking, L M AU - Clark, A M AU - Morrissey, R E AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 487 EP - 500 VL - 98 IS - 3 SN - 0041-008X, 0041-008X KW - Dioxins KW - 0 KW - Polychlorinated Dibenzodioxins KW - Tretinoin KW - 5688UTC01R KW - Index Medicus KW - Cleft Palate -- chemically induced KW - Animals KW - Dose-Response Relationship, Drug KW - Bone and Bones -- abnormalities KW - Body Weight -- drug effects KW - Mice, Inbred C57BL KW - Mice KW - Drug Synergism KW - Female KW - Pregnancy KW - Hydronephrosis -- chemically induced KW - Tretinoin -- toxicity KW - Polychlorinated Dibenzodioxins -- toxicity KW - Abnormalities, Drug-Induced -- etiology KW - Dioxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78995896?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-16 N1 - Date created - 1989-06-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of the Ki-ras protooncogene in spontaneously occurring and chemically induced lung tumors of the strain A mouse. AN - 78994283; 2654935 AB - The strain A mouse has a high incidence of spontaneous lung tumors and is susceptible to lung tumor induction by chemical carcinogens. By utilizing transfection assay, Southern blot analysis, and DNA amplification techniques, we have detected an activated Ki-ras gene in the DNAs of both spontaneously occurring and chemically induced lung tumors of strain A mice. The point mutations in the spontaneous lung tumors were in both codon 12 (60%) and codon 61 (30%). In contrast, 100% of the mutations in the Ki-ras gene detected in methylnitrosourea-induced lung tumors and 93% of the mutations in the Ki-ras genes detected in benzo[a]pyrene-induced lung tumors were in codon 12, whereas 90% of the mutations in the Ki-ras genes detected in ethyl carbamate-induced lung tumors were in codon 61. The selectivity of mutations in the Ki-ras oncogene observed in chemically induced tumors, as compared to spontaneous tumors, suggests that these chemicals directly induce point mutations in the Ki-ras protooncogene. These data indicate that the strain A mouse lung tumor model is a very sensitive system to detect the ability of chemicals to activate the Ki-ras protooncogene in lung tissue. JF - Proceedings of the National Academy of Sciences of the United States of America AU - You, M AU - Candrian, U AU - Maronpot, R R AU - Stoner, G D AU - Anderson, M W AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 3070 EP - 3074 VL - 86 IS - 9 SN - 0027-8424, 0027-8424 KW - Codon KW - 0 KW - DNA, Neoplasm KW - Proto-Oncogene Proteins KW - Benzo(a)pyrene KW - 3417WMA06D KW - Methylnitrosourea KW - 684-93-5 KW - Proto-Oncogene Proteins p21(ras) KW - EC 3.6.5.2 KW - Index Medicus KW - Animals KW - Exons KW - Mice KW - Nucleic Acid Hybridization KW - Gene Amplification KW - Mice, Inbred A KW - Transfection KW - DNA, Neoplasm -- genetics KW - Mutation KW - Cell Transformation, Neoplastic KW - Lung Neoplasms -- genetics KW - Gene Expression Regulation KW - Lung Neoplasms -- chemically induced KW - Proto-Oncogenes KW - Proto-Oncogene Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78994283?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-09 N1 - Date created - 1989-06-09 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Acta Pathol Jpn. 1971 Feb;21(1):13-56 [5110006] N Engl J Med. 1988 Sep 1;319(9):525-32 [2841597] Adv Cancer Res. 1978;26:197-226 [204165] Proc Natl Acad Sci U S A. 1982 Mar;79(6):1945-9 [7043469] Br J Cancer. 1983 Jul;48(1):1-15 [6191767] Nature. 1983 Dec 15-21;306(5944):658-61 [6318112] Nature. 1984 Feb 16-22;307(5952):658-60 [6694757] Toxicol Appl Pharmacol. 1984 Feb;72(2):313-23 [6695378] Carcinogenesis. 1984 Sep;5(9):1165-71 [6205783] Carcinogenesis. 1985 Feb;6(2):237-42 [3918802] Nature. 1985 Feb 28-Mar 6;313(6005):812-5 [2983224] Science. 1985 May 3;228(4699):596-7 [3983645] EMBO J. 1985 May;4(5):1199-203 [4006913] Mutat Res. 1985 Nov-Dec;152(2-3):147-56 [3906388] Proc Natl Acad Sci U S A. 1986 Jan;83(1):33-7 [3510430] Proc Natl Acad Sci U S A. 1986 Mar;83(5):1222-6 [3513171] Proc Natl Acad Sci U S A. 1987 Jan;84(2):344-8 [3540961] Mol Cell Biol. 1987 Jan;7(1):379-87 [3031469] Cancer Res. 1987 Jun 15;47(12):3212-9 [3581065] Gene. 1986;50(1-3):313-20 [3582981] N Engl J Med. 1987 Oct 8;317(15):929-35 [3041218] Science. 1987 Sep 11;237(4820):1309-16 [3629242] Science. 1988 Jan 29;239(4839):487-91 [2448875] Proc Natl Acad Sci U S A. 1988 Jun;85(11):3875-9 [3131765] Somat Cell Mol Genet. 1988 Jul;14(4):393-400 [3041622] Carcinogenesis. 1988 Sep;9(9):1607-10 [3044637] Adv Cancer Res. 1975;21:1-58 [1108612] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Establishment of a human in vitro mesothelial cell model system for investigating mechanisms of asbestos-induced mesothelioma. AN - 78991433; 2541616 AB - Normal human mesothelial (NHM) cells were transfected with a plasmid containing SV40 early region DNA. Individual colonies of transformed cells from several donors were subcultured for periods of 5 to 6 months and 60 to 70 population doublings (PDs) before senescence, in contrast to a culture lifespan of approximately 1 month and 15 PDs for NHM cells. One such culture, designated MeT-5A, escaped senescence and has been passaged continuously for more than 2 years. These cells had a single integrated copy of SV40 early region DNA in their genome, expressed SV40 large T antigen, and exhibited features of mesothelial cells including sensitivity to the cytotoxic effects of asbestos fibers. One year after injection subcutaneously or intraperitoneally in athymic nude mice, these cells remain nontumorigenic, and therefore are a potential model system for in vitro fiber carcinogenesis studies. JF - The American journal of pathology AU - Ke, Y AU - Reddel, R R AU - Gerwin, B I AU - Reddel, H K AU - Somers, A N AU - McMenamin, M G AU - LaVeck, M A AU - Stahel, R A AU - Lechner, J F AU - Harris, C C AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 979 EP - 991 VL - 134 IS - 5 SN - 0002-9440, 0002-9440 KW - Antigens, Polyomavirus Transforming KW - 0 KW - Glycoproteins KW - Growth Substances KW - Plasminogen Inactivators KW - RNA, Messenger KW - Asbestos, Amosite KW - 12172-73-5 KW - Asbestos KW - 1332-21-4 KW - Plasminogen Activators KW - EC 3.4.21.- KW - Abridged Index Medicus KW - Index Medicus KW - Karyotyping KW - Animals KW - Plasminogen Activators -- antagonists & inhibitors KW - Humans KW - RNA, Messenger -- analysis KW - Mice, Nude KW - Mice KW - Plasmids KW - Glycoproteins -- genetics KW - Simian virus 40 -- physiology KW - Antigens, Polyomavirus Transforming -- analysis KW - Cell Survival KW - Transfection KW - Cells, Cultured KW - Growth Substances -- pharmacology KW - Carcinogenicity Tests KW - Simian virus 40 -- immunology KW - Cell Transformation, Neoplastic KW - Cell Transformation, Viral KW - Mesothelioma -- etiology KW - Pleural Neoplasms -- pathology KW - Mesothelioma -- genetics KW - Asbestos -- pharmacology KW - Pleural Neoplasms -- genetics KW - Mesothelioma -- pathology KW - Asbestos -- adverse effects KW - Pleural Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78991433?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-20 N1 - Date created - 1989-06-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Virology. 1973 Apr;52(2):456-67 [4705382] In Vitro Cell Dev Biol. 1988 Nov;24(11):1077-84 [2461356] Nature. 1975 Dec 11;258(5535):487-90 [1105198] J Mol Biol. 1977 Jun 15;113(1):237-51 [881736] Methods Enzymol. 1979;58:152-64 [423757] Methods Enzymol. 1979;58:164-78 [423758] Am J Pathol. 1979 Mar;94(3):529-38 [426038] Proc Natl Acad Sci U S A. 1979 Mar;76(3):1373-6 [286319] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] Cell. 1981 Jan;23(1):175-82 [6260373] In Vitro. 1981 Jan;17(1):1-19 [6260624] IARC Sci Publ. 1980;(30):87-96 [7239674] In Vitro. 1981 Feb;17(2):98-106 [7275143] N Engl J Med. 1982 Jun 17;306(24):1446-55 [7043267] J Mol Appl Genet. 1982;1(4):327-41 [6286831] J Natl Cancer Inst. 1983 Jan;70(1):3-8 [6571918] Cell. 1982 Dec;31(3 Pt 2):693-703 [6186388] Cell. 1983 Aug;34(1):245-53 [6192933] J Cell Sci. 1983 Sep;63:77-99 [6313714] Cancer Res. 1984 Jul;44(7):2991-9 [6202404] J Cell Physiol. 1985 May;123(2):151-60 [2984216] Proc Natl Acad Sci U S A. 1985 Jun;82(11):3884-8 [2987952] Biochim Biophys Acta. 1986;823(3):161-94 [2423124] J Clin Invest. 1986 Dec;78(6):1673-80 [3097076] J Cell Biol. 1987 Feb;104(2):263-75 [3543023] Mol Cell Biol. 1987 May;7(5):2031-4 [3037341] Cancer Res. 1987 Dec 1;47(23):6180-4 [3479241] Int J Cancer. 1988 Feb 15;41(2):218-23 [3276635] Cancer Res. 1988 Apr 1;48(7):1904-9 [2450641] J Mol Biol. 1975 Nov 5;98(3):503-17 [1195397] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sublingual versus subcutaneous buprenorphine in opiate abusers. AN - 78990676; 2721107 AB - To compare the pharmacologic profiles of sublingually and subcutaneously administered buprenorphine, 10 healthy male subjects with histories of opiate abuse were given sublingually administered buprenorphine (1, 2, and 4 mg), subcutaneously administered buprenorphine (1 and 2 mg), and placebo in a double-blind, double-dummy, placebo-controlled study. All active buprenorphine dosages produced a significant degree of miosis but no significant changes in body temperature, blood pressure, or respiratory or heart rate. Buprenorphine produced varying degrees of euphoria related to dose and route of administration but little dysphoria and sedation, as assessed by subscales of the Addiction Research Center Inventory. Subject "liking" for buprenorphine was reported by both observers and subjects. The relative potency of sublingually to subcutaneously administered buprenorphine was calculated for both physiologic and behavioral parameters and found to be approximately two thirds. The results indicated that both sublingual and subcutaneous buprenorphine have a similar profile of effects in opiate abusers. JF - Clinical pharmacology and therapeutics AU - Jasinski, D R AU - Fudala, P J AU - Johnson, R E AD - National Institute on Drug Abuse, Addiction Research Center, Baltimore, MD 21224. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 513 EP - 519 VL - 45 IS - 5 SN - 0009-9236, 0009-9236 KW - Narcotics KW - 0 KW - Buprenorphine KW - 40D3SCR4GZ KW - Abridged Index Medicus KW - Index Medicus KW - Analysis of Variance KW - Body Temperature -- drug effects KW - Double-Blind Method KW - Humans KW - Respiration -- drug effects KW - Drug Evaluation KW - Heart Rate -- drug effects KW - Pupil -- drug effects KW - Adult KW - Injections, Subcutaneous KW - Blood Pressure -- drug effects KW - Administration, Sublingual KW - Male KW - Buprenorphine -- therapeutic use KW - Buprenorphine -- pharmacology KW - Substance-Related Disorders -- drug therapy KW - Buprenorphine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78990676?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-30 N1 - Date created - 1989-06-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of phi X174 as a shuttle vector for the study of in vivo mammalian mutagenesis. AN - 78985980; 2524662 AB - The most promising new techniques for the study of in vivo mammalian mutagenesis make use of transgenic mice carrying a recoverable vector. Mutation systems in mammals can be based on the selection of altered phenotypes among cells sampled from the whole animal, but they are then limited to the very few cell types in which the marker gene is expressed. Such systems require both in vivo and in vitro cell proliferation for expression and verification of the mutations. To avoid these complications, the study of mutations in most tissues must be based on the detection of genetic alterations in a vector that is independent of the phenotype of the mammalian cell. The vector is only a small portion of the mammalian genome, and many of the procedures for recovering the vector are inhibited by the host DNA. For this reason, partial purification is necessary. The purification is made possible by using vectors which are not cut by restriction enzymes that cut the host DNA to pieces of an average size considerably smaller than the vector. The efficiency for measuring mutation frequencies depends on the number of vectors which can be recovered from a certain amount of DNA and is affected by the number of vectors per mammalian genome and the transfection efficiency of the partially-purified vector. In order to avoid selection against or for the spontaneous or induced mutations, the transfection efficiency of the vector from the transformed DNA and of the pure vector DNA should be of the same order of magnitude. Differences in the response to mutagens between the mammalian genome and the procaryotic vector may be expected due to the lack of unique mammalian topographical features in the vectors. Any mutation induction which depends preferentially on these unique features of the mammalian genome may not be detected in a shuttle vector system unless the vector has been engineered or specifically designed to include such topographical characters. The shortcoming of short-term tests that use mutagenicity for predicting human carcinogenicity is usually lack of correlation between mutagenesis in the short-term tests and the corresponding results in carcinogenesis bioassays in mammals. One factor which could contribute to the lack of correlation between the short-term test systems and the bioassays is that we are comparing mutations in totally different genes in different organisms. By using the phi X174 shuttle system, one of the variables may be eliminated.(ABSTRACT TRUNCATED AT 400 WORDS) 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 - 1989/05// PY - 1989 DA - May 1989 SP - 11 EP - 21 VL - 212 IS - 1 SN - 0027-5107, 0027-5107 KW - DNA, Recombinant KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Mice KW - Mammals -- genetics KW - Mice, Transgenic -- genetics KW - Genetic Vectors KW - Bacteriophage phi X 174 -- genetics KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78985980?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-27 N1 - Date created - 1989-06-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Insertional mutagenesis of the vaccinia virus gene encoding a type I DNA topoisomerase: evidence that the gene is essential for virus growth. AN - 78982948; 2541548 AB - Vaccinia virus encodes a type I DNA topoisomerase whose function in virus replication is not known. To determine whether topoisomerase is required for growth of vaccinia in cell culture, we attempted to isolate null mutations in the topoisomerase gene through insertional mutagenesis. Plasmids containing mutant topoisomerase alleles were constructed by intragenic insertion of the Escherichia coli gpt gene. Recombinant viruses containing the gpt insertion were isolated by selection for growth in the presence of mycophenolic acid. Analysis of the genome structures of drug-resistant viruses revealed that in every case (n = 22) both the wild-type and the gpt-inserted allele were present in viral DNA. We interpret the retention of the wild-type allele as indicative of the essential nature of the topoisomerase gene for vaccinia virus growth. JF - Virology AU - Shuman, S AU - Golder, M AU - Moss, B AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 302 EP - 306 VL - 170 IS - 1 SN - 0042-6822, 0042-6822 KW - DNA, Viral KW - 0 KW - DNA Topoisomerases, Type I KW - EC 5.99.1.2 KW - Index Medicus KW - Blotting, Southern KW - DNA Mutational Analysis KW - Restriction Mapping KW - DNA, Viral -- genetics KW - Vaccinia virus -- genetics KW - Vaccinia virus -- enzymology KW - Vaccinia virus -- growth & development KW - DNA Topoisomerases, Type I -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78982948?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-13 N1 - Date created - 1989-06-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Gadolinium-DTPA enhanced dynamic MR imaging in the evaluation of cisplatinum nephrotoxicity. AN - 78981773; 2723175 AB - Gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA) enhanced dynamic magnetic resonance (MR) imaging was used to monitor the nephrotoxic effects of cis-platinum (cis-diamminedichloroplatinum; CDDP), a chemotherapeutic agent that produces damage in the proximal convoluted tubule. Ten New Zealand white rabbits (NZWs) were divided into two groups and were evaluated at two clinically relevant doses of CDDP. Group 1 (four NZWs) received CDDP intravenously at 125 mg/m2 over 1 h. Rabbits in Group 2 (six NZWs) were infused with CDDP at 40 mg/m2 each day for 5 consecutive days. Dynamic MR images were performed in the axial plane at 1.5 T using a gradient recalled acquisition in the steady state sequence with an echo time of 11 ms, a repetition time of 20 ms, and a flip angle of 10 degrees after a bolus injection of Gd-DTPA 0.1 mmol/kg. Thirty-two sequential post Gd-DTPA images (5.12 s/image) were obtained over 2 min 45 s at a single location. All rabbits underwent baseline normal and serial post CDDP Gd-DTPA enhanced dynamic MR scans. Analysis of the alterations in the normal pattern of renal enhancement caused by CDDP was facilitated by using a stacked profile image and quantitative region of interest measurements of signal intensity. Normally, after the injection of Gd-DTPA, a dark band promptly appears in the outer cortex of the kidneys and migrates centripetally toward the papilla, reflecting the tubular concentration of Gd-DTPA. In Group 1 rabbits, nephrotoxicity due to CDDP was observed as early as 9 h after administration of the drug, with a complete disappearance of the dark band by 7 days. In Group 2 rabbits, the band disappeared gradually and reappeared 2-10 days after the completion of CDDP treatment, indicative of tubular damage and recovery with return of the concentrating ability of the kidney. These results illustrate the feasibility of using Gd-DTPA dynamic MR as a sensitive monitor of drug induced alterations of renal function. JF - Journal of computer assisted tomography AU - Frank, J A AU - Choyke, P L AU - Girton, M E AU - Austin, H A AU - Sievenpiper, C AU - Inscoe, S W AU - Black, J L AU - Carvlin, M J AU - Dwyer, A J AD - Diagnostic Radiology Department, Warren Grant Magnuson Clinical Center, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892. PY - 1989 SP - 448 EP - 459 VL - 13 IS - 3 SN - 0363-8715, 0363-8715 KW - Contrast Media KW - 0 KW - Organometallic Compounds KW - Pentetic Acid KW - 7A314HQM0I KW - Gadolinium KW - AU0V1LM3JT KW - Gadolinium DTPA KW - K2I13DR72L KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Animals KW - Kidney Concentrating Ability KW - Rabbits KW - Magnetic Resonance Imaging -- methods KW - Cisplatin -- toxicity KW - Acute Kidney Injury -- chemically induced KW - Acute Kidney Injury -- physiopathology KW - Image Enhancement -- methods KW - Acute Kidney Injury -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78981773?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-28 N1 - Date created - 1989-06-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparative biodistributions of yttrium- and indium-labeled monoclonal antibody B72.3 in athymic mice bearing human colon carcinoma xenografts. AN - 78976260; 2785585 AB - The biodistribution of yttrium- and indium-labeled monoclonal antibody (MAb) B72.3 IgG using three different chelate conjugates (SCN-Bz-EDTA, CA-DTPA, and SCN-Bz-DTPA) was compared in athymic mice bearing LS-174T tumors. The 88Y-SCN-Bz-DTPA-B72.3 yielded 40% ID/g at 5-7 days in the tumors, while the 88Y-SCN-Bz-EDTA-B72.3 and 88Y-CA-DTPA-B72.3 showed only 6-8% ID/g. The yttrium uptake in the bone with the SCN-Bz-EDTA and CA-DTPA conjugated IgG was over 14 and 11% ID/g, respectively, while 88Y-SCN-Bz-DTPA-B72.3 showed only 3% ID/g. In contrast, the 111In-labeled B72.3 uptake in the bone with all three chelate conjugates was 2-3% ID/g. The differences in yttrium- versus indium-labeled MAb biodistributions demonstrate the difficulty in using 111In-labeled MAbs to predict the biodistribution and dosimetry of 90Y-labeled MAbs unless chelate conjugates such as SCN-Bz-DTPA are used. JF - Journal of nuclear medicine : official publication, Society of Nuclear Medicine AU - Roselli, M AU - Schlom, J AU - Gansow, O A AU - Raubitschek, A AU - Mirzadeh, S AU - Brechbiel, M W AU - Colcher, D AD - Laboratory of Tumor Immunology and Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 672 EP - 682 VL - 30 IS - 5 SN - 0161-5505, 0161-5505 KW - Antibodies, Monoclonal KW - 0 KW - Chelating Agents KW - Immunoglobulin G KW - Immunotoxins KW - Indium Radioisotopes KW - Yttrium Radioisotopes KW - Index Medicus KW - Neoplasm Transplantation KW - Chelating Agents -- pharmacokinetics KW - Animals KW - Chelating Agents -- therapeutic use KW - Humans KW - Transplantation, Heterologous KW - Mice KW - Tissue Distribution KW - Immunoglobulin G -- metabolism KW - Immunoglobulin G -- therapeutic use KW - Female KW - Yttrium Radioisotopes -- metabolism KW - Yttrium Radioisotopes -- therapeutic use KW - Colonic Neoplasms -- radiotherapy KW - Mice, Nude -- metabolism KW - Antibodies, Monoclonal -- metabolism KW - Carcinoma -- radiotherapy KW - Indium Radioisotopes -- therapeutic use KW - Immunotoxins -- therapeutic use KW - Colonic Neoplasms -- metabolism KW - Immunotoxins -- metabolism KW - Carcinoma -- metabolism KW - Indium Radioisotopes -- metabolism KW - Antibodies, Monoclonal -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78976260?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-22 N1 - Date created - 1989-06-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - cDNA-directed expression of rat testosterone 7 alpha-hydroxylase using the modified vaccinia virus, T7-RNA-polymerase system and evidence for 6 alpha-hydroxylation and delta 6-testosterone formation. AN - 78970777; 2714287 AB - The modified vaccinia virus, T7-RNA-polymerase cDNA-expression system was used to express rat cytochrome P-450a. Various parameters such as host-cell type and density, and duration of infection were tested to optimize the level of expression of cytochrome P-450a enzyme activity. Cytochrome P-450a expressed from the cDNA sequence was exclusively incorporated into the membrane-containing portions of the cell lysates, as expected from its normal association in the liver endoplasmic reticulum. The enzyme displayed a carbon-monoxide-reduced-cytochrome-P-450a difference spectrum with a Soret maximum of 450 nm. Activity measurements revealed that cytochrome P-450a produced three metabolites of testosterone; 7 alpha-hydroxytestosterone and 6 alpha-hydroxytestosterone and delta 6-testosterone at a ratio of about 38:1:1. Under the appropriate conditions, the vaccinia-virus, T7-RNA-polymerase system produces high levels of a single form of cytochrome P-450 in cells that are virtually devoid of endogenous cytochrome P-450. Analysis of the cytochrome P-450 in its natural membrane-bound state, as opposed to artificial-lipid reconstitution studies of purified enzymes, allows accurate and confident measurements of substrate specificities. JF - European journal of biochemistry AU - Aoyama, T AU - Korzekwa, K AU - Nagata, K AU - Gillette, J AU - Gelboin, H V AU - Gonzales, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/05/01/ PY - 1989 DA - 1989 May 01 SP - 331 EP - 336 VL - 181 IS - 2 SN - 0014-2956, 0014-2956 KW - Testosterone KW - 3XMK78S47O KW - DNA KW - 9007-49-2 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 - testosterone 7-alpha-hydroxylase, hamster KW - DNA-Directed RNA Polymerases KW - EC 2.7.7.6 KW - Index Medicus KW - T-Phages -- enzymology KW - Rats KW - Immunoblotting KW - Animals KW - Transfection KW - Cytochrome P-450 Enzyme System -- genetics KW - Kinetics KW - Testosterone -- biosynthesis KW - Hydroxylation KW - Vaccinia virus -- genetics KW - DNA-Directed RNA Polymerases -- metabolism KW - DNA -- genetics KW - Steroid Hydroxylases -- metabolism KW - Transcription, Genetic KW - Steroid Hydroxylases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78970777?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-22 N1 - Date created - 1989-06-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Eur J Biochem 1989 Oct 1;184(3):729 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Myelostimulatory activity of recombinant human interleukin-2 in mice. AN - 78970339; 2785408 AB - In a series of studies designed to extend our understanding of interleukin-2 (IL-2) and to study the effect of biologic response modifiers on bone marrow, we observed that administering recombinant human (rH) IL-2 to normal mice resulted in an increase in the frequency of colony-forming units-culture (CFU-C) in bone marrow. In addition, rH IL-2 was able to accelerate host recovery from cyclophosphamide (CTX)- or radiation-induced bone marrow depression and peripheral blood leukopenia. Not only can rH IL-2 accelerate, in a dose-dependent manner, the return of bone marrow, peripheral blood cellularity, and CFU-C frequency to normal levels following cytoreduction by CTX or irradiation, but it also significantly increases CFU-C frequency to greater than normal levels. Furthermore, rH IL-2 can significantly prolong survival of animals receiving a lethal dose of irradiation or CTX. Thus, multiple mechanisms are responsible for the synergistic therapeutic activity associated with rH IL-2 and CTX. rH IL-2 does not act only as an immunomodulatory agent in the presence or absence of suppressor T cells, but also accelerates host recovery from cytoreductive agents, resulting in decreased leukopenia and perhaps resistances to secondary infection. Thus, rH IL-2 plus chemotherapy may increase therapeutic activity against neoplastic disease, not only by adding immune stimulation to the direct antitumor effect of the drug but also by allowing delivery of higher, more effective doses of chemotherapy. JF - Blood AU - Talmadge, J E AU - Schneider, M AU - Keller, J AU - Ruscetti, F AU - Longo, D AU - Pennington, R AU - Bowersox, O AU - Tribble, H AD - Division of Cancer Treatment, National Cancer Institute-Frederick Cancer Research Facility. Y1 - 1989/05/01/ PY - 1989 DA - 1989 May 01 SP - 1458 EP - 1467 VL - 73 IS - 6 SN - 0006-4971, 0006-4971 KW - Interleukin-2 KW - 0 KW - Recombinant Proteins KW - Cyclophosphamide KW - 8N3DW7272P KW - Abridged Index Medicus KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Animals KW - Drug Administration Schedule KW - Recombinant Proteins -- pharmacology KW - Gamma Rays KW - Dose-Response Relationship, Drug KW - T-Lymphocytes -- physiology KW - Mice KW - Mice, Nude KW - Bone Marrow Cells KW - Mice, Inbred C57BL KW - Colony-Forming Units Assay KW - Cyclophosphamide -- pharmacology KW - Interleukin-2 -- pharmacology KW - Hematopoietic Stem Cells -- cytology KW - Bone Marrow -- radiation effects KW - Bone Marrow -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78970339?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-13 N1 - Date created - 1989-06-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential responses to growth factors by normal human mesothelial cultures from individual donors. AN - 78967366; 2497107 AB - A significant interindividual variation in the growth rates is found in normal cultured human mesothelial (NHM) cells derived from different donors. This variation is observed when the mesothelial cells are incubated in medium containing serum and when the potencies of several separate growth factors are measured by using defined media. Depending on the donor, gamma-interferon and interleukin-2 can be toxic, have no effect, or stimulate the growth rate of NHM cells. Cultured NHM cells can be induced to multiply by growth factors that are released by activated macrophages. Thus, interindividual variation in NHM cell growth control could play a role in the pathogenesis of mesothelioma for a person exposed to asbestos. JF - Journal of cellular physiology AU - Lechner, J F AU - LaVeck, M A AU - Gerwin, B I AU - Matis, E A AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 295 EP - 300 VL - 139 IS - 2 SN - 0021-9541, 0021-9541 KW - Growth Substances KW - 0 KW - Interleukin-2 KW - Epidermal Growth Factor KW - 62229-50-9 KW - Interferon-gamma KW - 82115-62-6 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Interleukin-2 -- pharmacology KW - Humans KW - Adult KW - Cell Division -- drug effects KW - Interferon-gamma -- pharmacology KW - Epidermal Growth Factor -- pharmacology KW - DNA -- biosynthesis KW - Epithelium -- drug effects KW - Epithelial Cells KW - Growth Substances -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78967366?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-09 N1 - Date created - 1989-06-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prevention of skin cancer in xeroderma pigmentosum with oral isotretinoin. AN - 78967193; 2721244 AB - To confirm reports that skin cancer can be prevented with retinoid treatment, a three-year controlled prospective study was conducted of oral isotretinoin in five patients with xeroderma pigmentosum who had a history of multiple cutaneous basal cell or squamous cell carcinomas. Patients were treated with isotretinoin, 2 mg/kg per day for two years, and then evaluated for an additional year without using the drug. Before, during, and after treatment, biopsy specimens of all suspicious lesions were examined, and skin cancers were removed surgically. The patients had a total of 121 tumors in the two years before treatment. During two years of treatment with isotretinoin, there were twenty-five tumors, with an average reduction in skin cancers of 63 percent (p = 0.019). After use of the drug was discontinued, the tumor frequency increased a mean of 8.5 times over the frequency during treatment (p = 0.007). Although all patients experienced mucocutaneous toxic effects, and abnormalities in triglyceride levels, results of liver function tests, or skeletal findings occurred in some, high-dosage oral isotretinoin was effective in the chemoprophylaxis of skin cancers in patients with xeroderma pigmentosum. JF - Cutis AU - Moshell, A N AD - Skin Diseases Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, Maryland 20892. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 485 EP - 490 VL - 43 IS - 5 SN - 0011-4162, 0011-4162 KW - Tretinoin KW - 5688UTC01R KW - Index Medicus KW - Administration, Oral KW - Prospective Studies KW - Humans KW - Adult KW - Follow-Up Studies KW - Child KW - Adolescent KW - Male KW - Female KW - Carcinoma, Basal Cell -- prevention & control KW - Tretinoin -- administration & dosage KW - Carcinoma, Squamous Cell -- prevention & control KW - Xeroderma Pigmentosum -- drug therapy KW - Skin Neoplasms -- prevention & control KW - Tretinoin -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78967193?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-03 N1 - Date created - 1989-07-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phenytoin hepatotoxicity masked by corticosteroids. AN - 78967084; 2719513 AB - The association of phenytoin and liver toxicity is well documented. This article describes a patient who underwent a transsphenoidal resection of a pituitary tumor who developed phenytoin-induced hepatotoxicity that was masked by the simultaneous administration of corticosteroids for treatment of cerebral edema. In a patient receiving both medications, the systemic manifestations of the hypersensitivity to phenytoin may go unrecognized, leading to delayed identification of a potentially lethal complication of this commonly prescribed anticonvulsant. JF - Archives of internal medicine AU - Lisker-Melman, M AU - Hoofnagle, J H AD - Digestive Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 1196 EP - 1197 VL - 149 IS - 5 SN - 0003-9926, 0003-9926 KW - Phenytoin KW - 6158TKW0C5 KW - Dexamethasone KW - 7S5I7G3JQL KW - Abridged Index Medicus KW - Index Medicus KW - Postoperative Complications -- drug therapy KW - Humans KW - Chemical and Drug Induced Liver Injury KW - Seizures -- etiology KW - Seizures -- drug therapy KW - Middle Aged KW - Pituitary Neoplasms -- surgery KW - Male KW - Brain Edema -- drug therapy KW - Dexamethasone -- adverse effects KW - Drug Hypersensitivity -- etiology KW - Phenytoin -- adverse effects KW - Liver Diseases -- diagnosis KW - Drug Hypersensitivity -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78967084?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-15 N1 - Date created - 1989-06-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - An evaluation of the possible neurotoxicity of metabolites of phenylalanine. AN - 78963994; 2654351 JF - The Journal of pediatrics AU - Kaufman, S AD - Laboratory of Neurochemistry, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 895 EP - 900 VL - 114 IS - 5 SN - 0022-3476, 0022-3476 KW - Phenethylamines KW - 0 KW - Phenylacetates KW - Phenylpyruvic Acids KW - Phenylalanine KW - 47E5O17Y3R KW - phenylacetic acid KW - ER5I1W795A KW - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Phenylketonurias -- urine KW - Animals KW - Phenethylamines -- urine KW - Phenylpyruvic Acids -- urine KW - Humans KW - Phenylacetates -- urine KW - Phenylalanine -- metabolism KW - Brain -- drug effects KW - Phenylalanine -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78963994?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-12 N1 - Date created - 1989-06-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Pediatr. 1990 Apr;116(4):665-6 [2319411] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Myeloid growth factor(s) regulation of ornithine decarboxylase: effects of antiproliferative signals interferon-gamma and cAMP. AN - 78963581; 2469492 AB - Colony-stimulating factors (CSFs) stimulate the activation and steady-state mRNA accumulation of an important regulatory enzyme for macromolecular synthesis, ornithine decarboxylase (ODC). Cloned murine CSF-dependent cell lines exhibited a rapid activation of ODC enzyme activity, detectable within ten minutes of stimulations with either interleukin-3 (IL-3), GM-CSF, or G-CSF. This early phase of enzyme activation did not require early protein or mRNA synthesis. The subsequent protracted rise in ODC activity occurring four to six hours after CSF treatment was dependent on increases in steady-state ODC mRNA accumulation and de novo protein synthesis. CSF, therefore, modulates both posttranslational activation of preexisting ODC and stabilization and accumulation of ODC mRNA. Antiproliferative signals, such as cAMP or interferon-gamma (IFN-gamma), effectively inhibited the CSF-directed increase in steady-state ODC mRNA. Cotreatment of the murine NSF 60.8 cell line with IFN-gamma and GM-CSF decreased steady-state ODC mRNA greater than 80% as compared with GM-CSF-treated cells alone. IFN treatment did not cause any appreciable destabilization of mature ODC mRNA, suggesting that its major effect may be at the level of ODC mRNA transcription or posttranscriptional processing. These data indicate that the ODC gene-protein system is an important molecular locus of the effects of myeloid proliferative and antiproliferation signals. JF - Blood AU - Farrar, W L AU - Harel-Bellan, A AD - Laboratory of Molecular Immunoregulation, National Cancer Institute, Frederick, MD 21701-1013. Y1 - 1989/05/01/ PY - 1989 DA - 1989 May 01 SP - 1468 EP - 1475 VL - 73 IS - 6 SN - 0006-4971, 0006-4971 KW - Colony-Stimulating Factors KW - 0 KW - Growth Substances KW - Interleukin-2 KW - RNA, Messenger KW - Recombinant Proteins KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - Dactinomycin KW - 1CC1JFE158 KW - Interferon-gamma KW - 82115-62-6 KW - Granulocyte-Macrophage Colony-Stimulating Factor KW - 83869-56-1 KW - Cycloheximide KW - 98600C0908 KW - Cyclic AMP KW - E0399OZS9N KW - Ornithine Decarboxylase KW - EC 4.1.1.17 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Dactinomycin -- pharmacology KW - Animals KW - Recombinant Proteins -- pharmacology KW - Blotting, Northern KW - Cycloheximide -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - Gene Expression Regulation -- drug effects KW - RNA, Messenger -- genetics KW - Cell Line KW - Ornithine Decarboxylase -- metabolism KW - Interleukin-2 -- pharmacology KW - Growth Substances -- pharmacology KW - Cyclic AMP -- pharmacology KW - Interferon-gamma -- pharmacology KW - Colony-Stimulating Factors -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78963581?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-13 N1 - Date created - 1989-06-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Decreased ligand binding to the hepatic glucocorticoid and epidermal growth factor receptors after 2,3,4,7,8-pentachlorodibenzofuran and 1,2,3,4,7,8-hexachlorodibenzofuran treatment of pregnant mice. AN - 78962860; 2718174 AB - 2,3,4,7,8-Pentachlorodibenzofuran (PeCDF) and 1,2,3,4,7,8-hexachlorodibenzofuran (HCDF) are environmental contaminants which mimic many of the toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Like TCDD, these polychlorinated dibenzofurans (PCDFs) induce hepatic benzo[a]pyrene hydroxylase activity (BPH) and possess high affinity for the Ah receptor. Another similarity of these PCDFs to TCDD is their ability to induce teratogenic effects such as cleft palate and hydronephrosis in mice. Recent studies have shown that TCDD modifies the equilibrium binding kinetics of the rat liver cytosolic glucocorticoid receptor (GRc) and the hepatic plasma membrane epidermal growth factor (EGF) receptor. To gain a better understanding of the action of halogenated hydrocarbons on these cytosolic and membrane-bound receptor systems during pregnancy, we investigated the biochemical effects of PeCDF and HCDF on the binding kinetics of maternal mouse liver GRc and EGF receptors and the induction of BPH activities. Pregnant C57BL/6N mice were treated once daily on gestation Days 10 through 13 with PeCDF (0-30 micrograms/kg) or HCDF (0-300 micrograms/kg). Hepatic [3H]dexamethasone and [125I]EGF equilibrium binding studies indicated that all doses of PeCDF tested (10, 20, and 30 micrograms/kg) significantly reduced the GRc and EGF receptor maximum binding capacities but did not affect the binding affinities of these receptors when compared to corn oil-treated control pregnant mice. Similar effects were observed for doses of HCDF greater than or equal to 100 micrograms/kg. These data suggest that the dibenzofuran-mediated decreases in GRc and EGF receptor binding capacities are similar to those caused by TCDD. Although the mechanism of action is not yet clear, our results indicate that halogenated aromatic compounds in addition to TCDD have profound effects on both steroid and growth factor receptor systems. JF - Toxicology and applied pharmacology AU - Ryan, R P AU - Sunahara, G I AU - Lucier, G W AU - Birnbaum, L S AU - Nelson, K G AD - Laboratory of Biochemical Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 454 EP - 464 VL - 98 IS - 3 SN - 0041-008X, 0041-008X KW - Benzofurans KW - 0 KW - Polychlorinated Dibenzodioxins KW - Receptors, Glucocorticoid KW - 1,2,3,4,7,8-hexachlorodibenzofuran KW - 70648-26-9 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - 2,3,4,7,8-pentachlorodibenzofuran KW - U4C2RV3124 KW - Index Medicus KW - Animals KW - Dose-Response Relationship, Drug KW - Polychlorinated Dibenzodioxins -- toxicity KW - Mice, Inbred C57BL KW - Mice KW - Female KW - Pregnancy KW - Receptor, Epidermal Growth Factor -- drug effects KW - Receptors, Glucocorticoid -- drug effects KW - Receptor, Epidermal Growth Factor -- metabolism KW - Liver -- drug effects KW - Receptors, Glucocorticoid -- metabolism KW - Benzofurans -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78962860?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-16 N1 - Date created - 1989-06-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genetic analysis of the rnc operon of Escherichia coli. AN - 78947163; 2540151 AB - RNase III, an Escherichia coli double-stranded endoribonuclease, is known to be involved in maturation of rRNA and regulation of several bacteriophage and Escherichia coli genes. Clones of the region of the E. coli chromosome containing the gene for RNase III (rnc) were obtained by screening genomic libraries in lambda with DNA known to map near rnc. A phage clone with the rnc region was randomly mutagenized with a delta Tn10 element, and the insertions were recombined onto the chromosome, generating a series of strains with delta Tn10 insertions in the rnc region. Two insertions that had Rnc- phenotypes were located. One of them lay in the rnc gene, and one was in the rnc leader sequence. Polarity studies showed that rnc is in an operon with two other genes, era and recO. The sequence of the recO gene beyond era indicated it could encode a protein of approximately 26 kilodaltons and, like rnc and era, had codon usage consistent with a low level of expression. Experiments using antibiotic cassettes to disrupt the genes rnc, era, and recO showed that era is essential for E. coli growth but that rnc and recO are dispensable. JF - Journal of bacteriology AU - Takiff, H E AU - Chen, S M AU - Court, D L AD - Laboratory of Molecular Oncology, National Cancer Institute-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 2581 EP - 2590 VL - 171 IS - 5 SN - 0021-9193, 0021-9193 KW - Bacterial Proteins KW - 0 KW - DNA Transposable Elements KW - Escherichia coli Proteins KW - Endoribonucleases KW - EC 3.1.- KW - Ribonuclease III KW - EC 3.1.26.3 KW - ribonuclease III, E coli KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Index Medicus KW - Base Sequence KW - DNA Mutational Analysis KW - Restriction Mapping KW - Molecular Sequence Data KW - Genetic Complementation Test KW - GTP-Binding Proteins -- genetics KW - Genes, Bacterial KW - Bacterial Proteins -- genetics KW - Operon KW - Escherichia coli -- genetics KW - Endoribonucleases -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78947163?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-07 N1 - Date created - 1989-06-07 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M26415; GENBANK; M26416 N1 - SuppNotes - Cited By: J Biol Chem. 1977 May 10;252(9):3064-73 [323260] Mol Gen Genet. 1973 Oct 16;126(1):53-9 [4591369] Biochim Biophys Acta. 1978 Sep 21;505(1):95-127 [361078] Virology. 1979 Dec;99(2):241-56 [160127] Cell. 1980 Feb;19(2):393-401 [6153577] Biochem Biophys Res Commun. 1980 Oct 16;96(3):1063-70 [6159890] Genetics. 1980 Aug;95(4):785-95 [6162715] J Bacteriol. 1980 Aug;143(2):926-33 [6259126] Gene. 1980 Dec;12(3-4):301-9 [6265323] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6106-10 [6273848] Microbiol Rev. 1981 Dec;45(4):502-41 [6173734] Proc Natl Acad Sci U S A. 1982 Jan;79(2):238-42 [6281759] Cell. 1982 Jul;29(3):727-8 [7151167] J Bacteriol. 1983 May;154(2):569-72 [6341355] J Bacteriol. 1983 Jun;154(3):1485-8 [6343356] J Biol Chem. 1974 Feb 25;249(4):1314-6 [4592261] J Mol Biol. 1975 Dec 15;99(3):487-99 [765478] Microbiol Rev. 1983 Jun;47(2):180-230 [6348505] Gene. 1983 Jul;23(1):75-84 [6311677] J Biol Chem. 1983 Oct 10;258(19):12034-42 [6311836] J Biol Chem. 1983 Oct 10;258(19):12073-80 [6311837] J Mol Biol. 1984 Jan 15;172(2):185-201 [6229640] Proc Natl Acad Sci U S A. 1984 Jan;81(1):185-8 [6364133] J Biol Chem. 1984 Mar 10;259(5):3202-9 [6321499] Gene. 1983 Dec;26(2-3):171-9 [6323258] J Bacteriol. 1984 Jun;158(3):910-9 [6327648] J Virol. 1984 Dec;52(3):966-72 [6238175] Proc Natl Acad Sci U S A. 1985 Feb;82(3):849-53 [2983317] Gene. 1984 Dec;32(3):369-79 [6099322] J Biol Chem. 1985 Jun 25;260(12):7206-13 [2987248] Nucleic Acids Res. 1985 Jul 11;13(13):4677-85 [3895158] Nucleic Acids Res. 1985 Jul 25;13(14):5041-54 [2991850] J Bacteriol. 1985 Sep;163(3):1060-6 [2993230] Mol Gen Genet. 1985;199(3):381-7 [3162077] Mol Gen Genet. 1985;201(1):25-9 [3903434] J Bacteriol. 1985 Dec;164(3):1124-35 [2999072] J Mol Biol. 1986 May 5;189(1):131-41 [3023619] Proc Natl Acad Sci U S A. 1986 Dec;83(23):8849-53 [3097637] Microbiol Rev. 1986 Dec;50(4):428-51 [2432388] Nucleic Acids Res. 1987 Jan 26;15(2):717-29 [3547328] Annu Rev Biochem. 1987;56:615-49 [3113327] Annu Rev Biochem. 1987;56:779-827 [3304147] Proc Natl Acad Sci U S A. 1987 Sep;84(18):6511-5 [2957696] EMBO J. 1987 Jul;6(7):2165-70 [3308454] Mol Gen Genet. 1987 Aug;209(1):28-32 [2823071] Oncogene. 1988 Jun;2(6):539-44 [2838786] J Mol Biol. 1988 Jun 20;201(4):683-95 [2459389] J Bacteriol. 1982 May;150(2):633-42 [6279565] J Mol Biol. 1969 Mar 28;40(3):391-413 [4903714] J Bacteriol. 1970 May;102(2):377-81 [4315893] Bacteriol Rev. 1972 Dec;36(4):525-57 [4568763] Proc Natl Acad Sci U S A. 1973 Dec;70(12):3296-3300 [4587248] J Bacteriol. 1978 Aug;135(2):528-41 [98520] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Female gene expression in the seminal vesicle of mice after prenatal exposure to diethylstilbestrol. AN - 78943979; 2707167 AB - Previous studies from our laboratory on the feminization of the male mouse reproductive tract after prenatal exposure to diethylstilbestrol (DES) showed that the mRNA for the major estrogen-inducible uterine secretory protein, lactoferrin (LF), was constitutively expressed in the seminal vesicle of male mice exposed prenatally to DES, but not in the seminal vesicle of control mice. After castration, treatment with 17 beta-estradiol (20 micrograms/kg.day) for 3 days induced the LF mRNA in the seminal vesicle of both control and prenatally DES-exposed mice; however, the levels in DES-treated tissues were approximately 6-fold higher than those in control tissue. This report describes the presence of LF in seminal vesicle tissues and secretions of prenatally DES-exposed mice, as determined by immunohistochemistry and Western blot analysis. Further, these data are correlated with immunolocalization of the estrogen receptor in the seminal vesicle tissue. We conclude that the seminal vesicle of prenatally DES-exposed male mice has acquired two key characteristics of female tissues, namely LF production/regulation and estrogen receptor localization/distribution similar to that in uterine tissues. JF - Endocrinology AU - Newbold, R R AU - Pentecost, B T AU - Yamashita, S AU - Lum, K AU - Miller, J V AU - Nelson, P AU - Blair, J AU - Kong, H AU - Teng, C AU - McLachlan, J A AD - Developmental Endocrinology and Pharmacology Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 2568 EP - 2576 VL - 124 IS - 5 SN - 0013-7227, 0013-7227 KW - Receptors, Estrogen KW - 0 KW - Diethylstilbestrol KW - 731DCA35BT KW - Lactoferrin KW - EC 3.4.21.- KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Mice KW - Body Fluids -- metabolism KW - Receptors, Estrogen -- metabolism KW - Lactoferrin -- metabolism KW - Immunohistochemistry KW - Male KW - Female KW - Pregnancy KW - Orchiectomy KW - Feminization KW - Seminal Vesicles -- physiology KW - Seminal Vesicles -- metabolism KW - Seminal Vesicles -- secretion KW - Diethylstilbestrol -- pharmacology KW - Gene Expression Regulation -- drug effects KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78943979?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-06 N1 - Date created - 1989-06-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Drug-induced allergic hepatitis: does isaxonine fall into this category? AN - 78943146; 2707741 JF - Hepatology (Baltimore, Md.) AU - Pohl, L R AD - Section of Pharmacological Chemistry, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 785 EP - 788 VL - 9 IS - 5 SN - 0270-9139, 0270-9139 KW - Pyrimidines KW - 0 KW - isaxonine KW - 883G6DMT63 KW - Index Medicus KW - Rats KW - Animals KW - Humans KW - Pyrimidines -- adverse effects KW - Chemical and Drug Induced Liver Injury -- etiology KW - Liver -- drug effects KW - Pyrimidines -- toxicity KW - Chemical and Drug Induced Liver Injury -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78943146?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-30 N1 - Date created - 1989-05-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A phase I study of intraarterial iododeoxyuridine in patients with colorectal liver metastases. AN - 78941328; 2709091 AB - Regional delivery of iododeoxyuridine (IdUrd) to patients with colorectal liver metastases was examined in a phase I study. The maximum-tolerated intraarterial (IA) dose (MTD) was 1,333 mg/m2/d administered continuously for 14 days. The dose-limiting toxicity was thrombocytopenia. Thrombocytopenia and leukopenia were correlated with the amount of IdUrd incorporated into DNA of peripheral granulocytes. In contrast to our experience with 5-fluorodeoxyuridine, there was no evidence of hepatobiliary toxicity. In 11 patients who received IA IdUrd alone, seven had a greater than or equal to 50% decrease in carcinoembryonic antigen (CEA) levels, with five having tumor volume reductions of 65%, 48%, 46%, 44%, and 27%. Thus, IA IdUrd alone has antitumor efficacy. Patients subsequently received IdUrd in combination with external beam radiation to a total dose of 2,400 cGy without acute local toxicity. In addition to these favorable clinical findings, we have previously shown that IdUrd is selectively incorporated into tumor DNA compared with normal liver in these patients. Further phase II evaluations of this approach are warranted. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Chang, A E AU - Collins, J M AU - Speth, P A AU - Smith, R AU - Rowland, J B AU - Walton, L AU - Begley, M G AU - Glatstein, E AU - Kinsella, T J AD - Surgery Branch, National Cancer Institute, Bethesda, Md. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 662 EP - 668 VL - 7 IS - 5 SN - 0732-183X, 0732-183X KW - Antineoplastic Agents KW - 0 KW - DNA, Neoplasm KW - Idoxuridine KW - LGP81V5245 KW - Index Medicus KW - Hematologic Diseases -- chemically induced KW - Drug Evaluation KW - Hepatic Artery KW - Combined Modality Therapy KW - Humans KW - Middle Aged KW - DNA, Neoplasm -- metabolism KW - Male KW - Female KW - Antineoplastic Agents -- administration & dosage KW - Colorectal Neoplasms -- pathology KW - Colorectal Neoplasms -- metabolism KW - Liver Neoplasms -- drug therapy KW - Idoxuridine -- pharmacokinetics KW - Liver Neoplasms -- secondary KW - Idoxuridine -- adverse effects KW - Colorectal Neoplasms -- drug therapy KW - Idoxuridine -- administration & dosage KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78941328?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-05 N1 - Date created - 1989-06-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment of HIV tissue culture infection with monoclonal antibody-ricin A chain conjugates. AN - 78939890; 2540236 AB - mAb 907 is directed against the envelope protein of the HIV. The epitope recognized by this antibody is expressed in moderate density on the surface of tissue culture cells infected with the LAV/HTLV-IIIB strain of HIV. We have coupled antibody 907 to ricin A chain (RAC). The antibody-RAC conjugate inhibited protein synthesis and cell growth in HIV-infected cells. An irrelevant antibody conjugated to RAC had no effect. Most important, treatment of infected cells with the conjugate markedly inhibited the production of infectious virus, as measured by the production of viral foci on susceptible monolayer cells. Exposure of HIV-infected target cells to the conjugate for as short a period as 1 h resulted in cell death. Serum of AIDS patients inhibited, but did not completely suppress, the toxicity of the 907-RAC conjugate. A second antibody, designated BM-1, which recognizes a carbohydrate Ag on the surface of virally infected cells, was conjugated to RAC. The BM-1-RAC conjugate did not kill HIV-infected cells, highlighting the importance of the target Ag. Immunotoxins produced with antibodies that recognize Ag on the surface of HIV-infected cells may have utility in the therapy of AIDS. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Pincus, S H AU - Wehrly, K AU - Chesebro, B AD - Laboratory of Microbial Structure and Function, National Institute of Allergy and Infectious Diseases, Hamilton, MT 59840. Y1 - 1989/05/01/ PY - 1989 DA - 1989 May 01 SP - 3070 EP - 3075 VL - 142 IS - 9 SN - 0022-1767, 0022-1767 KW - Antibodies, Monoclonal KW - 0 KW - HIV Envelope Protein gp120 KW - Immunotoxins KW - Lewis Blood-Group System KW - Protein Synthesis Inhibitors KW - Retroviridae Proteins KW - Ricin KW - 9009-86-3 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Virus Replication KW - Acute Disease KW - Retroviridae Proteins -- analysis KW - Humans KW - Cell Survival KW - Lewis Blood-Group System -- immunology KW - Culture Techniques KW - Protein Synthesis Inhibitors -- toxicity KW - Dose-Response Relationship, Immunologic KW - Kinetics KW - Binding, Competitive KW - Cell Line KW - Ricin -- toxicity KW - HIV -- physiology KW - HIV -- immunology KW - Immunotoxins -- toxicity KW - Antibodies, Monoclonal -- toxicity KW - Acquired Immunodeficiency Syndrome -- immunology KW - HIV -- analysis KW - Acquired Immunodeficiency Syndrome -- microbiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78939890?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-31 N1 - Date created - 1989-05-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Novel use of polymerase chain reaction to amplify cellular DNA adjacent to an integrated provirus. AN - 78935149; 2704070 AB - We describe a modification of the polymerase chain reaction technique which allows amplification of cellular DNA adjacent to an integrated provirus given sequence information for the provirus only. The modified technique should be generally useful for studies of insertional mutagenesis and other situations in which one wishes to isolate DNA adjacent to a region of known sequence. JF - Journal of virology AU - Silver, J AU - Keerikatte, V AD - Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 1924 EP - 1928 VL - 63 IS - 5 SN - 0022-538X, 0022-538X KW - DNA, Circular KW - 0 KW - DNA, Viral KW - Oligonucleotide Probes KW - Index Medicus KW - Animals KW - Recombination, Genetic KW - Molecular Biology -- methods KW - Mice KW - Proviruses -- genetics KW - Retroviridae -- genetics KW - DNA, Viral -- genetics KW - Cell Transformation, Viral KW - Gene Amplification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78935149?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-18 N1 - Date created - 1989-05-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1968 Sep 10;243(17):4556-63 [4879168] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Proc Natl Acad Sci U S A. 1978 May;75(5):2170-4 [209457] Science. 1979 Apr 6;204(4388):69-71 [219475] Science. 1979 Apr 6;204(4388):71-3 [219476] Proc Natl Acad Sci U S A. 1980 Jan;77(1):614-8 [6244569] Proc Natl Acad Sci U S A. 1981 Aug;78(8):4833-7 [6272277] J Virol. 1982 Feb;41(2):435-48 [6281459] J Virol. 1982 Aug;43(2):629-40 [6287036] Nucleic Acids Res. 1983 Aug 25;11(16):5603-20 [6310506] J Virol. 1984 Feb;49(2):471-8 [6319746] Proc Natl Acad Sci U S A. 1984 Nov;81(21):6812-6 [6093122] J Virol. 1985 Jan;53(1):100-6 [2981327] J Virol. 1985 Sep;55(3):768-77 [2991595] Science. 1985 Dec 20;230(4732):1350-4 [2999980] Science. 1986 Sep 5;233(4768):1076-8 [3461561] Science. 1987 Jan 16;235(4786):305-11 [3541204] J Virol. 1987 Mar;61(3):701-7 [3027396] Nucleic Acids Res. 1987 Sep 25;15(18):7640 [2821511] Nature. 1987 Nov 26-Dec 2;330(6146):384-6 [3683554] Methods Enzymol. 1987;155:335-50 [3431465] Science. 1988 Jan 29;239(4839):487-91 [2448875] Science. 1988 Jan 29;239(4839):491-4 [3340835] Erratum In: J Virol 1990 Jun;64(6):3150 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cyclosporin A-mediated inhibition of mitogen-induced gene transcription is specific for the mitogenic stimulus and cell type. AN - 78923958; 2496166 AB - We have examined the effect of cyclosporin A (CSA) on the mitogen-induced expression of 11 genes previously cloned from mitogen-activated T lymphocytes. Levels of induced gene expression in the human T cell line Jurkat were determined by mRNA blotting and nuclear run-on assay, after stimulation with one or combinations of the mitogens PMA, PHA, and the ionophore A23187. In the presence of CSA, gene expression induced with PMA alone was not inhibited, whereas PHA-induced increases in gene expression were inhibited by CSA. For one group of genes, including IL-2 and two novel genes with sequences suggestive of lymphokines, A23187 plus PMA-induced gene expression was inhibited by CSA. In contrast, another group of induced genes was unaffected by CSA after A23187 and PMA induction. This finding implies that A23187 and PMA stimulate gene induction by more than one mechanism, and that not all activation signals mediated through calcium fluxes are sensitive to CSA. In addition, 8 of the 11 genes were expressed in the fibroblast cell line Mrc 5 after stimulation with PMA, A23187, or serum; CSA had no effect on genes induced with these agents in Mrc 5 cells in both mRNA blotting and run-on experiments, although 5 of these genes were markedly inhibited by CSA in Jurkat after PMA/PHA induction. These data indicate that separate pathways for induction of identical genes exist, and that the inciting stimulus and cell type are determining factors in the ability of CSA to inhibit gene expression. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Gunter, K C AU - Irving, S G AU - Zipfel, P F AU - Siebenlist, U AU - Kelly, K AD - Laboratory of Pathology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/05/01/ PY - 1989 DA - 1989 May 01 SP - 3286 EP - 3291 VL - 142 IS - 9 SN - 0022-1767, 0022-1767 KW - Cyclosporins KW - 0 KW - Mitogens KW - Phytohemagglutinins KW - Calcimycin KW - 37H9VM9WZL KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Fibroblasts -- drug effects KW - Humans KW - Transcriptional Activation KW - Cell Line KW - Lymphocyte Activation -- drug effects KW - Transcription, Genetic -- drug effects KW - Gene Expression Regulation -- drug effects KW - Cyclosporins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78923958?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-31 N1 - Date created - 1989-05-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Poly(A+)RNA levels of growth-, differentiation- and transformation-associated genes in the progressive development of hepatocellular carcinoma in the rat. AN - 78915859; 2468594 AB - The development of chemically induced hepatocellular carcinoma in the rat proceeds through a series of premalignant changes that may ultimately progress to a primary malignant tumor. Using the selection technique based on diminished binding of preneoplastic hepatocytes to tissue culture plates precoated with asialofetuin, we have isolated poly(A+)RNA from early preneoplastic foci as well as preneoplastic persistent nodules and primary hepatocellular carcinoma induced by the Solt-Farber protocol in the Fischer rat. The steady-state poly(A+)RNA levels of genes traditionally associated with growth, differentiation and/or transformation were then determined to address the question of their temporal expression in the multistep nature of cancer development. Ornithine decarboxylase- and P53-specific transcripts did not significantly change in preneoplastic foci but were increased in later-stage preneoplastic nodules and hepatocellular carcinoma. Albumin-specific transcripts were decreased in all hepatocellular carcinoma but there was no consistent coordinated increase in alpha-fetoprotein-specific transcripts. c-myc and raf transcripts increased at the very early preneoplastic foci stage and continued to increase throughout the neoplastic process. No L-myc or N-myc transcripts could be detected in any RNA sample. c-Ha-ras-specific transcripts were essentially unaltered in all RNA samples whereas no c-Ki-ras or N-ras transcripts could be detected throughout the neoplastic process. In addition, no dominant-acting transforming mutations in the ras gene family were detected by DNA transfection experiments using NIH/3T3 cells. JF - Hepatology (Baltimore, Md.) AU - Huber, B E AU - Heilman, C A AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 756 EP - 762 VL - 9 IS - 5 SN - 0270-9139, 0270-9139 KW - Asialoglycoprotein Receptor KW - 0 KW - DNA Probes KW - RNA, Messenger KW - RNA, Neoplasm KW - Receptors, Immunologic KW - Poly A KW - 24937-83-5 KW - RNA KW - 63231-63-0 KW - Index Medicus KW - Receptors, Immunologic -- genetics KW - Rats KW - Animals KW - Blotting, Northern KW - Transcription, Genetic KW - Male KW - Poly A -- isolation & purification KW - Liver Neoplasms, Experimental -- genetics KW - Precancerous Conditions -- genetics KW - RNA, Neoplasm -- isolation & purification KW - Oncogenes KW - RNA -- isolation & purification KW - Gene Expression Regulation KW - Proto-Oncogenes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78915859?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-30 N1 - Date created - 1989-05-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Unmyristylated Moloney murine leukemia virus Pr65gag is excluded from virus assembly and maturation events. AN - 78900703; 2649693 AB - The gag precursor polyprotein of Moloney murine leukemia virus (MuLV) is normally modified by myristylation of the N-terminal glycine. Previous work showed that the Pr65gag lacking the myristylation site does not associate with cellular membranes or assemble into virus particles. We now report that it also is not cleaved to the mature gag cleavage products within the cell and that it sediments as a free 65-kilodalton monomer in detergent-free cell extracts containing 0.3 M NaCl. Even when the cells containing the mutant are productively infected with wild-type MuLV, the mutant Pr65gag is not processed into cleavage products and is not incorporated into the virions produced by these cells. Thus, the mutant gag molecules seem unable to participate in the normal processes of self-assembly and maturation. We propose that myristate-mediated membrane association is an essential first step in MuLV assembly. This association may also play a role in budding of MuLV. JF - Journal of virology AU - Schultz, A M AU - Rein, A AD - Laboratory of Molecular Virology and Carcinogenesis, NCI-Frederick Cancer Research Facility, Frederick, Maryland 21701. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 2370 EP - 2373 VL - 63 IS - 5 SN - 0022-538X, 0022-538X KW - Gene Products, gag KW - 0 KW - Myristic Acids KW - Protein Precursors KW - Retroviridae Proteins KW - Myristic Acid KW - 0I3V7S25AW KW - Peptide Hydrolases KW - EC 3.4.- KW - Index Medicus KW - Protein Precursors -- physiology KW - DNA Mutational Analysis KW - Cell Compartmentation KW - Protein Processing, Post-Translational KW - Peptide Hydrolases -- metabolism KW - Cell Membrane -- metabolism KW - Virus Replication KW - Retroviridae Proteins -- physiology KW - Moloney murine leukemia virus -- growth & development KW - Myristic Acids -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78900703?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-18 N1 - Date created - 1989-05-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1971 Jul;68(7):1520-4 [4327005] J Virol. 1987 Apr;61(4):1045-53 [3493352] J Virol. 1976 Jul;19(1):13-8 [181592] J Virol. 1976 Jul;19(1):19-25 [59816] Virology. 1976 Sep;73(2):532-6 [183368] J Virol. 1977 Jun;22(3):626-33 [195081] Proc Natl Acad Sci U S A. 1977 Aug;74(8):3446-50 [410020] Cell. 1978 Jul;14(3):601-9 [80281] J Virol. 1979 Dec;32(3):1015-27 [229256] J Gen Virol. 1980 Sep;50(1):1-21 [6255080] Virology. 1982 Apr 30;118(2):380-8 [6178211] Proc Natl Acad Sci U S A. 1983 Jan;80(2):339-43 [6340098] J Virol. 1983 May;46(2):355-61 [6302307] Virology. 1983 May;127(1):134-48 [6305011] Mol Immunol. 1983 Dec;20(12):1353-62 [6197636] J Virol. 1985 Mar;53(3):899-907 [3882995] Proc Natl Acad Sci U S A. 1985 Mar;82(6):1618-22 [3885215] Virology. 1985 Sep;145(2):280-92 [2411050] Virology. 1984 Apr 30;134(2):368-74 [6545073] Proc Natl Acad Sci U S A. 1986 Oct;83(19):7246-50 [3489936] Virology. 1971 Aug;45(2):401-10 [4106352] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential induction of fetal mouse liver and lung cytochromes P-450 by beta-naphthoflavone and 3-methylcholanthrene. AN - 76291471; 2468428 AB - Previous studies have shown that the incidences of liver and lung tumors in mice exposed transplacentally to 3-methyl-cholanthrene (MC) were significantly influenced by the sensitivity of both mothers and fetuses to induction of cytochrome(s) P-450 by polycyclic aromatic hydrocarbons. In order to delineate further the biochemical and molecular processes underlying the observed biological effects, the inductive effect of MC and beta-naphthoflavone (beta NF) on cytochrome P-450 was determined at the biochemical and molecular levels. C57BL/6 females were mated with DBA/2 males and treated i.p. on day 17 of gestation with olive oil alone, 150 mg/kg of beta NF or different doses of MC. At various times after injection the mothers were sacrificed and the fetuses removed for biochemical and molecular studies. MC caused maximal induction of aryl hydrocarbon hydroxylase (AHH) activity by 8 h in both the liver and lung. beta NF caused nearly maximal induction of AHH activity by 8 h in the lung but had little effect on liver AHH activity at this time. Maximal induction with beta NF occurred by 24 h in both organs. Addition of monoclonal antibody 1-7-1, specific for the MC-inducible forms of cytochrome P-450 (P-450IA1 and A2), to the incubation mixtures resulted in a 55-70% inhibition of AHH activity in both lung and liver assays, regardless of the inducing agent used, while having no effect on AHH activity from oil-treated mice. RNA blot analysis carried out in parallel with enzyme assays demonstrated that the levels of enzyme activity correlated very well with the levels of steady-state RNAs. MC caused maximal induction of P-450IA1 RNA levels 4 h after injection in both organs and a biphasic secondary increase was observed in the lung. Maximal levels of P-450IA1 RNA were seen at 12-16 h following injection of beta NF. However, the ratio of P-450IA1 RNAs present at 16 versus 2 h in the beta NF-treated liver appeared greater than that in the lung. P-450IA2 was also induced in fetal liver and lung, but at low levels relative to P-450IA1. The results indicate that the increase in functional AHH activity was primarily due to induction of cytochrome P-450IA1. The differences in induction kinetics observed for cytochromes P-450IA1 and A2 suggest that these enzymes exhibit both tissue- and inducer-dependent specificity. JF - Carcinogenesis AU - Miller, M S AU - Jones, A B AU - Chauhan, D P AU - Park, S S AU - Anderson, L M AD - Perinatal Carcinogenesis Section, National Cancer Institute, Frederick, Maryland 21701-1013. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 875 EP - 891 VL - 10 IS - 5 SN - 0143-3334, 0143-3334 KW - Benzoflavones KW - 0 KW - Flavonoids KW - Methylcholanthrene KW - 56-49-5 KW - beta-Naphthoflavone KW - 6051-87-2 KW - RNA KW - 63231-63-0 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - Index Medicus KW - Fetus KW - Animals KW - Reference Values KW - Mice, Inbred C57BL KW - Enzyme Induction KW - Mice KW - RNA -- drug effects KW - Male KW - Female KW - RNA -- genetics KW - Pregnancy KW - Mice, Inbred DBA KW - Aryl Hydrocarbon Hydroxylases -- biosynthesis KW - Liver -- enzymology KW - Methylcholanthrene -- pharmacology KW - Liver -- drug effects KW - Cytochrome P-450 Enzyme System -- genetics KW - Lung -- drug effects KW - Lung -- embryology KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Lung -- enzymology KW - Flavonoids -- pharmacology KW - Liver -- embryology KW - Benzoflavones -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76291471?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-08 N1 - Date created - 1989-06-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lack of in vitro synergy between etoposide and cis-diamminedichloroplatinum(II). AN - 76289658; 2706626 AB - Claims of synergy between etoposide and cisplatin have been based upon preclinical in vivo murine P388 models or upon human clinical trials in tumors such as lung cancer. Such in vivo studies are useful in exploring therapeutic synergy, i.e., an improved therapeutic strategy. The term "synergy" in this context is sometimes, however, taken to imply greater than additive kill of tumor cells. Unfortunately, it is virtually impossible to document supra-additive tumor cell kill in vivo, since in vivo curves of therapeutic effect are not linear and drugs are therefore not additive with themselves. Therapeutic synergy may, in fact, occur when two drugs are merely additive (or even antagonistic) with regard to cytotoxicity if the drugs have nonoverlapping host toxicity. The demonstration of true supra-additive cell kill would imply an interaction of the two agents at a cellular level and would have profound implications for biochemical studies. In order to determine whether the reported therapeutic synergy of etoposide and cisplatin is due, in part, to supra-additive cell kill, we used an in vitro tetrazolium-based colorimetric assay for cytotoxicity (MTT assay) and an isobologram analysis to test combinations of the two drugs against four human small cell and four human non-small cell lung carcinoma lines. Using a rigorous test for in vitro synergy, we could not establish a greater than additive cytotoxic effect on our cell lines. It thus appears that the clinical synergy between etoposide and cisplatin is not due to a supra-additive effect at the cellular level. Our results have implications for a variety of fields in which claims of "synergy" often appear. JF - Cancer research AU - Tsai, C M AU - Gazdar, A F AU - Venzon, D J AU - Steinberg, S M AU - Dedrick, R L AU - Mulshine, J L AU - Kramer, B S AD - National Cancer Institute, Naval Hospital, Bethesda 20814-5101. Y1 - 1989/05/01/ PY - 1989 DA - 1989 May 01 SP - 2390 EP - 2397 VL - 49 IS - 9 SN - 0008-5472, 0008-5472 KW - Etoposide KW - 6PLQ3CP4P3 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Cell Survival -- drug effects KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Antineoplastic Combined Chemotherapy Protocols -- pharmacology KW - Drug Synergism KW - Etoposide -- pharmacology KW - Cisplatin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76289658?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-01 N1 - Date created - 1989-06-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Do women with childhood exposure to cigarette smoking have increased fecundability? AN - 75767442; 2705428 AB - The authors earlier conducted a retrospective study of time to pregnancy among a group of pregnant women in Minnesota, in order to investigate the relation between cigarette smoking and fecundability. Further analysis of these data shows that women who had been exposed as children to cigarette smokers had increased fertility. This finding lacks biologic plausibility. However, the authors found a similar association in a group of North Carolina women whose fecundability had been measured prospectively. Furthermore, both groups showed an apparent dose-response effect. The authors briefly describe this unexpected finding so that it might be more fully explored in other studies. JF - American journal of epidemiology AU - Wilcox, A J AU - Baird, D D AU - Weinberg, C R AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 1079 EP - 1083 VL - 129 IS - 5 SN - 0002-9262, 0002-9262 KW - Tobacco Smoke Pollution KW - 0 KW - Index Medicus KW - Population KW - United States KW - North America KW - Minnesota KW - Fertility KW - Americas KW - Research Methodology KW - Population Dynamics KW - Retrospective Studies KW - Studies KW - Developed Countries KW - Fecundability KW - Pregnancy KW - Smoking KW - Northern America KW - Prospective Studies KW - Fecundity KW - Behavior KW - North Carolina KW - Demographic Factors KW - Reproduction KW - Maternal-fetal Exchange KW - Humans KW - Female KW - Mothers KW - Models, Statistical KW - Fathers KW - Prenatal Exposure Delayed Effects KW - Fertility -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75767442?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-25 N1 - Date created - 1989-05-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reduced fecundability in women with prenatal exposure to cigarette smoking. AN - 75765400; 2705427 AB - Animal studies have suggested that fertility may be impaired by transplacental exposures, but little is known about human prenatal exposures and subsequent adult reproduction. A possible relation between prenatal exposure to cigarette smoking and adult fecundability in women was explored, with the use of data from a prospective study of 221 North Carolina couples. These couples were recruited during 1983-1985, at the time they stopped using birth control in order to become pregnant. The relative fecundability of exposed compared with unexposed women was estimated by applying a discrete-time proportional probabilities model to the cycle-by-cycle conception rates. Women with prenatal exposure to their mother's cigarette smoking had reduced fecundability. The fecundability ratio associated with prenatal exposure to mother's smoking, adjusted for age, frequency of intercourse, current smoking status, age at menarche, and childhood exposure to cigarette smoking, was 0.5 (95% confidence interval 0.4-0.8). This association was not changed by further adjustment for other possible confounding variables, including educational level, reproductive history, body weight, and consumption of alcohol and caffeine. Thus, women whose mothers smoked while pregnant with them may be on average substantially less fecund than women whose mothers did not smoke during pregnancy. JF - American journal of epidemiology AU - Weinberg, C R AU - Wilcox, A J AU - Baird, D D AD - Statistics and Biomathematics Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/05// PY - 1989 DA - May 1989 SP - 1072 EP - 1078 VL - 129 IS - 5 SN - 0002-9262, 0002-9262 KW - Tobacco Smoke Pollution KW - 0 KW - Index Medicus KW - Population KW - Fetus KW - Fertility KW - Research Methodology KW - Population Dynamics KW - Statistical Studies KW - Social Behavior KW - Studies KW - Longterm Effects KW - Correlation Studies KW - Fecundability KW - Pregnancy KW - Smoking KW - Fecundity KW - Behavior KW - Risk Factors KW - Demographic Factors KW - Reproduction KW - Time Factors KW - Biology KW - Humans KW - Adult KW - Menarche KW - Smoking -- adverse effects KW - Fathers KW - Female KW - Mothers KW - Infertility, Female -- etiology KW - Tobacco Smoke Pollution -- adverse effects KW - Models, Statistical KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75765400?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-25 N1 - Date created - 1989-05-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The preparation and biochemical characterization of intact capsids of equine infectious anemia virus. AN - 78969900; 2541703 AB - Capsids of equine infectious anemia virus have been isolated as cone-shaped particles 60 x 120 nm in size. Detergent treatment of whole virus followed by two cycles of rate-zonal centrifugation in Ficoll produces these capsids in a yield of approximately 10%. The major protein components are the gag-encoded p11 nucleocapsid protein and p26 capsid protein, which are present in equimolar amounts. Substantial cleavage of p11 to p6 and p4 can be observed under conditions where the viral protease packaged in the capsid is enzymatically active. JF - Biochemical and biophysical research communications AU - Roberts, M M AU - Oroszlan, S AD - Laboratory of Molecular Virology and Carcinogenesis, NCI-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1989/04/28/ PY - 1989 DA - 1989 Apr 28 SP - 486 EP - 494 VL - 160 IS - 2 SN - 0006-291X, 0006-291X KW - Detergents KW - 0 KW - RNA, Viral KW - Viral Core Proteins KW - Index Medicus KW - Centrifugation, Zonal KW - Electrophoresis, Polyacrylamide Gel KW - Hydrogen-Ion Concentration KW - Viral Core Proteins -- ultrastructure KW - RNA, Viral -- isolation & purification KW - Viral Core Proteins -- isolation & purification KW - Capsid -- isolation & purification KW - Infectious Anemia Virus, Equine -- enzymology KW - Infectious Anemia Virus, Equine -- analysis KW - Capsid -- ultrastructure KW - Capsid -- enzymology KW - Infectious Anemia Virus, Equine -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78969900?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-16 N1 - Date created - 1989-06-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Functionally distinct NF-kappa B binding sites in the immunoglobulin kappa and IL-2 receptor alpha chain genes. AN - 78961555; 2497520 AB - The interleukin-2 receptor alpha (IL-2R alpha) chain gene contains a sequence similar to the immunoglobulin (Ig) kappa (kappa) enhancer NF-kappa B binding site. This site, which is bound by the nuclear protein, NF-kappa B, is critical for Ig kappa gene expression. The major T cell nuclear factor that binds to the IL-2R alpha site in vitro appears indistinguishable from NF-kappa B. NF-kappa B binds to IL-2R alpha and kappa sequences with similar affinities; however, only the kappa site potently activates transcription from heterologous promoters. Thus, high-affinity NF-kappa B binding in vitro cannot be equated with transcriptional activation in vivo. Mutation of the NF-kappa B binding site in the context of an IL-2 R alpha promoter construct markedly diminished promoter activity in human T cell lymphotropic virus type I (HTLV-I)-transformed MT-2 cells but not in phorbol myristate acetate-stimulated Jurkat T cells. JF - Science (New York, N.Y.) AU - Cross, S L AU - Halden, N F AU - Lenardo, M J AU - Leonard, W J AD - Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1989/04/28/ PY - 1989 DA - 1989 Apr 28 SP - 466 EP - 469 VL - 244 IS - 4903 SN - 0036-8075, 0036-8075 KW - DNA-Binding Proteins KW - 0 KW - Immunoglobulin kappa-Chains KW - NF-kappa B KW - Receptors, Interleukin-2 KW - Transcription Factors KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - AIDS/HIV KW - Animals KW - HIV-1 -- genetics KW - HeLa Cells KW - Humans KW - Human T-lymphotropic virus 1 KW - Transcription, Genetic KW - Mice KW - Binding Sites KW - T-Lymphocytes -- metabolism KW - Promoter Regions, Genetic KW - Base Sequence KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Line, Transformed KW - Mutation KW - Transcription Factors -- metabolism KW - Enhancer Elements, Genetic KW - Gene Expression Regulation KW - Receptors, Interleukin-2 -- genetics KW - Immunoglobulin kappa-Chains -- genetics KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78961555?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-16 N1 - Date created - 1989-06-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Maintenance of alveolitis in patients with chronic beryllium disease by beryllium-specific helper T cells. AN - 78933540; 2469014 AB - Chronic beryllium disease is characterized by the accumulation of helper/inducer T cells, macrophages, and granulomas in the lungs. To evaluate the hypothesis that the proliferation of CD4+ (helper/inducer) T cells in the lungs of patients with this disorder is maintained by local activation of beryllium-specific T-cell clones, we studied T cells obtained from peripheral blood and by bronchoalveolar lavage in eight patients and five healthy controls. The proliferation of T cells in response to beryllium in vitro was confined to the CD4+ T cells from the patients and was dependent on the presentation of antigen in the presence of both major histocompatibility complex class II antigens and functional interleukin-2 receptors. T cells from the patients' lungs had a significantly greater response to beryllium than did T cells from their peripheral blood (stimulation index, 103 vs. 5; P less than 0.01). Lines and clones of cells developed from T cells from the patients' lungs showed dose-dependent proliferation in response to beryllium but did not respond to recall antigens or to other metals. Although all beryllium-specific T-cell clones were CD4+ and none were CD8+ (suppressor/cytotoxic), all beryllium-specific clones studied had different rearrangements of T-cell antigen receptors, suggesting that the response to beryllium involved T cells with diverse specificities for beryllium. We conclude that in patients with chronic beryllium disease, beryllium acts as a class II-restricted antigen, stimulating local proliferation and accumulation in the lung of beryllium-specific CD4+ (helper/inducer) T cells. Hence, chronic beryllium disease is a hypersensitivity disease in which beryllium is the specific antigen. JF - The New England journal of medicine AU - Saltini, C AU - Winestock, K AU - Kirby, M AU - Pinkston, P AU - Crystal, R G AD - Pulmonary Branch, National Heart, Lung, and Blood Institute, Bethesda, MD 20892. Y1 - 1989/04/27/ PY - 1989 DA - 1989 Apr 27 SP - 1103 EP - 1109 VL - 320 IS - 17 SN - 0028-4793, 0028-4793 KW - Antigens, Differentiation, T-Lymphocyte KW - 0 KW - Epitopes KW - Histocompatibility Antigens Class I KW - Histocompatibility Antigens Class II KW - Beryllium KW - OW5102UV6N KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Histocompatibility Antigens Class II -- analysis KW - Bronchoalveolar Lavage Fluid -- immunology KW - Lung -- immunology KW - Lymphocyte Activation KW - Antigens, Differentiation, T-Lymphocyte -- analysis KW - Adult KW - Chronic Disease KW - Histocompatibility Antigens Class I -- analysis KW - T-Lymphocytes -- immunology KW - Female KW - Male KW - Berylliosis -- immunology KW - Beryllium -- immunology KW - Alveolitis, Extrinsic Allergic -- immunology KW - Alveolitis, Extrinsic Allergic -- etiology KW - T-Lymphocytes, Helper-Inducer -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78933540?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-26 N1 - Date created - 1989-05-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Impulsivity, aggression, and neuroendocrine responses to serotonergic stimulation in substance abusers. AN - 78975996; 2720017 AB - Alterations in the activity of central serotonergic systems have been implicated in impulsive and aggressive behavior. We examined the neuroendocrine and psychological responses of 24 substance users with differing levels of aggressiveness and impulsivity to the oral administration of an indirect serotonin agonist fenfluramine (60 mg) or placebo given in a double-blind crossover design. All subjects were volunteers on a closed research ward and were abstinent from drugs for a minimum of 5 days. Baseline plasma prolactin (PRL) levels were greater in the groups with higher levels of self-reported aggressiveness and impulsivity. When adjusted for the baseline, PRL and cortisol responses 180 min after fenfluramine administration were significantly elevated in subjects with higher levels of aggressiveness and impulsivity. Peak cortisol levels were correlated with impulsivity. PRL and cortisol responses to fenfluramine were more strongly correlated with impulsivity than aggressiveness. Also, the more impulsive subjects reported a decrease in subjective states of depression, hostility and anxiety after drug treatment. These data further support the hypothesis of altered serotonergic activity in aggressive and impulsive behaviors. JF - Biological psychiatry AU - Fishbein, D H AU - Lozovsky, D AU - Jaffe, J H AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1989/04/15/ PY - 1989 DA - 1989 Apr 15 SP - 1049 EP - 1066 VL - 25 IS - 8 SN - 0006-3223, 0006-3223 KW - Receptors, Serotonin KW - 0 KW - Fenfluramine KW - 2DS058H2CF KW - Serotonin KW - 333DO1RDJY KW - Prolactin KW - 9002-62-4 KW - Hydrocortisone KW - WI4X0X7BPJ KW - Index Medicus KW - Receptors, Serotonin -- drug effects KW - Humans KW - Adult KW - Violence KW - Male KW - Psychological Tests KW - Prolactin -- blood KW - Substance-Related Disorders -- blood KW - Serotonin -- physiology KW - Aggression -- psychology KW - Impulsive Behavior -- psychology KW - Impulsive Behavior -- blood KW - Substance-Related Disorders -- psychology KW - Hydrocortisone -- blood KW - Aggression -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78975996?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-06 N1 - Date created - 1989-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cardiac consequences of massive acetaminophen overdose. AN - 78931380; 2929460 JF - The American journal of cardiology AU - Mann, J M AU - Pierre-Louis, M AU - Kragel, P J AU - Kragel, A H AU - Roberts, W C AD - Pathology Branch, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989/04/15/ PY - 1989 DA - 1989 Apr 15 SP - 1018 EP - 1021 VL - 63 IS - 13 SN - 0002-9149, 0002-9149 KW - Acetaminophen KW - 362O9ITL9D KW - Abridged Index Medicus KW - Index Medicus KW - Myocardium -- pathology KW - Humans KW - Electrocardiography KW - Adult KW - Myocardium -- ultrastructure KW - Male KW - Acetaminophen -- poisoning KW - Heart -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78931380?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-11 N1 - Date created - 1989-05-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of interleukin 2 and the interleukin 2 receptor in aging rats. AN - 78917267; 2495185 AB - Lymphocytes of aged animals exhibit a marked decrease in proliferative capacity in response to mitogen stimulation when compared to those of younger animals. In humans and mice the decreased proliferation is due at least in part (i) to the inability of lymphocytes to synthesize sufficient interleukin 2 (IL-2) and (ii) to decreased expression of IL-2 receptors (IL-2R) on the surface of aged lymphocytes. We compared proliferative abilities, IL-2 production, and IL-2R expression in splenocyte cultures of 4- to 5- and 22- to 24-month-old Fischer 344 rats stimulated with either concanavalin A (Con A) or A23187 and phorbol myristate acetate (PMA). Proliferation was significantly decreased in aged lymphocytes (30-50%) with both treatment protocols. However, unlike mice and humans we observed no difference in IL-2 activity, IL-2 mRNA levels, or IL-2R cell surface expression of lymphocytes from young and aged rats stimulated with either Con A or A23187 and PMA. These results indicate that factors other than decreased expression of IL-2 and IL-2R are responsible for the diminished proliferative capacity of aged rat lymphocytes following mitogen stimulation. JF - Cellular immunology AU - Holbrook, N J AU - Chopra, R K AU - McCoy, M T AU - Nagel, J E AU - Powers, D C AU - Adler, W H AU - Schneider, E L AD - Laboratory of Molecular Genetics, National Institute on Aging, Baltimore, Maryland 21224. Y1 - 1989/04/15/ PY - 1989 DA - 1989 Apr 15 SP - 1 EP - 9 VL - 120 IS - 1 SN - 0008-8749, 0008-8749 KW - Interleukin-2 KW - 0 KW - RNA, Messenger KW - Receptors, Interleukin-2 KW - Concanavalin A KW - 11028-71-0 KW - Calcimycin KW - 37H9VM9WZL KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Rats KW - Lymphocyte Activation -- drug effects KW - Animals KW - Rats, Inbred F344 KW - Blotting, Northern KW - RNA, Messenger -- metabolism KW - Spleen -- cytology KW - Cells, Cultured KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Gene Expression Regulation KW - Calcimycin -- pharmacology KW - Concanavalin A -- pharmacology KW - Aging KW - Interleukin-2 -- genetics KW - Receptors, Interleukin-2 -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78917267?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-23 N1 - Date created - 1989-05-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Responsiveness of fetal and adult CD4-, CD8- thymocytes to T cell activation. AN - 78917054; 2564859 AB - Day-14 fetal CD4-, CD8- thymocytes showed a greater proliferative response to PMA + IL-4 than did adult double-negative thymocytes. In contrast, adult double-negative thymocytes were more responsive to PMA + IL-1 + IL-2 or to IL-1 + IL-2 alone. The adult double-negative thymocytes showed significantly greater proliferation than fetal thymocytes after stimulation via anti-CD3 or anti-Thy-1 in the presence or absence of interleukins (IL-1 + IL-2 or IL-4). Adult CD4-, CD8- thymocytes also exhibited greater calcium mobilization following anti-CD3 stimulation IL-2-dependent activation with anti-Thy-1 or IL-1 + IL-2 in the absence of PMA resulted in marked expansion of CD 3+, F23.1+, CD4-, CD8- thymocytes, a population absent in fetal thymocytes but constituting 4% of pre-cultured CD4-, CD8- adult thymocytes. IL-4 + PMA failed to expand this CD 3+ population. It is hypothesized that before expression of functional TCR, T cell development may be more dependent on activation pathways not using IL-2; after TCR expression, IL-2-dependent pathways, including Thy-1-mediated stimulation, become functional. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Takashi, T AU - Steinberg, A D AU - June, C H AU - Gause, W C AD - Cellular Immunology Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, MD 20892. Y1 - 1989/04/15/ PY - 1989 DA - 1989 Apr 15 SP - 2641 EP - 2646 VL - 142 IS - 8 SN - 0022-1767, 0022-1767 KW - Antigens, CD3 KW - 0 KW - Antigens, CD8 KW - Antigens, Differentiation, T-Lymphocyte KW - Antigens, Surface KW - Antigens, Thy-1 KW - Interleukin-1 KW - Interleukin-2 KW - Interleukins KW - Receptors, Antigen, T-Cell KW - Interleukin-4 KW - 207137-56-2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Interleukin-2 -- pharmacology KW - Interleukin-1 -- pharmacology KW - Receptors, Antigen, T-Cell -- immunology KW - Mice KW - Receptors, Antigen, T-Cell -- analysis KW - Antigens, Surface -- immunology KW - Calcium -- metabolism KW - Interleukins -- pharmacology KW - Mice, Inbred C57BL KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Female KW - Lymphocyte Activation KW - Antigens, Differentiation, T-Lymphocyte -- analysis KW - Fetus -- immunology KW - Antigens, Differentiation, T-Lymphocyte -- immunology KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78917054?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-22 N1 - Date created - 1989-05-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The alpha subunit of tryptophan synthase. Evidence that aspartic acid 60 is a catalytic residue and that the double alteration of residues 175 and 211 in a second-site revertant restores the proper geometry of the substrate binding site. AN - 78912725; 2649498 AB - Our studies, which are aimed at understanding the catalytic mechanism of the alpha subunit of tryptophan synthase from Salmonella typhimurium, use site-directed mutagenesis to explore the functional roles of aspartic acid 60, tyrosine 175, and glycine 211. These residues are located close to the substrate binding site of the alpha subunit in the three-dimensional structure of the tryptophan synthase alpha 2 beta 2 complex. Our finding that replacement of aspartic acid 60 by asparagine, alanine, or tyrosine results in complete loss of activity in the reaction catalyzed by the alpha subunit supports a catalytic role for aspartic acid 60. Since the mutant form with glutamic acid at position 60 has partial activity, glutamic acid 60 may serve as an alternative catalytic base. The mutant form in which tyrosine 175 is replaced by phenylalanine has substantial activity; thus the phenolic hydroxyl of tyrosine 175 is not essential for catalysis or substrate binding. Yanofsky and colleagues have identified many missense mutant forms of the alpha subunit of tryptophan synthase from Escherichia coli. Two of these inactive mutant forms had either tyrosine 175 replaced by cysteine or glycine 211 replaced by glutamic acid. Surprisingly, a second-site revertant which contained both of these amino acid changes was partially active. These results indicated that the second mutation must compensate in some way for the first. We now extend the studies of the effects of specific amino acid replacements at positions 175 and 211 by two techniques: 1) characterization of several mutant forms of the alpha subunit from S. typhimurium prepared by site-directed mutagenesis and 2) computer graphics modeling of the substrate binding site of the alpha subunit using the x-ray coordinates of the wild type alpha 2 beta 2 complex from S. typhimurium. We conclude that the restoration of alpha subunit activity in the doubly altered second-site revertant results from restoration of the proper geometry of the substrate binding site. JF - The Journal of biological chemistry AU - Nagata, S AU - Hyde, C C AU - Miles, E W AD - Section on Pharmacology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1989/04/15/ PY - 1989 DA - 1989 Apr 15 SP - 6288 EP - 6296 VL - 264 IS - 11 SN - 0021-9258, 0021-9258 KW - Glycerophosphates KW - 0 KW - Indoles KW - Ligands KW - Recombinant Proteins KW - Aspartic Acid KW - 30KYC7MIAI KW - indolepropanol phosphate KW - 40716-80-1 KW - Tryptophan Synthase KW - EC 4.2.1.20 KW - Index Medicus KW - Models, Molecular KW - DNA Mutational Analysis KW - Indoles -- pharmacology KW - Glycerophosphates -- pharmacology KW - Substrate Specificity KW - Salmonella typhimurium -- enzymology KW - Protein Conformation KW - Cloning, Molecular KW - Binding Sites KW - Tryptophan Synthase -- physiology KW - Tryptophan Synthase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78912725?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-18 N1 - Date created - 1989-05-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Isolation and characterization of proteins cross-linked to DNA by the antitumor agent methylene dimethanesulfonate and its hydrolytic product formaldehyde. AN - 78893621; 2703496 AB - This study attempted to characterize proteins cross-linked to DNA of Yoshida lymphosarcoma cells treated with methylene dimethanesulfonate (MDMS) and its hydrolytic products formaldehyde (HCHO) and methanesulfonic acid (MSA). MDMS and HCHO treatments produced a similar extent and type of DNA-protein cross-linking in Yoshida lymphosarcoma cells. All five major histones (H1, H2a, H2b, H3, and H4) were among the nuclear proteins cross-linked to DNA. Certain discrete differences were also apparent in these studies. MDMS cross-linked proteins of 29 and 48 kDa to DNA that were not observed following HCHO treatment alone, and HCHO cross-linked a 26-kDa protein to DNA that was not observed following MDMS treatment. Because semicarbazide prevented all MDMS-induced DNA-protein cross-linking, HCHO must be the component responsible for this lesion. The 26-kDa protein has been identified as an H4-H2b dimer. The formation of this dimer is particularly sensitive to MSA release on hydrolysis of MDMS because, in the presence of MSA, HCHO preferentially cross-linked an H2a-H2b dimer and a 48-kDa non-histone protein to DNA. Differences in DNA-protein cross-linking between these two agents are therefore proposed to arise from discrete changes in chromatin structure induced directly by MSA release. JF - The Journal of biological chemistry AU - O'Connor, P M AU - Fox, B W AD - Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/04/15/ PY - 1989 DA - 1989 Apr 15 SP - 6391 EP - 6397 VL - 264 IS - 11 SN - 0021-9258, 0021-9258 KW - Chromatin KW - 0 KW - Cross-Linking Reagents KW - DNA-Binding Proteins KW - Histones KW - Semicarbazides KW - methylene dimethanesulfonate KW - 156-72-9 KW - Formaldehyde KW - 1HG84L3525 KW - carbamylhydrazine KW - 37QUC23K2X KW - Methyl Methanesulfonate KW - AT5C31J09G KW - Index Medicus KW - Rats KW - Animals KW - Blotting, Western KW - Sarcoma, Experimental -- analysis KW - Hydrogen-Ion Concentration KW - Semicarbazides -- pharmacology KW - Histones -- analysis KW - Molecular Weight KW - Formaldehyde -- pharmacology KW - DNA-Binding Proteins -- analysis KW - Chromatin -- drug effects KW - Chromatin -- ultrastructure KW - Methyl Methanesulfonate -- analogs & derivatives KW - Methyl Methanesulfonate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78893621?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-18 N1 - Date created - 1989-05-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The beta subunit of tryptophan synthase. Clarification of the roles of histidine 86, lysine 87, arginine 148, cysteine 170, and cysteine 230. AN - 78893580; 2495283 AB - Our studies, which are aimed at understanding the catalytic mechanism of the beta subunit of tryptophan synthase from Salmonella typhimurium, use site-directed mutagenesis to clarify the functional roles of several putative active site residues. Although previous chemical modification studies have suggested that histidine 86, arginine 148, and cysteine 230 are essential residues in the beta subunit, our present findings that beta subunits with single amino acid replacements at these positions have partial activity show that these 3 residues are not essential for catalysis or substrate binding. These conclusions are consistent with the recently determined three-dimensional structure of the tryptophan synthase alpha 2 beta 2 complex. Amino acid substitution of lysine 87, which forms a Schiff base with pyridoxal phosphate in the wild type beta subunit, yields an inactive form of the beta subunit which binds alpha subunit, pyridoxal phosphate, and L-serine. We also report a rapid and efficient method for purifying wild type and mutant forms of the alpha 2 beta 2 complex from S. typhimurium from an improved enzyme source. The enzyme, which is produced by a multicopy plasmid encoding the trpA and trpB genes of S. typhimurium expressed in Escherichia coli, is crystallized from crude extracts by the addition of 6% poly(ethylene glycol) 8000 and 5 mM spermine. This new method is also used in the accompanying paper to purify nine alpha 2 beta 2 complexes containing mutant forms of the alpha subunit. JF - The Journal of biological chemistry AU - Miles, E W AU - Kawasaki, H AU - Ahmed, S A AU - Morita, H AU - Nagata, S AD - Section on Pharmacology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1989/04/15/ PY - 1989 DA - 1989 Apr 15 SP - 6280 EP - 6287 VL - 264 IS - 11 SN - 0021-9258, 0021-9258 KW - Recombinant Proteins KW - 0 KW - Histidine KW - 4QD397987E KW - Pyridoxal Phosphate KW - 5V5IOJ8338 KW - Arginine KW - 94ZLA3W45F KW - Tryptophan Synthase KW - EC 4.2.1.20 KW - Lysine KW - K3Z4F929H6 KW - Cysteine KW - K848JZ4886 KW - Index Medicus KW - Spectrum Analysis KW - Recombinant Proteins -- metabolism KW - DNA Mutational Analysis KW - Pyridoxal Phosphate -- metabolism KW - Salmonella typhimurium -- enzymology KW - Cloning, Molecular KW - Binding Sites KW - Tryptophan Synthase -- physiology KW - Tryptophan Synthase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78893580?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-18 N1 - Date created - 1989-05-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - From the National Institutes of Health. AN - 78917802; 2926919 JF - JAMA AU - Wyngaarden, J B AD - National Institutes of Health. Y1 - 1989/04/07/ PY - 1989 DA - 1989 Apr 07 SP - 1864 VL - 261 IS - 13 SN - 0098-7484, 0098-7484 KW - Cyclosporins KW - 0 KW - Caffeine KW - 3G6A5W338E KW - Sodium Fluoride KW - 8ZYQ1474W7 KW - Abridged Index Medicus KW - Index Medicus KW - Sodium Fluoride -- therapeutic use KW - Humans KW - Female KW - Arthritis, Rheumatoid -- drug therapy KW - Cyclosporins -- therapeutic use KW - Caffeine -- adverse effects KW - Osteoporosis -- drug therapy KW - Fertility -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78917802?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-25 N1 - Date created - 1989-04-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cancer-related legislation. I. The 100th Congress. AN - 78891367; 2646454 JF - Journal of the National Cancer Institute AU - Knipmeyer, M C AD - Office of Legislation, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/04/05/ PY - 1989 DA - 1989 Apr 05 SP - 482 EP - 484 VL - 81 IS - 7 SN - 0027-8874, 0027-8874 KW - Antineoplastic Agents KW - 0 KW - Radon KW - Q74S4N8N1G KW - Index Medicus KW - AIDS/HIV KW - United States KW - Acquired Immunodeficiency Syndrome -- prevention & control KW - Humans KW - Mammography -- economics KW - Environmental Exposure KW - Smoking -- economics KW - Laboratories -- legislation & jurisprudence KW - Medicare -- legislation & jurisprudence KW - National Health Programs -- legislation & jurisprudence KW - Neoplasms -- prevention & control KW - Legislation as Topic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78891367?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-18 N1 - Date created - 1989-04-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Diethylstilbestrol metabolites and analogs. Stereochemical probes for the estrogen receptor binding site. AN - 78882439; 2925625 AB - Indenestrol A (IA) and indenestrol B (IB) are analogs and metabolites of diethylstilbestrol (DES). These compounds have high binding affinity with the estrogen receptor (ER) but possess weak uterotropic activity. Due to their chemical structures, IA and IB exist as mixtures of enantiomers. We investigated whether the poor biological activity of these compounds was due to differential activity of the enantiomers. We also utilized these compounds as probes to determine the extent of stereochemical sensitivity in the ER ligand binding site. The IA and IB enantiomers were separated to greater than 98% purity using a chiral high pressure liquid chromatography column. Their enantiomeric nature was confirmed by mass spectrometry and NMR. The purified IA enantiomer peak 1 was derivatized with 4-bromobenzoyl chloride. The resulting di(4-bronobenzoate) IA was analyzed by x-ray crystallography and the absolute enantiomeric conformation assigned is C(3)-R. The IA enantiomers designated IA-R and A-S were assayed by competitive binding to cytosolic ER. The competitive binding index was estradiol, 100; DES, 286; IA-Rac (racemic mixture of IA), 143; IA-R, 3; and IA-S, 285; the index showed that ER demonstrates a stereochemical chiral preference. The IB enantiomers did not show a binding preference: IB, 145; IB-1, 100; and IB-2, 143. The differences in the IA enantiomer binding were shown to be due to competitive interactions by Lineweaver-Burk analysis of saturation binding of estradiol to ER in the presence of 1-, 5-, and 10-fold molar excess of competitor. Differences in binding affinity of the enantiomers could be partially explained by differences in the association rate constant (k+1) determined by association rate inhibition studies in which IA-S was 15 times more active than IA-R. Nuclear estrogen receptor levels were measured 1 h after in vivo treatment with doses of 5-20 micrograms/kg. The IA-Rac produced only 60% of the levels is compared with DES. Nuclear ER levels were checked every 30 min up to 2 h with no apparent difference, indicating that the low early levels were not due to a delayed estrogen receptor retention. When the enantiomers were tested individually only a dose of 10 micrograms/kg IA-S translocated ER to a level comparable to DES, while IA-R showed low levels at several doses. These results suggest that the poor biological activity of IA may be related to the differential ER interaction of its enantiomers.(ABSTRACT TRUNCATED AT 400 WORDS) JF - The Journal of biological chemistry AU - Korach, K S AU - Chae, K AU - Levy, L A AU - Duax, W L AU - Sarver, P J AD - Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/04/05/ PY - 1989 DA - 1989 Apr 05 SP - 5642 EP - 5647 VL - 264 IS - 10 SN - 0021-9258, 0021-9258 KW - Receptors, Estrogen KW - 0 KW - Estradiol KW - 4TI98Z838E KW - Diethylstilbestrol KW - 731DCA35BT KW - Index Medicus KW - Molecular Structure KW - Animals KW - Cytosol -- metabolism KW - Stereoisomerism KW - X-Ray Diffraction KW - Cell Nucleus -- metabolism KW - Mice KW - Binding Sites KW - Estradiol -- metabolism KW - Mice, Inbred Strains KW - Kinetics KW - Binding, Competitive KW - Ovariectomy KW - Molecular Conformation KW - Female KW - Uterus -- metabolism KW - Diethylstilbestrol -- metabolism KW - Diethylstilbestrol -- analogs & derivatives KW - Receptors, Estrogen -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78882439?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-11 N1 - Date created - 1989-05-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Written Spelling Agraphia AN - 85504646; 8906415 AB - Written spelling agraphia is described as a disorder of single word writing occurring in conjunction with preserved oral spelling & written grapheme formation. The case histories of two patients exhibiting this syndrome are reported. Tests of letter block spelling; oral reading; writing of letters, numbers, & words; oral spelling; & tests of letter knowledge & letter visualization were administered. Results indicate that although the clinical presentations of the two patients are similar, the underlying disorders appear to be very different. One patient did poorly on tests of letter-block spelling, searching for named individual letter blocks, & a curved/straight letter imaging task. This patient was found to have lost the ability to arouse the images that guide written spelling. The second patient succeeded at these three tasks but wrote correctly formed but incorrectly chosen letters. This patient was found to have difficulty in transferring information from the activated letter image to the graphic motor pattern underlying production of a written response. Anatomical considerations are discussed with reference to both types of deficit. 1 Table, 4 Figures, 24 References. B. Annesser Murray JF - Brain and Language AU - Friedman, Rhonda B AU - Alexander, Michael P AD - Cognitive Neuroscience NIH/NINDS, Bldg 10 Room 5C-422 Bethesda MD 20892 Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 503 EP - 517 VL - 36 IS - 3 SN - 0093-934X, 0093-934X KW - written spelling agraphia, single word writing disorder KW - anatomical considerations KW - case histories KW - Oral Reading (or1a) KW - Word and Letter Association (wo2) KW - Language Pathology (la4) KW - Writing Disorders (wr1) KW - Orthography (or5) 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/85504646?accountid=14244 LA - English DB - Linguistics and Language Behavior Abstracts (LLBA) N1 - Date revised - 2003-10-01 N1 - Last updated - 2016-09-27 N1 - CODEN - BRLGAZ N1 - SubjectsTermNotLitGenreText - Language Pathology (la4); Writing Disorders (wr1); Orthography (or5); Oral Reading (or1a); Word and Letter Association (wo2) ER - TY - JOUR T1 - Premorbid personality assessments of first onset of major depression. AN - 85256380; pmid-2649038 AB - This is a report on personality traits associated with the first onset of major depression in a sample of high-risk subjects. The subjects are the first-degree relatives, spouses, and their controls of patients with affective disorders. None of these subjects had any history of mental disorder as of their initial evaluation. In the subsequent six years, 29 subjects had a first onset of major depression. These first onset subjects were compared with 370 subjects who continued to be free of illness during the six-year follow-up. Personality traits were assessed at the initial evaluation (ie, before the onset of depression in subjects with first onset) by means of scales from five self-report inventories. Lower emotional strength and resiliency significantly differentiated the first onset from the never ill group; overall differences were not found on measures of interpersonal dependency or extraversion. Age was a significant predictor of first onset, both alone (younger age predicted first onsets) and in interaction with personality measures. Among younger subjects (17 to 30 years of age), personality variables did not significantly discriminate between the two comparison groups. Among older subjects (31 to 41 years of age), however, decreased emotional strength, increased interpersonal dependency, and increased thoughtfulness were associated with first onset of depression. JF - Archives of General Psychiatry AU - Hirschfeld, R M AU - Klerman, G L AU - Lavori, P AU - Keller, M B AU - Griffith, P AU - Coryell, W AD - National Institute of Mental Health, Rockville, Md. PY - 1989 SP - 345 EP - 350 VL - 46 IS - 4 SN - 0003-990X, 0003-990X KW - Age Factors KW - Analysis of Variance KW - Comparative Study KW - Psychiatric Status Rating Scales KW - Human KW - Adult KW - Personality Inventory KW - Depressive Disorder KW - Female KW - Male KW - Personality Assessment UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85256380?accountid=14244 LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Blink reflex excitability recovery curves in patients with spasmodic dysphonia. AN - 85164664; pmid-2927683 AB - We studied 12 patients with spasmodic dysphonia (SD) and 12 healthy control subjects. The patients, who had no symptomatic involvement of the eyes, were evaluated for increased excitability of blink reflexes, which is characteristic of blepharospasm and generalized dystonia. We measured symptom severity from sound spectrograms of five sentences, including sentence production time, number of pitch phonatory breaks, and percentage of aperiodic phonation. We evoked blink reflexes by electrical and mechanical stimulation, and assessed excitability by obtaining excitability recovery curves and responses to trains of stimuli. Patients and controls differed from each other in test R2 amplitude attenuation across all intervals from 150 to 1,000 msec to electrical and mechanical stimulation. Our results indicate that patients with SD have increased excitability of blink reflexes, which suggests that the dystonia involves not only the larynx but also other anatomical structures. JF - Neurology AU - Cohen, L G AU - Ludlow, C L AU - Warden, M AU - Estegui, M AU - Agostino, R AU - Sedory, S E AU - Holloway, E AU - Dambrosia, J AU - Hallett, M AD - Human Motor Control Section, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892. PY - 1989 SP - 572 EP - 577 VL - 39 IS - 4 SN - 0028-3878, 0028-3878 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85164664?accountid=14244 LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - CRH and alpha-helical-CRH modulate behavioral measures of arousal in monkeys. AN - 79252397; 2798541 AB - Several neuropeptides involved in the control of pituitary-adrenal activation have also been shown to have behavioral effects which may be mediated by actions on brain mechanisms independent of pituitary release. The behavioral effects of intraventricular administration of CRH and the synthetic peptide antagonist alpha-helical-CRH were assessed in socially separated squirrel monkeys. Treated monkeys were presented with a sequence of behavioral challenges including undisturbed social separation, presentation of a mirror image, and presentation of a "predator" stimulus. The test sequence was repeated at several time intervals after administration of the peptides. CRH produced dose-related increases in several species-typical measures of arousal including motor activity, vigilance-checking, and marking. Pretreatment with alpha-helical-CRH prevented the increased motor activity but not the marking behavior associated with CRH. When administered alone, alpha-helical-CRH increased vigilance-checking. In addition, alpha-helical-CRH increased aggressive behaviors exhibited at the mirror stimulus. The data provide further support for a central role for CRH in the mediation of both activational and inhibitory behavioral responses to stressful stimuli. These data also suggest both antagonistic and partial agonist effects for alpha-helical-CRH. JF - Pharmacology, biochemistry, and behavior AU - Winslow, J T AU - Newman, J D AU - Insel, T R AD - Laboratory of Comparative Ethology, National Institute of Child Health and Human Development, Bethesda, MD 20874. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 919 EP - 926 VL - 32 IS - 4 SN - 0091-3057, 0091-3057 KW - Peptide Fragments KW - 0 KW - Corticotropin-Releasing Hormone KW - 9015-71-8 KW - corticotropin releasing hormone (9-41) KW - 96118-75-1 KW - Index Medicus KW - Animals KW - Drug Interactions KW - Dose-Response Relationship, Drug KW - Male KW - Stress, Physiological -- physiopathology KW - Injections, Intraventricular KW - Saimiri -- physiology KW - Arousal -- drug effects KW - Peptide Fragments -- pharmacology KW - Corticotropin-Releasing Hormone -- antagonists & inhibitors KW - Motor Activity -- drug effects KW - Peptide Fragments -- administration & dosage KW - Corticotropin-Releasing Hormone -- administration & dosage KW - Corticotropin-Releasing Hormone -- pharmacology KW - Cebidae -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79252397?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-07 N1 - Date created - 1989-11-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prostaglandins in cerebrospinal fluid of healthy human volunteers, abstinent alcoholics and rhesus monkeys. AN - 79155182; 2762559 AB - A sensitive and selective assay for measuring prostaglandins in cerebrospinal fluid has been developed, based on the selected-ion-monitoring, electron-capture negative ionization GC/MS detection for the MO-PFB-TMS derivatives of prostaglandins E2, E1, F2 alpha, F1 alpha, and 6-keto-F1 alpha. Improvements over previously published assay procedures have been made, and the new assay has been applied to measurement of prostaglandin concentrations in lumbar CSF of healthy human volunteers, abstinent alcoholic patients, in cisternal CSF of Rhesus monkeys, and continuously sampled lumbar CSF of awake Rhesus monkeys. Results indicated that the concentrations of PGE2, PGE1, PGF1 alpha, and 6-keto-PGF1 alpha were below 15 pg/mL CSF in lumbar CSF of healthy humans and abstinent alcoholics, and in cisternal CSF of Rhesus monkeys. In contrast, continuously sampled lumbar CSF of awake Rhesus monkeys contained more than 200 pg/mL of PGE2, PGF2 alpha, and 6-keto-PGF1 alpha, probably present as a result of local production. JF - Prostaglandins AU - Yergey, J A AU - Karanian, J W AU - Salem, N AU - Heyes, M P AU - Ravitz, B AU - Linnoila, M AD - Laboratory of Clinical Studies, NIAAA, Bethesda, MD 20892. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 505 EP - 517 VL - 37 IS - 4 SN - 0090-6980, 0090-6980 KW - Prostaglandins KW - 0 KW - Index Medicus KW - Animals KW - Reference Values KW - Gas Chromatography-Mass Spectrometry -- methods KW - Humans KW - Radioimmunoassay -- methods KW - Macaca mulatta KW - Male KW - Alcoholism -- rehabilitation KW - Prostaglandins -- cerebrospinal fluid KW - Alcoholism -- cerebrospinal fluid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79155182?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-20 N1 - Date created - 1989-09-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Developmental toxicity of perfluorodecanoic acid in C57BL/6N mice. AN - 79045744; 2731659 AB - Perfluorodecanoic acid (PFDA) is a representative of the perfluorinated carboxylic acids used as commercial wetting agents and flame retardants. Signs of PFDA toxicity have been reported to resemble those seen after exposure to TCDD. To determine if PFDA exhibits teratogenic effects similar to those of TCDD or is a developmental toxin, time-mated C57BL/6N mice were administered PFDA by gavage in corn oil (10 ml/kg) on gestation days (gd) 10-13 or gd 6-15 at levels of 0, 0.25, 0.5, 1.0, 2.0, 4.0, 8.0, 16.0, or 32.0 mg/kg/day or 0, 0.03, 0.3, 1.0, 3.0, 6.4, or 12.8 mg/kg/day, respectively. Dams were killed on gd 18 and maternal and fetal toxicity was assessed. Fetuses were examined for external, visceral, or skeletal malformations. Maternal body weight gain (corrected for the weight of the gravid uterus) was significantly reduced as a result of PFDA treatment at 6.4 and 12.8 mg/kg/day (gd 6-15) and 16.0 and 32.0 mg/kg/day (gd 10-13). Fetal viability was decreased only in those groups showing extensive maternal body weight loss. Fetal body weights were significantly reduced at levels as low as 0.1 mg/kg/day (gd 6-15) and 0.5 mg/kg/day (gd 10-13). No hydronephrosis, cleft palate, or edema was observed nor were any other soft tissue or skeletal malformations detected. Thus, PFDA does not produce malformations in C57BL/6N mice, and the developmental toxicity observed (increased fetal mortality and decreased live fetal body weight) was seen only at doses that were maternally toxic. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Harris, M W AU - Birnbaum, L S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 442 EP - 448 VL - 12 IS - 3 SN - 0272-0590, 0272-0590 KW - Decanoic Acids KW - 0 KW - Dioxins KW - Fluorocarbons KW - Teratogens KW - perfluorodecanoic acid KW - 335-76-2 KW - Index Medicus KW - Animals KW - Fetus -- drug effects KW - Reproduction -- drug effects KW - Body Weight -- drug effects KW - Mice, Inbred C57BL KW - Mice KW - Dioxins -- toxicity KW - Female KW - Pregnancy KW - Fluorocarbons -- toxicity KW - Decanoic Acids -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79045744?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-27 N1 - Date created - 1989-07-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transplacental initiation of liver, lung, neurogenic, and connective tissue tumors by N-nitroso compounds in mice. AN - 79027442; 2731672 AB - Epidemiological studies have implicated nitroso compounds as possible causative agents for human childhood cancers, including those of neurogenic origin. Published evidence from animal models, which is reviewed in this report, indicates that capacity for metabolic activation of nitrosamines is limited in rodent fetuses and that nitrosamines are correspondingly weak transplacental carcinogens. The C3H mouse fetus, however, has both moderate capability for activation of N-nitrosodimethylamine (NDMA) and proven susceptibility to transplacental causation of neurogenic tumors by a nitrosourea. We tested whether NDMA could act as a transplacental carcinogen in the C3H mouse, and whether it or N-nitrosodiethylamine (NDEA) would initiate neurogenic tumors. N-Nitrosoethylurea (NEU) served as positive control. C3H/HeNCr MTV- pregnant mice were treated ip on Gestation Day 16 or 19 with NDMA (0.1 mmol, 7.4 mg/kg, maximum nonfetotoxic dose), NDEA (0.5 mmol, 51 mg/kg), or NEU (0.4 mmol, 47 mg/kg). NDMA had significant transplacental carcinogenic effects, resulting in an increase in percentage female offspring with hepatocellular carcinomas and in average number of liver tumors after treatment on either gestational day, compared with controls. In the males there was a significant increase in numbers of liver tumors and carcinomas following Day 19 exposure. An increase in incidence of histiocytic and undifferentiated sarcomas was also of statistical significance. There was no change in number of pulmonary tumors. One intracranial schwannoma resulted. NDEA had no effect when given on Gestation Day 16, but caused a significant increase in liver and lung tumor numbers in both sexes when treatment was on Day 19. NEU induced the expected high incidence of lung tumors, significantly increased liver tumor incidence in females (Day 19 exposure), and produced schwannomas in 14 and 35% of the offspring after Days 16 or 19 treatment, respectively. The results show that NDMA at even a low dose had significant transplacental carcinogenic effects, including one schwannoma, which was most unlikely to have occurred spontaneously. However, this single neurogenic tumor contrasts with the absence of similar neoplasms in mice exposed transplacentally to NDEA, in view of the generally greater efficiency of ethylating agents as carcinogens for the nervous system in rodents. These data thus neither conclusively support nor refute the hypothesis that nitrosamines may initiate neurogenic tumors in fetuses. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Anderson, L M AU - Hagiwara, A AU - Kovatch, R M AU - Rehm, S AU - Rice, J M AD - Division of Cancer Etiology, National Cancer Institute, Frederick, Maryland 21701. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 604 EP - 620 VL - 12 IS - 3 SN - 0272-0590, 0272-0590 KW - Nitroso Compounds KW - 0 KW - Index Medicus KW - Maternal-Fetal Exchange KW - Animals KW - Mice, Inbred C3H KW - Mice KW - Fetus -- metabolism KW - Female KW - Pregnancy KW - Connective Tissue Diseases -- chemically induced KW - Neoplasms, Experimental -- chemically induced KW - Liver Neoplasms, Experimental -- chemically induced KW - Nitroso Compounds -- toxicity KW - Nervous System Neoplasms -- chemically induced KW - Lung Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79027442?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-27 N1 - Date created - 1989-07-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Kidney and urinary bladder lesions in F344/N rats and B6C3F1 mice after 13 weeks of 2,2-bis(bromomethyl)-1,3-propanediol administration. AN - 79022755; 2731663 AB - Thirteen-week toxicity studies of the flame retardant 2,2-bis(bromomethyl)-1,3-propanediol (BMP; dibromoneopentyl glycol; FR-1138; CAS No. 329690-0) were conducted in male and female F344/N rats and B6C3F1 mice. The chemical was administered by oral gavage in corn oil 5 days per week for 13 weeks to rats at doses of 0, 50, 100, 200, 400, and 800 mg/kg and to mice at doses of 0, 25, 50, 100, 200, and 400 mg/kg, or in the feed for 13 weeks at concentrations of 0, 1250, 2500, 5000, 10,000, and 20,000 ppm for rats and at 0, 625, 1250, 2500, 5000, and 10,000 ppm for mice. There was a dose-related decrease in body weight gain in rats and mice after chemical administration. Mortality attributed to toxicity of BMP was seen in the gavage study in 2/10 high-dose (800 mg/kg) male rats and 3/10 high-dose (400 mg/kg) male mice no dose-related mortality occurred in the feed study. Minimal degeneration in the renal papilla was seen in male rats at 800 mg/kg in the gavage study and at doses of 5000 ppm or more in the feed study. This was also present in one female rat at the 20,000 ppm dose. In male mice renal papillary necrosis occurred at 400 mg/kg after dosing by the gavage route and at 2500, 5000, and 10,000 ppm in the dosed-feed study. In female mice papillary necrosis occurred only at the 10,000 ppm dose in the feed study. Tubular cell regeneration of the renal cortex was also present in mice at the same dose levels at which the papillary necrosis was observed. Transitional cell hypeplasia of the urinary bladder was seen in male rats at 400 and 800 mg/kg and in both sexes of mice at 200 and 400 mg/kg. Hyperplasia of the urinary bladder was also seen when BMP was administered in the feed at doses of 20,000 ppm to male rats; at doses of 2500, 5000, and 10,000 ppm to male mice; and at doses of 5000 and 10,000 ppm to female mice. The kidney and urinary bladder are target organs when BMP is administered by gavage or the dosed-feed route; mice were more sensitive than rats for the development of kidney and bladder lesions. Male rats and mice were more sensitive than females for the development of renal papillary degeneration or necrosis. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Elwell, M R AU - Dunnick, J K AU - Brown, H R AU - Montgomery, C A AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 480 EP - 490 VL - 12 IS - 3 SN - 0272-0590, 0272-0590 KW - Flame Retardants KW - 0 KW - Propylene Glycols KW - 2,2-bis(bromomethyl)-1,3-propanediol KW - 3296-90-0 KW - Index Medicus KW - Rats KW - Mice, Inbred Strains KW - Animals KW - Rats, Inbred F344 KW - Blood Chemical Analysis KW - Necrosis -- chemically induced KW - Body Weight -- drug effects KW - Mice KW - Male KW - Female KW - Propylene Glycols -- toxicity KW - Urinary Bladder Diseases -- chemically induced KW - Flame Retardants -- toxicity KW - Kidney Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79022755?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-27 N1 - Date created - 1989-07-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Methionine lowers circulating levels of acetaldehyde after ethanol ingestion. AN - 79008707; 2658650 AB - Methionine, administered to ethanol treated mice and rats, significantly reduced circulating acetaldehyde levels without altering circulating levels of ethanol. Hepatic levels of acetaldehyde were also lowered by methionine. Methionine was effective when given prior to or after the administration of ethanol, but the time course of the action of methionine suggested the necessity for metabolic transformation of this amino acid in order for the acetaldehyde-lowering effect to be evidenced. Studies with humans, given methionine doses of approximately one-tenth of those used with mice, indicated that methionine can also lower acetaldehyde in humans ingesting ethanol. Given the toxic characteristics of acetaldehyde, methionine may prove effective in reducing the damaging effects of ethanol ingestion. JF - Alcoholism, clinical and experimental research AU - Tabakoff, B AU - Eriksson, C J AU - von Wartburg, J P AD - National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland 20892. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 164 EP - 171 VL - 13 IS - 2 SN - 0145-6008, 0145-6008 KW - Citrates KW - 0 KW - Ethanol KW - 3K9958V90M KW - Methionine KW - AE28F7PNPL KW - Acetaldehyde KW - GO1N1ZPR3B KW - Index Medicus KW - Rats KW - Animals KW - Humans KW - Mice, Inbred C57BL KW - Mice KW - Citrates -- pharmacology KW - Male KW - Female KW - Mice, Inbred DBA KW - Acetaldehyde -- blood KW - Ethanol -- pharmacology KW - Methionine -- administration & dosage KW - Methionine -- pharmacology KW - Methionine -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79008707?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-27 N1 - Date created - 1989-06-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nonrandom karyotypic changes in immortal and tumorigenic Syrian hamster cells induced by diethylstilbestrol. AN - 78956506; 2720639 AB - Treatment of Syrian hamster embryo cells with diethylstilbestrol (DES) resulted in the induction of immortal cell lines that progressed and formed tumors in nude mice. Four independently treated cell lines were analyzed cytogenetically at several passages during neoplastic progression. The immortal cell lines at the early passages had no structural abnormalities but did have numerical changes. For example, gain of chromosome 11 was found in all immortal cell lines, and gain of chromosome 19 was found in two of four cell lines. Tumorigenic cells showed not only a variety of numerical abnormalities but also structural abnormalities. Loss of a sex chromosome and gain of chromosome 19 were found in six of seven tumors. Gain of chromosome 11, which was found in all immortal cell lines, disappeared in five of seven tumors. Structural abnormalities involving chromosomes 2 and 3 were found in three of seven tumors. Many marker chromosomes were also found in the tumors. These results support our hypothesis that DES-induced nondisjunction is important in its ability to induce cell transformation and suggests that gain of chromosome 11 and/or 19 may play a role in DES-induced neoplastic progression. Furthermore, these results indicate that for the acquisition of tumorigenicity, additional numerical or structural changes are needed, suggesting that multiple genetic events are required in the multistep process of carcinogenesis. JF - Cancer genetics and cytogenetics AU - Ozawa, N AU - Oshimura, M AU - McLachlan, J A AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 271 EP - 282 VL - 38 IS - 2 SN - 0165-4608, 0165-4608 KW - Diethylstilbestrol KW - 731DCA35BT KW - Index Medicus KW - Neoplasm Transplantation KW - Animals KW - Tumor Cells, Cultured KW - Mesocricetus KW - Mice, Nude KW - Mice KW - Embryo, Mammalian KW - Cricetinae KW - Karyotyping KW - Neoplasms, Experimental -- chemically induced KW - Neoplasms, Experimental -- genetics KW - Chromosome Aberrations UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78956506?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-29 N1 - Date created - 1989-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Loss of heterozygosity at the c-raf locus in small cell lung carcinoma. AN - 78950686; 2566144 AB - The c-raf-1 oncogene is located at chromosome 3p25, near a region known to be specifically deleted in patients with renal cell carcinoma and small cell lung carcinoma (SCLC). From cytogenetic analyses of SCLC cell lines, we have estimated that one c-raf-1 allele was deleted in approximately 80% of the cases. However, c-raf-1 was generally thought to be distal to the most common deletion in SCLC, 3p14-23. Using restriction site polymorphisms (RFLPs) located within the c-raf-1 locus, we have examined DNA from 84 human lung carcinomas. In an analysis of 11 paired (normal versus tumor) SCLC DNA samples, all five informative cases showed loss of heterozygosity at this locus in the corresponding tumor sample. Analysis of 73 unpaired lung carcinoma DNAs showed that out of 31 non-SCLC samples, 19% were heterozygous for the BglI polymorphism and 25% showed heterozygosity with TaqI. However, all of the 42 SCLC samples were homozygous for both of these RFLPs. This striking loss of heterozygosity at the c-raf-1 locus in SCLC indicates that one allele of c-raf-1 is deleted in SCLC. The kinase activity of the c-raf protein appears to be constitutively activated in these cells. Whether this apparent activation results from genetic or epigenetic events is under investigation. JF - Oncogene AU - Sithanandam, G AU - Dean, M AU - Brennscheidt, U AU - Beck, T AU - Gazdar, A AU - Minna, J D AU - Brauch, H AU - Zbar, B AU - Rapp, U R AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, Maryland 21701. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 451 EP - 455 VL - 4 IS - 4 SN - 0950-9232, 0950-9232 KW - Proto-Oncogene Proteins KW - 0 KW - DNA KW - 9007-49-2 KW - Proto-Oncogene Proteins c-raf KW - EC 2.7.11.1 KW - Index Medicus KW - Proto-Oncogene Proteins -- analysis KW - Polymorphism, Restriction Fragment Length KW - Humans KW - DNA -- analysis KW - Heterozygote KW - Lung Neoplasms -- genetics KW - Proto-Oncogenes KW - Chromosome Mapping KW - Carcinoma, Small Cell -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78950686?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-12 N1 - Date created - 1989-06-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evaluation of nitroimidazole hypoxic cell radiosensitizers in a human tumor cell line high in intracellular glutathione. AN - 78932547; 2522917 AB - Five nitroimidazole hypoxic cell radiosensitizers were evaluated in a human lung adenocarcinoma cell line (A549) whose GSH level was 8-fold higher than Chinese hamster V79 cells. One millimolar concentrations of Misonidazole (MISO), SR-2508, RSU-1164, RSU-1172, and Ro-03-8799 sensitized hypoxic A549 cells to radiation, with Ro-03-8799 giving the highest sensitizer enhancement ration (SER) (2.3). However, MISO, SR-2508 and Ro-03-8799 were less effective in this cell line than in V79 cells, presumably due to higher GSH content of the A549 cells. Increased hypoxic radiosensitization was seen with 0.1 mM Ro-03-8799 after GSH depletion by BSO as compared to 0.1 mM Ro-03-8799 alone (SER-1.8 vs 1.3). The combination of GSH depletion and 0.1 mM Ro-03-8799 was considerably more toxic than 0.1 mM or 1.0 mM Ro-03-8799 alone. This sensitivity was much greater than has been observed for SR-2508. These data show that Ro-03-8799 was the most efficient hypoxic cell radiosensitizer in a human tumor cell line considerably higher in GSH than the rodent cell lines often used in hypoxic radiosensitization studies. Thus, Ro-03-8799 may be a more effective hypoxic cell sensitizer in human tumors that are high in GSH. JF - International journal of radiation oncology, biology, physics AU - DeGraff, W G AU - Russo, A AU - Gamson, J AU - Mitchell, J B AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 1021 EP - 1024 VL - 16 IS - 4 SN - 0360-3016, 0360-3016 KW - 1-(2-nitro-1-imidazoly)-3-(2,3-dimethylaziridino)-2-propanol KW - 0 KW - Nitroimidazoles KW - Radiation-Sensitizing Agents KW - Etanidazole KW - 30DKA3Q1HL KW - pimonidazole KW - 46JO4D76R2 KW - Misonidazole KW - 8FE7LTN8XE KW - Glutathione KW - GAN16C9B8O KW - Oxygen KW - S88TT14065 KW - Index Medicus KW - Oxygen -- metabolism KW - Misonidazole -- pharmacology KW - Humans KW - Misonidazole -- analogs & derivatives KW - Drug Evaluation, Preclinical KW - Cell Line KW - Tumor Cells, Cultured -- metabolism KW - Tumor Cells, Cultured -- drug effects KW - Radiation-Sensitizing Agents -- pharmacology KW - Glutathione -- metabolism KW - Nitroimidazoles -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78932547?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-19 N1 - Date created - 1989-05-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Longterm survival of normal, diploid Syrian hamster-cells in tumors induced by transfection with v-Ha-ras and v-myc oncogenes. AN - 78929549; 2653615 AB - Tumors were induced following transfection of normal, diploid hamster embryo cells with plasmids containing the viral Harvey ras and viral myc oncogenes. Direct cytogenetic studies of the tumors performed at 3-7 weeks after injection of the transfected hamster cells into nude mice revealed that 100% of the hamster cells were aneuploid and no detectable diploid cells in mitosis were observed. However, when tumor explants were cultured in vitro, diploid Syrian hamster cells were frequently detected at early passages. The percentage of diploid hamster cells in the cultures varied from 2 to 94% at the first passage. After several passages in vitro, only aneuploid hamster cells were observed. The diploid hamster cells in culture had a flat morphology and senesced. The aneuploid cells in the cultures were readily cloned and formed tumors after reinjection in nude mice. Reconstruction experiments consisting of injecting cloned, aneuploid tumor cells mixed with 6 X 10(6) normal Syrian hamster embryo cells were performed. Cell cultures derived from these mixed tumors contained both normal and aneuploid hamster cells indicating that normal cells survived in vivo during the growth of the tumor cells for up to 4 weeks. During this period, some normal cells transplanted in vivo did not die or terminally differentiate. Since normal cells can persist in vivo, tumor-derived cell cultures are mixed populations and caution should be exercised in interpreting quantitative molecular or cellular studies of these uncloned populations. JF - Cancer letters AU - Oshimura, M AU - Annab, L A AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 35 EP - 41 VL - 45 IS - 1 SN - 0304-3835, 0304-3835 KW - Index Medicus KW - Karyotyping KW - Animals KW - Aneuploidy KW - Cells, Cultured KW - Mesocricetus KW - Embryo, Mammalian KW - Cricetinae KW - Genes, ras KW - Transfection KW - Proto-Oncogenes KW - Cell Transformation, Neoplastic KW - Cell Survival UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78929549?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-14 N1 - Date created - 1989-06-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Screening for major depression among alcoholics: an application of receiver operating characteristic analysis. AN - 78926449; 2702922 AB - When comparing several screening tests designed to detect the same disease, methodological problems arise in determining which is most accurate. We have previously demonstrated that receiver operating characteristic (ROC) methodology can provide a set of statistical procedures which allow for objective comparisons of screening tests. In this report, ROC methodology is brought to a different substantive area: the detection of clinical depression among treated alcoholics. In a sample of hospitalized alcoholics, we compared the accuracies of several commonly used screening tests for depressive disorders, as well as comparing each of these with a screening test for anxiety disorders. No test offered a statistically significant advantage over any other, and all did poorly in detecting clinically diagnosed major depression. The performance of the screening tests was worst when the non-depressed comparison group included subjects with remitted disorder, but was still poor when the comparison group did not include such potentially 'noisy' subjects. Factors contributing to the difficulty of screening for clinical depression are discussed, as well as suggestions for improvements in future screening efforts. JF - Drug and alcohol dependence AU - Grant, B F AU - Hasin, D S AU - Harford, T C AD - Division of Biometry and Epidemiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 123 EP - 131 VL - 23 IS - 2 SN - 0376-8716, 0376-8716 KW - Index Medicus KW - ROC Curve KW - Humans KW - Adult KW - Schizophrenia -- epidemiology KW - Mood Disorders -- epidemiology KW - Male KW - Female KW - Depressive Disorder -- epidemiology KW - Depressive Disorder -- etiology KW - Mass Screening -- methods KW - Alcoholism -- psychology KW - Alcoholism -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78926449?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-19 N1 - Date created - 1989-05-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ethanol enhancement of isoproterenol-stimulated melatonin and cyclic AMP release from cultured pineal glands. AN - 78923843; 2540311 AB - Norepinephrine stimulates the synthesis of melatonin in the pineal gland. The action of norepinephrine is believed to be mediated primarily by beta adrenergic receptors, and involves activation of adenylate cyclase. Ethanol, 25 to 50 mM, added to cultured pineal glands in vitro, enhanced isoproterenol-induced stimulation of cyclic AMP and melatonin production. The action of ethanol was observed only at doses of isoproterenol that produced a submaximal effect, and ethanol alone had no effect on cyclic AMP or melatonin release. Butanol, at a concentration of 2 mM, was as effective as 50 mM ethanol in increasing isoproterenol-stimulated cyclic AMP and melatonin release, indicating that the response to alcohols was not due simply to changes in osmolarity, and may reflect a hydrophobic interaction of the alcohols with the cell membrane. The effects of ethanol on pineal cyclic AMP and melatonin release were reversible after a 15-min preincubation, but not after a 2-hr preincubation, suggesting that, over a long incubation period, ethanol may sensitize the pineal beta adrenergic receptor-coupled adenylate cyclase system to isoproterenol. The findings in this study are consistent with earlier work showing that ethanol increases cerebral cortical beta adrenergic receptor-coupled adenylate cyclase activity, and demonstrate that the effect of ethanol on the receptor-effector system can result in an endocrinological response. JF - The Journal of pharmacology and experimental therapeutics AU - Chung, C T AU - Tamarkin, L AU - Hoffman, P L AU - Tabakoff, B AD - Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 16 EP - 22 VL - 249 IS - 1 SN - 0022-3565, 0022-3565 KW - Butanols KW - 0 KW - Ethanol KW - 3K9958V90M KW - 1-Butanol KW - 8PJ61P6TS3 KW - Cyclic AMP KW - E0399OZS9N KW - Arylamine N-Acetyltransferase KW - EC 2.3.1.5 KW - Melatonin KW - JL5DK93RCL KW - Isoproterenol KW - L628TT009W KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - Butanols -- pharmacology KW - Drug Synergism KW - Arylamine N-Acetyltransferase -- analysis KW - Male KW - Melatonin -- secretion KW - Ethanol -- pharmacology KW - Cyclic AMP -- secretion KW - Pineal Gland -- drug effects KW - Pineal Gland -- secretion KW - Isoproterenol -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78923843?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-01 N1 - Date created - 1989-06-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of sister chromatid exchanges by tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in human and hamster cells. AN - 78922836; 2649269 AB - 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a nicotine derived N-nitrosamine, is a carcinogen that induces tumors in mice, rats and hamsters. To assess the ability of NNK to interact with the cellular DNA as an essential step in carcinogenesis, the induction of sister chromatid exchange (SCE) was examined in cultured normal human lymphocytes (HL) and Chinese hamster V79 cells. SCE formation is a sensitive indicator of carcinogen-DNA interaction that correlates with the induction of mutation and neoplastic cell transformation. HL and V79 cells were treated for 2 h with 20, 50, 100 and 200 micrograms/ml of NNK with and without application of metabolic activation S-9 mixture, and subsequently incubated for two rounds of replication in the presence of 5-bromodeoxyuridine required for SCE visualization. In V79 cells NNK produced a dose-dependent increase in SCE only with metabolic activation. In HL NNK induced a small but statistically significant increase in SCE with or without metabolic activation. These data provide the first evidence that NNK and/or its metabolic derivatives are able to induce DNA damage leading to SCE formation both in hamster and human cells. The differences in response between the two cell types suggests the existence of a difference in susceptibility associated with NNK metabolism and its interaction with cellular DNA. JF - Carcinogenesis AU - Zimonjic, D AU - Popescu, N C AU - DiPaolo, J A AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 753 EP - 755 VL - 10 IS - 4 SN - 0143-3334, 0143-3334 KW - Nitrosamines KW - 0 KW - 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone KW - 7S395EDO61 KW - Index Medicus KW - Animals KW - Cricetulus KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - Biotransformation KW - Humans KW - Lymphocytes KW - Cricetinae KW - Nitrosamines -- pharmacology KW - Sister Chromatid Exchange UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78922836?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-24 N1 - Date created - 1989-05-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutagenic specificity of a potent carcinogen, benzo[c]phenanthrene (4R,3S)-dihydrodiol (2S,1R)-epoxide, which reacts with adenine and guanine in DNA. AN - 78920194; 2648399 AB - Mutations were induced in the supF gene of the pS189 shuttle vector by treatment with optically active benzo[c]phenanthrene (4R,3S)-dihydrodiol (2S,1R)-epoxide in vitro and replication in human cells. The induced mutation frequency was 60-fold greater than the spontaneous rate, and most of the mutations analyzed were transversions (86%), which principally consisted of similar numbers of A.T----T.A and G.C----T.A changes. The unusual susceptibility of A.T pairs to mutation by this chemical agent is consistent with its chemical reactivity toward adenine and argues that the mutations are targeted to the adducts formed. The central base in the sequences 5'-AGA-3', 5'-AAC-3', and 5'-GAG-3' was particularly susceptible to mutation. Twelve "hotspots" in the supF gene accounted for most mutations seen. Some of these hotspots differed from those found by others for racemic benzo[a]pyrene dihydrodiol epoxide and, even when a hotspot was common, the mutagenic changes were not always the same. Although adenine insertion opposite a noninstructional lesion could account for most of the data, no single mutagenic mechanism could encompass all of it. The cellular machinery that converts chemical damage to mutations must determine the mutational result to a large extent, but the findings herein show that the chemical agent itself plays a large role in determining both the location and the nature of the mutations that arise. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Bigger, C A AU - Strandberg, J AU - Yagi, H AU - Jerina, D M AU - Dipple, A AD - Bionetics Research, Inc., National Cancer Institute-Frederick Cancer Research Facility, MD 21701. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 2291 EP - 2295 VL - 86 IS - 7 SN - 0027-8424, 0027-8424 KW - Carcinogens KW - 0 KW - DNA, Bacterial KW - Mutagens KW - Guanine KW - 5Z93L87A1R KW - Adenine KW - JAC85A2161 KW - Index Medicus KW - Base Sequence KW - Base Composition KW - Genetic Vectors KW - Molecular Sequence Data KW - Genes, Bacterial -- drug effects KW - Nucleic Acid Conformation KW - DNA, Bacterial -- genetics KW - Escherichia coli -- drug effects KW - Escherichia coli -- genetics KW - Mutagens -- pharmacology KW - DNA, Bacterial -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78920194?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-05 N1 - Date created - 1989-05-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 1984 Jun;44(6):2320-4 [6372992] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3787-91 [3108878] Carcinogenesis. 1988 May;9(5):691-6 [3284662] Nature. 1964 May 23;202:781-4 [14187619] J Mol Biol. 1967 Jun 14;26(2):365-9 [4291934] Virology. 1973 Apr;52(2):456-67 [4705382] Proc Natl Acad Sci U S A. 1975 Dec;72(12):5135-9 [1061098] J Biol Chem. 1976 Sep 10;251(17):5124-40 [821949] Nature. 1976 Sep 23;263(5575):285-9 [958482] J Gen Virol. 1977 Jul;36(1):59-74 [886304] Chem Biol Interact. 1980 Sep;31(3):255-63 [7408034] Science. 1980 Sep 19;209(4463):1392-6 [6251547] Proc Natl Acad Sci U S A. 1982 Mar;79(6):1945-9 [7043469] Proc Natl Acad Sci U S A. 1983 May;80(10):3010-4 [6304690] Proc Natl Acad Sci U S A. 1983 May;80(10):3015-9 [6574469] J Mol Biol. 1983 Jun 5;166(4):557-80 [6345791] Annu Rev Genet. 1983;17:215-38 [6364961] Proc Natl Acad Sci U S A. 1984 Mar;81(5):1494-8 [6369329] Cell. 1985 Mar;40(3):483-4 [2982494] Gene. 1985;38(1-3):233-7 [2998945] Adv Cancer Res. 1985;45:45-105 [3911748] Cancer Res. 1986 May;46(5):2257-61 [3697970] Proc Natl Acad Sci U S A. 1986 May;83(10):3402-6 [3010297] Carcinogenesis. 1986 Jul;7(7):1037-42 [3087641] Mol Cell Biol. 1987 Jan;7(1):379-87 [3031469] Nature. 1987 Jun 11-17;327(6122):535-6 [3587368] Proc Natl Acad Sci U S A. 1987 Jul;84(14):4944-8 [3474635] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intracellular calcium alterations in response to increased external calcium in normal and neoplastic keratinocytes. AN - 78916376; 2702726 AB - Normal keratinocytes proliferate when cultured in medium with 0.02-0.10 mM calcium and terminally differentiate when medium calcium is increased to greater than 0.1 mM. In contrast, neoplastic keratinocyte cell lines maintain the potential for continued cell renewal and survive when external calcium is increased. In order to determine whether elevation of extracellular calcium produced changes in intracellular free calcium (Cai) levels, Cai was measured in individual living keratinocytes by use of the fluorescent calcium probe fura-2. Most normal keratinocytes responded to increased extracellular calcium by a gradual 2- to 3-fold increase in Cai lasting for at least 28 min. A subpopulation displayed a sharp peak of Cai at 2 min. In contrast, the Cai level in neoplastic cells in either low or high calcium medium was 2- to 3-fold higher than that in normal cells, and all cells in the population showed a transient 4- to 9-fold elevation of Cai 2 min after external calcium was increased. Thus normal and neoplastic keratinocytes differ in the level of Cai under low calcium conditions and in their response to elevated external calcium. The regulation of Cai in keratinocytes may be important in determining their potential for terminal differentiation. JF - Carcinogenesis AU - Hennings, H AU - Kruszewski, F H AU - Yuspa, S H AU - Tucker, R W AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 777 EP - 780 VL - 10 IS - 4 SN - 0143-3334, 0143-3334 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Cells, Cultured KW - Mice KW - Mice, Inbred BALB C KW - Cell Line KW - Calcium -- metabolism KW - Skin -- metabolism KW - Skin Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78916376?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-24 N1 - Date created - 1989-05-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Suramin: an anticancer drug with a unique mechanism of action. AN - 78913453; 2926472 AB - We administered suramin, an anti-parasitic drug and reverse transcriptase inhibitor, to 15 patients with metastatic cancer. This compound is known to inhibit the binding of growth factors (eg, epidermal growth factor [EGF], platelet-derived growth factor [PDGF], tumor growth factor-beta [TGF-beta]) to their receptors and thus antagonize the ability of these factors to stimulate growth of tumor cells in vitro. There were no complete responses (CRs), four partial responses (PRs) (two of ten adrenal cortex, one of four renal, one of one adult T-cell leukemia-lymphoma [HTLV-1]), and two minimal responses (MRs) (two of ten adrenal cortex). Toxicity included proteinuria (14 patients), reversible liver function test abnormalities (eight), vortex keratopathy (five), adrenal insufficiency (three), coagulopathy secondary to increased circulating levels of glycosaminoglycans (11), and one case of a reversible acute demyelinating polyneuropathy resembling the Guillain-Barrè syndrome. We conclude that suramin is an active agent in the treatment of metastatic cancer, and further work is necessary to define its scope. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Stein, C A AU - LaRocca, R V AU - Thomas, R AU - McAtee, N AU - Myers, C E AD - Clinical Oncology Program, National Cancer Institute, Bethesda, MD 208292. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 499 EP - 508 VL - 7 IS - 4 SN - 0732-183X, 0732-183X KW - Antineoplastic Agents KW - 0 KW - Suramin KW - 6032D45BEM KW - Index Medicus KW - AIDS/HIV KW - Kidney Neoplasms -- drug therapy KW - Carcinoma -- secondary KW - Humans KW - Pilot Projects KW - Leukemia-Lymphoma, Adult T-Cell -- drug therapy KW - Carcinoma -- drug therapy KW - Adult KW - Adenocarcinoma -- secondary KW - Adrenal Cortex Neoplasms -- drug therapy KW - Middle Aged KW - Adenocarcinoma -- drug therapy KW - Female KW - Male KW - Remission Induction KW - Suramin -- adverse effects KW - Suramin -- pharmacology KW - Suramin -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78913453?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-08 N1 - Date created - 1989-05-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of fos RNA by DNA-damaging agents. AN - 78896170; 2466559 AB - We have found that a wide variety of DNA-damaging agents and heat shock increase fos RNA to different extents in Chinese hamster ovary cells. These include the monofunctional alkylating agents methylmethane sulfonate and N-methyl-N'-nitro-N-nitrosoguanidine, the cross-linking agents cis-Pt(II) diamminedichloride and mechlorethamine HCl, the DNA base-damaging agents 4-nitroquinoline-N-oxide and N-acetoxy-2-acetylaminofluorene, ultraviolet and near-ultraviolet radiation, hydrogen peroxide, and Adriamycin. Prolonged increases in fos RNA were observed, with persistence to 16 h following treatment. Variation in the amount of fos RNA induction by these agents and the diverse types and frequencies of cellular damage produced by them suggested that there might be several different mechanisms responsible for increased fos RNA. JF - Cancer research AU - Hollander, M C AU - Fornace, A J AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/04/01/ PY - 1989 DA - 1989 Apr 01 SP - 1687 EP - 1692 VL - 49 IS - 7 SN - 0008-5472, 0008-5472 KW - RNA KW - 63231-63-0 KW - DNA KW - 9007-49-2 KW - Methyl Methanesulfonate KW - AT5C31J09G KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Hot Temperature KW - Animals KW - Cisplatin -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Methyl Methanesulfonate -- pharmacology KW - Cricetinae KW - Oncogenes KW - DNA Damage KW - DNA -- radiation effects KW - RNA -- biosynthesis KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78896170?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-05 N1 - Date created - 1989-05-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of cytotoxic T cell lysis by anti-CD8 monoclonal antibodies: studies with CD3-targeted cytolysis of nominal antigen-negative targets. AN - 78895964; 2466891 AB - The function of the CD8 molecule in lympholysis mediated by cytotoxic T cells was investigated by examining possible contributions of ligands on the target cell to the inhibition of lysis observed with CD8-specific mAb. In order to evaluate a variety of target cells, including those not expressing the nominal Ag (NA) for which the CTL was specific, lysis was effected by cross-linking the CTL and the target cells with anti-CD3 mAb. Such CD3 redirected cytotoxicity was demonstrated to be inhibited by anti-CD8 mAb when low anti-CD3 mAb concentrations were used. The possibility that inhibition by anti-CD8 mAb resulted for competition for the FcR between the anti-CD3 mAb and anti-CD8 mAb was eliminated by targeting TNP-modified cells with an antibody heteroconjugate prepared from Fab fragments of anti-CD3 and anti-DNP antibodies. Inhibition of the lysis of target cells not expressing NA including those deficient in class I expression, demonstrated that neither NA nor class I expression was required for anti-CD8 mAb inhibition. Whether the anti-CD8 mAb inhibition required CD8 Ag interaction with any ligand on the target cell was further investigated by measuring exocytosis of enzyme granule from CTL activated with CD3-coated poly-styrene beads. CD8-specific mAb inhibited such CTL activation in this target cell-free system. A CD8(+), MHC class II-specific CTL clone, was used to show differential inhibition by anti-CD8 mAb, depending on the target cell, therefore providing evidence that anti-CD8 mAb binding does not generate an absolute off signal. These data are consistent with the hypothesis that anti-CD8 mAb affect the lytic process independent of the recognition of a ligand on the target cell by CD8. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Quinones, R R AU - Segal, D M AU - Henkart, P AU - Perez, P AU - Gress, R E AD - Experimental Immunology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/04/01/ PY - 1989 DA - 1989 Apr 01 SP - 2200 EP - 2206 VL - 142 IS - 7 SN - 0022-1767, 0022-1767 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Differentiation, T-Lymphocyte KW - Epitopes KW - Histocompatibility Antigens Class II KW - Immunoglobulin Fab Fragments KW - Macromolecular Substances KW - Receptors, Antigen, T-Cell KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Binding, Competitive KW - Cytotoxicity Tests, Immunologic KW - Cytoplasmic Granules -- physiology KW - Epitopes -- immunology KW - Cell-Free System KW - T-Lymphocytes, Cytotoxic -- physiology KW - Cytotoxicity, Immunologic KW - T-Lymphocytes, Cytotoxic -- immunology KW - Receptors, Antigen, T-Cell -- immunology KW - Antigens, Differentiation, T-Lymphocyte -- immunology KW - Antibodies, Monoclonal -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78895964?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-02 N1 - Date created - 1989-05-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tumor necrosis factor alpha induces expression of human immunodeficiency virus in a chronically infected T-cell clone. AN - 78893799; 2784570 AB - Tumor necrosis factor alpha (TNF-alpha), also known as cachectin, was demonstrated to induce the expression of human immunodeficiency virus (HIV) in a chronically infected T-cell clone (ACH-2). Concentrations of recombinant TNF-alpha as low as 50 pg/ml induced a significant increase over background of HIV expression in the ACH-2 cells as determined by supernatant reverse transcriptase activity. The HIV-inducing effects of TNF-alpha could not be explained by toxic effects on the cells. In addition, both the uninfected parental cell line (A3.01) and the infected ACH-2 cells were shown to have high-affinity receptors for TNF-alpha. Transient-transfection experiments demonstrated that the inductive effects of TNF-alpha were due to specific activation of the HIV long terminal repeat. These studies provide evidence that TNF-alpha may play a role in the mechanisms of pathogenesis of HIV infection. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Folks, T M AU - Clouse, K A AU - Justement, J AU - Rabson, A AU - Duh, E AU - Kehrl, J H AU - Fauci, A S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 2365 EP - 2368 VL - 86 IS - 7 SN - 0027-8424, 0027-8424 KW - Recombinant Proteins KW - 0 KW - Tumor Necrosis Factor-alpha KW - Index Medicus KW - AIDS/HIV KW - Clone Cells KW - Recombinant Proteins -- pharmacology KW - Promoter Regions, Genetic -- drug effects KW - Cell Survival -- drug effects KW - Transfection KW - Humans KW - Gene Expression Regulation -- drug effects KW - Cell Line KW - HIV-1 -- genetics KW - T-Lymphocytes -- microbiology KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Genes, Viral -- drug effects KW - HIV-1 -- growth & development KW - T-Lymphocytes -- drug effects KW - HIV-1 -- drug effects KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78893799?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-05 N1 - Date created - 1989-05-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1975 Sep;72(9):3666-70 [1103152] Anal Biochem. 1980 Sep 1;107(1):220-39 [6254391] Mol Biochem Parasitol. 1980 Oct;2(1):31-8 [7464858] Infect Immun. 1981 Jul;33(1):156-64 [7021422] J Exp Med. 1981 Sep 1;154(3):631-9 [7276825] Nature. 1984 Dec 20-1985 Jan 2;312(5996):724-9 [6392892] Nature. 1987 Jan 1-7;325(6099):67-70 [3025748] Proc Natl Acad Sci U S A. 1986 Dec;83(24):9759-63 [2432602] J Immunol. 1987 Mar 15;138(6):1719-23 [3493285] J Exp Med. 1987 Jun 1;165(6):1581-94 [3108447] Science. 1987 Nov 6;238(4828):800-2 [3313729] J Virol. 1988 Jan;62(1):139-47 [3257102] Proc Natl Acad Sci U S A. 1987 Dec;84(23):8642-6 [2825201] Science. 1987 Nov 20;238(4830):1144-6 [3500512] J Immunol. 1988 Jan 1;140(1):120-4 [3121735] J Immunol. 1988 Feb 15;140(4):1117-22 [2449497] J Infect Dis. 1988 Mar;157(3):413-20 [3278061] J Exp Med. 1988 Mar 1;167(3):937-53 [2965212] J Immunol. 1988 Apr 15;140(8):2621-4 [3258616] N Engl J Med. 1988 Jun 9;318(23):1481-6 [2835680] Am J Med. 1988 Sep;85(3):289-91 [3414726] J Exp Med. 1985 May 1;161(5):984-95 [3872925] Proc Natl Acad Sci U S A. 1985 Jul;82(13):4539-43 [2989831] Nature. 1985 Aug 8-14;316(6028):552-4 [2993897] Nucleic Acids Res. 1985 Sep 11;13(17):6361-73 [2995927] Nature. 1985 Dec 19-1986 Jan 1;318(6047):665-7 [3001529] Proc Natl Acad Sci U S A. 1986 Jan;83(2):446-50 [3455781] J Immunol. 1986 Apr 1;136(7):2445-50 [3005411] J Exp Med. 1986 Mar 1;163(3):632-43 [3512757] J Immunol. 1986 Jun 1;136(11):4049-53 [2422271] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] J Virol. 1983 Oct;48(1):218-28 [6310145] J Exp Med. 1984 Mar 1;159(3):828-43 [6421983] Science. 1984 Jul 27;225(4660):381-5 [6330891] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fecapentaene concentration and mutagenicity in 718 North American stool samples. AN - 78893630; 2649794 AB - The fecapentaenes (FP) are the predominant fecal mutagens identified to date, but they have not been shown to be carcinogenic. Epidemiologists looking for other fecal mutagens that may be related to colorectal cancer must disentangle from their investigations the pervasive mutagenic effect of the fecapentaenes. As a first step to studying the epidemiology of fecal mutagenicity independent of fecapentaenes, we compared FP measurements and Salmonella mutagenicity assay results for 718 acetone-extracted stool samples collected from a variety of subjects in the Washington DC metropolitan areas. In this large group, 50% of mutagenic samples contained elevated fecapentaenes. Specifically, three-quarters of the samples mutagenic in TA100 contained high FP levels. In contrast, mutagenicity in TA98 was not generally explainable by fecapentaenes, suggesting that non-fecapentaene TA98 mutagenicity should be one focus of future efforts to uncover colorectal carcinogens of etiologic importance. JF - Mutation research AU - Schiffman, M H AU - Van Tassell, R L AU - Andrews, A W AU - Wacholder, S AU - Daniel, J AU - Robinson, A AU - Smith, L AU - Nair, P P AU - Wilkins, T D AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 351 EP - 357 VL - 222 IS - 4 SN - 0027-5107, 0027-5107 KW - Mutagens KW - 0 KW - Polyenes KW - Index Medicus KW - North America KW - Mutagenicity Tests KW - Humans KW - Salmonella typhimurium -- drug effects KW - Feces -- analysis KW - Mutagens -- analysis KW - Polyenes -- analysis KW - Polyenes -- toxicity KW - Mutagens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78893630?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-25 N1 - Date created - 1989-05-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sex differences in the single-dose toxicokinetics of N-nitrosomethyl(2-hydroxyethyl)amine in the rat. AN - 78887396; 2924320 AB - The single-dose toxicokinetics of N-nitrosomethyl(2-hydroxyethyl)amine (NMHA) has been characterized in 8-week-old Fischer 344 rats by analysis using high-performance liquid chromatography of serial blood samples. An i.v. bolus dose of 0.6 mumol/kg to male rats revealed biphasic first-order elimination with a terminal half-life of 37.4 +/- 1.7 min for unchanged NMHA and 101 +/- 6 min for total radioactivity, and extensive conversion to polar metabolites was seen in the high-performance liquid chromatographic assays. The systemic blood clearance and apparent steady-state volume of distribution for unchanged NMHA were 13.1 +/- 0.9 ml/min/kg, and 685 +/- 31 ml/kg, respectively. Renal blood clearance and intrinsic hepatic clearance were estimated to be 0.805 +/- 0.024 and 16.7 +/- 2.1 ml/min/kg, respectively. A similar dose given to female rats yielded a terminal half-life for NMHA of 27.2 +/- 1.2 min, a steady-state volume of distribution of 652 +/- 23 ml/kg, and systemic blood, renal blood, and intrinsic hepatic clearances of 16.9 +/- 1.3, 1.45 +/- 0.14, and 22.5 +/- 0.3 ml/min/kg, respectively. The sex differences in terminal half-life and systemic blood, renal blood, and intrinsic hepatic clearances were significant at the P less than 0.05 level. Larger doses given by gavage, which appeared to be completely absorbed from the gut, indicated systemic bioavailabilities for unchanged NMHA of 78 +/- 10% and 69 +/- 1% for male and female rats, respectively. Binding of NMHA to plasma proteins was found to be negligible. Taken together the data allow for the conclusion that the observed sex differences in toxicokinetic parameters are due to differences in the intrinsic hepatic clearance of the compound. This difference in the ability of the liver to metabolize NMHA in vivo correlates with and may contribute to the greater susceptibility of female rats to hepatocarcinogenesis and of male rats to development of tumors in the nasal epithelium following oral exposure to NMHA. JF - Cancer research AU - Streeter, A J AU - Nims, R W AU - Hrabie, J A AU - Heur, Y H AU - Keefer, L K AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, Maryland 21701. Y1 - 1989/04/01/ PY - 1989 DA - 1989 Apr 01 SP - 1783 EP - 1789 VL - 49 IS - 7 SN - 0008-5472, 0008-5472 KW - Carcinogens KW - 0 KW - Nitrosamines KW - N-nitrosomethyl-(2-hydroxyethyl)amine KW - 26921-68-6 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Kidney -- metabolism KW - Liver Circulation KW - Sex Factors KW - DNA -- metabolism KW - Metabolic Clearance Rate KW - Protein Binding KW - Male KW - Female KW - Nitrosamines -- toxicity KW - Carcinogens -- pharmacokinetics KW - Nitrosamines -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78887396?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-05 N1 - Date created - 1989-05-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Squamous differentiation in normal and transformed rat tracheal epithelial cells. AN - 78885882; 2467758 AB - Morphological observations suggest that rate tracheal epithelial (RTE) cells undergo squamous differentiation when maintained in cell culture. The purpose of the studies presented here was to examine and define differentiation of cultured RTE cells with the help of markers previously shown to be specific for squamous differentiation. Furthermore, we wanted to determine whether neoplastic transformation of these cells causes significant disruption of their differentiation program. Our experiments showed that squamous differentiation occurs in normal primary RTE cell cultures. Epidermal transglutaminase (transglutaminase type I) activity increased approximately 20-fold in RTE cultures as a function of time. Cholesterol sulfate, another marker of squamous differentiation, increased only modestly with time. A significant number of cells formed cross-linked envelopes in cultures growth-arrested at a cell density of approximately 250 cells/mm2. However, no significant changes in keratin expression were detected. Neoplastically transformed RTE cells which exhibit a greatly increased growth capacity expressed the same three markers of squamous differentiation as normal RTE cells. However, transglutaminase type I activity was relatively low. The cross-linked envelope formation was independent of cell density in the transformed cells. Like in normal RTE cultures, cholesterol sulfate accumulation only increased moderately with increasing cell density. The keratin pattern of transformed RTE cell lines was identical to that of normal primary RTE cells. A well-differentiated squamous cell carcinoma derived from one of the neoplastic cell lines expressed in vivo keratin markers typical of keratinization (56 kd acidic keratin and 65-67 kd basic keratins). We draw the following conclusions. (i) The biochemical studies confirm that normal RTE cells undergo squamous differentiation. The pathway of terminal squamous differentiation is cell density dependent. (ii) In transformed RTE cells, growth as well as differentiation are less subject to regulation by cell density than in normal cells. (iii) Transformed RTE cells are differentiation competent; the main abnormality appears to be that in transformed cell populations proliferation and differentiation occur concomitantly. JF - Carcinogenesis AU - Nettesheim, P AU - Smits, H L AU - George, M A AU - Gray, T AU - Jetten, A M AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 743 EP - 748 VL - 10 IS - 4 SN - 0143-3334, 0143-3334 KW - Cholesterol Esters KW - 0 KW - Keratins KW - 68238-35-7 KW - Transglutaminases KW - EC 2.3.2.13 KW - cholesteryl sulfate KW - KU576NT9O9 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Epithelial Cells KW - Cells, Cultured KW - Male KW - Cell Division KW - Keratins -- metabolism KW - Transglutaminases -- metabolism KW - Cholesterol Esters -- metabolism KW - Trachea -- pathology KW - Trachea -- metabolism KW - Trachea -- cytology KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78885882?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-24 N1 - Date created - 1989-05-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retinoic acid treatment of fibroblasts causes a rapid decrease in [3H]inositol uptake. AN - 78882236; 2538335 AB - NIH 3T3 fibroblasts treated with all-trans-retinoic acid (RA) showed a dramatic decrease in the uptake of [3H]inositol compared to solvent-treated controls. The onset of RA-induced inhibition of [3H]inositol uptake was rapid with a 10-15% decrease occurring after 2-3 h of RA exposure and 60-70% reduction after 16 h of RA treatment. A progressive dose-dependent decrease in inositol uptake was found as the concentration of RA increased from 10(-8) to 10(-5) M and the effect was fully reversible within 48 h after RA removal. The Vmax and Kt for the controls were 10 nmol/2.5 x 10(6) cells/2 h and 51 microM; and for RA-treated cells the values were 4 nmol/2.5 x 10(6) cells/2 h and 52 microM. The decreased [3H]inositol uptake was not due to a change in the affinity (Kt) of the transporter for the inositol but to a decrease in the Vmax. The maximal effect on inositol uptake was dependent on RA treatment of the cells after they reached saturation density or if made quiescent by serum starvation. RA was the most active of the different retinoids examined in the order RA greater than 13-cis-RA = retinyl acetate greater than all-trans-retinol greater than 5,6-dihydroxyretinoic acid methyl ester greater than N-4-hydroxyphenyl retinamide. In contrast to this effect on inositol, the uptake of fucose, mannose, galactose, and glucose was either not affected or enhanced (for mannose and fucose) by RA treatment. RA inhibition of inositol uptake was also observed in 3T3-Swiss and Balb/3T3 cells but not in two virally transformed 3T3 cell lines. Phlorizin, amiloride, and monensin inhibited inositol uptake by 66, 74, and 58%, respectively, and this inhibition was additive when the cells were treated with RA as well as these inhibitors. A decreased incorporation of [3H]inositol into polyphosphoinositides was also observed in RA-treated cells but not to the same extent as for [3H]inositol uptake. In conclusion, RA treatment of 3T3 fibroblasts decreases the uptake of [3H]inositol by up to 70% within 8 to 10 h at near physiological concentrations in a reversible and specific manner. JF - Experimental cell research AU - Sinha, R AU - Creek, K E AU - Silverman-Jones, C AU - De Luca, L M AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 385 EP - 399 VL - 181 IS - 2 SN - 0014-4827, 0014-4827 KW - Inositol Phosphates KW - 0 KW - Phosphatidylinositols KW - Vitamin A KW - 11103-57-4 KW - Fenretinide KW - 187EJ7QEXL KW - retinol acetate KW - 3LE3D9D6OY KW - Inositol KW - 4L6452S749 KW - Tretinoin KW - 5688UTC01R KW - 5,6-dihydroxyretinoic acid methyl ester KW - 75664-64-1 KW - Ethylmaleimide KW - O3C74ACM9V KW - Index Medicus KW - Phosphatidylinositols -- metabolism KW - Animals KW - Vitamin A -- analogs & derivatives KW - Dose-Response Relationship, Drug KW - Inositol Phosphates -- metabolism KW - Vitamin A -- pharmacology KW - Biological Transport -- drug effects KW - Fibroblasts KW - Kinetics KW - Cell Line, Transformed KW - Ethylmaleimide -- pharmacology KW - Cell Line KW - Carbohydrate Metabolism KW - Cell Division KW - Tretinoin -- pharmacology KW - Tretinoin -- analogs & derivatives KW - Tretinoin -- metabolism KW - Inositol -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78882236?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-05 N1 - Date created - 1989-05-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Developmental and tissue-specific expression of nuclear proteins that bind the regulatory element of the major histocompatibility complex class I gene. AN - 78881606; 2926327 AB - Expression of MHC class I genes varies according to developmental stage and type of tissues. To study the basis of class I gene regulation in tissues in vivo, we examined binding of nuclear proteins to the conserved cis sequence of the murine H-2 gene, class I regulatory element (CRE), which contains two independent factor-binding sites, region I and region II. In gel mobility shift analyses we found that extracts from adult tissues that express class I genes, such as spleen and liver, had binding activity to region I. In contrast, extracts from brain, which does not express class I genes, did not show region I binding activity. In addition, fetal tissues that express class I gene at very low levels, also did not reveal region I binding activity. Binding activity to region I became detectable during the neonatal period when class I gene expression sharply increases. Most of these tissues showed binding activity to region II, irrespective of class I gene expression. Although region II contained a sequence similar to the AP-1 recognition site, AP-1 was not responsible for the region II binding activity detected in this work. These results illustrate a correlation between region I binding activity and developmental and tissue-specific expression of MHC class I genes. The CRE exerts an enhancer-like activity in cultured fibroblasts. We evaluated the significance of each factor binding to CRE. Single 2-bp mutations were introduced into the CRE by site-directed mutagenesis and the ability of each mutant to elicit the enhancer activity was tested in transient CAT assays. A mutation that eliminated region I protein binding greatly impaired enhancer activity. A mutation that eliminated region II binding also caused a lesser but measurable effect. We conclude that region I and region II are both capable of enhancing transcription of the class I gene. These results indicate that in vivo regulation of MHC class I gene expression is mediated by binding of trans-acting factors to the CRE. JF - The Journal of experimental medicine AU - Burke, P A AU - Hirschfeld, S AU - Shirayoshi, Y AU - Kasik, J W AU - Hamada, K AU - Appella, E AU - Ozato, K AD - Laboratory of Developmental and Molecular Immunity, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1989/04/01/ PY - 1989 DA - 1989 Apr 01 SP - 1309 EP - 1321 VL - 169 IS - 4 SN - 0022-1007, 0022-1007 KW - DNA-Binding Proteins KW - 0 KW - H-2 Antigens KW - Nuclear Proteins KW - Transcription Factors KW - Index Medicus KW - Animals KW - Enhancer Elements, Genetic KW - DNA Mutational Analysis KW - Transcription, Genetic KW - Mice KW - Tissue Distribution KW - Transcription Factors -- physiology KW - Regulatory Sequences, Nucleic Acid KW - H-2 Antigens -- genetics KW - Gene Expression Regulation KW - DNA-Binding Proteins -- physiology KW - Nuclear Proteins -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78881606?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-11 N1 - Date created - 1989-05-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell. 1986 Sep 12;46(6):795-805 [3530495] Nature. 1986 Aug 21-27;322(6081):743-6 [3748155] Proc Natl Acad Sci U S A. 1986 Dec;83(24):9537-41 [3467324] Proc Natl Acad Sci U S A. 1987 May;84(10):3380-4 [3106967] Proc Natl Acad Sci U S A. 1987 May;84(9):2653-7 [3554244] Cell. 1987 Jun 19;49(6):729-39 [3034432] Cell. 1987 Jun 19;49(6):741-52 [3034433] Science. 1987 Jun 5;236(4806):1237-45 [3296191] Mol Cell Biol. 1987 Jul;7(7):2625-30 [3475569] Mol Cell Biol. 1987 Aug;7(8):2745-52 [3670292] Mol Cell Biol. 1987 Sep;7(9):3349-52 [3313015] EMBO J. 1987 Nov;6(11):3317-24 [3322806] Proc Natl Acad Sci U S A. 1988 Feb;85(3):723-7 [3422454] Mol Cell Biol. 1987 Dec;7(12):4542-8 [3501825] Science. 1988 Mar 11;239(4845):1302-6 [3125612] Cell. 1988 Feb 12;52(3):415-23 [2964277] J Immunol. 1988 Jun 15;140(12):4378-87 [2453581] Nature. 1988 Aug 11;334(6182):494-8 [2900470] Proc Natl Acad Sci U S A. 1988 Aug;85(16):5884-8 [2457903] Annu Rev Biochem. 1988;57:159-97 [3052270] Transplantation. 1980 Apr;29(4):274-79 [6989046] Proc Natl Acad Sci U S A. 1982 May;79(10):3082-6 [6179076] J Neuroimmunol. 1981 Dec;1(4):429-56 [6125529] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] Cell. 1984 Dec;39(3 Pt 2):653-62 [6096017] Nature. 1985 Apr 18-24;314(6012):637-9 [3990797] Proc Natl Acad Sci U S A. 1985 Apr;82(8):2427-31 [2581247] Immunogenetics. 1985;22(5):441-52 [2998982] Nucleic Acids Res. 1985 Dec 20;13(24):8765-85 [3001650] Proc Natl Acad Sci U S A. 1986 Jan;83(2):446-50 [3455781] Cell. 1986 Jan 31;44(2):261-72 [3510743] Cell. 1986 Dec 5;47(5):767-76 [3779841] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Initiation of cell proliferation in livers of the viviparous fish Poeciliopsis lucida with 7,12-dimethylbenz[a]anthracene. AN - 78876133; 2494046 AB - Stimulation of liver cell proliferation by sublethal exposures to 7,12-dimethylbenz[a]anthracene (DMBA) is examined in the small, viviparous fish Poeciliopsis lucida. Poeciliopsis is susceptible to induction of liver tumors by repeated short-term exposures, under 24 hr, to waterborne DMBA at 5 ppm. Exposures to 5 ppm for 24 hr was lethal to fish under 1 month old and resulted in 60% mortality of adult females 20-25 mm in length. Response to 16-, 20-, and 22-hr exposures of 5 ppm DMBA, as measured by mitotic index, was similar in females of two size classes, 20-25 mm and 26-30 mm. Differences were observed in the onset of mitosis in livers of fish exposed for 16 hr vs 20 or 22 hr. Hepatocyte proliferation did not begin until 10-11 days after the 16-hr exposure and lasted for only 3 days. When exposure was increased to 20 or 22 hr, mitotic activity was observed earlier, 2 days following treatment, and continued for 6-8 days. The peak period of cell proliferation also varied, occurring 12 days after a 16-hr exposure, 4 days after a 20-hr exposure, and at least 10 days after a 22-hr exposure. The mitotic index was the highest on the final day specimens of the 22-hr treatment were collected. These results suggest that the toxic properties of DMBA in stimulating cell proliferation may function as an important cofactor in hepatocarcinogenesis. JF - Environmental research AU - Schultz, M E AU - Kaplan, L A AU - Schultz, R J AD - NIEHS Marine and Freshwater Biomedical Core Center, University of Connecticut, Storrs 06268. Y1 - 1989/04// PY - 1989 DA - April 1989 SP - 248 EP - 254 VL - 48 IS - 2 SN - 0013-9351, 0013-9351 KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - Index Medicus KW - Animals KW - Cell Division -- drug effects KW - Liver Neoplasms, Experimental -- chemically induced KW - Mitosis -- drug effects KW - Time Factors KW - Female KW - Liver -- cytology KW - Liver -- drug effects KW - 9,10-Dimethyl-1,2-benzanthracene -- toxicity KW - Cyprinodontiformes -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78876133?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-10 N1 - Date created - 1989-05-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modification of transplacental tumorigenesis by 3-methylcholanthrene in mice by genotype at the Ah locus and pretreatment with beta-naphthoflavone. AN - 78873308; 2538231 AB - Transplacental lung and liver tumorigenesis in the mouse by 3-methylcholanthrene (MC) was assessed as a function of inducibility of MC metabolism in fetus and in mother, and of pretreatment of the mothers with a noncarcinogenic inducer, beta-naphthoflavone (beta NF). Pregnant (C57BL/6 X DBA/2)F1 females (genotype Ahb Ahd, inducer responsive) mated to DBA/2 males received 45 or 100 mg/kg MC on gestation day 17, and DBA/2 females (genotype Ahd Ahd, nonresponsive) mated to F1 males were given 5 or 30 mg MC/kg. These crosses generated both responsive and nonresponsive offspring. Phenotype and tumor incidences were determined at 13 months of age. The transplacental action of MC was dose dependent and resulted in more lung and liver tumors in induction-responsive offspring than in nonresponsive littermates in most comparisons. beta NF alone did not result in increased numbers of tumors. Significant, complex effects were seen when the mothers were pretreated with beta NF (150 mg/kg) on gestation day 15, before MC on day 17. The beta NF pretreatment protected the fetuses of the F1 mothers: there was a significant overall 30 to 50% reduction in numbers of lung and liver tumors. The greatest effect was seen in the induction-responsive males, who experienced a 50% reduction in both incidence and multiplicity of lung tumors after 100 mg MC/kg, compared with males exposed to MC only. By contrast, beta NF pretreatment of DBA mothers had no general effect but rather potentiated the action of the 5 mg MC/kg dose on multiplicity of lung tumors in inducible males, causing a significant 4-fold increase. It also caused a 60% increase in inducible male liver tumor multiplicity when given before the 30 mg MC/kg dose. Thus, beta NF pretreatment was protective when the mother was inducible, especially in the inducible fetuses of such a mother, but when the mother was noninducible the beta NF pretreatment had no effect in some situations and potentiated the action of the carcinogen in others, mainly in inducible fetuses. These results underscore the fact that induced maternal and fetal metabolism contribute to risk of transplacental tumorigenesis by MC in qualitatively opposite ways. JF - Cancer research AU - Anderson, L M AU - Jones, A B AU - Riggs, C W AU - Kovatch, R M AD - Division of Cancer Etiology, National Cancer Institute-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1989/04/01/ PY - 1989 DA - 1989 Apr 01 SP - 1676 EP - 1681 VL - 49 IS - 7 SN - 0008-5472, 0008-5472 KW - Benzoflavones KW - 0 KW - Flavonoids KW - Receptors, Aryl Hydrocarbon KW - Receptors, Drug KW - Methylcholanthrene KW - 56-49-5 KW - beta-Naphthoflavone KW - 6051-87-2 KW - Index Medicus KW - Genotype KW - Animals KW - Mice, Inbred C57BL KW - Mice KW - Fetus -- metabolism KW - Male KW - Female KW - Pregnancy KW - Mice, Inbred DBA KW - Receptors, Drug -- genetics KW - Fetal Diseases -- chemically induced KW - Methylcholanthrene -- toxicity KW - Liver Neoplasms, Experimental -- chemically induced KW - Lung Neoplasms -- chemically induced KW - Flavonoids -- pharmacology KW - Methylcholanthrene -- metabolism KW - Benzoflavones -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78873308?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-05 N1 - Date created - 1989-05-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of Pertussigen (Pertussis Toxin) on the Mouse Protective Activity of Vaccines Made from Bordetella Species AN - 1492612594; 18826496 AB - Pertussigen [pertussis toxin (Ptx)] from Bordetella pertussis, when detoxified, induces protection in mice to intracerebral challenge (ic) with virulent B. pertussis. In its native form, minute nonprotective doses promote the development of immunity induced by other antigens of B. pertussis. As little as 4 ng of Ptx, given with a nonprotective dose of 8 10 super(7) killed cells of the phase III Sakairi strain, promoted detectable protection to ic challenge. Native Ptx in doses of 0.4 to 400 ng did not protect mice, and vaccines made from strains not producing Ptx induced only weak protection. The marked enhancing action of Ptx was also observed with 5 mu g of purified filamentous hemagglutinin and with vaccines made from other species of the Bordetella genus, such as B. parapertussis and B. bronchiseptica, but it was not observed with B. pertussis endotoxin. In addition, Ptx was still effective when given as late as 7 days after the vaccine. Antibodies to surface antigens of the challenge strain were demonstrated in sera of mice immunized with vaccines prepared with the different Bordetella species tested, but antibodies to Ptx were detected only in the sera of mice immunized with the wild-type B. pertussis strains. Glutaraldehyde detoxified Ptx does not have this action. Pretreatment of normal mice with Ptx, also enhanced the protective action of a mouse antiserum to a wild-type strain of B. pertussis. These observations show that antigens other than Ptx are responsible for the protection, and that Ptx acts non-specifically to enhance the mouse protective action of those antigens. JF - Microbiology and Immunology AU - Munoz, John J AU - Peacock, Marius G AD - Department of Health and Human Services, Public Health Service, National Institutes of Health, National Institute of Allergy and Infectious Diseases, Laboratory of Pathobiology, Rocky Mountain Laboratories, Hamilton, Montana, 59840, U.S.A. Y1 - 1989/04// PY - 1989 DA - Apr 1989 SP - 341 EP - 355 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 33 IS - 4 SN - 0385-5600, 0385-5600 KW - Immunology Abstracts; Microbiology Abstracts B: Bacteriology KW - Endotoxins KW - Pertussis KW - Bordetella pertussis KW - Antibodies KW - Bordetella KW - surface antigens KW - Hemagglutinins KW - Vaccines KW - Immunity KW - Glutaraldehyde KW - pertussis toxin KW - J 02350:Immunology KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492612594?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-12-01 N1 - Last updated - 2014-05-15 N1 - SubjectsTermNotLitGenreText - Endotoxins; Pertussis; Antibodies; surface antigens; Hemagglutinins; Immunity; Vaccines; Glutaraldehyde; pertussis toxin; Bordetella pertussis; Bordetella DO - http://dx.doi.org/10.1111/j.1348-0421.1989.tb01982.x ER - TY - JOUR T1 - Ethanol inhibits NMDA-activated ion current in hippocampal neurons. AN - 78923028; 2467382 AB - The ion current induced by the glutamate receptor agonist N-methyl-D-aspartate (NMDA) in voltage-clamped hippocampal neurons was inhibited by ethanol (EtOH). Inhibition increased in a concentration-dependent manner over the range 5 to 50 mM, a range that also produces intoxication. The amplitude of the NMDA-activated current was reduced 61 percent by 50 mM EtOH; in contrast, this concentration of EtOH reduced the amplitude of current activated by the glutamate receptor agonists kainate and quisqualate by only 18 and 15 percent, respectively. The potency for inhibition of the NMDA-activated current by several alcohols is linearly related to their intoxicating potency, suggesting that alcohol-induced inhibition of responses to NMDA receptor activation may contribute to the neural and cognitive impairments associated with intoxication. JF - Science (New York, N.Y.) AU - Lovinger, D M AU - White, G AU - Weight, F F AD - Section of Electrophysiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852. Y1 - 1989/03/31/ PY - 1989 DA - 1989 Mar 31 SP - 1721 EP - 1724 VL - 243 IS - 4899 SN - 0036-8075, 0036-8075 KW - Butanols KW - 0 KW - Calcium Channels KW - Chloride Channels KW - Chlorides KW - Ion Channels KW - Membrane Proteins KW - Oxadiazoles KW - Pentanols KW - Receptors, Glutamate KW - Receptors, N-Methyl-D-Aspartate KW - Receptors, Neurotransmitter KW - Sodium Channels KW - Aspartic Acid KW - 30KYC7MIAI KW - Ethanol KW - 3K9958V90M KW - gamma-Aminobutyric Acid KW - 56-12-2 KW - N-Methylaspartate KW - 6384-92-5 KW - Quisqualic Acid KW - 8OC22C1B99 KW - 1-Butanol KW - 8PJ61P6TS3 KW - isopentyl alcohol KW - DEM9NIT1J4 KW - Kainic Acid KW - SIV03811UC KW - Methanol KW - Y4S76JWI15 KW - Index Medicus KW - Calcium Channels -- physiology KW - Kainic Acid -- pharmacology KW - Electric Conductivity KW - gamma-Aminobutyric Acid -- pharmacology KW - Humans KW - Sodium Channels -- physiology KW - Receptors, Neurotransmitter -- drug effects KW - Chlorides -- physiology KW - Receptors, Neurotransmitter -- physiology KW - Pentanols -- pharmacology KW - Methanol -- pharmacology KW - Oxadiazoles -- pharmacology KW - Butanols -- pharmacology KW - Calcium Channels -- drug effects KW - Sodium Channels -- drug effects KW - Membrane Proteins -- physiology KW - Ethanol -- adverse effects KW - Aspartic Acid -- pharmacology KW - Aspartic Acid -- analogs & derivatives KW - Hippocampus -- physiology KW - Ethanol -- pharmacology KW - Ion Channels -- drug effects KW - Hippocampus -- cytology KW - Neurons -- physiology KW - Ion Channels -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78923028?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-08 N1 - Date created - 1989-05-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Flupirtine antinociception in the dog is primarily mediated by nonopioid supraspinal mechanisms. AN - 79064624; 2744078 AB - Flupirtine is a novel analgesic recently introduced with therapy. The present study assessed the role of opioid mechanisms in flupirtine-induced antinociception, localized its site of action along the neuraxis and evaluated its relative potency. Analgesic and general behavioral effects of flupirtine (0.3-10 mg/kg i.v.) were compared to those of the opioid analgesic pentazocine (0.3-5 mg/kg i.v.) in chronic spinal dogs. Flupirtine was slightly less effective than pentazocine in depressing the supraspinally mediated skin twitch nociceptive reflex. But in contrast to pentazocine, flupirtine only weakly depressed the flexor reflex, a spinally mediated nociceptive reflex. Statistically reliable potency estimates for antinociception were not obtained. Both drugs constricted pupils and lowered body temperature. In drug interaction studies, a relatively high dose (1 mg/kg i.v.) of the opioid antagonist naltrexone antagonized the effects of pentazocine but not those of flupirtine. It is concluded that flupirtine-induced antinociception is not opiate-receptor mediated, that its antinociceptive actions occur primarily at supraspinal sites and that its potency is less than that of pentazocine in the dog. JF - European journal of pharmacology AU - Vaupel, D B AU - Nickel, B AU - Becketts, K AD - Neuropharmacology Laboratory, National Institute on Drug Abuse, Addiction Research Center, Baltimore, MD 21224. Y1 - 1989/03/29/ PY - 1989 DA - 1989 Mar 29 SP - 447 EP - 456 VL - 162 IS - 3 SN - 0014-2999, 0014-2999 KW - Aminopyridines KW - 0 KW - Analgesics KW - Naltrexone KW - 5S6W795CQM KW - flupirtine KW - MOH3ET196H KW - Pentazocine KW - RP4A60D26L KW - Index Medicus KW - Animals KW - Pentazocine -- pharmacology KW - Reflex -- drug effects KW - Temperature KW - Naltrexone -- pharmacology KW - Dogs KW - Decerebrate State KW - Time Factors KW - Female KW - Analgesics -- pharmacology KW - Aminopyridines -- pharmacology KW - Aminopyridines -- adverse effects KW - Analgesics -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79064624?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-22 N1 - Date created - 1989-08-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human non-histone chromosomal protein HMG-17: identification, characterization, chromosome localization and RFLPs of a functional gene from the large multigene family. AN - 78945748; 2565024 AB - The multigene family of chromosomal protein HMG-17 is the largest known human retropseudogene family. A functional gene was identified and isolated by screening cDNA-selected genomic clones with a set of 5 oligonucleotides whose sequence corresponded to regions in which the sequence of the retropseudogenes differed from that of the cDNA and which did not span previously identified exon/intron junctions. A 7195 bp genomic fragment containing 6 exons, ranging in size from 30 to 817 bp, two of which encode the entire DNA binding domain of the protein, was sequenced. The gene has features which are typical to "housekeeping" genes and is characterized by a very high content of G + C residues in a 1.4 kb fragment starting 500 bp from the cap site and by an "HTF" island in the 5' region. Transcriptional regulatory signals, exon/intraon boundaries and features characteristic of "housekeeping" genes are evolutionary conserved between the human and chicken genes. The HMG-17 gene was localized to human chromosome 1p12-34. RFLP's useful for further mapping were detected. The experimental evidence presented leads to the assumption that the gene characterized is the only functional human HMG-17 gene. JF - Nucleic acids research AU - Landsman, D AU - McBride, O W AU - Bustin, M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/03/25/ PY - 1989 DA - 1989 Mar 25 SP - 2301 EP - 2314 VL - 17 IS - 6 SN - 0305-1048, 0305-1048 KW - High Mobility Group Proteins KW - 0 KW - Oligonucleotide Probes KW - DNA KW - 9007-49-2 KW - DNA Restriction Enzymes KW - EC 3.1.21.- KW - Index Medicus KW - Animals KW - Base Composition KW - Sequence Homology, Nucleic Acid KW - Biological Evolution KW - Exons KW - Humans KW - Transcription, Genetic KW - Mice KW - Amino Acid Sequence KW - Nucleic Acid Hybridization KW - Cloning, Molecular KW - Regulatory Sequences, Nucleic Acid KW - Base Sequence KW - Chickens KW - DNA -- genetics KW - Molecular Sequence Data KW - Introns KW - Cricetinae KW - Chromosomes, Human, Pair 1 KW - High Mobility Group Proteins -- genetics KW - Polymorphism, Restriction Fragment Length KW - Polymorphism, Genetic KW - Multigene Family KW - Chromosome Mapping UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78945748?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-22 N1 - Date created - 1989-05-22 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - X13546; GENBANK N1 - SuppNotes - Cited By: Science. 1976 Sep 3;193(4256):848-56 [948749] J Biol Chem. 1988 Sep 25;263(27):13500-3 [3417670] Nucleic Acids Res. 1980 Sep 11;8(17):3757-78 [6449690] Annu Rev Biochem. 1981;50:349-83 [6791577] J Exp Med. 1982 May 1;155(5):1480-90 [6802926] Nucleic Acids Res. 1982 Mar 25;10(6):2017-42 [6210882] Annu Rev Biochem. 1982;51:89-121 [6287925] Nature. 1982 Dec 23;300(5894):773-4 [7177197] Proc Natl Acad Sci U S A. 1983 Jan;80(1):278-82 [6572002] Nucleic Acids Res. 1982 Dec 20;10(24):8155-70 [6819544] Anal Biochem. 1983 Feb 15;129(1):216-23 [6305233] Proc Natl Acad Sci U S A. 1983 Nov;80(22):6735-9 [6196774] J Biol Chem. 1984 Jan 25;259(2):699-702 [6229533] Chromosoma. 1984;90(5):355-65 [6439496] Exp Cell Res. 1985 Feb;156(2):295-310 [3881264] J Biol Chem. 1985 Apr 25;260(8):5040-9 [3988744] Proc Natl Acad Sci U S A. 1986 Jan;83(1):130-4 [3001719] Nucleic Acids Res. 1986 Apr 25;14(8):3363-76 [3703677] J Biol Chem. 1986 Jun 5;261(16):7479-84 [3754870] Nature. 1986 May 15-21;321(6067):209-13 [2423876] Annu Rev Biochem. 1986;55:631-61 [2427017] Exp Cell Res. 1986 Oct;166(2):486-96 [3743668] EMBO J. 1987 Aug;6(8):2393-9 [3665881] J Biol Chem. 1988 Mar 15;263(8):3917-23 [2831214] J Mol Biol. 1987 Oct 5;197(3):405-13 [3441004] Proc Natl Acad Sci U S A. 1988 Jul;85(13):4775-8 [3387438] Cell. 1980 Jan;19(1):289-301 [6244103] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - New protein cross-linking reagents that are cleaved by mild acid. AN - 79025072; 2471550 AB - New homo- and heterobifunctional cross-linking reagents have been synthesized. These reagents are based on ortho ester, acetal, and ketal functionalities that undergo acid-catalyzed dissociation but are base stable. The protein-reactive group in all the homobifunctional reagents is a maleimide group; the heterobifunctional acetal cross-linker has a maleimide group at one end and an N-hydroxysuccinimide ester at the other. These reagents have been used to cross-link diphtheria toxin (DT) to itself to give covalently cross-linked DT dimer or to conjugate DT monomer to the anti-CD5 antibody, T101. The hydrolysis of these cross-linked proteins was studied as a function of pH. Cleavage rates vary from minutes to hours at the pH of acidified cellular vesicles (approximately pH 5.4), ortho esters being the fastest, acetals the slowest, and ketals intermediate, but the cross-linked products are approximately 100 times more stable at the vascular pH of 7.4 and 1000 times more stable at a storage pH of 8.4 in all cases. The utility of these reagents in the reversible blockade of a toxic protein functional domain was demonstrated by using cross-linked DT dimer where the blocking and unblocking of toxin binding sites correlates with cellular toxicity. Of the different cross-linkers described, the acetone ketal, bis(maleimidoethoxy)propane (BMEP), appears to be the most promising in the construction of highly efficacious immunotoxins. JF - Biochemistry AU - Srinivasachar, K AU - Neville, D M AD - Laboratory of Molecular Biology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1989/03/21/ PY - 1989 DA - 1989 Mar 21 SP - 2501 EP - 2509 VL - 28 IS - 6 SN - 0006-2960, 0006-2960 KW - Antigens, CD5 KW - 0 KW - Antigens, Differentiation KW - Cross-Linking Reagents KW - Diphtheria Toxin KW - Proteins KW - Index Medicus KW - Antigen-Antibody Reactions KW - Hydrogen-Ion Concentration KW - Hydrolysis KW - Structure-Activity Relationship KW - Magnetic Resonance Spectroscopy KW - Cross-Linking Reagents -- chemical synthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79025072?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-27 N1 - Date created - 1989-07-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Determination of carcinogen-DNA adducts by immunoassay. AN - 79103194; 2664949 JF - Journal of UOEH AU - Poirier, M C AU - Liou, S H AU - Reed, E AU - Strickland, P T AU - Tockman, M S AD - National Cancer Institute, Bethesda, MD. Y1 - 1989/03/20/ PY - 1989 DA - 1989 Mar 20 SP - 353 EP - 367 VL - 11 Suppl SN - 0387-821X, 0387-821X KW - Antibodies, Monoclonal KW - 0 KW - Antigens KW - Carcinogens KW - DNA Adducts KW - Immune Sera KW - benzo(a)pyrene-DNA adduct KW - Benzo(a)pyrene KW - 3417WMA06D KW - DNA KW - 9007-49-2 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Smoke Inhalation Injury -- immunology KW - DNA Damage KW - Blood Cells -- analysis KW - Humans KW - Neoplasms -- blood KW - Immune Sera -- immunology KW - Cisplatin -- blood KW - Antigens -- analysis KW - Cisplatin -- therapeutic use KW - Benzo(a)pyrene -- analysis KW - Smoke Inhalation Injury -- blood KW - Cisplatin -- analysis KW - Antigens -- immunology KW - Male KW - Neoplasms -- drug therapy KW - Cell Nucleus -- immunology KW - Benzo(a)pyrene -- blood KW - Neoplasms -- analysis KW - Enzyme-Linked Immunosorbent Assay -- methods KW - Cell Nucleus -- analysis KW - Blood Cells -- immunology KW - Benzo(a)pyrene -- immunology KW - Female KW - Remission Induction KW - DNA -- blood KW - DNA -- analysis KW - DNA -- immunology KW - Carcinogens -- analysis KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79103194?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-14 N1 - Date created - 1989-08-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of polymerase chain reaction catalyzed by Taq DNA polymerase for site-specific mutagenesis. AN - 79100637; 2744478 AB - The polymerase chain reaction catalyzed by Taq DNA polymerase has been used for site-specific mutagenesis. The amplification was primed by two oligodeoxyribonucleotides complementary to insulin receptor cDNA. To direct the synthesis of mutant DNA, mismatches were introduced into one of the primers. Six different mutations were constructed by this technique. Of twelve clones whose sequences were determined, ten (83%) had the correct sequence. This technique, which does not require the use of single-stranded DNA templates, provides a simple and efficient approach to site-specific mutagenesis. JF - Gene AU - Kadowaki, H AU - Kadowaki, T AU - Wondisford, F E AU - Taylor, S I AD - Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD. Y1 - 1989/03/15/ PY - 1989 DA - 1989 Mar 15 SP - 161 EP - 166 VL - 76 IS - 1 SN - 0378-1119, 0378-1119 KW - DNA, Recombinant KW - 0 KW - Oligodeoxyribonucleotides KW - Receptor, Insulin KW - EC 2.7.10.1 KW - Taq Polymerase KW - EC 2.7.7.- KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - Index Medicus KW - Chemistry KW - Oligodeoxyribonucleotides -- genetics KW - Plasmids KW - Cloning, Molecular KW - Gene Amplification KW - Base Sequence KW - Receptor, Insulin -- genetics KW - Genetic Vectors KW - Chemical Phenomena KW - Oligodeoxyribonucleotides -- biosynthesis KW - Templates, Genetic KW - Catalysis KW - Mutation KW - DNA-Directed DNA Polymerase -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79100637?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-25 N1 - Date created - 1989-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Kinetics of pulmonary surfactant phosphatidylcholine metabolism in the lungs of silica-treated rats. AN - 78927697; 2538945 AB - Exposure of rats to silica by intratracheal injection increased the intra- and extracellular compartments of pulmonary surfactant phospholipid. These changes were dose and time dependent, but both pools were not affected equally. Seven days after the instillation of 10 mg of silica, the intracellular pool increased 13.3-fold, from 1.49 +/- 0.30 to 19.86 +/- 0.77 mg of surfactant phospholipid per pair of lungs, and the extracellular pool increased 7.4-fold, from 1.87 +/- 0.79 to 13.79 +/- 0.72 mg of surfactant phospholipid per pair of lungs. To investigate the physiologic processes responsible for these massive accumulations of surfactant. [14C]choline was injected into the tail veins of control and silica-treated rats and the specific activity of surfactant phospholipids within the intracellular and extracellular pools was determined at various times between 0 and 26 hr after injection. All of the processes measured were increased in response to silica exposure, but not to the same extent. At 1 hr, incorporation of [14C]choline into the intracellular surfactant pool was increased 12.6-fold above controls, from 4.8 +/- 1.1 x 10(3) to 60.6 +/- 26.6 x 10(3) dpm. The flux of [14C]choline-labeled phospholipid from the intracellular to the extracellular pool was increased 7.3-fold, from 102 +/- 10 to 749 +/- 39 micrograms/hr in silica-treated animals, but its disappearance from the extracellular pool was increased only 5.0-fold, from 87 +/- 8 to 434 +/- 21 micrograms/hr. The half-life of [14C]choline-labeled phospholipids in the intracellular pool of surfactant was increased from 10.1 +/- 1.0 to 18.3 +/- 5.3 hr and that in the extracellular surfactant pool from 14.8 +/- 1.4 to 21.9 +/- 4.9 hr. Expansion of the intra- and extracellular pools of surfactant phospholipids may be explained on the basis of a metabolic imbalance in which the intracellular production of surfactant is increased above its secretion rate into the extracellular compartment, and the secretion rate is elevated above the rate at which surfactant phospholipids are cleared from the alveoli. JF - Toxicology and applied pharmacology AU - Dethloff, L A AU - Gladen, B C AU - Gilmore, L B AU - Hook, G E AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/03/15/ PY - 1989 DA - 1989 Mar 15 SP - 1 EP - 11 VL - 98 IS - 1 SN - 0041-008X, 0041-008X KW - Phosphatidylcholines KW - 0 KW - Phospholipids KW - Pulmonary Surfactants KW - Silicon Dioxide KW - 7631-86-9 KW - Choline KW - N91BDP6H0X KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Pulmonary Alveoli -- metabolism KW - Kinetics KW - Phospholipids -- metabolism KW - Choline -- metabolism KW - Male KW - Pulmonary Surfactants -- metabolism KW - Silicon Dioxide -- administration & dosage KW - Lung -- drug effects KW - Silicon Dioxide -- toxicity KW - Phosphatidylcholines -- metabolism KW - Lung -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78927697?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-02 N1 - Date created - 1989-05-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Combination cytokine immunotherapy with tumor necrosis factor alpha, interleukin 2, and alpha-interferon and its synergistic antitumor effects in mice. AN - 78891196; 2784349 AB - The antitumor activity of combination therapy with recombinant human tumor necrosis factor alpha (rhTNF-alpha), recombinant human interleukin 2 (rhIL-2), and recombinant hybrid alpha-interferon A/D (rhIFN-alpha A/D) was assessed against established weakly immunogenic (MCA-106) and nonimmunogenic (MCA-102) sarcomas at both s.c. and visceral (hepatic) sites. C57BL/6 mice were treated with a single i.v. dose of rhTNF-alpha followed by rhIL-2 (75,000 units) and rhIFN-alpha A/D (75,000 units) i.p. twice daily for 5 consecutive days. Substantial improvements were observed when the combination of rhTNF-alpha, rhIL-2, and rhIFN-alpha A/D was administered, as measured by regression of tumor, prolongation of survival, and improved cure rates, compared with any combination of two cytokines or any cytokine alone against the MCA-106 sarcoma. These findings were consistent in both the s.c. and single hepatic tumor models. For example, treatment of the MCA-106 s.c. tumor bearers with the triple cytokine combination resulted in cures of 16 of 18, 17 of 18, and 12 of 18 mice receiving rhTNF-alpha dosages of 2, 4, and 6 micrograms, respectively, compared with 2 of 18, 7 of 18, and 9 of 18 at 2, 4, and 6 micrograms of rhTNF-alpha plus rhIL-2 without rhIFN-alpha A/D. Established 10-day single liver tumor weights when treated with the triple combination therapy were 54 and 25 mg in treatment groups receiving 2 and 4 micrograms of rhTNF-alpha, compared with 376 and 302 mg with the same amounts of rhTNF-alpha alone (P less than 0.004). Mice bearing hepatic sarcomas treated with triple cytokine combination therapy had cure rates of 50% and 67% at rhTNF-alpha doses of 2 and 4 micrograms, compared with no survivors with rhTNF-alpha alone. No improved antitumor effects resulted from therapy with any cytokine alone or in combination against the nonimmunogenic MCA-102 sarcoma. Possible in vivo mechanisms by which these three cytokines synergize are discussed. JF - Cancer research AU - McIntosh, J K AU - Mulé, J J AU - Krosnick, J A AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/03/15/ PY - 1989 DA - 1989 Mar 15 SP - 1408 EP - 1414 VL - 49 IS - 6 SN - 0008-5472, 0008-5472 KW - Interferon Type I KW - 0 KW - Interleukin-2 KW - Recombinant Proteins KW - Tumor Necrosis Factor-alpha KW - Index Medicus KW - Animals KW - Sarcoma, Experimental -- therapy KW - Liver Neoplasms, Experimental -- mortality KW - Liver Neoplasms, Experimental -- therapy KW - Mice, Inbred C57BL KW - Mice KW - Drug Synergism KW - Recombinant Proteins -- administration & dosage KW - Female KW - Interleukin-2 -- administration & dosage KW - Interferon Type I -- administration & dosage KW - Tumor Necrosis Factor-alpha -- administration & dosage KW - Neoplasms, Experimental -- therapy KW - Neoplasms, Experimental -- mortality KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78891196?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-26 N1 - Date created - 1989-04-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vivo differentiation of rat liver oval cells into hepatocytes. AN - 78879416; 2466557 AB - The Solt-Farber protocol, in the absence of an initiating agent, was used to examine the precursor-product relationship between oval cells and hepatocytes in rat liver. The animals were administered 2-acetylaminofluorene (AAF) by gavage for 2 wk combined with partial hepatectomy 1 wk after administering AAF Two dose levels of AAF were used: 9- and 21-mg total dose for animals in Groups I and II, respectively. [3H]Thymidine was administered i.p. to one-half of the animals at Day 6 post-partial hepatectomy. Animals were sacrificed 7, 9, 11, and 13 days after surgery. Only oval cells became labeled on Day 7 in both groups. On Day 9 both labeled oval cells and labeled basophilic hepatocytes were present in Group I, whereas in Group II only oval cells remained labeled. On Days 11 and 13 both oval cells and basophilic hepatocytes were labeled in both groups. The total amount of radioactivity in Group II livers remained the same on Day 9 when only labeled oval cells were present and on Days 11 and 13 when both labeled oval cells and labeled basophilic hepatocytes were present. The calculated half-life for basophilic hepatocytes was about 50 h. The differentiation of oval cells into basophilic hepatocytes was delayed in Group II as compared to Group I, and the higher dose of AAF also induced the formation of both intestinal metaplasia and bile duct formation. In situ hybridization with an alpha-fetoprotein probe showed a strong expression in groups of typical oval cells and in cells arranged in duct-like structures. In addition a transient expression of AFP was also observed in the areas of basophilic hepatocytes 9 to 11 days after partial hepatectomy. Administration of AAF decreased the level of albumin mRNA in preexisting hepatocytes and caused a significant decrease of serum albumin. In contrast, oval cells showed a strong albumin expression, and basophilic hepatocytes formed islands of albumin-expressing cells. Oval cells and the foci of early basophilic hepatocytes lacked glucose-6-phosphatase activity. At Day 13 significant numbers of basophilic hepatocytes were positive for glucose-6-phosphatase. Oval cells were strongly gamma-glutamyltranspeptidase positive, whereas the foci of basophilic hepatocytes were negative for gamma-glutamyltranspeptidase. Only occasionally were transiently gamma-glutamyltranspeptidase-positive hepatocytes observed in basophilic foci. In summary our data indicate that oval cells can differentiate to hepatocytes and may have an important physiological function as a source of major serum proteins when hepatocytes are unable to synthesize these proteins. JF - Cancer research AU - Evarts, R P AU - Nagy, P AU - Nakatsukasa, H AU - Marsden, E AU - Thorgeirsson, S S AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/03/15/ PY - 1989 DA - 1989 Mar 15 SP - 1541 EP - 1547 VL - 49 IS - 6 SN - 0008-5472, 0008-5472 KW - RNA, Messenger KW - 0 KW - Serum Albumin KW - alpha-Fetoproteins KW - DNA KW - 9007-49-2 KW - 2-Acetylaminofluorene KW - 9M98QLJ2DL KW - gamma-Glutamyltransferase KW - EC 2.3.2.2 KW - Glucose-6-Phosphatase KW - EC 3.1.3.9 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Serum Albumin -- genetics KW - gamma-Glutamyltransferase -- analysis KW - Glucose-6-Phosphatase -- analysis KW - Hepatectomy KW - RNA, Messenger -- analysis KW - alpha-Fetoproteins -- genetics KW - DNA -- biosynthesis KW - Male KW - Liver -- pathology KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78879416?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-26 N1 - Date created - 1989-04-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pentostatin in hairy cell leukemia: treatment by the special exception mechanism. AN - 78870423; 2783980 AB - An analysis of the clinical outcomes in 66 patients with hairy cell leukemia treated with pentostatin under the Special Exception mechanism of the Division of Cancer Treatment, National Cancer Institute, between 1983 and 1987 has revealed a favorable balance of risk and benefit. Hematologic parameters and performance status were improved in most patients treated outside the clinical trials mechanism. The treating physicians considered 37 patients (56%) to be complete responders and 15 patients (23%) to be partial responders. Four patients (6%) died while receiving pentostatin. Life-threatening leukopenia (wbc count, less than 1,000/mm3) was reported in 24% of patients, and severe or life-threatening infection occurred in 11%. The experience gained with these patients supplements the information presently being collected from the controlled clinical trials and supports the development of a group C treatment protocol. JF - Journal of the National Cancer Institute AU - Grem, J L AU - King, S A AU - Cheson, B D AU - Leyland-Jones, B AU - Wittes, R E AD - Investigational Drug Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/03/15/ PY - 1989 DA - 1989 Mar 15 SP - 448 EP - 453 VL - 81 IS - 6 SN - 0027-8874, 0027-8874 KW - Antineoplastic Agents KW - 0 KW - Ribonucleosides KW - Coformycin KW - 11033-22-0 KW - Pentostatin KW - 395575MZO7 KW - Index Medicus KW - Aged, 80 and over KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Male KW - Female KW - Leukemia, Hairy Cell -- pathology KW - Coformycin -- adverse effects KW - Coformycin -- therapeutic use KW - Leukemia, Hairy Cell -- drug therapy KW - Ribonucleosides -- therapeutic use KW - Antineoplastic Agents -- therapeutic use KW - Coformycin -- analogs & derivatives KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78870423?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-04 N1 - Date created - 1989-04-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carbachol-induced reverse transformation of Chinese hamster ovary cells transfected with and expressing the m5 muscarinic acetylcholine receptor. AN - 78882411; 2466702 AB - Reverse transformation was induced in Chinese hamster ovary (CHO) cells transfected with and stably expressing the m5 subtype of the muscarinic acetylcholine receptor when stimulated with the muscarinic agonist, carbachol. Atropine, a muscarinic antagonist, blocked the carbachol-stimulated reverse transformation. CHO cells not transfected with the muscarinic receptor did not change with added carbachol. PMA induced reverse transformation without increasing cAMP accumulation in CHO cells. Carbachol, prostaglandin E2, and cholecystokinin increased cAMP accumulation but only carbachol caused reverse transformation. Carbachol-stimulated cAMP accumulation occurred at a higher concentration (EC50 10 microM) than did carbachol-stimulated reverse transformation (EC50 63 nM). Muscarinic m5 acetylcholine receptor transfected into CHO cells can induce reverse transformation which may be independent of cAMP. JF - FEBS letters AU - Felder, C C AU - Ma, A L AU - Conklin, B R AD - National Institute of Mental Health, Section on Pharmacology, Bethesda, MD 20892. Y1 - 1989/03/13/ PY - 1989 DA - 1989 Mar 13 SP - 75 EP - 79 VL - 245 IS - 1-2 SN - 0014-5793, 0014-5793 KW - Receptors, Muscarinic KW - 0 KW - Bucladesine KW - 63X7MBT2LQ KW - Carbachol KW - 8Y164V895Y KW - Cholecystokinin KW - 9011-97-6 KW - Cyclic AMP KW - E0399OZS9N KW - Dinoprostone KW - K7Q1JQR04M KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - 1-Methyl-3-isobutylxanthine KW - TBT296U68M KW - Index Medicus KW - Cyclic AMP -- biosynthesis KW - Animals KW - Dinoprostone -- pharmacology KW - Ovary KW - Kinetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cholecystokinin -- pharmacology KW - Bucladesine -- pharmacology KW - 1-Methyl-3-isobutylxanthine -- pharmacology KW - Female KW - Cell Line KW - Cricetinae KW - Receptors, Muscarinic -- genetics KW - Transfection KW - Cell Transformation, Neoplastic -- drug effects KW - Carbachol -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78882411?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-28 N1 - Date created - 1989-04-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antagonism of the intoxicating effects of ethanol by the potent benzodiazepine receptor ligand Ro 19-4603. AN - 76290994; 2539880 AB - The effects of the imidazothienodiazepinone Ro 19-4603 were investigated in mice. Ro 19-4603 (0.03-0.3 mg/kg) caused a dose-related reduction in seizure threshold to i.v. bicuculline. Doses of 0.1-3 mg/kg induced seizures in some but not all mice, consistent with its suggested action as a partial benzodiazepine receptor inverse agonist. Ro 19-4603 (0.01-0.3 mg/kg) attenuated the intoxicating effects of ethanol (2.4 g/kg) and was as effective as Ro 15-4513 in this respect. JF - Brain research AU - Lister, R G AU - Durcan, M J AD - Laboratory of Clinical Studies, NIAAA, Bethesda, MD 20892. Y1 - 1989/03/13/ PY - 1989 DA - 1989 Mar 13 SP - 141 EP - 144 VL - 482 IS - 1 SN - 0006-8993, 0006-8993 KW - Azepines KW - 0 KW - Convulsants KW - Receptors, GABA-A KW - Ethanol KW - 3K9958V90M KW - Ro 19-4603 KW - 99632-94-7 KW - Index Medicus KW - Seizures -- chemically induced KW - Animals KW - Dose-Response Relationship, Drug KW - Mice KW - Male KW - Azepines -- pharmacology KW - Receptors, GABA-A -- physiology KW - Ethanol -- pharmacology KW - Convulsants -- pharmacology KW - Receptors, GABA-A -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76290994?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-01 N1 - Date created - 1989-06-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Determination of the three-dimensional solution structure of the antihypertensive and antiviral protein BDS-I from the sea anemone Anemonia sulcata: a study using nuclear magnetic resonance and hybrid distance geometry-dynamical simulated annealing. AN - 78963614; 2566326 AB - The three-dimensional solution structure of the antihypertensive and antiviral protein BDS-I from the sea anemone Anemonia sulcata has been determined on the basis of 489 interproton and 24 hydrogen-bonding distance restraints supplemented by 23 phi backbone and 21 chi 1 side-chain torsion angle restraints derived from nuclear magnetic resonance (NMR) measurements. A total of 42 structures is calculated by a hybrid metric matrix distance geometry-dynamical simulated annealing approach. Both the backbone and side-chain atom positions are well defined. The average atomic rms difference between the 42 individual SA structures and the mean structure obtained by averaging their coordinates is 0.67 +/- 0.12 A for the backbone atoms and 0.90 +/- 0.17 A for all atoms. The core of the protein is formed by a triple-stranded antiparallel beta-sheet composed of residues 14-16 (strand 1), 30-34 (strand 2), and 37-41 (strand 3) with an additional mini-antiparallel beta-sheet at the N-terminus (residues 6-9). The first and second strands of the triple-stranded antiparallel beta-sheet are connected by a long exposed loop (residues 17-30). A number of side-chain interactions are discussed in light of the structure. JF - Biochemistry AU - Driscoll, P C AU - Gronenborn, A M AU - Beress, L AU - Clore, G M AD - Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1989/03/07/ PY - 1989 DA - 1989 Mar 07 SP - 2188 EP - 2198 VL - 28 IS - 5 SN - 0006-2960, 0006-2960 KW - Antihypertensive Agents KW - 0 KW - Antiviral Agents KW - BDS-I antiviral protein, Anemonia sulcata KW - Cnidarian Venoms KW - Protons KW - Index Medicus KW - Animals KW - Sea Anemones KW - Magnetic Resonance Spectroscopy -- methods KW - Models, Molecular KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Protein Conformation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78963614?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-29 N1 - Date created - 1989-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A proton nuclear magnetic resonance study of the antihypertensive and antiviral protein BDS-I from the sea anemone Anemonia sulcata: sequential and stereospecific resonance assignment and secondary structure. AN - 78961917; 2566325 AB - The sequential resonance assignment of the 1H NMR spectrum of the antihypertensive and antiviral protein BDS-I from the sea anemone Anemonia sulcata is presented. This is carried out with two-dimensional NMR techniques to identify through-bond and through-space (less than 5 A) connectivities. Added spectral complexity arises from the fact that the sample is an approximately 1:1 mixture of two BDS-I isoproteins, (Leu-18)-BDS-I and (Phe-18)-BDS-I. Complete assignments, however, are obtained, largely due to the increased resolution and sensitivity afforded at 600 MHz. In addition, the stereospecific assignment of a large number of beta-methylene protons is achieved from an analysis of the pattern of 3J alpha beta coupling constants and the relative magnitudes of intraresidue NOEs involving the NH, C alpha H, and C beta H protons. Regular secondary structure elements are deduced from a qualitative interpretation of the nuclear Overhauser enhancement, 3JHN alpha coupling constant, and amide NH exchange data. A triple-stranded antiparallel beta-sheet is found to be related to that found in partially homologous sea anemone polypeptide toxins. JF - Biochemistry AU - Driscoll, P C AU - Clore, G M AU - Beress, L AU - Gronenborn, A M AD - Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1989/03/07/ PY - 1989 DA - 1989 Mar 07 SP - 2178 EP - 2187 VL - 28 IS - 5 SN - 0006-2960, 0006-2960 KW - Antihypertensive Agents KW - 0 KW - Antiviral Agents KW - BDS-I antiviral protein, Anemonia sulcata KW - Cnidarian Venoms KW - Index Medicus KW - Animals KW - Sea Anemones KW - Magnetic Resonance Spectroscopy -- methods KW - Energy Transfer KW - Amino Acid Sequence KW - Protein Conformation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78961917?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-29 N1 - Date created - 1989-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Resistance of paraquat and adriamycin in human breast tumor cells: role of free radical formation. AN - 78887187; 2537656 AB - Generation and enhanced detoxification of toxic free radicals by glutathione peroxidase and glutathione transferase in human breast tumor cells have been suggested to play an important role in toxicity and in resistance to adriamycin. We have examined the biochemical basis of paraquat-induced free radical formation and the mechanism of resistance to this agent in human breast tumor cell lines. We have also compared the similarities and differences between adriamycin and paraquat in their mode of free radical formation and tumor cell kill. Anaerobic incubation of paraquat resulted in the formation of the paraquat cation radical in both the sensitive and resistant cells which increased with time and was enhanced by NADPH addition. Our studies show that while both adriamycin and paraquat form hydroxyl radicals (.OH) in these cell lines, adriamycin was 2-3 fold better at reducing oxygen. The formation of .OH was inhibited by exogenously added superoxide dismutase and catalase, indicating the involvement of both superoxide anion radical and hydrogen peroxide. In the adriamycin-resistant cell line, less .OH was formed by each of these drugs. While the .OH appeared to be formed outside by both adriamycin and paraquat in the drug-sensitive cells, experiments using chromium oxalate as a spin-broadening agent suggest that the drug-induced .OH formation in the resistant cells is an intracellular event. The adriamycin-resistant cell line was also cross-resistant to paraquat, suggesting a common mechanism of toxicity for both drugs. However, adriamycin was significantly more toxic (4000-times) to the sensitive cells suggesting that either other mechanisms or site-specific free radical formation are also important in biochemical mechanisms of adriamycin toxicity. JF - Biochimica et biophysica acta AU - Sinha, B K AU - Dusre, L AU - Collins, C AU - Myers, C E AD - Biochemical Pharmacology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/03/06/ PY - 1989 DA - 1989 Mar 06 SP - 304 EP - 310 VL - 1010 IS - 3 SN - 0006-3002, 0006-3002 KW - Hydroxides KW - 0 KW - Chromium KW - 0R0008Q3JB KW - Hydroxyl Radical KW - 3352-57-6 KW - Doxorubicin KW - 80168379AG KW - DNA KW - 9007-49-2 KW - Paraquat KW - PLG39H7695 KW - Daunorubicin KW - ZS7284E0ZP KW - Index Medicus KW - Breast Neoplasms -- pathology KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Daunorubicin -- metabolism KW - DNA -- metabolism KW - Chromium -- pharmacology KW - Drug Resistance KW - Female KW - Paraquat -- pharmacology KW - Paraquat -- metabolism KW - Doxorubicin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78887187?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-18 N1 - Date created - 1989-04-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential down-regulation of protein kinase C isozymes. AN - 78872099; 2917998 AB - Types I, II, and III protein kinase C have been shown to be products of, respectively, gamma, beta, and alpha genes of this enzyme family (Huang, F. L., Yoshida, Y., Nakabayashi, H., Knopf, J. L., Young, W. S., III, and Huang, K.-P. (1987) Biochem. Biophys. Res. Commun. 149, 946-952). Incubation of the highly purified rat brain protein kinase C isozymes with trypsin (kinase/trypsin (w/w) = 100) under identical conditions results in a preferential degradation of types I and II enzymes, whereas the type III enzyme was relatively resistant to tryptic proteolysis. Degradation of the type III enzyme by trypsin could be facilitated with the addition of Ca2+, phosphatidylserine, and dioleoylglycerol; none of these components alone was effective. Limited proteolysis of the three protein kinase C isozymes generated distinctive fragments for each isozyme, indicating that each isozyme has different trypsin-sensitive sites. Tryptic digestion of the type III protein kinase C was used as a model to determine the effects of various modulators on protein kinase C degradation. While Ca2+ and phosphatidylserine together were sufficient to convert the type III protein kinase C from a trypsin-insensitive to a -sensitive form, addition of dioleoylglycerol greatly reduced the Ca2+ requirement for such a conversion. Among the various phospholipids tested, in the presence of either dioleoylglycerol or phorbol ester, phosphatidylserine, cardiolipin, and phosphatidic acid were the most effective, and phosphatidylcholine and phosphatidylethanolamine were the least effective in supporting the digestion of type III protein kinase. Other acidic phospholipids, such as lysophosphatidylserine and phosphatidylinositol, were also effective in supporting the degradation in the presence of phorbol ester but not in the presence of dioleoylglycerol. The relevance of these proteolytic reactions to physiological responses was assessed with phorbol ester on rat basophilic leukemia RBL-2H3 cells, which contained both types II and III protein kinase C. Immunoblot analysis with the isozyme-specific antibodies revealed that phorbol ester induced a faster degradation of type II than that of type III isozyme in these cells. The results demonstrate that the various protein kinase C isozymes have different susceptibilities to proteolysis in vitro, when tested with trypsin, as well as to endogenous proteases in intact cells. JF - The Journal of biological chemistry AU - Huang, F L AU - Yoshida, Y AU - Cunha-Melo, J R AU - Beaven, M A AU - Huang, K P AD - Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1989/03/05/ PY - 1989 DA - 1989 Mar 05 SP - 4238 EP - 4243 VL - 264 IS - 7 SN - 0021-9258, 0021-9258 KW - Diglycerides KW - 0 KW - Isoenzymes KW - Peptide Fragments KW - Protein Kinase C KW - EC 2.7.11.13 KW - Trypsin KW - EC 3.4.21.4 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Rats KW - Animals KW - Diglycerides -- pharmacology KW - Cell Membrane -- enzymology KW - Cytosol -- enzymology KW - Peptide Fragments -- analysis KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Trypsin -- pharmacology KW - Molecular Weight KW - Protein Kinase C -- metabolism KW - Isoenzymes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78872099?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-03 N1 - Date created - 1989-04-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Divided attention, as measured by dichotic speech performance, in dementia of the Alzheimer type. AN - 85164630; pmid-2919988 AB - To determine if impaired dichotic performance in patients with dementia of the Alzheimer type is due to the inability to divide attention or the inability to perceive degraded auditory stimuli, we measured performance on tasks of both dichotic and degraded monotic speech materials. We also examined whether perception of degraded speech stimuli presented monaurally is related to abnormalities of temporal lobe anatomy and physiology, as we have shown for dichotic performance. Although the patients were impaired on both dichotic and monotic tests, significantly greater impairment was seen on the dichotic test. Our earlier finding of a significant relation between dichotic performance and measures of anterior temporal lobe atrophy and reduced glucose metabolism was replicated, but no significant relation was found between monotic tests and measures to temporal lobe integrity. We conclude that the inability to divide attention, rather than abnormal processing of degraded stimuli per se, is reflected in poor dichotic performance in patients with dementia of the Alzheimer type, and that dichotic performance, unlike degraded monotic perception, depends directly on the integrity of temporal cortex in these patients. JF - Archives of Neurology AU - Grady, C L AU - Grimes, A M AU - Patronas, N AU - Sunderland, T AU - Foster, N L AU - Rapoport, S I AD - Laboratory of Neurosciences, National Institute on Aging, Bethesda, MD 20892. PY - 1989 SP - 317 EP - 320 VL - 46 IS - 3 SN - 0003-9942, 0003-9942 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85164630?accountid=14244 LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Derivative fluorescence spectral analysis of polycyclic aromatic hydrocarbon-DNA adducts in human placenta. AN - 79591424; 2519708 AB - Metabolic activation in humans of chemical carcinogens found in the environment results in the formation of carcinogen-DNA adducts in vivo. Some polycyclic aromatic hydrocarbon-DNA adducts in human DNA can be hydrolyzed under mildly acidic conditions to yield tetrahydrotetrol derivatives which may then be detected by synchronous fluorescence spectroscopy. In an analysis of human placental DNA, second derivative spectroscopy alone was unable to resolve the synchronous fluorescent signature for r-7,t-8,t-9,c-10-tetrahydroxy-7,8,9,10-tetrahydrobenzo[alpha]pyrene from a crude extract, because a complex array of other fluorescent materials was also present. Purification of the sample by a combination of chromatographic procedures including immunoaffinity chromatography and HPLC has now been shown to yield r-7,t-8,t-9,c-10-tetrahydroxy-7,8,9,10-tetrahydrobenzo[alpha]pyrene residues from human DNA that are spectroscopically pure at the second derivative level. Immunoaffinity columns were prepared with rabbit antiserum raised against DNA that had been modified with (+/-)-r-7,t-8-dihydroxy-t-9,10-epoxy-7,8,9,10-tetrahydrobenzo[alpha]pyre ne. This antiserum has now been shown to recognize DNA samples that have been modified with six different polycyclic aromatic hydrocarbon diol epoxides and is probably only specific for a broad spectrum of polycyclic aromatic hydrocarbon-DNA adducts. Adducts were eluted from the immunoaffinity columns, hydrolyzed with acid, and extracted into isoamyl alcohol, before being subjected to high-performance liquid chromatography. These experiments reveal important limitations of second derivative fluorescence spectroscopy as a tool in the analysis of complex environmental mixtures. Furthermore, they extensively define the ability of anti-benzo[alpha]pyrenediol epoxide-DNA antibodies to recognize different types of polycyclic aromatic hydrocarbon-DNA adducts. JF - Chemical research in toxicology AU - Weston, A AU - Manchester, D K AU - Poirier, M C AU - Choi, J S AU - Trivers, G E AU - Mann, D L AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. PY - 1989 SP - 104 EP - 108 VL - 2 IS - 2 SN - 0893-228X, 0893-228X KW - Polycyclic Compounds KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Chromatography, Affinity KW - Fluorescence KW - Spectrometry, Fluorescence KW - Biotransformation KW - Humans KW - In Vitro Techniques KW - Enzyme-Linked Immunosorbent Assay KW - Female KW - Cross Reactions KW - Chromatography, High Pressure Liquid KW - Pregnancy KW - Placenta -- chemistry KW - Polycyclic Compounds -- pharmacokinetics KW - DNA -- metabolism KW - Polycyclic Compounds -- toxicity KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79591424?accountid=14244 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 - Tolerance to tumor necrosis factor. AN - 79579863; 2520273 JF - Nutrition (Burbank, Los Angeles County, Calif.) AU - Norton, J A AU - Fraker, D L AD - Surgical Metabolism Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. PY - 1989 SP - 131 EP - 135 VL - 5 IS - 2 SN - 0899-9007, 0899-9007 KW - Tumor Necrosis Factor-alpha KW - 0 KW - Index Medicus KW - Eating -- drug effects KW - Neoplasms, Experimental -- complications KW - Animals KW - Cachexia -- prevention & control KW - Drug Tolerance -- physiology KW - Humans KW - Lethal Dose 50 KW - Cachexia -- etiology KW - Shock, Septic -- prevention & control KW - Tumor Necrosis Factor-alpha -- toxicity KW - Tumor Necrosis Factor-alpha -- antagonists & inhibitors KW - Tumor Necrosis Factor-alpha -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79579863?accountid=14244 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 - Relapse and recovery in drug abuse: research and practice. AN - 79231807; 2551830 AB - Relapse and recovery are two related areas which are central to drug abuse treatment research and practice. The view of drug addiction and dependence as a chronic, relapsing disease is supported by both research and clinical experience. Recent research shows that many drug abusers have relatively short "addiction careers" and suggests that a better understanding of relapse (and its prevention) may assist treatment providers in more effectively moving clients toward recovery. JF - The International journal of the addictions AU - Leukefeld, C G AU - Tims, F M AD - Division of Clinical Research, National Institute on Drug Abuse, Rockville, Maryland 20857. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 189 EP - 201 VL - 24 IS - 3 SN - 0020-773X, 0020-773X KW - Index Medicus KW - Motivation KW - Humans KW - Recurrence KW - Aftercare KW - Substance-Related Disorders -- therapy KW - Substance-Related Disorders -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79231807?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-06 N1 - Date created - 1989-11-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Clinical metabolic studies in cancer research. AN - 79060919; 2662176 AB - Clinical metabolic studies are being used increasingly to study the role of nutrition in cancer etiology and prevention. These studies have important applications in at least five areas. The kinetics and toxicity of potential chemoprevention agents can be investigated in preparation for intervention studies. Nutrient levels proposed as compliance markers in intervention studies can be assessed under rigorous control. Potential mechanisms of action of nutrients can be evaluated. And intermediate endpoints, markers of biologic damage, can be measured before and after controlled dietary manipulations. As a result of these contributions, clinical metabolic studies are taking on a new and important role in the interdisciplinary approach to cancer research. JF - Preventive medicine AU - Taylor, P R AU - Schatzkin, A AU - Patterson, B H AU - Schiffman, M H AU - Albanes, D AD - National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 194 EP - 202 VL - 18 IS - 2 SN - 0091-7435, 0091-7435 KW - Antineoplastic Agents KW - 0 KW - Biomarkers KW - Index Medicus KW - Humans KW - Antineoplastic Agents -- pharmacokinetics KW - Antineoplastic Agents -- toxicity KW - Research Design KW - Neoplasms -- prevention & control KW - Research KW - Nutritional Physiological Phenomena KW - Neoplasms -- etiology KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79060919?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-01 N1 - Date created - 1989-08-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reduction of the intoxicating effects of ethanol by drugs acting at the benzodiazepine-GABA receptor complex. AN - 79060363; 2544902 AB - The ability of the benzodiazepine receptor partial inverse agonists Ro 15-4513, Ro 15-3505 and FG 7142, and the picrotoxin site ligands pentylenetetrazole and Ro 5-3663 to reduce ethanol-induced intoxication were investigated. Ro 15-4513 (0.3-3 mg/kg), Ro 15-3505 (3 mg/kg), pentylenetetrazole (20 and 25 mg/kg) and Ro 5-3663 (4 mg/kg) all significantly attenuated the intoxicating effects of ethanol. In contrast, FG 7142 (20 and 40 mg/kg) failed to reduce ethanol intoxication, but reversed the effect of Ro 15-4513. This pattern of results differs from that obtained using other behavioral paradigms. Since drugs which reduce the effects of GABA generally reduce the intoxicating effects of ethanol, it is suggested that the beta-carbolines may be unusual in their interaction with ethanol. JF - Pharmacology, biochemistry, and behavior AU - Durcan, M J AU - Lister, R G AD - Laboratory of Clinical Studies, NIAAA, Bethesda, MD 20892. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 667 EP - 670 VL - 32 IS - 3 SN - 0091-3057, 0091-3057 KW - Azides KW - 0 KW - Benzodiazepinones KW - Carbolines KW - Receptors, GABA-A KW - Picrotoxin KW - 124-87-8 KW - Benzodiazepines KW - 12794-10-4 KW - Ethanol KW - 3K9958V90M KW - FG 7142 KW - 60PO70N1BP KW - Ro 15-3505 KW - 78756-33-9 KW - Ro 15-4513 KW - 91917-65-6 KW - Index Medicus KW - Animals KW - Drug Interactions KW - Picrotoxin -- pharmacology KW - Azides -- pharmacology KW - Mice KW - Carbolines -- pharmacology KW - Benzodiazepinones -- pharmacology KW - Benzodiazepines -- pharmacology KW - Male KW - Receptors, GABA-A -- physiology KW - Ethanol -- toxicity KW - Receptors, GABA-A -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79060363?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-01 N1 - Date created - 1989-08-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prolonged occurrence of cocaine in human saliva and urine after chronic use. AN - 79046466; 2733393 AB - Cocaine was detected by immunoassay in saliva and urine of chronic cocaine addicts for 5-10 days during abstinence. Confirmation by a less sensitive but highly specific GC/MS assay of unmetabolized cocaine was successful in saliva through the first 24 h of collection and for the initial 4-5 days in urine. Cocaine saliva concentrations and subject scores for cocaine craving and depression declined during this time and correlated significantly. The presence of unmetabolized cocaine in these biofluids long after the last drug administration suggests that multiple dosing and high exposure to cocaine in man leads to accumulation in deep body compartments and subsequent slow release back into circulation and eventual excretion. The prolonged presence of cocaine in saliva and urine may have implications in testing for cocaine use and in treatment of cocaine withdrawal. JF - Journal of analytical toxicology AU - Cone, E J AU - Weddington, W W AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland 21224. PY - 1989 SP - 65 EP - 68 VL - 13 IS - 2 SN - 0146-4760, 0146-4760 KW - benzoylecgonine KW - 5353I8I6YS KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Humans KW - Adult KW - Time Factors KW - Male KW - Cocaine -- analysis KW - Cocaine -- analogs & derivatives KW - Cocaine -- urine KW - Saliva -- analysis KW - Cocaine -- pharmacokinetics KW - Substance-Related Disorders -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79046466?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-27 N1 - Date created - 1989-07-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mortality among forest and soil conservationists. AN - 78935581; 2930251 AB - The mortality of forest conservationists and soil conservationists in the United States Department of Agriculture (USDA) who died during January 1, 1970-December 31, 1979 (N = 1,411 white males) while actively employed or while receiving a pension was evaluated. The proportionate mortality analysis was used to identify cancers that might be elevated in this occupational group compared to the total U.S. white male population, whereas case-control analyses more rigorously evaluated the disease association with occupation. Controls were selected from employees at USDA who died of any cause of death other than that cause of death represented by the case. In case-control analyses, non-Hodgkin's lymphoma (NHL) and colon cancer demonstrated a statistically significant linear trend (p less than .05) with duration of employment as either a forest or soil conservationist, which suggests an occupational etiology for both diseases. Soil conservationists who were last employed after 1960 experienced significantly elevated risks for NHL (OR = 2.6) and colon cancer (OR = 1.8), whereas those last employed before 1960 were not at an increased risk. Among forest conservationists, the risk for both NHL and colon cancer appeared to be elevated before and after 1960. JF - Archives of environmental health AU - Alavanja, M C AU - Blair, A AU - Merkle, S AU - Teske, J AU - Eaton, B AU - Reed, B AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland. PY - 1989 SP - 94 EP - 101 VL - 44 IS - 2 SN - 0003-9896, 0003-9896 KW - Abridged Index Medicus KW - Index Medicus KW - United States KW - Kidney Neoplasms -- mortality KW - Risk KW - Lymphoma, Non-Hodgkin -- mortality KW - Humans KW - Colonic Neoplasms -- mortality KW - Male KW - Neoplasms -- mortality KW - Occupational Diseases -- mortality KW - Conservation of Natural Resources UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78935581?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-03 N1 - Date created - 1989-05-03 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - Additive and multiplicative models and multistage carcinogenesis theory. AN - 78930882; 2710973 AB - In light of the Armitage-Doll multistage carcinogenesis theory, this paper examines the assumption that an additive relative risk relationship is indicative of two carcinogens that affect the same stage in the cancer process. We present formulas to compute excess cancer risks for a variety of patterns for limited exposure durations to two carcinogens that affect the first and penultimate stages; and using an index of synergy proposed by Thomas (1982), we find a number of these patterns to produce additive, or nearly additive, relative risk relationships. The consistent feature of these patterns is that the two exposure periods are of short duration and occur close together. JF - Risk analysis : an official publication of the Society for Risk Analysis AU - Brown, C C AU - Chu, K C AD - Biometry Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 99 EP - 105 VL - 9 IS - 1 SN - 0272-4332, 0272-4332 KW - Carcinogens, Environmental KW - 0 KW - Index Medicus KW - Risk KW - Epidemiologic Methods KW - Humans KW - Time Factors KW - Cocarcinogenesis KW - Carcinogens, Environmental -- adverse effects KW - Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78930882?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-30 N1 - Date created - 1989-05-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of supF, an Escherichia coli tyrosine suppressor tRNA gene, as a mutagenic target in shuttle-vector plasmids. AN - 78926453; 2494447 AB - The Escherichia coli tyrosine amber suppressor tRNA gene, supF, has been utilized as a mutagenic target in several shuttle-vector plasmids. Data on mutagenic inactivation of suppressor activity was obtained from induced mutagenesis experiments with plasmids pZ189 and p3AC, and from studies on alterations of the supF gene transduced into E. coli. 162 single or tandem base-substitution mutations that reduce or eliminate suppressor activity were identified at 86 sites within 158 base pairs. The 2 transition and 4 transversion mutations possible in double-stranded DNA were all detectable. At 56 sites two different inactivating mutations were found; and at 20 sites all 3 possible base substitution mutations inactivated suppressor function. Most of the mutations were clustered within the mature tRNA region: 144 of the base-substitution mutations were found at 74 sites within the 85-bp mature tRNA region. Insertions of 1 or 2 bases at 4 sites and deletions of 1 to 3 bases at 15 sites were found to inactivate supF function. A few silent mutations which do not inactivate suppressor function were found: single base-substitutions at 4 sites, 14 pairs of silent double mutations, and a large deletion including the promoter region. The supF gene is thus an extremely sensitive target for mutagenic inactivation in shuttle-vector plasmids. JF - Mutation research AU - Kraemer, K H AU - Seidman, M M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. PY - 1989 SP - 61 EP - 72 VL - 220 IS - 2-3 SN - 0027-5107, 0027-5107 KW - RNA, Transfer, Amino Acid-Specific KW - 0 KW - RNA, Transfer, Tyr KW - beta-Galactosidase KW - EC 3.2.1.23 KW - Index Medicus KW - Genes, Bacterial KW - Base Sequence KW - Molecular Sequence Data KW - Escherichia coli -- genetics KW - beta-Galactosidase -- genetics KW - Structure-Activity Relationship KW - RNA, Transfer, Tyr -- genetics KW - Mutagenicity Tests -- methods KW - Genetic Vectors KW - RNA, Transfer, Amino Acid-Specific -- genetics KW - Suppression, Genetic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78926453?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-10 N1 - Date created - 1989-05-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular analysis of spontaneous mutations at the gpt locus in Chinese hamster ovary (AS52) cells. AN - 78923628; 2494446 AB - AS52 cells are Chinese hamster ovary (CHO) cells that carry a single functional copy of the bacterial gpt gene and allow the isolation of 6-thioguanine-resistant (6TGr)mutants arising from mutation at the chromosally integrated gpt locus. The gpt locus in AS52 cells is extremely stable, giving rise to 6TGr mutants at frequencies comparable to the endogenous CHO hprt locus. In this study, we describe the spectrum of spontaneous mutations observed in AS52 cells by Southern blot and DNA sequence analyses. Using the polymerase chain reaction (PCR) and the Thermus aquaticus (Taq) polymerase, we have enzymatically amplified 6TGr mutant gpt sequences in vitro. The PCR product was then sequenced without further cloning manipulations to directly identify gpt structural gene mutations. Deletions predominant among the 62 spontaneous 6TGr-AS52 mutant clones analyzed in this study. Of these, 79% (49/62) of the mutations were identified as deletions either by Southern blotting, PCR amplification or DNA sequence analysis. Among these deletions is a predominant 3-base deletion that was observed in 31% (19/62) of the mutants. These data provide a basis for future comparisons of induced point mutational spectra derived in the AS52 cell line, and demonstrate the utility of PCR in the generation of DNA sequence spectra derived from chromosomally integrated mammalian loci. JF - Mutation research AU - Tindall, K R AU - Stankowski, L F AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1989 SP - 241 EP - 253 VL - 220 IS - 2-3 SN - 0027-5107, 0027-5107 KW - Pentosyltransferases KW - EC 2.4.2.- KW - Hypoxanthine Phosphoribosyltransferase KW - EC 2.4.2.8 KW - Thioguanine KW - FTK8U1GZNX KW - Index Medicus KW - Animals KW - Thioguanine -- toxicity KW - Base Sequence KW - Cricetulus KW - Blotting, Southern KW - Cell Line KW - Gene Amplification KW - Cricetinae KW - Pentosyltransferases -- genetics KW - Mutagenicity Tests -- methods KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78923628?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-10 N1 - Date created - 1989-05-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Studies on direct and indirect effects of DNA damage on mutagenesis in monkey cells using an SV40-based shuttle vector. AN - 78916827; 2538742 AB - We are using an SV40-based shuttle vector, pZ189, to study mechanisms of mutagenesis in mammalian cells. The vector can be treated with mutagens in vitro and replicated in animal cells; resulting mutants can be selected and amplified in bacteria for DNA sequencing. This versatile vector system has allowed us to explore several different questions relating to the mutagenic process. We have studied the direct effects of template damage caused by UV or benzo[a]pyrene diolepoxide by treating vector DNA with these agents and then replicating the damaged DNA in monkey cells. Mutational mechanisms were deduced from the spectrum of mutations induced in the supF target gene of the vector DNA. To study the role of indirect effects of DNA damage on mutagenesis in mammalian cells, we have treated the cells and the vector DNA separately with DNA-damaging agents. We find that pretreatment of cells with DNA-damaging agents, or with conditioned medium from damaged cells, causes an enhancement of mutagenesis of a UV-damaged vector. Thus, DNA damage can act indirectly to enhance the mutagenic process. We also have preliminary evidence that pZ189 can be used in an in vitro DNA replication system to study the process of mutation fixation on the biochemical level. We believe that the pZ189 vector will prove to be as useful for in vitro studies of mutational mechanisms as it has been for in vivo studies. JF - Mutation research AU - Dixon, K AU - Roilides, E AU - Hauser, J AU - Levine, A S AD - Section on Viruses and Cellular Biology, National Institute of Child Health and Human Development, Bethesda, MD 20892. PY - 1989 SP - 73 EP - 82 VL - 220 IS - 2-3 SN - 0027-5107, 0027-5107 KW - Mitomycins KW - 0 KW - RNA, Transfer, Tyr KW - Mitomycin KW - 50SG953SK6 KW - 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide KW - 55097-80-8 KW - Index Medicus KW - Animals KW - Ultraviolet Rays KW - Escherichia coli -- genetics KW - Haplorhini KW - Base Sequence KW - Cells, Cultured KW - Molecular Sequence Data KW - Suppression, Genetic KW - Mitomycins -- pharmacology KW - DNA Replication KW - Mutagenicity Tests -- methods KW - DNA Damage KW - Simian virus 40 -- genetics KW - Genetic Vectors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78916827?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-10 N1 - Date created - 1989-05-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Optimal two-stage designs for phase II clinical trials. AN - 78916793; 2702835 AB - The primary objective of a phase II clinical trial of a new drug or regimen is to determine whether it has sufficient biological activity against the disease under study to warrant more extensive development. Such trials are often conducted in a multi-institution setting where designs of more than two stages are difficult to manage. This paper presents two-stage designs that are optimal in the sense that the expected sample size is minimized if the regimen has low activity subject to constraints upon the size of the type 1 and type 2 errors. Two-stage designs which minimize the maximum sample size are also determined. Optimum and "minimax" designs for a range of design parameters are tabulated. These designs can also be used for pilot studies of new regimens where toxicity is the endpoint of interest. JF - Controlled clinical trials AU - Simon, R AD - Biometric Research Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 1 EP - 10 VL - 10 IS - 1 SN - 0197-2456, 0197-2456 KW - Index Medicus KW - Humans KW - Statistics as Topic KW - Neoplasms -- drug therapy KW - Drug Evaluation -- methods KW - Research Design UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78916793?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-12 N1 - Date created - 1989-05-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of differential drug uptake, efflux, and binding of etoposide in sensitive and resistant human tumor cell lines: implications for the mechanisms of drug resistance. AN - 78915429; 2564628 AB - In order to study the mechanism of etoposide (VP-16) resistance in human tumor cells and to assess the role of P-170 glycoprotein in VP-16 accumulation, we have examined the uptake and efflux of VP-16 in both sensitive and multidrug-resistant MCF-7 human breast and HL60 human promyelocytic leukemia cells. The drug-resistant cells, MCF-7/ADR and HL60/ADR, were selected for resistance to adriamycin and were 200- to 250-fold resistant to VP-16. Whereas MCF-7/ADR cells overexpress the P-170 glycoprotein and show the multidrug-resistant phenotype, HL60/ADR cells do not overexpress the P-170 glycoprotein. Although there was a 2-fold decrease in accumulation of VP-16 in MCF-7/ADR cells, this decrease did not correlate with a 250-fold resistance to the drug. VP-16 efflux was rapid and almost complete from MCF-7 cell lines and it was decreased at 4 degrees. Further, there was a significant increase in VP-16 accumulation in the MCF-7/ADR cells in the presence of glucose-free medium supplemented with sodium azide. However, no change in the pattern of VP-16 efflux was observed. Under these conditions, addition of glucose caused release of VP-16 from MCF-7/ADR cells, suggesting energy-dependent modifications in the drug binding. Coincubation of vincristine with VP-16 also increased the drug accumulation and decreased the rate of efflux of VP-16 in both sensitive and resistant MCF-7 cells, suggesting that vincristine and VP-16 may compete for similar binding and efflux mechanisms in these cell lines. In contrast, daunorubicin increased VP-16 accumulation only in the sensitive MCF-7 cell line, whereas the efflux rate of VP-16 was not significantly changed in either cell line. HL60 sensitive cells accumulated 4- to 5-fold more VP-16 than the resistant subline. Both sensitive and resistant cells showed an important noneffluxable pool of the drug, 3-fold larger for sensitive cells (79 +/- 12 versus 25 +/- 2 pmol of VP-16/mg of protein, for sensitive and resistant cells, respectively). The efflux of VP-16 was temperature dependent only in sensitive cells. VP-16 accumulation in HL60/ADR cells was increased in glucose-free medium supplemented with sodium azide; however, the noneffluxable pool of VP-16 was not significantly changed. In contrast, although these conditions had no effect on the drug accumulation in the parental line, they caused a decrease in the noneffluxable pool of VP-16, suggesting an energy-dependent binding and retention of VP-16.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Molecular pharmacology AU - Politi, P M AU - Sinha, B K AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 271 EP - 278 VL - 35 IS - 3 SN - 0026-895X, 0026-895X KW - Azides KW - 0 KW - Membrane Glycoproteins KW - P-Glycoprotein KW - Vincristine KW - 5J49Q6B70F KW - Etoposide KW - 6PLQ3CP4P3 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Sodium Azide KW - 968JJ8C9DV KW - Index Medicus KW - Membrane Glycoproteins -- physiology KW - Tumor Cells, Cultured -- drug effects KW - Dose-Response Relationship, Drug KW - Humans KW - Vincristine -- pharmacology KW - Azides -- pharmacology KW - Adenosine Triphosphate -- analysis KW - Female KW - Etoposide -- pharmacology KW - Etoposide -- pharmacokinetics KW - Leukemia, Promyelocytic, Acute -- metabolism KW - Drug Resistance KW - Breast Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78915429?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-26 N1 - Date created - 1989-04-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interleukin 1 potentiates the secretion of beta-endorphin induced by secretagogues in a mouse pituitary cell line (AtT-20). AN - 78904479; 2538829 AB - Previous work has shown that corticotropin releasing factor, vasoactive intestinal peptide, phorbol ester, and forskolin cause the secretion of adrenocorticotropic hormone and beta-endorphin from the AtT-20 mouse pituitary cell line. Human recombinant interleukin 1 alpha and 1 beta also stimulated adrenocorticotropic hormone and beta-endorphin secretion from AtT-20 cells in a time- and dose-related manner. The effect appeared only after pretreatment with interleukin 1 (IL-1) for at least 18 hr and was maximum at 24 hr. After pretreatment of the cells over a period of time with IL-1, the secretion induced by corticotropin releasing factor and vasoactive intestinal peptide was increased in more than an additive manner. The enhancement of corticotropin releasing factor-induced beta-endorphin release produced by IL-1 was apparent after 12 hr and reached a maximum at 24 hr. IL-1 did not affect forskolin-induced cAMP generation but enhanced the effect of forskolin on beta-endorphin secretion. This suggests that IL-1 does not induce adenylate cyclase and that forskolin causes the secretion of beta-endorphin by a mechanism independent of cAMP. IL-1 enhanced phorbol ester-induced beta-endorphin secretion. After prolonged treatment with phorbol ester (an activator of protein kinase C), the secretion induced by phorbol ester was abolished as well as the enhancement induced by IL-1. However, prolonged treatment with phorbol ester had no effect on IL-1-induced beta-endorphin secretion. These observations suggest that IL-1 enhances peptide-generated secretion of beta-endorphin by inducing protein kinase C. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Făgăraşan, M O AU - Eskay, R AU - Axelrod, J AD - National Institute on Alcohol Abuse and Alcoholism, Laboratory of Metabolism and Molecular Biology, Bethesda, MD 20892. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 2070 EP - 2073 VL - 86 IS - 6 SN - 0027-8424, 0027-8424 KW - Interleukin-1 KW - 0 KW - Recombinant Proteins KW - Colforsin KW - 1F7A44V6OU KW - Vasoactive Intestinal Peptide KW - 37221-79-7 KW - beta-Endorphin KW - 60617-12-1 KW - Corticotropin-Releasing Hormone KW - 9015-71-8 KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Vasoactive Intestinal Peptide -- pharmacology KW - Animals KW - Cyclic AMP -- biosynthesis KW - Recombinant Proteins -- pharmacology KW - Mice KW - Pituitary Neoplasms KW - Corticotropin-Releasing Hormone -- pharmacology KW - Protein Kinase C -- metabolism KW - Colforsin -- pharmacology KW - Tumor Cells, Cultured KW - Kinetics KW - Enzyme Activation -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Drug Synergism KW - Interleukin-1 -- pharmacology KW - beta-Endorphin -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78904479?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-28 N1 - Date created - 1989-04-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biol Reprod. 1980 May;22(4):955-63 [6249409] J Immunol. 1986 Jun 15;136(12):4509-14 [2940296] Proc Natl Acad Sci U S A. 1981 Jun;78(6):3363-7 [6267587] Biochem Biophys Res Commun. 1982 Jun 30;106(4):1364-71 [6288045] Endocrinology. 1983 Feb;112(2):550-7 [6129133] J Biol Chem. 1983 Mar 10;258(5):2875-81 [6298209] J Neurosci. 1983 Apr;3(4):725-32 [6300355] Science. 1984 May 4;224(4648):452-9 [6143403] J Neurochem. 1984 Jun;42(6):1659-66 [6144727] Endocrinology. 1985 Oct;117(4):1389-96 [2992912] Science. 1985 Nov 29;230(4729):1035-7 [2997929] Endocrinology. 1986 Jan;118(1):212-7 [3000734] Science. 1986 Aug 8;233(4764):652-4 [3014662] Neurosci Lett. 1987 Jul 22;78(2):211-6 [2442676] Endocrinology. 1987 Oct;121(4):1580-2 [2820704] Proc Natl Acad Sci U S A. 1988 Sep;85(17):6306-9 [2901097] J Biol Chem. 1988 Nov 5;263(31):15876-9 [2846527] Neuroendocrinology. 1988 Aug;48(2):160-6 [2851750] Science. 1987 Oct 23;238(4826):519-21 [2821620] Science. 1987 Oct 23;238(4826):522-4 [2821621] Science. 1987 Oct 23;238(4826):524-6 [2443979] FASEB J. 1988 Feb;2(2):108-15 [3277884] Proc Natl Acad Sci U S A. 1988 Aug;85(15):5556-60 [2899892] Arch Biochem Biophys. 1980 Aug;203(1):37-48 [6250490] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Control of growth and squamous differentiation in normal human bronchial epithelial cells by chemical and biological modifiers and transferred genes. AN - 78897806; 2538323 AB - The majority of human lung cancers arise from bronchial epithelial cells. The normal pseudostratified bronchial epithelium is composed of basal, mucous, and ciliated cells. This multi-differentiated epithelium usually responds to xenobiotics and physical injury by undergoing basal cell hyperplasia, mucous cell hyperplasia, and squamous metaplasia. One step of the multistage process of carcinogenesis is thought to involve aberrations in control of the squamous metaplastic processes. Decreased responsiveness to regulators of terminal squamous differentiation may confer a selective clonal expansion advantage to an initiated cell. We studied the effects of endogenous [e.g., transforming growth factor beta 1 (TGF-beta 1) and serum] and exogenous [e.g., 12-O-tetradecanoyl-13-phorbol-acetate (TPA), tobacco smoke condensate, and aldehydes] modifiers of normal human bronchial epithelial (NHBE) cell in a serum-free culture system. NHBE cells are growth inhibited by all of these compounds and induced to undergo squamous differentiation by TGF-beta 1 or TPA. In contrast, lung carcinoma cell lines are relatively resistant to inducers of terminal squamous differentiation which may provide them with a selective growth advantage. Chemical agents and activated protooncogenes (ras,raf,myc) altered the response to endogenous and exogenous inducers of squamous differentiation and caused extended cellular lifespan, aneuploidy, and/or tumorigenicity. The data suggest a close relationship between dysregulation of terminal differentiation pathways and neoplastic transformation of human bronchial epithelial cells. JF - Environmental health perspectives AU - Pfeifer, A M AU - Lechner, J F AU - Masui, T AU - Reddel, R R AU - Mark, G E AU - Harris, C C AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 209 EP - 220 VL - 80 SN - 0091-6765, 0091-6765 KW - Smoke KW - 0 KW - nickel sulfate KW - 4FLT4T3WUN KW - Transforming Growth Factors KW - 76057-06-2 KW - Nickel KW - 7OV03QG267 KW - Cyclic AMP KW - E0399OZS9N KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Humans KW - Cyclic AMP -- physiology KW - Proto-Oncogenes KW - Transforming Growth Factors -- physiology KW - Epithelial Cells KW - Cells, Cultured KW - Nickel -- pharmacology KW - Transfection KW - In Vitro Techniques KW - Calcium -- physiology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Division KW - Bronchi -- cytology KW - Cell Differentiation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78897806?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-10 N1 - Date created - 1989-05-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Immunol. 1985 May;134(5):3120-3 [3920313] Mol Cell Biol. 1987 Mar;7(3):1171-9 [3561413] Anticancer Res. 1987 Jan-Feb;7(1):1-12 [3032070] Blood. 1987 May;69(5):1542-5 [3105625] Cancer Res. 1987 Jun 1;47(11):2950-4 [3471320] Cell. 1987 May 22;49(4):437-8 [3471351] J Cell Biochem. 1987 Mar;33(3):213-24 [3553218] J Clin Invest. 1987 Jun;79(6):1629-34 [3034978] Nature. 1987 May 28-Jun 3;327(6120):293-7 [3587348] Mol Cell Biol. 1987 May;7(5):2031-4 [3037341] Gan To Kagaku Ryoho. 1987 Jun;14(6 Pt 2):2140-6 [3300556] Cancer Res. 1987 Aug 15;47(16):4386-90 [2886219] Proc Natl Acad Sci U S A. 1987 Aug;84(16):5923-7 [3112776] Science. 1987 Aug 28;237(4818):1039-41 [3616625] J Cell Biol. 1987 Aug;105(2):965-75 [2887577] J Cell Biol. 1978 Mar;76(3):705-11 [24643] Cancer Res. 1979 Mar;39(3):1008-13 [427740] J Supramol Struct. 1979;11(1):79-93 [522485] Cell. 1980 Apr;19(4):1025-32 [7379122] Cell Biol Int Rep. 1980 Jan;4(1):23-8 [6446408] Anal Biochem. 1980 Mar 1;102(2):255-70 [6999941] Cell. 1980 Nov;22(2 Pt 2):629-32 [6160916] Exp Cell Res. 1980 Dec;130(2):474-7 [7449865] Proc Natl Acad Sci U S A. 1986 Feb;83(4):1092-6 [2869482] Clin Physiol Biochem. 1986;4(1):99-111 [3514058] J Cell Biol. 1986 May;102(5):1955-64 [2422182] J Cell Biochem. 1986;30(3):195-218 [3084503] Proc Natl Acad Sci U S A. 1986 Apr;83(8):2438-42 [2871553] Carcinogenesis. 1986 Jun;7(6):937-42 [2423264] Cell. 1986 Jul 18;46(2):301-9 [3459590] Science. 1986 Jul 25;233(4762):461-4 [3014659] Science. 1986 Aug 1;233(4763):532-4 [3487831] Cancer Res. 1986 Sep;46(9):4665-71 [3089593] In Vitro Cell Dev Biol. 1986 Jul;22(7):423-8 [2426243] Proc Natl Acad Sci U S A. 1986 Aug;83(15):5539-43 [3526333] J Cell Physiol Suppl. 1986;4:73-81 [3528185] In Vitro Cell Dev Biol. 1986 Jun;22(6):332-6 [3759789] Exp Cell Res. 1986 Dec;167(2):539-49 [3464447] Carcinogenesis. 1986 Dec;7(12):2033-9 [3779897] J Natl Cancer Inst. 1986 Dec;77(6):1187-95 [3467112] Mol Cell Biol. 1986 Dec;6(12):4214-20 [3540608] Science. 1987 Jan 16;235(4786):305-11 [3541204] Cancer Res. 1987 Feb 1;47(3):707-12 [3467839] Cell. 1987 Jan 30;48(2):251-60 [3026638] Cell. 1987 Feb 13;48(3):417-28 [2879636] J Natl Cancer Inst. 1987 Mar;78(3):419-23 [3469455] Cancer Res. 1987 Apr 15;47(8):2045-9 [3828994] Carcinogenesis. 1984 Feb;5(2):209-15 [6421503] Differentiation. 1984;25(3):229-37 [6698333] Cell. 1984 Jul;37(3):1053-62 [6331674] Proc Natl Acad Sci U S A. 1984 Sep;81(17):5435-9 [6591199] Cancer Res. 1984 Nov;44(11):5124-6 [6488172] Proc Natl Acad Sci U S A. 1984 Nov;81(21):6757-61 [6208555] Science. 1984 Nov 9;226(4675):705-7 [6093254] In Vitro. 1984 Aug;20(8):652-62 [6500605] Science. 1985 Jan 25;227(4685):375-81 [2981433] Nature. 1985 Jan 31-Feb 6;313(6001):404-6 [3855502] Proc Natl Acad Sci U S A. 1985 Feb;82(3):815-9 [3156372] Science. 1985 Mar 8;227(4691):1174-9 [3975607] Science. 1981 Mar 27;211(4489):1452-4 [6970413] Nature. 1981 Apr 2;290(5805):411-3 [6261139] Nature. 1981 Sep 3;293(5827):72-4 [6791032] Exp Cell Res. 1982 Jan;137(1):155-67 [6173242] J Cell Physiol. 1982 Feb;110(2):219-29 [7040427] Carcinogenesis. 1982;3(5):525-31 [6178528] Nature. 1982 Oct 14;299(5884):640-4 [6289129] Cancer Res. 1982 Dec;42(12):5139-46 [6291749] In Vitro. 1982 Jul;18(7):633-42 [7141447] Nature. 1983 Jun 30;303(5920):775-9 [6866079] Nature. 1983 Jul 7-13;304(5921):35-9 [6306471] Environ Health Perspect. 1983 Apr;50:247-57 [6409604] J Cell Biol. 1983 Oct;97(4):1179-90 [6137487] Cancer Res. 1983 Dec;43(12 Pt 1):5915-21 [6640540] Carcinogenesis. 1984 Jan;5(1):109-12 [6606503] Nature. 1984 Feb 9-15;307(5951):521-7 [6320011] Cancer Res. 1985 Jun;45(6):2522-6 [3986791] Cancer Res. 1985 Jun;45(6):2748-52 [3921248] Carcinog Compr Surv. 1985;8:159-71 [3986819] Cell. 1985 Jul;41(3):665-76 [2408759] In Vitro Cell Dev Biol. 1985 Feb;21(2):99-107 [4040133] Carcinogenesis. 1985 Jul;6(7):1011-5 [2410159] Mol Cell Biol. 1985 Jun;5(6):1400-7 [2993863] Nature. 1985 Aug 22-28;316(6030):701-5 [3861940] Nature. 1985 Aug 29-Sep 4;316(6031):823-6 [2993906] J Cell Physiol. 1985 Aug;124(2):207-12 [2995414] J Cell Physiol. 1985 Oct;125(1):82-90 [3900103] Nature. 1985 Nov 7-13;318(6041):69-73 [2997622] Proc Natl Acad Sci U S A. 1985 Nov;82(21):7330-4 [2997786] Br J Cancer. 1985 Oct;52(4):479-93 [2415144] Carcinogenesis. 1985 Dec;6(12):1755-9 [4064250] Proc R Soc Lond B Biol Sci. 1985 Oct 22;226(1242):107-19 [2866518] Cancer Res. 1986 Feb;46(2):583-7 [3606750] Nature. 1985 Dec 19-1986 Jan 1;318(6047):667-70 [4079980] Cancer Res. 1986 Mar;46(3):1465-70 [3510727] Cancer Res. 1986 Mar;46(3):1530-4 [3002619] Nucleic Acids Res. 1986 Jan 24;14(2):843-52 [3945555] J Natl Cancer Inst. 1986 Mar;76(3):363-70 [3005742] Nature. 1986 Feb 20-26;319(6055):680-2 [3005866] Nature. 1986 Mar 13-19;320(6058):134-9 [3754034] Cancer Res. 1987 Apr 15;47(8):2148-55 [3030544] J Cell Physiol. 1987 Mar;130(3):397-409 [3494020] N Engl J Med. 1987 Oct 8;317(15):929-35 [3041218] J Biol Chem. 1987 Oct 15;262(29):14090-9 [2443501] Science. 1987 Oct 23;238(4826):533-6 [2821623] Cell. 1987 Nov 20;51(4):513-4 [3119222] Mol Cell Biol. 1987 Nov;7(11):4017-23 [2828924] Cancer Res. 1988 Apr 1;48(7):1904-9 [2450641] Adv Biochem Psychopharmacol. 1988;44:45-55 [3041752] Somat Cell Mol Genet. 1987 Jul;13(4):429-40 [3331832] Differentiation. 1988 Jun;38(1):60-6 [2846394] Science. 1985 Apr 5;228(4695):89-91 [3975633] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Free radical intermediates during peroxidase oxidation of 2-t-butyl-4-methoxyphenol, 2,6-di-t-butyl-4-methylphenol, and related phenol compounds. AN - 78894130; 2537599 AB - 2-t-butyl-4-methoxyphenol (BHA) and 2,6-di-t-butyl-4-methylphenol (BHT) are widely used antioxidant food additives that are generally recognized as safe by the Food and Drug Administration. Previously reported studies have suggested that the ip LD50 of BHA may be as much as 2 orders of magnitude lower than its oral LD50. Metabolic activation of BHA to reactive intermediates possibly may be responsible for this result and may be related to other reported toxic effects. BHT has been reported to cause haemorrhagic lung damage and possible hepatocarcinogenicity in test animals. The present studies report investigations by electron spin resonance spectroscopy of free radical metabolites of BHA, BHT and related compounds. The primary, unstable phenoxy free radical of BHA has been generated by oxidation with horseradish peroxidase and hydrogen peroxide and detected by ESR spectroscopy. A scheme has been proposed for the peroxidatic oxidation of BHA. The ESR spectrum of the di-BHA dimer, one product of BHA oxidation, has been observed, analyzed, and reported. ESR studies have been extended to other phenol derivatives structurally related to BHA and suspected to be substrates for peroxidase. Similarly it has been found that BHT and structurally related phenols are substrates for peroxidation by horseradish peroxidase and hydrogen peroxide. In agreement with previous chemical and biochemical studies, it has been found that ortho-disubstituted phenols are oxidized to more stable phenoxy radicals than are ortho-monosubstituted phenols. The ESR hyperfine coupling constants for the phenoxy radicals studied are in agreement with those for similar radicals produced by chemical oxidation. Attention has been drawn to the biochemical and toxicological implications of these and related studies of BHA and BHT peroxidation. JF - Archives of biochemistry and biophysics AU - Valoti, M AU - Sipe, H J AU - Sgaragli, G AU - Mason, R P AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 423 EP - 432 VL - 269 IS - 2 SN - 0003-9861, 0003-9861 KW - Antioxidants KW - 0 KW - Free Radicals KW - Phenols KW - Butylated Hydroxytoluene KW - 1P9D0Z171K KW - Horseradish Peroxidase KW - EC 1.11.1.- KW - Peroxidases KW - 2-tert-butyl-4-methylphenol KW - Y9VVU7G7J4 KW - Index Medicus KW - Electron Spin Resonance Spectroscopy KW - Structure-Activity Relationship KW - Butylated Hydroxytoluene -- analogs & derivatives KW - Peroxidases -- metabolism KW - Horseradish Peroxidase -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78894130?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-28 N1 - Date created - 1989-03-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Relationship of oxidative damage to the hepatocarcinogenicity of the peroxisome proliferators di(2-ethylhexyl)phthalate and Wy-14,643. AN - 78894090; 2924396 AB - Quantitative comparisons of the time course of biochemical and morphological changes induced by peroxisome proliferators resulting in low and high incidences of hepatic cancer have not been conducted previously under bioassay conditions. [4-Chloro-6-(2,3-xylidino)-2-pyrimidyl-thio]acetic acid (Wy-14,643) at 0.1% in the diet produced a much higher incidence of hepatic cancer in male rats than 1.2% di(2-ethylhexyl)phthalate (DEHP) in the diet. Both diets, however, caused similar degrees of peroxisome proliferation. To investigate this difference in carcinogenicity, H2O2-detoxification mechanisms and indices of oxidative damage were evaluated in male F-344 rats fed 1.2% DEHP or 0.1% Wy-14,643 for up to one year. DEHP or Wy-14,643 treatment increased hepatic catalase activity approximately 25% from 8 to 365 days. DEHP or Wy-14,643 treatment decreased hepatic glutathione peroxidase activity by 50% from 8 to 365 days. Glutathione concentrations were not affected by 151 days of DEHP or Wy-14,643 feeding. The similar effects of DEHP and Wy on H2O2 detoxification enzymes and glutathione concentrations suggests that these factors are not responsible for the widely different carcinogenicities of Wy-14,643 and DEHP. Hepatic vitamin E concentrations were 50% lower in rats receiving Wy-14,643 for 151 days as compared to rats fed DEHP or control diets. Lipofuscin, which was contained within lysosomes, was increased 3-fold after 39 days of DEHP and remained at this level up to 365 days of treatment. In comparison, lipofuscin was increased 4-fold after 18 days of Wy-14,643 and continued to accumulate in a linear manner reaching values 30-fold over controls after 365 days of treatment. DEHP treatment for 39-365 days increased the activities of the lysosomal enzymes alpha-fucosidase, beta-galactosidase and N-acetylglucosaminidase 50-100%. The same enzyme activities were increased approximately 4-fold after 39-365 days of Wy-14,643. Lysosomal cathepsin B activity was unchanged by DEHP but doubled by 151 and 365 days of Wy-14,643. Acid phosphatase activity was unchanged by DEHP but increased by 50% after 151 and 365 days of Wy-14,643. In addition, conjugated dienes were increased (approximately 45%) only in rats receiving Wy-14,643 for 151 and 365 days. These data show for the first time that the magnitude and time course of lipofuscin deposition, induction of lysosomal enzymes and conjugated diene accumulation, is correlated closely with the degree of carcinogenicity. Wy-14,643-induced decreases in hepatic vitamin E concentrations could contribute to the observed accumulation of conjugated dienes at later time points.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Carcinogenesis AU - Conway, J G AU - Tomaszewski, K E AU - Olson, M J AU - Cattley, R C AU - Marsman, D S AU - Popp, J A AD - Chemical Industry Institute of Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 513 EP - 519 VL - 10 IS - 3 SN - 0143-3334, 0143-3334 KW - Anticholesteremic Agents KW - 0 KW - Lipofuscin KW - Phthalic Acids KW - Pyrimidines KW - Vitamin E KW - 1406-18-4 KW - pirinixic acid KW - 86C4MRT55A KW - Hydrogen Peroxide KW - BBX060AN9V KW - Diethylhexyl Phthalate KW - C42K0PH13C KW - Index Medicus KW - Rats KW - Oxidation-Reduction KW - Animals KW - Rats, Inbred F344 KW - Enzyme Induction -- drug effects KW - Hydrogen Peroxide -- metabolism KW - Cell Division -- drug effects KW - Lysosomes -- enzymology KW - Vitamin E -- physiology KW - Male KW - Lipofuscin -- metabolism KW - Pyrimidines -- toxicity KW - Diethylhexyl Phthalate -- toxicity KW - Liver Neoplasms, Experimental -- chemically induced KW - Microbodies -- drug effects KW - Phthalic Acids -- toxicity KW - Anticholesteremic Agents -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78894090?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-25 N1 - Date created - 1989-04-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Subendothelial matrix of cultured endothelial cells contains fully processed high molecular weight von Willebrand factor. AN - 78891197; 2784474 AB - Von Willebrand factor (vWf) is an adhesive glycoprotein composed of identical subunits linked by disulfide bonds to form multimers of varying sizes. VWf is found in platelets and plasma, where it functions in the adhesion of platelets to exposed subendothelium. Subendothelial matrix contains vWf, but the multimeric composition of matrix vWf, its binding site in matrix, and the mechanism by which it is delivered to matrix are unknown. Using human umbilical vein endothelial cell (HUVE) cultures, we have partially characterized subendothelial matrix vWf. Matrix from HUVE was solubilized in sodium dodecyl sulfate and electrophoresed on 1.25% agarose gels. The extracted vWf was composed of extremely high molecular weight (HMW) multimers of vWf not normally found in plasma. The vWf content of HUVE supernatant, extract, and matrix was quantitated and characterized by radioimmunoassay, agarose gel electrophoresis, and densitometry. The matrix-bound or -associated vWf represented 4% to 18% of total HUVE vWf. Western blot analysis of matrix vWf after reduction showed a subunit species of 220 kd. Long-term incubation of HUVE with phorbol 12-myristate 13-acetate (PMA), a compound that causes release of HMW vWf from Weibel-Palade bodies in HUVE, resulted in a marked decrease in matrix vWf (0.2% to 1% of the total vWf). The multimeric pattern of the remaining matrix vWf continued to show predominantly HMW multimers.(ABSTRACT TRUNCATED AT 250 WORDS) JF - The Journal of laboratory and clinical medicine AU - Tannenbaum, S H AU - Rick, M E AU - Shafer, B AU - Gralnick, H R AD - Clinical Pathology Department, Clinical Center, National Institutes of Health, Bethesda, MD 20892. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 372 EP - 378 VL - 113 IS - 3 SN - 0022-2143, 0022-2143 KW - von Willebrand Factor KW - 0 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Cells, Cultured KW - Humans KW - Hemostasis KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Molecular Weight KW - von Willebrand Factor -- analysis KW - Endothelium, Vascular -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78891197?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-24 N1 - Date created - 1989-04-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - S-adenosylmethionine, S-adenosylhomocysteine and DNA methylation levels in the liver of rats fed methapyrilene and analogs. AN - 78891166; 2924400 AB - The antihistamine methapyrilene (hydrochloride) and four close structural analogs, methaphenilene, methafurylene, thenyldiamine and clorothen, were given to rats at a concentration of 0.1% in drinking water for 34 weeks. Only methapyrilene produced notable histopathological changes in the liver, bile duct hyperplasia and focal cellular change. Methapyrilene produced an early and persistent elevation in the ratio of S-adenosylmethionine to S-adenosylhomocysteine, which was 2.8 times the control levels at 34 weeks; none of the other antihistamines produced so high a ratio or altered the ratio as early. Methapyrilene, but not the other antihistamines, produced a significant increase in the methylation of liver DNA at 20 and 34 weeks, as measured by the level of 5-methyldeoxycytidine. The increase in deoxycytosine methylation is so far the only detected effect of the carcinogen methapyrilene on DNA which is absent in rats treated with its non-carcinogenic analogs. JF - Carcinogenesis AU - Hernandez, L AU - Allen, P T AU - Poirier, L A AU - Lijinsky, W AD - NCI-Frederick Cancer Research Facility, BRI-Basic Research Program, Frederick, MD 21701. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 557 EP - 562 VL - 10 IS - 3 SN - 0143-3334, 0143-3334 KW - Aminopyridines KW - 0 KW - Carcinogens KW - Homocysteine KW - 0LVT1QZ0BA KW - Deoxycytidine KW - 0W860991D6 KW - S-Adenosylmethionine KW - 7LP2MPO46S KW - DNA KW - 9007-49-2 KW - S-Adenosylhomocysteine KW - 979-92-0 KW - Methapyrilene KW - A01LX40298 KW - 5-methyldeoxycytidine KW - B200GV71QM KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Deoxycytidine -- metabolism KW - Deoxycytidine -- analogs & derivatives KW - Deoxycytidine -- analysis KW - Methylation KW - Male KW - Liver -- pathology KW - Liver -- drug effects KW - DNA -- metabolism KW - Methapyrilene -- toxicity KW - Liver -- metabolism KW - S-Adenosylmethionine -- analysis KW - Homocysteine -- analogs & derivatives KW - Aminopyridines -- toxicity KW - S-Adenosylhomocysteine -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78891166?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-25 N1 - Date created - 1989-04-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Guanine nucleotide-binding proteins (G proteins) in activation of adenylyl cyclase: lessons learned from cholera and "travelers' diarrhea". AN - 78890122; 2494276 JF - The Journal of laboratory and clinical medicine AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, Bethesda, MD 20892. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 258 EP - 268 VL - 113 IS - 3 SN - 0022-2143, 0022-2143 KW - Bacterial Toxins KW - 0 KW - Enterotoxins KW - Escherichia coli Proteins KW - heat-labile enterotoxin, E coli KW - Cholera Toxin KW - 9012-63-9 KW - Poly(ADP-ribose) Polymerases KW - EC 2.4.2.30 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Abridged Index Medicus KW - Index Medicus KW - Travel KW - Animals KW - Enzyme Activation KW - Humans KW - Cholera Toxin -- pharmacology KW - Poly(ADP-ribose) Polymerases -- analysis KW - Enterotoxins -- pharmacology KW - Bacterial Toxins -- pharmacology KW - Adenylyl Cyclases -- analysis KW - GTP-Binding Proteins -- physiology KW - Diarrhea -- etiology KW - Cholera -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78890122?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-24 N1 - Date created - 1989-04-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of sympathetic blockade on diurnal variation of hemodynamic patterns. AN - 78887025; 2923262 AB - Heart rate, stroke volume, and intra-arterial blood pressure were monitored continuously in each of four monkeys, 18 consecutive h/day for several weeks. The mean heart rate, stroke volume, cardiac output, systolic and diastolic blood pressure, and total peripheral resistance were calculated for each minute and reduced to hourly means. After base-line data were collected for approximately 20 days, observation was continued for equal periods of time under conditions of alpha-sympathetic blockade, beta-sympathetic blockade, and double sympathetic blockade. This was achieved by intra-arterial infusion of prazosin, atenolol, or a combination of both in concentration sufficient for at least 75% reduction of response to injection of agonists. The results confirmed previous findings of a diurnal pattern characterized by a fall in cardiac output and a rise in total peripheral resistance throughout the night. This pattern was not eliminated by selective blockade, of alpha- or beta-sympathetic receptors or by double sympathetic blockade; in fact, it was exacerbated by sympathetic blockade, indicating that the sympathetic nervous system attenuates these events. Because these findings indicate that blood volume redistribution is probably not the mechanism mediating the observed effects, we have hypothesized that a diurnal loss in plasma volume may mediate the fall in cardiac output and that the rise in total peripheral resistance reflects a homeostatic regulation of arterial pressure. JF - The American journal of physiology AU - Talan, M I AU - Engel, B T AD - Laboratory of Behavioral Sciences, National Institute on Aging, Baltimore, Maryland 21224. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - R778 EP - R785 VL - 256 IS - 3 Pt 2 SN - 0002-9513, 0002-9513 KW - Atenolol KW - 50VV3VW0TI KW - Isoproterenol KW - L628TT009W KW - Prazosin KW - XM03YJ541D KW - Index Medicus KW - Animals KW - Drug Interactions KW - Reference Values KW - Vascular Resistance -- drug effects KW - Cardiac Output -- drug effects KW - Isoproterenol -- pharmacology KW - Heart Rate -- drug effects KW - Diastole -- drug effects KW - Macaca mulatta KW - Systole -- drug effects KW - Blood Pressure -- drug effects KW - Stroke Volume -- drug effects KW - Male KW - Hemodynamics -- drug effects KW - Sympathetic Nervous System -- physiology KW - Sympathetic Nervous System -- drug effects KW - Prazosin -- pharmacology KW - Circadian Rhythm -- drug effects KW - Atenolol -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78887025?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-12 N1 - Date created - 1989-04-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of long-acting somatostatin analog SMS 201-995 in patients with pancreatic islet cell tumors. AN - 78881839; 2537716 AB - Natural somatostatin reduces plasma concentrations of many peptides, and is of short term benefit in patients with islet cell tumors, but has to be given as a continuous intravenous infusion. We review the published experience with the long acting synthetic somatostatin analogue SMS 201-995 in patients with islet cell tumors. Fifteen of 18 patients with vasoactive intestinal peptide-producing tumors, 8 of 8 patients with glucagonomas, 7 of 7 patients with unresectable insulinomas, and 3 of 3 patients with growth hormone releasing factor-producing tumors had a good sustained symptomatic response to SMS 201-995. Patients with benign insulinomas responded variably and are best treated by surgery. Patients with gastrinomas are best treated by oral gastric antisecretory agents. In all these syndromes, the clinical response to SMS 201-995 did not necessarily parallel the change in plasma concentration of marker peptide, suggesting that SMS 201-995 may have actions at various sites. The effect of SMS 201-995 on tumor size has been assessed in 46 patients, less than 20% of whom showed a reduction in tumor size. Side effects have been mild, but include steatorrhea and gastrointestinal disturbances. More studies will be required to fully assess the effects of long-term administration of SMS 201-995. JF - Digestive diseases and sciences AU - Maton, P N AU - Gardner, J D AU - Jensen, R T AD - Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 28S EP - 39S VL - 34 IS - 3 Suppl SN - 0163-2116, 0163-2116 KW - Octreotide KW - RWM8CCW8GP KW - Abridged Index Medicus KW - Index Medicus KW - Vipoma -- drug therapy KW - Insulinoma -- drug therapy KW - Humans KW - Glucagonoma -- drug therapy KW - Gastrinoma -- drug therapy KW - Octreotide -- therapeutic use KW - Octreotide -- adverse effects KW - Pancreatic Neoplasms -- drug therapy KW - Adenoma, Islet Cell -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78881839?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-20 N1 - Date created - 1989-04-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Dig Dis Sci. 1989 Nov;34(11):1803-4 [2573486] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vitro polymerization of histones by carcinogenic nickel compounds. AN - 78878047; 2924407 AB - This study was undertaken to explore whether nuclear chromatin constituents can participate in and/or be affected by redox reactions catalyzed by nickel, like those of nickel complexes with small peptides, e.g. tetraglycine (G4) and oxygen. Calf thymus DNA, nucleohistone (NH) or free histones were incubated at 37 degrees C, pH 7.6, for up to 96 h with nickel(II)acetate (NiAcet) or nickel subsulfide (Ni3S2) and/or G4. The effects on DNA and NH were studied by means of melting profiles. Free individual histones and histones extracted from NH prior to and after exposure to nickel compounds and/or G4 were examined by electrophoresis on polyacrylamide gels. Two-day exposure of DNA to NiAcet, G4, or NiAcet + G4 had no significant effect on its melting temperature. Incubation of NH with NiAcet, however, markedly increased its melting temperature by 2.2 +/- 0.3 degrees C after 24 h and 3.0 +/- 0.5 degrees C after 96 h (P less than 0.01 versus NH alone at either time). Incubation of NH with NiAcet + G4 also resulted in a significant rise of the melting temperature by 1.4 +/- 0.3 degrees C after 24 h (P less than 0.05) and 5.5 +/- 0.3 degrees C after 96 h (P less than 0.0001). G4 alone had no effect. Exposure of NH to NiAcet + G4, but not to the individual chemicals, slowly decreased solubility of the histone components in 0.2 M H2SO4. Only trace amounts of histones could be extracted from NH with acid after 72-h exposure to NiAcet + G4. Treatment of free histones with NiAcet, Ni3S2 and/or G4 resulted in a slow random polymerization of the proteins by NiAcet + G4, Ni3S2 + G4 and Ni3S2 alone, but not NiAcet or G4 alone. The action of Ni3S2 alone was slower than that of either nickel compound combined with G4. The present findings indicate that nickel carcinogens NiAcet and Ni3S2, in the presence of G4 or even alone (Ni3S2), are capable of causing protein-protein and perhaps also protein-DNA crosslinking. Reactions of this type may be involved in the mechanism(s) of nickel carcinogenesis. JF - Carcinogenesis AU - Kasprzak, K S AU - Bare, R M AD - Inorganic Carcinogenesis Section, National Cancer Institute, Frederick, MD. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 621 EP - 624 VL - 10 IS - 3 SN - 0143-3334, 0143-3334 KW - Acetates KW - 0 KW - Carcinogens KW - Histones KW - Oligopeptides KW - Polymers KW - nickel subsulfide KW - 12035-72-2 KW - glycyl-glycyl-glycyl-glycine KW - 637-84-3 KW - Nickel KW - 7OV03QG267 KW - DNA KW - 9007-49-2 KW - Acetic Acid KW - Q40Q9N063P KW - Index Medicus KW - Oxidation-Reduction KW - DNA -- metabolism KW - Polymers -- metabolism KW - Oligopeptides -- pharmacology KW - Histones -- metabolism KW - Nickel -- toxicity KW - Acetates -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78878047?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-25 N1 - Date created - 1989-04-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Multistep process of squamous differentiation in tracheobronchial epithelial cells in vitro: analogy with epidermal differentiation. AN - 78876714; 2647475 AB - The lung, in particular the bronchial epithelium, is a major site for tumor formation in humans. Environmental factors, such as cigarette smoke, in conjunction with genetic factors are important determinants in this disease. Malignant cells exhibit alterations in their control of proliferation and differentiation. It is believed that the acquisition of defects in the regulation of these processes is important in the process of carcinogenesis. A clear insight into the basic mechanisms of the regulation of proliferation and differentiation is required to understand the molecular mechanisms involved in tumor development and in other pathological conditions. Studies using in vitro cell culture systems of tracheobronchial epithelial cells provide useful models in which to study the regulation of differentiation and proliferation. The clonogenic cells derived from the treacheobronchial epithelium are pluripotent: They have self-renewal capacity and can differentiate along either a normal, mucosecretory, or a squamous cell pathway. Squamous differentiation in tracheobronchial epithelial cells has many morphological, biochemical, and regulatory properties in common with epidermal differentiation. This pathway of differentiation is a multistep process consisting of at least three stages. In the initial stage, cells become committed to terminal cell division. This is followed by the expression of the squamous differentiated phenotype and finally cornification. Various factors, such as several growth factors, retinoids, calcium ions, and phorbol esters, regulate the program of differentiation at different stages. Studies have indicated that the controls of proliferation and differentiation are interrelated. Cell lines established from tracheobronchial epithelial cells expressing SV 40 large T-antigen, as well as carcinoma cell lines, exhibit altered responses to growth and differentiation regulatory factors. Alterations in the commitment to terminal cell division must be a crucial step in the transition of a normal to a malignant cell. JF - Environmental health perspectives AU - Jetten, A M AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 149 EP - 160 VL - 80 SN - 0091-6765, 0091-6765 KW - Retinoids KW - 0 KW - Transforming Growth Factors KW - 76057-06-2 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Clone Cells -- cytology KW - Epithelial Cells KW - Carcinoma, Squamous Cell -- pathology KW - Humans KW - In Vitro Techniques KW - Calcium -- physiology KW - Rabbits KW - Transforming Growth Factors -- physiology KW - Retinoids -- physiology KW - Cell Transformation, Neoplastic KW - Bronchi -- cytology KW - Epidermis -- cytology KW - Cell Differentiation KW - Trachea -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78876714?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-10 N1 - Date created - 1989-05-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell. 1985 Mar;40(3):685-95 [2578891] Biochim Biophys Acta. 1985 Jun 30;845(3):349-57 [3859337] 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Invest. 1988 Jun;58(6):706-17 [3379917] Lab Invest. 1988 Jul;59(1):25-35 [3260640] Lab Invest. 1971 Jan;24(1):55-66 [4322702] Proc Natl Acad Sci U S A. 1981 Feb;78(2):1077-80 [6940125] Cancer Res. 1981 Jun;41(6):2294-304 [7016311] Cell. 1981 Sep;25(3):617-25 [6169442] J Cell Biol. 1981 Sep;90(3):732-7 [6895225] J Cell Biol. 1981 Sep;90(3):738-42 [6895226] Exp Cell Res. 1982 Jan;137(1):155-67 [6173242] J Clin Invest. 1982 Feb;69(2):277-83 [6276439] Cell Tissue Kinet. 1982 Mar;15(2):119-30 [7066955] Cancer Res. 1982 Jun;42(6):2344-9 [6122503] J Invest Dermatol. 1983 Aug;81(2):125-30 [6192180] J Cell Biol. 1983 Sep;97(3):686-91 [6193127] Proc Natl Acad Sci U S A. 1986 Nov;83(21):8206-10 [3022285] Carcinogenesis. 1986 Dec;7(12):2033-9 [3779897] Biochem Soc Trans. 1986 Oct;14(5):930-3 [3781092] J Biol Chem. 1986 Dec 25;261(36):17073-80 [3465727] J Cell Biol. 1986 Nov;103(5):1945-55 [2430980] Cell. 1987 Feb 13;48(3):409-15 [2879635] J Biol Chem. 1987 Mar 15;262(8):3897-902 [3493244] J Cell Physiol. 1987 Feb;130(2):173-81 [3818799] Proc Natl Acad Sci U S A. 1987 Apr;84(8):2302-6 [2436229] Cancer Res. 1987 Jul 1;47(13):3523-7 [2884032] Exp Lung Res. 1987;12(4):311-29 [3582283] J Invest Dermatol. 1987 Jul;89(1):51-8 [2885378] Lab Invest. 1987 Jun;56(6):654-64 [2439773] Lab Invest. 1987 Aug;57(2):219-29 [3613528] J Natl Cancer Inst. 1982 Oct;69(4):895-905 [6956765] Mol Cell Biol. 1982 Sep;2(9):1115-7 [6891021] Cell. 1983 Jan;32(1):247-55 [6186392] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Case-control study of colorectal cancer and fecapentaene excretion. AN - 78875769; 2917361 AB - The fecapentaenes are potent mutagens found in high concentrations in the stools of some individuals. These compounds are produced in vivo by common species of the colonic microflora, from precursors of unknown origin. The fecapentaenes have been postulated to increase the risk of colorectal cancer. To test this hypothesis, we measured fecapentaene excretion in 69 patients with adenocarcinoma of the colon or rectum, newly diagnosed at three Washington, DC area hospitals. The cases were compared with 114 surgical controls, frequency matched to the cases on age, sex, and hospital. We attempted to measure fecapentaene excretion 4 times for each subject: before surgery; and at 1 mo; 3 mo; and 6 mo following surgery. Contrary to our study hypothesis, we found fecapentaene excretion during the four study periods to be similar or even lower in cases compared to controls. An indirect measurement of fecapentaene precursors also tended to be lower in cases. The case-control differences could not be explained as effects of bleeding or of the colorectal diagnostic workup, which was assessed in a separate group of 86 patients. We conclude from these data that the excretion of fecapentaenes does not increase the risk of colorectal cancer, at least when measured near the time of diagnosis. JF - Cancer research AU - Schiffman, M H AU - Van Tassell, R L AU - Robinson, A AU - Smith, L AU - Daniel, J AU - Hoover, R N AU - Weil, R AU - Rosenthal, J AU - Nair, P P AU - Schwartz, S AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/03/01/ PY - 1989 DA - 1989 Mar 01 SP - 1322 EP - 1326 VL - 49 IS - 5 SN - 0008-5472, 0008-5472 KW - Mutagens KW - 0 KW - Polyenes KW - 1-(1-glycero)dodeca-1,3,5,7,9-pentaene KW - 84000-59-9 KW - Index Medicus KW - Humans KW - Aged KW - Middle Aged KW - Male KW - Female KW - Feces -- analysis KW - Mutagens -- analysis KW - Colorectal Neoplasms -- metabolism KW - Polyenes -- analysis KW - Colorectal Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78875769?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-24 N1 - Date created - 1989-03-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Absolute stereochemistry of the major 7,12-dimethylbenz[alpha]anthracene- DNA adducts formed in mouse cells. AN - 78872031; 2494001 AB - In recent work we assigned partial structures to individual 7,12-dimethylbenz[alpha]anthracene (DMBA)--deoxyribonucleoside bisphosphates separated by TLC after postlabeling with [32P]ATP. We have now been able to postlabel DNA adducts formed in cells exposed to either the (4R,3R)- or (4S,3S)-dihydrodiol of DMBA and thereby to assign absolute stereochemistry to the 2-, 3- and 4- positions in the major DMBA-DNA adducts. It is found that the major anti dihydrodiol epoxide-DNA adducts arise from the (4R,3S)-dihydrodiol (2S,1R)-epoxide and that the major syn dihydrodiol epoxide-DNA adducts arise from the (4S,3R)-dihydrodiol (2S,1R)-epoxide. JF - Carcinogenesis AU - Vericat, J A AU - Cheng, S C AU - Dipple, A AD - BRI Basic Research Program, NCI-Frederick Cancer Research Facility, MD 21701. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 567 EP - 570 VL - 10 IS - 3 SN - 0143-3334, 0143-3334 KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Cells, Cultured KW - Mice KW - Molecular Conformation KW - DNA -- metabolism KW - 9,10-Dimethyl-1,2-benzanthracene -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78872031?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-25 N1 - Date created - 1989-04-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The influence of alcoholism on the course of depression. AN - 78869861; 2522114 AB - The clinical course of 289 patients with primary non-bipolar major depression without concurrent alcoholism was compared with that of 79 patients with non-bipolar major depression with concurrent alcoholism. Neither patient group suffered from dysthymia or current drug abuse. Contrary to expectations, the two groups did not differ on time to recovery from the major depression, time to relapse into a subsequent major depression, or various cross-sectional clinical ratings at 2 years. The two groups did differ on psychosocial status. Although they were equally impaired at index, the alcoholism group maintained significantly lower levels of psychosocial functioning throughout the 2-year follow-up period. Interpersonal relation with spouse was particularly worse among the alcoholic group. JF - Journal of affective disorders AU - Hirschfeld, R M AU - Kosier, T AU - Keller, M B AU - Lavori, P W AU - Endicott, J AD - National Institute of Mental Health, Rockville, MD 20857. PY - 1989 SP - 151 EP - 158 VL - 16 IS - 2-3 SN - 0165-0327, 0165-0327 KW - Index Medicus KW - Social Adjustment KW - Humans KW - Interpersonal Relations KW - Adult KW - Middle Aged KW - Follow-Up Studies KW - Male KW - Female KW - Psychological Tests KW - Depressive Disorder -- psychology KW - Alcohol Drinking -- psychology KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78869861?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-14 N1 - Date created - 1989-04-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Auditory event-related potentials in adolescents at risk for drug abuse. AN - 78867714; 2920193 AB - We evaluated sensory and cognitive information processing in noninstitutionalized delinquent male adolescents and in age-matched low delinquency controls. Detailed psychometric testing documented the nature of the aggressive behavior of these young men. Deficits in information processing, as assessed by event-related potential (ERP) techniques, were observed at several levels of the auditory system in the delinquent group. The delinquent group showed delays in wave V of the brainstem auditory evoked potential, shorter N100 latency, and decreased slow wave amplitude of cognitive event-related potentials when subjects were asked to perform a mental task in a noisy environment. It remains to be determined whether or not such information-processing deficiencies are common among delinquent populations and how they might influence the development of delinquent behavior and drug abuse. JF - Biological psychiatry AU - Herning, R I AU - Hickey, J E AU - Pickworth, W B AU - Jaffe, J H AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1989/03/01/ PY - 1989 DA - 1989 Mar 01 SP - 598 EP - 609 VL - 25 IS - 5 SN - 0006-3223, 0006-3223 KW - Index Medicus KW - Personality Tests KW - Risk Factors KW - Humans KW - Adolescent KW - Male KW - Social Environment KW - Arousal KW - Evoked Potentials, Auditory KW - Substance-Related Disorders -- psychology KW - Substance-Related Disorders -- genetics KW - Juvenile Delinquency -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78867714?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-17 N1 - Date created - 1989-04-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Bacterial lipopolysaccharides prime human neutrophils for enhanced production of leukotriene B4. AN - 78866172; 2537852 AB - Neutrophils can be "primed" for an enhanced respiratory burst by lipopolysaccharide (LPS) in concentrations measurable in patients with septic shock. Leukotriene B4 (LTB4) is the primary eicosanoid product of neutrophils and is felt to be a mediator of host defense and inflammation. We investigated the in vitro effects of LPS on neutrophil production of LTB4 and the omega-oxidation metabolites of LTB4. Incubation of neutrophils with LPS in concentrations ranging from 0.01 to 100 ng/ml did not result in production of LTB4 or metabolites in the absence of a second stimulus. Priming neutrophils with LPS and then stimulating with opsonized zymosan, phorbol-myristate-acetate or a low concentration of the calcium ionophore A23187 resulted in enhanced production of LTB4. LPS priming of neutrophils occurred in a concentration dependent manner. LPS did not result in LTB4 production in response to the chemoattractant peptide FMLP. LPS priming of neutrophils had no effect on cytosolic calcium concentrations of resting or zymosan-stimulated cells. These results suggest that LPS might effect host defense and tissue injury by potentiating the effect of other stimulants on neutrophil production of LTB4. This LPS induced enhancement may represent an important pathogenetic pathway in patients with gram negative sepsis. JF - The Journal of clinical investigation AU - Doerfler, M E AU - Danner, R L AU - Shelhamer, J H AU - Parrillo, J E AD - Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 970 EP - 977 VL - 83 IS - 3 SN - 0021-9738, 0021-9738 KW - Lipopolysaccharides KW - 0 KW - Opsonin Proteins KW - Leukotriene B4 KW - 1HGW4DR56D KW - Calcimycin KW - 37H9VM9WZL KW - N-Formylmethionine Leucyl-Phenylalanine KW - 59880-97-6 KW - Zymosan KW - 9010-72-4 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Abridged Index Medicus KW - Index Medicus KW - Oxidation-Reduction KW - N-Formylmethionine Leucyl-Phenylalanine -- pharmacology KW - Cytosol -- metabolism KW - Zymosan -- pharmacology KW - Calcium -- blood KW - Kinetics KW - Humans KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Calcimycin -- pharmacology KW - Salmonella KW - Neutrophils -- metabolism KW - Neutrophils -- drug effects KW - Leukotriene B4 -- blood KW - Lipopolysaccharides -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78866172?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-14 N1 - Date created - 1989-04-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochem Biophys Res Commun. 1987 Apr 29;144(2):794-800 [3034265] J Immunol. 1987 May 15;138(10):3396-402 [3033073] Am Rev Respir Dis. 1987 Jul;136(1):161-9 [3037955] J Clin Invest. 1987 Sep;80(3):605-12 [3624479] Crit Care Med. 1987 Oct;15(10):923-9 [3652707] Biochem Biophys Res Commun. 1988 Jan 29;150(2):532-9 [2829878] Nature. 1988 Mar 24;332(6162):362-4 [3352735] J Exp Med. 1965 Aug 1;122:207-35 [14316942] N Engl J Med. 1970 Dec 10;283(24):1313-6 [5478453] Adv Prostaglandin Thromboxane Res. 1978;5:39-94 [364961] J Biol Chem. 1979 Apr 25;254(8):2643-6 [429307] Proc Natl Acad Sci U S A. 1979 Jun;76(6):2640-3 [288052] Nature. 1980 Jul 17;286(5770):264-5 [6250050] J Immunol. 1980 Oct;125(4):1789-91 [7410854] Nature. 1981 Feb 19;289(5799):646-50 [7464931] J Biol Chem. 1981 Jul 25;256(14):7228-34 [6788763] Prostaglandins Med. 1981 Jun;6(6):557-70 [6267638] FEBS Lett. 1981 Dec 21;136(1):141-4 [6274698] J Biol Chem. 1982 Jul 10;257(13):7847-51 [7085651] Inflammation. 1982 Jun;6(2):189-200 [6179872] Int J Immunopharmacol. 1982;4(3):195-204 [6809647] Biochem Biophys Res Commun. 1982 Oct 29;108(4):1531-7 [6295385] Nature. 1983 Feb 17-23;301(5901):621-3 [6828143] Biochem Biophys Res Commun. 1983 Jul 29;114(2):638-45 [6411090] Immunology. 1983 Sep;50(1):65-73 [6309653] Br Med Bull. 1983 Jul;39(3):219-22 [6313113] Br Med Bull. 1983 Jul;39(3):243-8 [6313115] Br Med Bull. 1983 Jul;39(3):260-4 [6354351] J Biol Chem. 1984 Mar 10;259(5):3111-6 [6321496] J Exp Med. 1984 Mar 1;159(3):844-60 [6699545] J Biol Chem. 1984 Apr 10;259(7):4070-5 [6323454] J Biol Chem. 1984 Apr 10;259(7):4076-82 [6323455] J Clin Invest. 1984 Apr;73(4):889-97 [6323538] Science. 1984 May 11;224(4649):622-5 [6231726] J Biol Chem. 1984 Aug 25;259(16):10048-52 [6236211] J Biol Chem. 1984 Aug 25;259(16):10181-7 [6088485] Nature. 1984 Aug 23-29;310(5979):691-3 [6236373] Nature. 1984 Nov 22-28;312(5992):315-21 [6095092] J Exp Med. 1984 Dec 1;160(6):1656-71 [6096475] J Immunol. 1985 Apr;134(4):2624-30 [2982947] Biochem Biophys Res Commun. 1986 Jan 14;134(1):367-71 [3004439] Prostaglandins. 1986 Feb;31(2):227-37 [3008216] Am Rev Respir Dis. 1986 May;133(5):797-804 [3706888] Am Rev Respir Dis. 1986 May;133(5):805-8 [3010781] J Exp Med. 1986 Jul 1;164(1):165-79 [2941513] Science. 1986 Jul 18;233(4761):305-12 [3014651] Proc Natl Acad Sci U S A. 1986 Aug;83(16):5817-21 [3461461] Science. 1986 Dec 19;234(4783):1519-26 [3024320] Biochem J. 1986 Jun 15;236(3):829-37 [3790093] Biochem Biophys Res Commun. 1986 Dec 15;141(2):399-404 [3026382] Biochem J. 1987 Jan 1;241(1):55-62 [3032161] J Biol Chem. 1987 May 5;262(13):6308-12 [3571258] Methods Enzymol. 1987;141:355-71 [3037248] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Renal toxicity of interleukin-2 administration in patients with metastatic renal cell cancer: effect of pre-therapy nephrectomy. AN - 78865041; 2783983 AB - Systemic administration of interleukin-2 and lymphokine-activated killer cells is a new approach to the immunotherapy of advanced cancer. Metastatic renal cell cancer is one of the histological types of tumors particularly susceptible to this treatment approach although renal toxicity often is a dose-limiting side effect. We compared the renal functional changes observed during interleukin-2 therapy in 52 consecutive patients with advanced renal cancer to that of 83 consecutive patients with metastatic nonrenal cancer. Of the 52 patients with renal cancer 41 had recently undergone nephrectomy. The over-all peak serum creatinine values and the percentage increase of serum creatinine over baseline for all patients studied were significantly higher in cycle 2 of interleukin-2 therapy than in cycle 1: 3.8 +/- 0.2 versus 2.6 +/- 0.1 mg. per dl. and 241.7 +/- 16.5 versus 140.3 +/- 11.0 per cent, respectively. In patients with pre-therapy serum creatinine values of 0.4 to 0.9 mg. per dl. there were no significant differences in the mean peak serum creatinine nor in the percentage increase over baseline between renal and nonrenal cancer patients during cycle 1. In cycle 2 of therapy these values were higher in the renal cancer group (3.6 +/- 0.8 versus 2.4 +/- 0.2 mg. per dl. and 310.4 +/- 103.5 versus 214 +/- 30.4 per cent, respectively) but they did not reach statistical significance (P2 = 0.08 and 0.25, respectively). Renal and nonrenal cancer patients with pre-therapy serum creatinine levels of 1.0 to 1.4 mg. per dl. achieved similar high values in cycle 2 of interleukin-2 therapy (3.9 +/- 0.3 versus 3.9 +/- 0.4 mg. per dl. and 222.7 +/- 23.2 versus 248.7 +/- 33.5 per cent, respectively), although the initial increase (cycle 1) was higher in the renal cancer patients (3.3 +/- 0.3 versus 2.4 +/- 0.2 mg. per dl. and 172.3 +/- 25.9 versus 116.1 +/- 18.0 per cent, respectively). Baseline serum creatinine greater than or equal to 1.5 mg. per dl. was associated with an over-all higher peak serum creatinine and higher percentage increase of serum creatinine over baseline than that below 1.5 mg. per dl. baseline: 4.4 mg.per dl. and 171.1 +/- 36.3 per cent in cycle 1 and 6.5 +/- 0.7 mg. per dl. and 296.1 +/- 44.0 per cent in cycle 2, respectively (p less than 0.01). There was no association between peak serum creatinine and interval from nephrectomy to interleukin-2 therapy.(ABSTRACT TRUNCATED AT 400 WORDS) JF - The Journal of urology AU - Belldegrun, A AU - Webb, D E AU - Austin, H A AU - Steinberg, S M AU - Linehan, W M AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, Bethesda, Maryland. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 499 EP - 503 VL - 141 IS - 3 SN - 0022-5347, 0022-5347 KW - Interleukin-2 KW - 0 KW - Lymphokines KW - Recombinant Proteins KW - Creatinine KW - AYI8EX34EU KW - Abridged Index Medicus KW - Index Medicus KW - Lymphokines -- immunology KW - Killer Cells, Natural -- transplantation KW - Risk Factors KW - Humans KW - Recombinant Proteins -- adverse effects KW - Creatinine -- blood KW - Recombinant Proteins -- therapeutic use KW - Male KW - Female KW - Kidney Neoplasms -- therapy KW - Interleukin-2 -- adverse effects KW - Carcinoma, Renal Cell -- therapy KW - Nephrectomy KW - Interleukin-2 -- therapeutic use KW - Immunization, Passive KW - Kidney -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78865041?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-30 N1 - Date created - 1989-03-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Infrequent activation of K-ras, H-ras, and other oncogenes in hepatocellular neoplasms initiated by methyl(acetoxymethyl)nitrosamine, a methylating agent, and promoted by phenobarbital in F344 rats. AN - 78859651; 2645046 AB - Fischer 344/Ncr rats of both sexes were subjected to partial hepatectomy and then initiated 21-24 h later by a single injection of methyl(acetoxymethyl)nitrosamine at 0.1 mmol/kg body weight via the portal vein. Beginning 3 weeks later, development of hepatocellular neoplasms in initiated rats was promoted by feeding 0.05% phenobarbital (PB) in the diet. Not only intrahepatic lesions but also a variety of extrahepatic tumors were induced. High-molecular-weight DNAs were prepared from 67 samples of grossly normal liver containing multiple preneoplastic foci/areas of microscopic dimensions, 137 hepatocellular adenomas (nodules), 93 hepatocellular carcinomas (HCC), 10 cholangiomas, and 25 extrahepatic tumors in 95 rats and tested for transforming activity in the NIH 3T3 transfection assay. DNA preparations from 7 of 93 HCCs, 2 of 10 cholangiomas, 2 of 137 nodules, 1 histiocytic sarcoma, and 1 thyroid carcinoma were positive in the transfection assay. Southern blot analysis showed that NIH 3T3 transformants induced by DNA from 5 HCCs, 1 hepatocellular adenoma, 1 cholangioma, 1 histiocytic sarcoma, and 1 thyroid carcinoma contained an activated K-ras gene of rat origin. Rat-derived H-ras was identified in transformants from 2 additional HCCs and rat c-raf from 1 hepatocellular adenoma. The transforming gene from one cholangioma showed no sequence homology to the ras genes, neu, or c-raf. Immunoprecipitation analysis of ras Mr 21,000 protein in 11 transformants indicated that, based upon protein electrophoretic mobilities, activation of the ras genes consistently resulted from mutations in codon 12 of these genes. Selective oligonucleotide analysis revealed that a G----A transition in the second base of codon 12 of K-ras was present in the 9 K-ras-positive transformants and also in DNAs prepared from the original tumors. In contrast, oligonucleotide hybridization experiments with DNAs from 35 hepatocellular tumors that were negative in transfection assays revealed the presence of mutant K-ras in 1 of 15 HCCs; no mutation could be detected in 20 transfection-negative adenomas. The infrequency of detection of a specific oncogene, more frequent detection of oncogenes in malignant tumors, and failure to observe activated oncogenes in preneoplastic lesions suggest that activation of ras oncogenes may occur as a late and infrequent event in the evolution of some rat hepatocellular neoplasms and that mutation of a specific ras locus is not an obligatory early event in the genesis of these neoplasms. JF - Cancer research AU - Watatani, M AU - Perantoni, A O AU - Reed, C D AU - Enomoto, T AU - Wenk, M L AU - Rice, J M AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, Maryland 21701. Y1 - 1989/03/01/ PY - 1989 DA - 1989 Mar 01 SP - 1103 EP - 1109 VL - 49 IS - 5 SN - 0008-5472, 0008-5472 KW - Carcinogens KW - 0 KW - Proto-Oncogene Proteins KW - methyl(acetoxymethyl)nitrosamine KW - 56856-83-8 KW - Proto-Oncogene Proteins p21(ras) KW - EC 3.6.5.2 KW - Dimethylnitrosamine KW - M43H21IO8R KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Transfection KW - Proto-Oncogene Proteins -- analysis KW - Nucleic Acid Hybridization KW - Male KW - Female KW - Genes, ras KW - Liver Neoplasms, Experimental -- genetics KW - Phenobarbital -- pharmacology KW - Liver Neoplasms, Experimental -- pathology KW - Dimethylnitrosamine -- toxicity KW - Liver Neoplasms, Experimental -- chemically induced KW - Dimethylnitrosamine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78859651?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-24 N1 - Date created - 1989-03-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 1-Aminocyclopropane carboxylic acid: a potent and selective ligand for the glycine modulatory site of the N-methyl-D-aspartate receptor complex. AN - 78856520; 2465385 AB - 1-Aminocyclopropane carboxylic acid (ACPC) competitively inhibited (IC50, 38 +/- 7 nM) [3H]glycine binding to rat forebrain membranes but did not affect [3H]strychnine binding to rat brainstem/spinal cord membranes. Like glycine, ACPC enhanced 3H-labelled (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate ([3H]MK-801) binding to N-methyl-D-aspartate receptor-coupled cation channels (EC50, 135 +/- 76 nM and 206 +/- 78 nM for ACPC and glycine, respectively) but was approximately 40% less efficacious in this regard. The maximum increase in [3H]MK-801 binding produced by a combination of ACPC and glycine was not different from that elicited by glycine, but both compounds potentiated glutamate-stimulated [3H]MK-801 binding. These findings indicate that ACPC is a potent and selective ligand at the glycine modulatory site associated with the N-methyl-D-aspartate receptor complex. JF - Journal of neurochemistry AU - Marvizón, J C AU - Lewin, A H AU - Skolnick, P AD - Laboratory of Neuroscience, NIDDK, Bethesda, MD 20892. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 992 EP - 994 VL - 52 IS - 3 SN - 0022-3042, 0022-3042 KW - Amino Acids KW - 0 KW - Amino Acids, Cyclic KW - Cations KW - Dibenzocycloheptenes KW - Glutamates KW - Ion Channels KW - Receptors, N-Methyl-D-Aspartate KW - Receptors, Neurotransmitter KW - 1-aminocyclopropane-1-carboxylic acid KW - 3K9EJ633GL KW - Glutamic Acid KW - 3KX376GY7L KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - Strychnine KW - H9Y79VD43J KW - Glycine KW - TE7660XO1C KW - Index Medicus KW - Animals KW - Diencephalon -- metabolism KW - Telencephalon -- metabolism KW - Brain Stem -- metabolism KW - Spinal Cord -- metabolism KW - Strychnine -- metabolism KW - Synaptic Membranes -- metabolism KW - Dibenzocycloheptenes -- metabolism KW - Ion Channels -- metabolism KW - Rats, Inbred Strains KW - Rats KW - Glutamates -- pharmacology KW - Binding, Competitive KW - Male KW - Receptors, Neurotransmitter -- metabolism KW - Glycine -- metabolism KW - Receptors, Neurotransmitter -- drug effects KW - Amino Acids -- metabolism KW - Amino Acids -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78856520?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-24 N1 - Date created - 1989-03-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human and rat kidney cell metabolism of 2-acetylaminofluorene and benzo(a)pyrene. AN - 78855809; 2917350 AB - The metabolism and mutagenic activation of the model carcinogens benzo(a)pyrene [B(a)P] and 2-acetylaminofluorene (AAF) by human and rat kidney cells were measured. A slicing technique followed by enzyme digestion was utilized to obtain the kidney cells. Although levels of total metabolism of B(a)P by rat and human kidney cells were similar, analysis of specific metabolites of B(a)P indicated that species differences existed. Human kidney cells produced the organic-soluble metabolites B(a)P-9,10-diol, B(a)P-4,5-diol, B(a)P-7,8-diol, B(a)P-3,6-quinone, and B(a)P-9-phenol. Rat kidney cells produced organic-soluble B(a)P-pre-9,10-diols, B(a)P-9,10-diol, B(a)P-4,5-diol, and B(a)P-6,12-quinone. Both species produced sulfate and glucuronide conjugates of all products. For AAF, kidney cells from some human tissues produced up to four times the level of total metabolites compared to rat kidney cells. Organic-soluble metabolites were qualitatively similar between the species and consisted of 2-aminofluorene (AF), N-hydroxy-AAF and ring-hydroxylated products at the 1, 3, 5/9, 7, and 8 positions. Sulfate and glucuronide conjugates of these metabolites were also detected. Human interindividual variation with kidney cells was about 2.5-fold for total AAF metabolism and up to 6-fold for individual AAF metabolites. For B(a)P metabolism, human interindividual variation in total metabolism was low while for specific metabolites there was up to a 4-fold variation. Levels of AAF and AF cell-mediated Salmonella typhimurium mutagenesis were significantly higher with human cells as compared to rat kidney cells. It appears that the differences between human and rodent kidney cell metabolism of chemical carcinogens vary with the chemical class and understanding these differences will be necessary in the extrapolation of rodent carcinogenesis data to humans. JF - Cancer research AU - Rudo, K M AU - Dauterman, W C AU - Langenbach, R AD - Cellular and Genetic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/03/01/ PY - 1989 DA - 1989 Mar 01 SP - 1187 EP - 1192 VL - 49 IS - 5 SN - 0008-5472, 0008-5472 KW - Mutagens KW - 0 KW - Benzo(a)pyrene KW - 3417WMA06D KW - 2-Acetylaminofluorene KW - 9M98QLJ2DL KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Biotransformation KW - Mutagens -- metabolism KW - Humans KW - Liver -- metabolism KW - Species Specificity KW - Male KW - Kidney -- metabolism KW - 2-Acetylaminofluorene -- metabolism KW - Benzo(a)pyrene -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78855809?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-24 N1 - Date created - 1989-03-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of RNase H activity and viral replication by single mutations in the 3' region of Moloney murine leukemia virus reverse transcriptase. AN - 78847181; 2464706 AB - Selected conserved amino acids in the putative RNase H domain of reverse transcriptase (RT) were modified in a molecularly cloned infectious provirus and in a Moloney murine leukemia virus RT expression vector by site-directed mutagenesis. Substitution of either of two conserved aspartic acid residues in proviral DNA prevented production of infectious particles in transfected NIH 3T3 cells, and the same modifications depressed RT-associated RNase H activity by more than 25-fold with little or no effect on polymerase activity. JF - Journal of virology AU - Repaske, R AU - Hartley, J W AU - Kavlick, M F AU - O'Neill, R R AU - Austin, J B AD - Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 1460 EP - 1464 VL - 63 IS - 3 SN - 0022-538X, 0022-538X KW - RNA-Directed DNA Polymerase KW - EC 2.7.7.49 KW - Endoribonucleases KW - EC 3.1.- KW - Ribonuclease H KW - EC 3.1.26.4 KW - Index Medicus KW - DNA Mutational Analysis KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Structure-Activity Relationship KW - Virus Replication KW - Moloney murine leukemia virus -- enzymology KW - Moloney murine leukemia virus -- genetics KW - RNA-Directed DNA Polymerase -- metabolism KW - Endoribonucleases -- genetics KW - RNA-Directed DNA Polymerase -- genetics KW - Endoribonucleases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78847181?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-21 N1 - Date created - 1989-03-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1983 Jun;80(12):3618-22 [6304725] Cell. 1983 Mar;32(3):853-69 [6299578] Nature. 1983 Oct 27-Nov 2;305(5937):827-9 [6195530] Nature. 1984 Jun 21-27;309(5970):728 [6203043] Cell. 1984 Jul;37(3):1043-52 [6204767] J Virol. 1984 Aug;51(2):470-8 [6205170] J Virol. 1984 Sep;51(3):813-21 [6206236] DNA. 1984 Dec;3(6):479-88 [6096101] Cell. 1985 Jan;40(1):9-17 [2981635] Proc Natl Acad Sci U S A. 1985 Feb;82(3):677-81 [2983308] EMBO J. 1985 May;4(5):1267-72 [2408886] Cell. 1985 Aug;42(1):369-82 [2410140] J Biol Chem. 1985 Aug 5;260(16):9326-35 [2410413] Nature. 1985 Aug 15-21;316(6029):641-3 [2412125] J Virol. 1986 Feb;57(2):422-32 [2418214] Science. 1986 Mar 28;231(4745):1567-72 [3006247] Cell. 1986 May 9;45(3):375-85 [2421920] Proc Natl Acad Sci U S A. 1986 Oct;83(20):7648-52 [2429313] Nature. 1987 Apr 16-22;326(6114):662-9 [3031510] Virology. 1987 May;158(1):88-102 [3033897] Nature. 1987 Jun 25-Jul 1;327(6124):716-7 [2439916] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1777-81 [2450347] Nature. 1987 Aug 6-12;328(6130):543-7 [3649576] J Virol. 1976 Jul;19(1):19-25 [59816] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] J Virol. 1979 Feb;29(2):494-500 [219244] J Mol Biol. 1967 Jun 14;26(2):365-9 [4291934] Virology. 1970 Dec;42(4):1136-9 [4099080] Nat New Biol. 1971 Dec 22;234(51):240-3 [4331605] Virology. 1973 Apr;52(2):456-67 [4705382] J Virol. 1975 Apr;15(4):843-54 [46925] Virology. 1975 May;65(1):128-34 [167514] Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4 [388439] Nature. 1981 Oct 15-21;293(5833):543-8 [6169994] Cell. 1982 Jun;29(2):403-15 [6180831] Cell. 1982 Oct;30(3):797-805 [6183006] J Biol Chem. 1983 Jan 25;258(2):1276-81 [6296074] Cell. 1983 Jul;33(3):781-9 [6191868] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nuclear run-on transcription from primary embryonic lens tissue. AN - 78845363; 2645183 AB - We have devised an in vitro RNA elongation assay (nuclear "run-on" transcription) that is suitable for use with small amounts of primary embryonic tissue. The assay is sensitive enough to detect transcription of single-copy genes in 8 X 10(5) nuclei isolated from embryonic chicken lens epithelia, and gives no detectable hybridization to unrelated DNAs, such as phi X or pBR322. We have used this assay to examine transcription of delta-crystallin and six proto-oncogenes in lens epithelia of 6-day-old embryonic chickens. The results indicate that delta-crystallin, c-myc, p53, and c-fos are actively transcribed in these cells, while c-myb, N-ras, and c-mil are not transcribed at detectable levels. JF - Developmental biology AU - Zelenka, P S AU - Pallansch, L A AU - Vatal, M AD - Laboratory of Molecular and Developmental Biology, National Eye Institute, Bethesda, Maryland 20892. Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 69 EP - 72 VL - 132 IS - 1 SN - 0012-1606, 0012-1606 KW - Amanitins KW - 0 KW - Crystallins KW - Proto-Oncogene Proteins KW - Index Medicus KW - Animals KW - Amanitins -- pharmacology KW - Chick Embryo KW - In Vitro Techniques KW - Cell Nucleus -- physiology KW - Transcription, Genetic KW - Gene Expression Regulation KW - Nucleic Acid Hybridization KW - Crystallins -- genetics KW - Cell-Free System KW - Lens, Crystalline -- physiology KW - Lens, Crystalline -- embryology KW - Proto-Oncogenes KW - Proto-Oncogene Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78845363?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-29 N1 - Date created - 1989-03-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - An Exploration of Phonation Types in Wu Dialects of Chinese AN - 58206350; 8908572 AB - The three-way contrast of initial stops & affricates in terms of voicing & aspiration is the most characteristic feature of the Wu dialects of Chinese. However, the phonetic nature of the "voiced" category has been an area of controversy. Recent instrumental phonetic studies have shown that there is no vocal cord vibration during the closure of either type in initial position in isolated monosyllabic words or in stressed position in running speech. An exploration of the possible role of breathy phonation in the distinction is reported. Contrasting word pairs with initial "voiced" & voiceless stops spoken by speakers of four different Wu dialects (N = 10) were recorded, & measurements were made of the energy difference between harmonics at the onset, middle, & offset of the vowel. Air flow & air pressure during closure & release of syllables with bilabial consonants was also studied. Results indicated the presence of the difference in phonation type in the two segment types, but only in initial position in monosyllables or in stressed position in running speech. No phonation contrast is found in unstressed position in running speech. Tables, Figures, References. Modified HA JF - University of California Working Papers in Phonetics AU - Cao Jianfen AU - Maddieson, Ian AD - Instit Linguistics Chinese Academy Social Sciences, 5 Jianguomen Nei Da Jie 5 Hao Beijing People's Republic China Y1 - 1989/03// PY - 1989 DA - March 1989 SP - 139 EP - 160 VL - 72 IS - Mar SN - 1067-9030, 1067-9030 KW - Chinese Wu dialects phonation types, initial stops/affricates three-way contrast, voicing/aspiration basis KW - Chinese (ch2) KW - Phonation Structures (ph5) KW - Phonetics (ph9) KW - article KW - 6110: phonetics; phonetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/58206350?accountid=14244 LA - English DB - Linguistics and Language Behavior Abstracts (LLBA) N1 - Date revised - 2012-11-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Phonetics (ph9); Chinese (ch2); Phonation Structures (ph5) ER - TY - JOUR T1 - Distribution and possible metabolic role of class III alcohol dehydrogenase in the human brain. AN - 76293482; 2650803 AB - In human brain, the sole alcohol dehydrogenase (ADH) present in significant quantity has been shown to be Class III (chi) ADH and this ADH is ineffective in generating potentially toxic and reactive acetaldehyde from ethanol at concentrations attainable in living brain tissue. We have extended this finding to show that Class I ADH potentially present is undetectable even when concentrated several hundred-fold. Purified Class III ADH from human brain is identical in its pattern of tryptic peptides and in other properties to Class III ADH from human liver. Immunohistochemical staining and western immunoblots using polyclonal antibodies reveal that Class III ADH is widely distributed in brian and most concentrated in the subependymal layer and perivascular areas. Class III ADH closely resembles omega-hydroxyfatty acid dehydrogenase and a possible role for the brain enzyme is in the oxidation of long chain fatty alcohols and omega-hydroxyfatty acids. JF - Brain research AU - Giri, P R AU - Linnoila, M AU - O'Neill, J B AU - Goldman, D AD - Laboratory on Clinical Studies, NIAAA, DICBR, Bethesda, MD 20892. Y1 - 1989/02/27/ PY - 1989 DA - 1989 Feb 27 SP - 131 EP - 141 VL - 481 IS - 1 SN - 0006-8993, 0006-8993 KW - Amino Acids KW - 0 KW - Alcohol Oxidoreductases KW - EC 1.1.- KW - Index Medicus KW - Kinetics KW - Hydrogen-Ion Concentration KW - Humans KW - Amino Acids -- analysis KW - Brain -- enzymology KW - Alcohol Oxidoreductases -- classification KW - Alcohol Oxidoreductases -- analysis KW - Alcohol Oxidoreductases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76293482?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-02 N1 - Date created - 1989-06-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential seizure sensitivities to picrotoxinin in two inbred strains of mice (DBA/2J and BALB/c ByJ): parallel changes in GABA receptor-mediated chloride flux and receptor binding. AN - 76291131; 2539878 AB - Two strains of mice were shown to possess a differential sensitivity to picrotoxinin-induced convulsions; picrotoxinin elicited both tonic and clonic seizures at lower doses in the DBA/2J (DBA) strain compared to the BALB/c ByJ (BALB) strain. Less protection of picrotoxinin-induced tonic seizures was afforded by pentobarbital in the DBA strain. Biochemical studies revealed that picrotoxin inhibited 36Cl- efflux from forebrain synaptoneurosomes only in the DBA strain. In addition, picrotoxin inhibited pentobarbital-induced 36Cl- efflux to a greater extent in the DBA strain. No differences were observed in the binding of [3H]muscimol or [35S]t-butylbicyclophosphorothionate (TBPS) to forebrain homogenates, while pentobarbital was a less potent inhibitor of [35S]TBPS binding in the DBA strain. These findings suggest a genetic basis for the behavioral differences in convulsant sensitivity as well as for the neurochemical differences in allosteric coupling between convulsant and depressant/anticonvulsant sites associated with the GABA receptor-gated Cl- channel. JF - Brain research AU - Schwartz, R D AU - Seale, T W AU - Skolnick, P AU - Paul, S M AD - Clinical Neuroscience Branch, NIMH, Bethesda, MD 20892. Y1 - 1989/02/27/ PY - 1989 DA - 1989 Feb 27 SP - 169 EP - 174 VL - 481 IS - 1 SN - 0006-8993, 0006-8993 KW - Bridged Bicyclo Compounds KW - 0 KW - Bridged Bicyclo Compounds, Heterocyclic KW - Chlorides KW - Receptors, GABA-A KW - Picrotoxin KW - 124-87-8 KW - Muscimol KW - 2763-96-4 KW - tert-butylbicyclophosphorothionate KW - 70636-86-1 KW - Pentobarbital KW - I4744080IR KW - Index Medicus KW - Frontal Lobe -- physiopathology KW - Animals KW - Dose-Response Relationship, Drug KW - Mice KW - Bridged Bicyclo Compounds -- metabolism KW - Species Specificity KW - Muscimol -- metabolism KW - Male KW - Synaptosomes -- physiology KW - Pentobarbital -- pharmacology KW - Seizures -- chemically induced KW - Mice, Inbred BALB C -- physiology KW - Receptors, GABA-A -- physiology KW - Seizures -- physiopathology KW - Receptors, GABA-A -- drug effects KW - Mice, Inbred DBA -- physiology KW - Chlorides -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76291131?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-02 N1 - Date created - 1989-06-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chromosomal protein HMG-14. Identification, characterization, and chromosome localization of a functional gene from the large human multigene family. AN - 78852624; 2563381 AB - The human HMG-14 multigene family is one of the largest retropseudogene families known. To identify and isolate a functional human HMG-14 gene, genomic clones, selected with the cDNA, were screened with a set of 6 oligonucleotides. A single genomic clone was isolated suggesting that the human genome contains few, and perhaps only one, functional genes. An 8882-base pair (bp) genomic clone containing the complete, 6804-bp-long human gene together with 850 bp 5' to the start of transcription and 1228 bp 3' to the end of transcription was sequenced. The gene is comprised of 6 exons ranging in size from 30 to 839 bp, two of which code for the entire DNA binding site of the protein, and has several features typical of "housekeeping" genes. Using human-rodent somatic cell hybrids, the HMG-14 gene was localized to human chromosome 21. A restriction fragment length polymorphism, useful for further analysis and mapping, has been detected. The present article, which describes the first isolation and characterization of a gene coding for chromosomal protein HMG-14, indicates that genes coding for HMG-14 and HMG-17 may share several distinctive characteristics. Comparison with the human and chicken HMG-17 genes reveals that all contain 6 exons, that all have exons of similar size, that all have 5' regions highly enriched in GC residues and that all have features typical of housekeeping genes. JF - The Journal of biological chemistry AU - Landsman, D AU - McBride, O W AU - Soares, N AU - Crippa, M P AU - Srikantha, T AU - Bustin, M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/02/25/ PY - 1989 DA - 1989 Feb 25 SP - 3421 EP - 3427 VL - 264 IS - 6 SN - 0021-9258, 0021-9258 KW - DNA, Recombinant KW - 0 KW - High Mobility Group Proteins KW - Oligonucleotide Probes KW - DNA KW - 9007-49-2 KW - DNA Restriction Enzymes KW - EC 3.1.21.- KW - Index Medicus KW - Animals KW - Sequence Homology, Nucleic Acid KW - Exons KW - Humans KW - Transcription, Genetic KW - Mice KW - Nucleic Acid Hybridization KW - Base Sequence KW - Chickens KW - Polymorphism, Restriction Fragment Length KW - Chromosomes, Human, Pair 21 KW - DNA -- genetics KW - Introns KW - Molecular Sequence Data KW - High Mobility Group Proteins -- genetics KW - Chromosome Mapping UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78852624?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-21 N1 - Date created - 1989-03-21 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M21339; GENBANK N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phorbol ester-mediated down-regulation of an interferon-inducible gene. AN - 78836461; 2464596 AB - Interferons (IFNs) induce the expression of a variety of cellular RNAs and inhibit phorbol ester induction of other genes. Experiments reported here indicate that phorbol esters can also specifically inhibit the expression of an IFN-induced RNA (IFN-IND-1). Phorbol esters exert their effects by inhibiting IFN-induced transcription of the gene that encodes IFN-IND-1 (ISG-54K); inhibitors of protein synthesis reverse the effects of these compounds. The actions of phorbol esters are only seen in those types of cultured cells where cycloheximide in the presence of IFN prevents long term IFN treatment of cells from inducing a "desensitized state." In desensitized cells, IFN is not able to reinduce the transcription of the RNA. Our results indicate that a protein kinase C-dependent pathway requiring protein synthesis may be one mechanism by which IFN is able to down regulate the transcription of genes whose expression it initially induces. JF - The Journal of biological chemistry AU - Akai, H AU - Larner, A C AD - Laboratory of Pathology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/02/25/ PY - 1989 DA - 1989 Feb 25 SP - 3252 EP - 3255 VL - 264 IS - 6 SN - 0021-9258, 0021-9258 KW - Interferon Type I KW - 0 KW - Recombinant Proteins KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - RNA KW - 63231-63-0 KW - Cycloheximide KW - 98600C0908 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Transcription, Genetic -- drug effects KW - Tumor Cells, Cultured KW - Humans KW - Cycloheximide -- pharmacology KW - Fibroblasts -- metabolism KW - Melanoma KW - Interferon Type I -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Gene Expression Regulation -- drug effects KW - RNA -- genetics KW - RNA -- biosynthesis KW - Phorbol 12,13-Dibutyrate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78836461?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-21 N1 - Date created - 1989-03-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Glucocorticoids potentiate kainic acid-induced seizures and wet dog shakes. AN - 78944733; 2713658 AB - Glucocorticoid effects on kainic acid-induced motor seizures and wet dog shakes in rats were investigated by adrenalectomy and dexamethasone treatment. One-day adrenalectomy attenuated kainic acid-induced wet dog shakes and seizure activity. These effects were restored by dexamethasone. Administration of dexamethasone to non-adrenalectomized rats potentiated kainic acid-induced wet dog shakes and severity of seizure activity. These results suggest that glucocorticoids may play an important role in modulating the severity of kainic acid-induced seizures and wet dog shakes. JF - Brain research AU - Lee, P H AU - Grimes, L AU - Hong, J S AD - Laboratory of Molecular and Integrative Neuroscience, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/02/20/ PY - 1989 DA - 1989 Feb 20 SP - 322 EP - 325 VL - 480 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Glucocorticoids KW - 0 KW - Dexamethasone KW - 7S5I7G3JQL KW - Kainic Acid KW - SIV03811UC KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Drug Interactions KW - Dose-Response Relationship, Drug KW - Adrenalectomy KW - Male KW - Seizures -- chemically induced KW - Glucocorticoids -- physiology KW - Seizures -- physiopathology KW - Dexamethasone -- pharmacology KW - Glucocorticoids -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78944733?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-16 N1 - Date created - 1989-06-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Peroxidase-mediated formation of glutathione conjugates from polycyclic aromatic dihydrodiols and insecticides. AN - 78861375; 2492794 AB - Using two peroxidative systems (prostaglandin H synthase/arachidonic acid and horseradish peroxidase/H2O2) we observed GSH conjugate formation with a number of compounds including polycyclic aromatic hydrocarbon-diols (PAH-diols), insecticides, and steroids. Several of the conjugates were characterized by chromatography, uv-vis spectrophotometry, and FAB mass spectroscopy. Conjugate formation is dependent upon a functioning peroxidase, GSH, and is markedly enhanced (3- to 10-fold) by the inclusion of a number of reducing cosubstrates including phenol, uric acid, phenylbutazone, and acetaminophen. The mechanism of conjugate formation appears to involve addition of thiyl radical to alkene bonds conjugated to an electron releasing group probably by resonance stabilization of the carbon-centered radical intermediate. Thiyl radicals are formed either directly by GSH reduction of the peroxidase or indirectly by GSH reduction of radicals formed from reducing cosubstrates. The nitrone spin trap, 5,5-dimethyl-1-pyrroline N-oxide, which traps thiyl radicals, totally inhibits production of GSH conjugates in both peroxidative systems. Conjugation of PAH-diols, some of which are penultimate carcinogens, would prevent their metabolism to the diol-epoxides, an ultimate carcinogenic species of PAH. Conjugation by peroxidases appears to be a general pathway for glutathione conjugate formation that may lead to potential detoxification of chemicals. JF - Archives of biochemistry and biophysics AU - Foureman, G L AU - Eling, T E AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/02/15/ PY - 1989 DA - 1989 Feb 15 SP - 55 EP - 68 VL - 269 IS - 1 SN - 0003-9861, 0003-9861 KW - Arachidonic Acids KW - 0 KW - Dihydroxydihydrobenzopyrenes KW - Free Radicals KW - Insecticides KW - Sulfhydryl Compounds KW - benzo(a)pyrene 7,8-dihydrodiol KW - 13345-25-0 KW - Arachidonic Acid KW - 27YG812J1I KW - Hydrogen Peroxide KW - BBX060AN9V KW - Horseradish Peroxidase KW - EC 1.11.1.- KW - Peroxidases KW - Prostaglandin-Endoperoxide Synthases KW - EC 1.14.99.1 KW - Glutathione KW - GAN16C9B8O KW - Index Medicus KW - Rats KW - Animals KW - Spectrophotometry, Ultraviolet KW - Gas Chromatography-Mass Spectrometry KW - Glutathione -- chemical synthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78861375?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-16 N1 - Date created - 1989-03-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transduction of cytochrome P3-450 by retroviruses: constitutive expression of enzymatically active microsomal hemoprotein in animal cells. AN - 78860142; 2914941 AB - Cell lines were established which produce replication-defective ecotropic and amphotropic host range recombinant retroviruses containing the cDNA for mouse cytochrome P3-450 as well as the bacterial Neo gene for G418 resistance. The G418-resistant clones derived from virus-infected cultures were analyzed for the expression, subcellular localization, and catalytic activities of the cytochrome P3-450. Southern blot analysis of the genomic DNAs indicates that the viral DNA was stably integrated into the cellular DNA. Western blot analysis of the proteins showed that the size of the constitutively expressed product was Mr 54,000, indistinguishable from the cytochrome P3-450 found in mouse liver microsomes. Spectral characterization of the P3-450 proteins indicates that the newly synthesized apoprotein incorporated heme and integrated into the microsomes. Enzymatic analysis of the cell homogenates in vitro and of the dividing cells in situ showed very high acetanilide hydroxylase activity and very low aryl hydrocarbon hydroxylase activity, a diagnostic feature of the cytochrome P3-450. The precise transmission of the recombinant retroviral sequences into the target cells and the exceptional fidelity of expression of the enzyme in cells will allow the analysis of an increasing number of cloned genes of cytochrome P-450s by defining the individual enzyme specificities, their physiological role in cells, and consequences of their functional expression, such as in toxicity, mutagenesis, and carcinogenesis. JF - The Journal of biological chemistry AU - Battula, N AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/02/15/ PY - 1989 DA - 1989 Feb 15 SP - 2991 EP - 2996 VL - 264 IS - 5 SN - 0021-9258, 0021-9258 KW - DNA, Recombinant KW - 0 KW - Hemeproteins KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - acetanilide hydroxylase KW - Index Medicus KW - Animals KW - Aryl Hydrocarbon Hydroxylases -- metabolism KW - Genes KW - DNA, Recombinant -- metabolism KW - Transfection KW - HeLa Cells KW - Cells, Cultured KW - Humans KW - Genetic Vectors KW - Genes, Viral KW - Aryl Hydrocarbon Hydroxylases -- genetics KW - Cell Line KW - Cytochrome P-450 Enzyme System -- genetics KW - Microsomes, Liver -- metabolism KW - Transduction, Genetic KW - Hemeproteins -- genetics KW - Cytochrome P-450 Enzyme System -- metabolism KW - Retroviridae -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78860142?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-21 N1 - Date created - 1989-03-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Decrease in interleukin 2-induced vascular leakage in the lungs of mice by administration of recombinant interleukin 1 alpha in vivo. AN - 78829676; 2783561 AB - The administration of interleukin 2 (IL-2) to mice and humans is limited by the induction of a dose-dependent increase in vascular permeability causing a vascular leak syndrome (VLS). We have investigated the impact of the injection of recombinant interleukin 1 alpha (IL-1 alpha) on the VLS induced by IL-2 by measuring the extravasation of 125I-albumin into tissues and by assessing wet and dry lung weights. IL-1 alpha alone did not induce any significant extravasation of radiolabeled albumin. IL-2 alone, however, caused a significant increase in the extravasation compared to control lungs. IL-1 alpha injection along with IL-2 significantly reduced the IL-2-induced extravasation of radiolabeled albumin [9,886 +/- 533 (SEM) cpm were observed in IL-2 and IL-1 alpha-treated lungs compared to 14,172 +/- 2,628 cpm in lungs treated with IL-2 alone (P less than 0.02)]. IFN-alpha in combination with IL-2 produced more severe vascular leakage than caused by IL-2 alone. IL-1 alpha also significantly decreased (P less than 0.05) the vascular permeability induced by the combination of IFN-alpha and IL-2. We observed 44,811 +/- 13,131 cpm in IFN-alpha- and IL-2-treated lungs compared to 18,350 +/- 2,622 cpm in IFN-alpha-, IL-2-, and IL-1 alpha-treated lungs. The IL-2- and IFN-alpha-induced increase in lung water weight was also reduced significantly by the addition of IL-1 alpha. The decrease in vascular leakage was dependent on the dose and timing of IL-1 alpha administered. When recombinant IL-1 alpha was given as a single i.p. injection, 24 h before the injection of IL-2 (or Hanks' balanced salt solution) or IL-2 and IFN-alpha no abrogation of the VLS was observed. Although IL-1 alpha decreased VLS significantly in mice treated with IFN-alpha and IL-2 the survival of mice was not improved by the simultaneous administration of IL-1 alpha. Histologically, treatment with IFN-alpha and IL-2 produced marked perivascular and intraalveolar edema which was completely eliminated by the addition of IL-1 alpha. However, some perivascular edema in IL-1 alpha-treated mice remained which was equivalent to that caused by IL-2 alone. Treatment of MCA-106 induced pulmonary metastases was enhanced by the administration of IFN-alpha and IL-2 together.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Cancer research AU - Puri, R K AU - Travis, W D AU - Rosenberg, S A AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/02/15/ PY - 1989 DA - 1989 Feb 15 SP - 969 EP - 976 VL - 49 IS - 4 SN - 0008-5472, 0008-5472 KW - Interferon Type I KW - 0 KW - Interleukin-1 KW - Interleukin-2 KW - Recombinant Proteins KW - Index Medicus KW - Animals KW - Reference Values KW - Lung Neoplasms -- secondary KW - Mice, Inbred C57BL KW - Interferon Type I -- therapeutic use KW - Lung Neoplasms -- therapy KW - Mice KW - Female KW - Interleukin-1 -- pharmacology KW - Recombinant Proteins -- pharmacology KW - Interleukin-2 -- therapeutic use KW - Pulmonary Circulation -- drug effects KW - Lung -- drug effects KW - Lung -- pathology KW - Interleukin-2 -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78829676?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-07 N1 - Date created - 1989-03-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The pharmacokinetics of zidovudine administered by continuous infusion in children. AN - 78827376; 2643914 AB - To define the pharmacokinetics of zidovudine (azidothymidine) in children with human immunodeficiency virus infection. Plasma, urine, and cerebrospinal fluid were obtained following a single 80 mg/m2 body surface dose infused over 1 hour (n = 9), and during a continuous infusion of 0.5 (n = 3), 0.9 (n = 8), 1.4 (n = 7), or 1.8 (n = 3) mg/kg body weight per hour. Outpatient clinic and inpatient ward of the Pediatric Branch of the National Cancer Institute. Twenty-one children (seventeen boys) ranging in age from 14 months to 12 years with symptomatic human immunodeficiency virus infection who were being treated on a phase I-II study of continuous intravenous infusion zidovudine. Zidovudine disappearance following bolus administration was rapid and biexponential with half-lives of 9.6 and 92 minutes, and a total clearance of 705 +/- 330 mL/min.m2. Zidovudine remained above 1 mumol/L, the optimal virostatic concentration in vitro, for only 1.5 hours. In contrast, with continuous infusion steady-state plasma zidovudine concentrations (Css) were maintained above 1 mumol/L continuously, even at the lowest infusion rate. At steady state the ratio of cerebrospinal fluid zidovudine concentration to plasma was 24% +/- 9%. Patients who developed severe neutropenia (absolute neutrophil count less than 0.5 X 10(9)/L) on the continuous infusion regimen had significantly higher plasma Css. Six of eight had a Css greater than 3.0 mumol/L. Pharmacokinetic parameters show that continuous infusion is better than an intermittent schedule in maintaining minimal virostatic concentrations of the drug with a lower daily dose. JF - Annals of internal medicine AU - Balis, F M AU - Pizzo, P A AU - Murphy, R F AU - Eddy, J AU - Jarosinski, P F AU - Falloon, J AU - Broder, S AU - Poplack, D G AD - National Institutes of Health, Bethesda, Maryland. Y1 - 1989/02/15/ PY - 1989 DA - 1989 Feb 15 SP - 279 EP - 285 VL - 110 IS - 4 SN - 0003-4819, 0003-4819 KW - Zidovudine KW - 4B9XT59T7S KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Infant KW - Body Weight KW - Drug Administration Schedule KW - Age Factors KW - Infusions, Intravenous KW - Half-Life KW - Humans KW - Clinical Trials as Topic KW - Neutropenia -- chemically induced KW - Child KW - Male KW - Female KW - Child, Preschool KW - Zidovudine -- therapeutic use KW - Zidovudine -- pharmacokinetics KW - Acquired Immunodeficiency Syndrome -- blood KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Zidovudine -- administration & dosage KW - Acquired Immunodeficiency Syndrome -- cerebrospinal fluid KW - Acquired Immunodeficiency Syndrome -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78827376?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-27 N1 - Date created - 1989-02-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sigma-G RNA polymerase controls forespore-specific expression of the glucose dehydrogenase operon in Bacillus subtilis. AN - 78876070; 2493633 AB - The gene encoding glucose dehydrogenase (gdh) is part of an operon whose expression is transcriptionally activated specifically in the developing forespore of Bacillus subtilis at stage III of sporulation. The in vivo startpoint of gdh transcription was determined using primer extension analysis. Deletion mapping and site-specific mutagenesis experiments indicated that the region responsible for regulated expression of gdh in vivo was limited to the "-35" and "-10" regions preceding the transcriptional start site. RNA polymerase containing omega G (E omega G) transcribed gdh in vitro with a start site identical to that found in vivo, and transcription of gdh by E omega G in vitro also did not require any specific sequences upstream from "-35" region. These results suggest that the appearance of E omega G in the forespore at stage III of sporulation is sufficient to cause temporal and compartment-specific expression of the gdh operon. JF - Nucleic acids research AU - Nakatani, Y AU - Nicholson, W L AU - Neitzke, K D AU - Setlow, P AU - Freese, E AD - Laboratory of Molecular Biology, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892. Y1 - 1989/02/11/ PY - 1989 DA - 1989 Feb 11 SP - 999 EP - 1017 VL - 17 IS - 3 SN - 0305-1048, 0305-1048 KW - DNA, Ribosomal KW - 0 KW - Sigma Factor KW - Transcription Factors KW - Carbohydrate Dehydrogenases KW - EC 1.1.- KW - Glucose Dehydrogenases KW - EC 1.1.1.- KW - DNA-Directed RNA Polymerases KW - EC 2.7.7.6 KW - Index Medicus KW - Protein Biosynthesis KW - Chromosome Deletion KW - Base Sequence KW - DNA Mutational Analysis KW - Molecular Sequence Data KW - Gene Expression Regulation KW - Lac Operon KW - Nucleotide Mapping KW - Cloning, Molecular KW - Glucose Dehydrogenases -- genetics KW - Bacillus subtilis -- enzymology KW - Transcription Factors -- physiology KW - Bacillus subtilis -- genetics KW - Carbohydrate Dehydrogenases -- genetics KW - Sigma Factor -- physiology KW - Operon KW - DNA-Directed RNA Polymerases -- physiology KW - Spores, Bacterial -- physiology KW - Spores, Bacterial -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78876070?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-12 N1 - Date created - 1989-04-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Mol Biol. 1971 Mar 14;56(2):209-21 [4994568] J Bacteriol. 1988 Nov;170(11):5086-92 [3141376] J Mol Biol. 1973 Jun 25;77(2):255-77 [4587752] Anal Biochem. 1976 May 7;72:248-54 [942051] Bacteriol Rev. 1976 Dec;40(4):908-62 [12736] J Bacteriol. 1977 Oct;132(1):282-93 [21162] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Mol Gen Genet. 1979 Jan 5;168(1):111-5 [107388] Methods Enzymol. 1980;65(1):499-560 [6246368] J Bacteriol. 1980 Dec;144(3):1119-25 [6777366] Proc Natl Acad Sci U S A. 1983 Feb;80(3):785-9 [6219387] Proc Natl Acad Sci U S A. 1983 Apr;80(8):2305-9 [6300908] Methods Enzymol. 1983;101:20-78 [6310323] Cell. 1983 Nov;35(1):275-83 [6414720] Proc Natl Acad Sci U S A. 1984 Jan;81(2):439-43 [6420789] Mol Cell Biol. 1984 Mar;4(3):520-8 [6325881] J Bacteriol. 1985 Feb;161(2):556-62 [3918016] J Bacteriol. 1986 Apr;166(1):238-43 [3082854] Mol Gen Genet. 1986 Aug;204(2):229-36 [3020362] Annu Rev Genet. 1986;20:625-69 [3101583] J Bacteriol. 1988 Jan;170(1):239-44 [3121585] Methods Enzymol. 1987;154:498-511 [3431461] J Biol Chem. 1971 May 25;246(10):3189-95 [4995746] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Passive smoking on commercial airline flights. AN - 78845344; 2913384 AB - In-flight exposure to nicotine, urinary cotinine levels, and symptom self-reports were assessed in a study of nine subjects (five passengers and four attendants) on four routine commercial flights each of approximately four hours' duration. Urine samples were collected for 72 hours following each flight. Exposures to nicotine measured during the flights using personal exposure monitors were found to be variable, with some nonsmoking areas attaining levels comparable to those in smoking sections. Attendants assigned to work in nonsmoking areas were not protected from smoke exposure. The type of aircraft ventilation was important in determining the levels of in-flight nicotine exposure. The environmental tobacco smoke levels that occurred produced measurable levels of cotinine (a major metabolite of nicotine) in the urine of passengers and attendants. Passengers who experienced the greatest smoke exposure had the highest levels of urinary cotinine. Changes in eye and nose symptoms between the beginning and end of the flights were significantly related both to nicotine exposure during the flight and to the subsequent urinary excretion of cotinine. In addition, subjects' perceptions of annoyance and smokiness in the airplane cabin were also related to in-flight nicotine exposure and urinary excretion measures. JF - JAMA AU - Mattson, M E AU - Boyd, G AU - Byar, D AU - Brown, C AU - Callahan, J F AU - Corle, D AU - Cullen, J W AU - Greenblatt, J AU - Haley, N J AU - Hammond, K AD - National Cancer Institute, Division of Cancer Prevention and Control, Bethesda, MD 20892. Y1 - 1989/02/10/ PY - 1989 DA - 1989 Feb 10 SP - 867 EP - 872 VL - 261 IS - 6 SN - 0098-7484, 0098-7484 KW - Air Pollutants KW - 0 KW - Tobacco Smoke Pollution KW - Nicotine KW - 6M3C89ZY6R KW - Cotinine KW - K5161X06LL KW - Abridged Index Medicus KW - Index Medicus KW - Environmental Monitoring KW - Cotinine -- urine KW - Humans KW - Nicotine -- analysis KW - Air Pollutants -- analysis KW - Male KW - Female KW - Aircraft KW - Tobacco Smoke Pollution -- adverse effects KW - Tobacco Smoke Pollution -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78845344?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-09 N1 - Date created - 1989-03-09 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: JAMA. 1989 Nov 24;262(20):2838 [2535641] JAMA. 1989 Nov 24;262(20):2837-8 [2627218] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In situ phosphorylation of human platelet myosin heavy and light chains by protein kinase C. AN - 78840150; 2914906 AB - Treatment of human platelets with 162 nM 12-O-tetradecanoylphorbol-13-acetate (TPA) resulted in phosphorylation of a number of peptides, including myosin heavy chain and the 20-kDa myosin light chain. The site phosphorylated on the myosin heavy chain was localized by two-dimensional peptide mapping to a serine residue(s) in a single major tryptic phosphopeptide. This phosphopeptide co-migrated with a tryptic peptide that was produced following in vitro phosphorylation of platelet myosin heavy chain using protein kinase C. The sites phosphorylated in the 20-kDa myosin light chain in intact cells were analyzed by two-dimensional mapping of tryptic peptides and found to correspond to Ser1 and Ser2 in the turkey gizzard myosin light chain. In vitro phosphorylation of purified human platelet myosin by protein kinase C showed that in addition to Ser1 and Ser2, a third site corresponding to Thr9 in turkey gizzard myosin light chain is also phosphorylated. The phosphorylatable myosin light chains from human platelets were found to consist of two major isoforms present in approximately equal amounts, but differing in their molecular weights and isoelectric points. A third, minor isoform was also visualized by two-dimensional gel electrophoresis. Following treatment with TPA, both the mono- and diphosphorylated forms of each isoform could be visualized, and the sites of phosphorylation were identified. The phosphate content rose from negligible amounts found prior to treatment with TPA to 1.2 mol of phosphate/mol of myosin light chain and 0.7 mol of phosphate/mol of myosin heavy chain following treatment. These results suggest that TPA mediates phosphorylation of both myosin light and heavy chains in intact platelets by activation of protein kinase C. JF - The Journal of biological chemistry AU - Kawamoto, S AU - Bengur, A R AU - Sellers, J R AU - Adelstein, R S AD - Laboratory of Molecular Cardiology, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989/02/05/ PY - 1989 DA - 1989 Feb 05 SP - 2258 EP - 2265 VL - 264 IS - 4 SN - 0021-9258, 0021-9258 KW - Myosin Subfragments KW - 0 KW - Peptide Fragments KW - Phosphopeptides KW - Protein Kinase C KW - EC 2.7.11.13 KW - Trypsin KW - EC 3.4.21.4 KW - Myosins KW - EC 3.6.4.1 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Phosphopeptides -- isolation & purification KW - Phosphorylation KW - Kinetics KW - Humans KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Protein Kinase C -- blood KW - Blood Platelets -- enzymology KW - Peptide Fragments -- isolation & purification KW - Myosins -- isolation & purification KW - Myosins -- blood KW - Peptide Fragments -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78840150?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-13 N1 - Date created - 1989-03-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: J Biol Chem 1989 May 15;264(14):8442 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Participation of a guanine nucleotide-binding protein cascade in cholera toxin activation of adenylate cyclase. AN - 79030505; 2499682 AB - Guanine nucleotide-binding (G) proteins are involved in several transmembrane signaling systems. Choleragen (cholera toxin) activates adenylate cyclase by catalyzing the ADP-ribosylation of Gs alpha, the stimulatory G protein of the cyclase system. This reaction is enhanced by another guanine nucleotide-binding protein termed ADP-ribosylation factor or ARF that was purified from bovine brain membranes [R. A. Kahn and A. G. Gilman, Journal of Biological Chemistry (1986) 261, 7906-7911]. It was recently found that this ARF also increases the NAD:agmatine and NAD:protein ADP-ribosyltransferase, NAD glycohydrolase and auto-ADP-ribosylation activities of the toxin. We have purified and characterized two soluble proteins from bovine brain that act in a similar fashion to enhance choleragen activity in each of these reactions. The membrane and soluble factors are all proteins of approximately 19 kDa that require GTP or GTP analogues for activity and are ADP-ribosylated by the toxin. The ARF proteins apparently interact directly with choleragen in a GTP-dependent fashion to increase its catalytic activity and thus are part of a G protein cascade through which the toxin activates adenylate cyclase. The physiological function of the ARF proteins, as well as their possible relationships to the ras oncogene products and/or the family of G proteins that includes Gs alpha, remains to be determined. JF - Journal of molecular and cellular cardiology AU - Vaughan, M AU - Tsai, S C AU - Noda, M AU - Adamik, R AU - Moss, J AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 97 EP - 102 VL - 21 Suppl 1 SN - 0022-2828, 0022-2828 KW - Membrane Proteins 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 - Animals KW - Cattle KW - Membrane Proteins -- metabolism KW - In Vitro Techniques KW - Enzyme Activation -- drug effects KW - Rabbits KW - Signal Transduction KW - GTP-Binding Proteins -- metabolism KW - Cholera Toxin -- pharmacology KW - Adenylyl Cyclases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79030505?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-18 N1 - Date created - 1989-07-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Protamine sulfate as an effective alternative to polybrene in retroviral-mediated gene-transfer: implications for human gene therapy. AN - 79018721; 2786000 AB - The polycation protamine sulfate was compared to polybrene, the usual agent employed, for its ability to increase the efficiency of retroviral infection. The murine retroviral vector SAX, which contains the neoR gene and the human adenosine deaminase (ADA) cDNA, was used as a marker of cell infection. SAX viral supernate was titered on NIH 3T3 cells in varying concentrations of polycation. The highest infection efficiency for protamine was seen at 5 micrograms/ml and was 7-fold greater than infections performed in the absence of polycation. Infection efficiency using protamine averaged 92% +/- 11 (SEM) of the highest efficiency obtained with polybrene. Total ADA activity attained when human-ADA deficient T cells were exposed to SAX supernate in the presence of protamine was 83% of that attained with polybrene. The infection rate of mouse bone marrow early progenitor cells (CFU-S) was similar with each polycation. In summary, for supernate infections, concentrations of 5-10 micrograms/ml of protamine provided essentially the same infection efficiency as polybrene with low toxicity on a range of cell types. Since protamine is approved for human use by the U.S. Food and Drug Administration it provides an effective alternative to polybrene when developing human gene therapy protocols. JF - Journal of virological methods AU - Cornetta, K AU - Anderson, W F AD - Laboratory of Molecular Hematology, National Heart, Lung and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 187 EP - 194 VL - 23 IS - 2 SN - 0166-0934, 0166-0934 KW - Cations KW - 0 KW - Polyamines KW - Polymers KW - Protamines KW - polycations KW - Index Medicus KW - Bone Marrow Cells KW - Animals KW - Cells, Cultured KW - T-Lymphocytes -- microbiology KW - Humans KW - Mice KW - Cell Line KW - Mice, Inbred DBA KW - Transfection KW - Protamines -- pharmacology KW - Retroviridae -- drug effects KW - Genetic Vectors KW - Retroviridae -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79018721?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-05 N1 - Date created - 1989-07-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transforming growth factor-beta 1 enhances the suppression of human hematopoiesis by tumor necrosis factor-alpha or recombinant interferon-alpha. AN - 78976366; 2715197 AB - The effects of transforming growth factor-beta 1 (TGF-beta 1) on human hematopoiesis were evaluated in combination with two other regulatory cytokines, namely, recombinant human tumor necrosis factor-alpha (TNF-alpha) and recombinant human interferon-alpha (rIFN-alpha). Combinations of TNF-alpha and TGF-beta 1 resulted in a synergistic suppression of colony formation by erythroid progenitor cells (BFU-E) and an additive suppression of granulocyte-macrophage (CFU-GM) and multipotential (CFU-GEMM) progenitor cells. In addition, TGF-beta 1 synergized with rIFN-alpha to suppress CFU-GM formation, while the combined suppressive effects of both cytokines on CFU-GEMM and BFU-E were additive. When TGF-beta 1 was tested with TNF-alpha or IFN-alpha on granulocyte/macrophage colony-stimulating factor (GM-CSF)-stimulated bone marrow cells in a 5-day proliferation assay, the antiproliferative effects of TGF-beta 1 and TNF-alpha were additive, while those with TGF-beta 1 and rIFN-alpha were synergistic. A similar pattern was seen in the suppression of the myeloblastic cell line KG-1 where TGF-beta 1 in combination with TNF-alpha resulted in an additive suppression while inhibition by TGF-beta 1 and IFN-alpha was synergistic. These results demonstrate for the first time the cooperative effects between TGF-beta and TNF-alpha and IFN-alpha in the suppression of hematopoietic cell growth, raising the possibility that TGF-beta might be used in concert with TNF-alpha or IFN-alpha in the treatment of various myeloproliferative disorders. JF - Journal of cellular biochemistry AU - Sing, G K AU - Keller, J R AU - Ellingsworth, L R AU - Ruscetti, F W AD - Division of Cancer Treatment, National Cancer Institute-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 107 EP - 115 VL - 39 IS - 2 SN - 0730-2312, 0730-2312 KW - Interferon Type I KW - 0 KW - Recombinant Proteins KW - Tumor Necrosis Factor-alpha KW - Transforming Growth Factors KW - 76057-06-2 KW - Index Medicus KW - Humans KW - Cell Division -- drug effects KW - Leukemia, Myeloid, Acute -- pathology KW - Drug Synergism KW - Leukemia, Experimental -- pathology KW - Cell Line KW - Hematopoietic Stem Cells -- drug effects KW - Interferon Type I -- pharmacology KW - Hematopoiesis -- drug effects KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Transforming Growth Factors -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78976366?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-15 N1 - Date created - 1989-06-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Two-year toxicity and carcinogenicity studies of ampicillin trihydrate and penicillin VK in rodents. AN - 78972599; 2497039 AB - Toxicology and carcinogenesis studies of ampicillin trihydrate and penicillin VK, two widely used beta-lactam antibiotics, were performed in F344/N rats and B6C3F1 mice. In these studies ampicillin trihydrate was administered for 2 years to rats at doses of 0, 750, or 1500 mg/kg and to mice at doses of 0, 1500, or 3000 mg/kg, and penicillin VK was administered to rats and mice at doses of 0, 500, or 1000 mg/kg. Both drugs were administered by oral gavage in corn oil. Toxic lesions of the stomach were seen in rats and mice after ampicillin trihydrate administration and in mice after penicillin VK administration. In male rats that received ampicillin trihydrate there was a marginal increase in incidence of mononuclear cell leukemia and pheochromocytomas of the adrenal gland medulla. There was no evidence for carcinogenic activity in female rats or male and female mice after ampicillin trihydrate administration or in rats and mice after penicillin VK administration. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Dunnick, J K AU - Eustis, S L AU - Huff, J E AU - Haseman, J K AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 252 EP - 257 VL - 12 IS - 2 SN - 0272-0590, 0272-0590 KW - Carcinogens KW - 0 KW - Ampicillin KW - 7C782967RD KW - Penicillin V KW - Z61I075U2W KW - Index Medicus KW - Rats KW - Mice, Inbred Strains KW - Animals KW - Rats, Inbred F344 KW - Body Weight -- drug effects KW - Mice KW - Male KW - Female KW - Penicillin V -- toxicity KW - Ampicillin -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78972599?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-22 N1 - Date created - 1989-06-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Functional identification of regulatory elements within the promoter region of platelet-derived growth factor 2. AN - 78952025; 2651898 AB - Human platelet-derived growth factor (PDGF) is composed of two polypeptide chains, PDGF-1 and PDGF-2, the human homolog of the v-sis oncogene. Deregulation of PDGF-2 expression can confer a growth advantage to cells possessing the cognate receptor and, thus, may contribute to the malignant phenotype. We investigated the regulation of PDGF-2 mRNA expression during megakaryocytic differentiation of K562 cells. Induction by 12-O-tetradecanoylphorbol-13-acetate (TPA) led to a greater than 200-fold increase in PDGF-2 transcript levels in these cells. Induction was dependent on protein synthesis and was not enhanced by cycloheximide exposure. In our initial investigation of the PDGF-2 promoter, a minimal promoter region, which included sequences extending only 42 base pairs upstream of the TATA signal, was found to be as efficient as 4 kilobase pairs upstream of the TATA signal in driving expression of a reporter gene in uninduced K562 cells. We also functionally identified different regulatory sequence elements of the PDGF-2 promoter in TPA-induced K562 cells. One region acted as a transcriptional silencer, while another region was necessary for maximal activity of the promoter in megakaryoblasts. This region was shown to bind nuclear factors and was the target for trans-activation in normal and tumor cells. In one tumor cell line, which expressed high PDGF-2 mRNA levels, the presence of the positive regulatory region resulted in a 30-fold increase in promoter activity. However, the ability of the minimal PDGF-2 promoter to drive reporter gene expression in uninduced K562 cells and normal fibroblasts, which contained no detectable PDGF-2 transcripts, implies the existence of other negative control mechanisms beyond the regulation of promoter activity. JF - Molecular and cellular biology AU - Pech, M AU - Rao, C D AU - Robbins, K C AU - Aaronson, S A AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 396 EP - 405 VL - 9 IS - 2 SN - 0270-7306, 0270-7306 KW - Platelet-Derived Growth Factor KW - 0 KW - Proto-Oncogene Proteins KW - Proto-Oncogene Proteins c-sis KW - RNA, Messenger KW - Transcription Factors KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Chromosome Deletion KW - Tumor Cells, Cultured -- metabolism KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Cell Differentiation KW - RNA, Messenger -- genetics KW - Transcription Factors -- genetics KW - RNA, Messenger -- biosynthesis KW - Base Sequence KW - Molecular Sequence Data KW - Tumor Cells, Cultured -- pathology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Gene Expression Regulation KW - Promoter Regions, Genetic KW - Platelet-Derived Growth Factor -- genetics KW - Proto-Oncogene Proteins -- genetics KW - Genes, Regulator UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78952025?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-26 N1 - Date created - 1989-05-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Virology. 1968 Oct;36(2):254-61 [4300880] Proc Natl Acad Sci U S A. 1986 Sep;83(17):6455-9 [3529084] Blood. 1975 Mar;45(3):321-34 [163658] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] Exp Cell Res. 1981 Dec;136(2):255-61 [6171440] Nature. 1982 Jan 14;295(5845):116-9 [6173755] J Biol Chem. 1982 May 10;257(9):5161-71 [6279659] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] Cell. 1983 Dec;35(3 Pt 2):603-10 [6606489] Nucleic Acids Res. 1984 Feb 10;12(3):1687-96 [6322116] Nucleic Acids Res. 1983 Dec 10;11(23):8287-301 [6324080] Nucleic Acids Res. 1984 Sep 25;12(18):7035-56 [6091052] Cell. 1984 Nov;39(1):89-97 [6091919] Proc Natl Acad Sci U S A. 1984 Nov;81(21):6772-4 [6208557] Cell. 1985 May;41(1):301-12 [2986848] Science. 1985 Nov 22;230(4728):912-6 [3904002] Nature. 1986 Jan 9-15;319(6049):154-8 [3079885] Nature. 1986 Jan 9-15;319(6049):158-60 [3941744] Nucleic Acids Res. 1986 Jan 24;14(2):765-78 [3003695] Nucleic Acids Res. 1986 Feb 11;14(3):1303-17 [3513122] Proc Natl Acad Sci U S A. 1986 May;83(10):3371-5 [3458188] Nature. 1986 Oct 9-15;323(6088):555-8 [3020435] Mol Cell Biol. 1986 Apr;6(4):1050-7 [2431274] Mol Cell Biol. 1986 May;6(5):1847-50 [3466024] Nucleic Acids Res. 1986 Dec 22;14(24):10009-26 [3808945] Nucleic Acids Res. 1986 Dec 22;14(24):9679-98 [3027659] Cell. 1987 Jun 19;49(6):729-39 [3034432] Cell. 1987 Jun 19;49(6):741-52 [3034433] Cold Spring Harb Symp Quant Biol. 1986;51 Pt 2:959-66 [3472769] EMBO J. 1987 May;6(5):1213-8 [3475202] Cell. 1987 Dec 4;51(5):783-93 [3119226] Mol Cell Biol. 1988 Jan;8(1):284-92 [3275870] Oncogene. 1987 Mar;1(1):79-85 [3325876] Cell. 1981 Dec;27(3 Pt 2):467-76 [6101201] Proc Natl Acad Sci U S A. 1986 Apr;83(8):2392-6 [3517869] Proc Natl Acad Sci U S A. 1986 Apr;83(8):2453-7 [3010310] Nature. 1986 Jun 12-18;321(6071):702-6 [3520340] Cell. 1986 Jul 18;46(2):155-69 [3013421] Exp Cell Res. 1970 Jul;61(1):1-5 [5431618] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Toxicity and carcinogenicity of nitrofurazone in F344/N rats and B6C3F1 mice. AN - 78943514; 2714718 AB - Toxicology and carcinogenesis studies were conducted by feeding diets containing nitrofurazone (99% pure) to groups of F344/N rats and B6C3F1 mice for 14 days, 13 wk or 2 yr. In the 14-day studies, in which doses ranged from 630 to 10,000 ppm, nitrofurazone was more toxic to mice than to rats. Accordingly, in the 13-wk studies, doses for rats ranged from 150 to 2500 ppm and for mice from 70 to 1250 ppm. At the higher doses, convulsive seizures and gonadal hypoplasia were observed in both species. Evidence of toxicity in rats also included degenerative arthropathy. For the 2-yr studies, rats were exposed to 0, 310 or 620 ppm nitrofurazone and the survival of male rats given 620 ppm was lower than that of controls (33/50, 30/50 and 20/50 in the control, 310- and 620-ppm groups, respectively). Nitrofurazone administration increased the incidences of mammary gland fibroadenomas in female rats (8/49, 36/50 and 36/50 in the control, 310- and 620-ppm groups, respectively). In male rats it was associated with a marginal increase in sebaceous gland adenomas and trichoepitheliomas of the skin, mesotheliomas of the tunica vaginalis, and tumours of the perputial gland. Nitrofurazone caused testicular degeneration (atrophy of germinal epithelium and aspermatogenesis) in rats, and degeneration of vertebral and knee articular cartilage in rats of both sexes. In mice, dietary concentrations of nitrofurazone for the 2-yr studies were 0, 150 or 310 ppm. In mice of each sex, nitrofurazone administration induced stimulus-sensitive convulsive seizures, primarily during the first year of study. In male mice, there was no evidence of any chemically-related carcinogenic effects, but there was a treatment-related decrease in survival (39/50, 31/50 and 27/50 in the control, 150- and 310-ppm groups, respectively). In female mice nitrofurazone induced ovarian lesions with increased incidences of benign mixed tumours (0/47, 17/50 and 20/50 in control, low- and high-dose groups, respectively) and granulosa cell tumours (1/47, 4/50 and 9/50 in control, low- and high-dose groups, respectively). JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association AU - Kari, F W AU - Huff, J E AU - Leininger, J AU - Haseman, J K AU - Eustis, S L AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 129 EP - 137 VL - 27 IS - 2 SN - 0278-6915, 0278-6915 KW - Nitrofurazone KW - X8XI70B5Z6 KW - Index Medicus KW - Rats KW - Eating -- drug effects KW - Mammary Neoplasms, Experimental -- chemically induced KW - Animals KW - Rats, Inbred F344 KW - Dose-Response Relationship, Drug KW - Body Weight -- drug effects KW - Carcinogenicity Tests KW - Ovarian Neoplasms -- chemically induced KW - Mice KW - Male KW - Female KW - Nitrofurazone -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78943514?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-16 N1 - Date created - 1989-06-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Developmental toxicity of 2,3,4,7,8-pentachlorodibenzofuran in the Fischer 344 rat. AN - 78936715; 2714534 AB - Fischer 344 rats were exposed acutely to 2,3,4,7,8-pentachlorodibenzofuran (4-PeCDF) during the organogenic period to evaluate its potential as an inducer of teratogenic and embryolethal effects. All dams were treated by gavage with a single dose of 0, 30, 100, or 300 micrograms 4-PeCDF/kg body wt on gestation Day (gd) 8, 10, or 12. An additional treatment group was included on gd 12 and administered 10 micrograms 4-PeCDF/kg body wt po. All animals were killed on gd 20 and maternal and fetal toxicities were assessed. Determination of embryotoxicity involved both soft tissue and skeletal examinations. 4-PeCDF induced a dose-related decrease in corrected maternal weight gain following treatment on gd 8 and 10, as well as resulted in a concomitant increase in the liver/body weight ratios, first evident at 30 micrograms/kg for all 3 days of exposure. The maternal thymus weight decreased relative to body weight compared with those of controls. Embryo-fetal toxicity was evident from the high mortality (greater than 80%) observed at 300 micrograms/kg for all 3 days of exposure. Mean fetal weight, a sensitive indicator of fetal toxicity, decreased compared to that of controls at 30, 100, and 300 micrograms/kg following treatment on either gd 8, 10, or 12.4-PeCDF induced cleft palate in survivors at a dose of 300 micrograms/kg for all 3 days of exposure. In conclusion, 4-PeCDF is maternally and fetally toxic regardless of the gestation day of exposure, but induced terata only at doses where overt maternal and fetal toxicity were observed, in contrast to previously reported studies in the mice where teratogenic effects were observed at nonfetotoxic dose levels. Thus, the mouse may be a more sensitive model for evaluating specific toxic responses induced prenatally following exposure to the structurally related polyhalogenated aromatic hydrocarbons which include the dioxins, furans, biphenyls, and naphthalenes. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Couture, L A AU - Harris, M W AU - Birnbaum, L S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 358 EP - 366 VL - 12 IS - 2 SN - 0272-0590, 0272-0590 KW - Benzofurans KW - 0 KW - Teratogens KW - 2,3,4,7,8-pentachlorodibenzofuran KW - U4C2RV3124 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Fetus -- drug effects KW - Gestational Age KW - Body Weight -- drug effects KW - Male KW - Female KW - Pregnancy KW - Organ Size -- drug effects KW - Benzofurans -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78936715?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-22 N1 - Date created - 1989-06-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of beta-polymerase mRNA by DNA-damaging agents in Chinese hamster ovary cells. AN - 78933105; 2710127 AB - Only a few of the genes involved in DNA repair in mammalian cells have been isolated, and induction of a DNA repair gene in response to DNA damage has not yet been established. DNA polymerase beta (beta-polymerase) appears to have a synthetic role in DNA repair after certain types of DNA damage. Here we show that the level of beta-polymerase mRNA is increased in CHO cells after treatment with several DNA-damaging agents. JF - Molecular and cellular biology AU - Fornace, A J AU - Zmudzka, B AU - Hollander, M C AU - Wilson, S H AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 851 EP - 853 VL - 9 IS - 2 SN - 0270-7306, 0270-7306 KW - RNA, Messenger KW - 0 KW - Methylnitronitrosoguanidine KW - 12H3O2UGSF KW - Methyl Methanesulfonate KW - AT5C31J09G KW - DNA Polymerase I KW - EC 2.7.7.- KW - Index Medicus KW - Animals KW - Ultraviolet Rays KW - Gene Expression Regulation -- radiation effects KW - Cricetulus KW - Ovary KW - Cells, Cultured KW - Gene Expression Regulation -- drug effects KW - Female KW - Cricetinae KW - DNA Damage KW - DNA Polymerase I -- genetics KW - DNA Polymerase I -- biosynthesis KW - RNA, Messenger -- genetics KW - RNA, Messenger -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78933105?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-26 N1 - Date created - 1989-05-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Chem Biol Interact. 1971 Feb;3(1):29-47 [5156325] Curr Genet. 1986;11(2):107-12 [3329047] Biochemistry. 1980 Apr 29;19(9):1782-90 [6246934] FEBS Lett. 1981 Mar 23;125(2):227-30 [7014256] J Biol Chem. 1982 Sep 10;257(17):10204-9 [6179938] J Biol Chem. 1983 Jan 10;258(1):108-18 [6848490] Biochim Biophys Acta. 1983 Apr 15;739(3):301-11 [6403037] Nature. 1983 Aug 11-17;304(5926):552-4 [6877378] J Biol Chem. 1983 Aug 25;258(16):9990-4 [6411709] Anal Biochem. 1983 Dec;135(2):318-25 [6660508] Microbiol Rev. 1984 Mar;48(1):60-93 [6371470] Biochemistry. 1984 Mar 27;23(7):1383-91 [6426505] J Biol Chem. 1984 Aug 25;259(16):10252-9 [6088490] J Biol Chem. 1985 Sep 5;260(19):10412-7 [2411723] Mutat Res. 1985 Nov;146(3):295-300 [4058446] J Biol Chem. 1986 Mar 15;261(8):3536-43 [3005291] Biochem Biophys Res Commun. 1986 Apr 14;136(1):341-7 [2423078] Carcinogenesis. 1986 Jun;7(6):927-32 [3708756] Proc Natl Acad Sci U S A. 1986 Jul;83(14):5106-10 [2873575] J Biol Chem. 1988 Nov 15;263(32):16992-8 [3182828] Nucleic Acids Res. 1988 Oct 25;16(20):9587-96 [2460824] Nucleic Acids Res. 1986 Jul 25;14(14):5793-811 [2426659] Mol Cell Biol. 1987 May;7(5):2012-8 [3600656] Nucleic Acids Res. 1987 Jul 10;15(13):5017-30 [3299263] Biochim Biophys Acta. 1988 Feb 28;949(2):149-57 [3277667] Biochemistry. 1977 Nov 1;16(22):4927-34 [911803] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fidelity of two retroviral reverse transcriptases during DNA-dependent DNA synthesis in vitro. AN - 78932008; 2469002 AB - We determined the fidelity of avian myeloblastosis virus and Moloney murine leukemia virus reverse transcriptases (RTs) during DNA synthesis in vitro using the M13mp2 lacZ alpha gene as a mutational target. Both RTs commit an error approximately once for every 30,000 nucleotides polymerized. DNA sequence analysis of mutants generated in a forward mutation assay capable of detecting many types of errors demonstrated that avian myeloblastosis virus RT produced a variety of different mutations. The majority (58%) were single-base substitutions; all of which resulted from the misincorporation of either dAMP or dGMP. Minus-one frameshifts were also common, composing about 30% of the mutations. In addition to single-base events, eight mutants contained sequence changes involving from 2 to 59 bases. The frequency of these mutants suggests that, at least during DNA synthesis in vitro, RTs also commit errors by mechanisms other than classical base miscoding and misalignment. We examined the ability of RTs to synthesize DNA from a mismatched primer terminus at a sequence where the mismatched base was complementary to the next base in the template. Unlike cellular DNA polymerases which polymerize from the mismatched template-primer, RTs preferred to polymerize from a rearranged template-primer containing a matched terminal base pair and an unpaired base in the template strand. The unusual preference for this substrate suggests that the interactions between RTs and the template-primer are different from those of cellular DNA polymerases. The overall error rate of RT in vitro is sufficient to account for the estimated mutation rate of these viruses. JF - Molecular and cellular biology AU - Roberts, J D AU - Preston, B D AU - Johnston, L A AU - Soni, A AU - Loeb, L A AU - Kunkel, T A AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 469 EP - 476 VL - 9 IS - 2 SN - 0270-7306, 0270-7306 KW - Codon KW - 0 KW - DNA, Viral KW - RNA-Directed DNA Polymerase KW - EC 2.7.7.49 KW - Index Medicus KW - Moloney murine leukemia virus -- enzymology KW - Mutagenicity Tests KW - Base Sequence KW - Codon -- genetics KW - Avian Myeloblastosis Virus -- genetics KW - Molecular Sequence Data KW - Avian Myeloblastosis Virus -- enzymology KW - Moloney murine leukemia virus -- genetics KW - Genes, Viral KW - Mutation KW - Retroviridae -- enzymology KW - DNA, Viral -- biosynthesis KW - RNA-Directed DNA Polymerase -- metabolism KW - Retroviridae -- genetics KW - DNA, Viral -- genetics KW - RNA-Directed DNA Polymerase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78932008?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-26 N1 - Date created - 1989-05-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1972 Jan 10;247(1):241-8 [4336040] Virology. 1961 Feb;13:158-63 [13775833] Biochem Biophys Res Commun. 1973 May 15;52(2):401-6 [4123058] J Biol Chem. 1974 Jul 10;249(13):4086-93 [4137275] J Biol Chem. 1975 Jan 25;250(2):470-8 [163228] J Virol. 1975 Apr;15(4):843-54 [46925] Biochem Biophys Res Commun. 1974 Nov 27;61(2):410-4 [4375985] J Biol Chem. 1976 Feb 25;251(4):982-6 [55415] Biochemistry. 1976 Apr 6;15(7):1510-6 [769823] Biochemistry. 1976 Jun 29;15(13):2817-23 [949478] J Biol Chem. 1977 Apr 10;252(7):2281-9 [66234] J Biol Chem. 1977 Jun 10;252(11):3605-10 [863897] Biochim Biophys Acta. 1977 Oct 4;478(3):305-15 [199256] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Cell. 1978 Jul;14(3):601-9 [80281] J Virol. 1978 Oct;28(1):279-91 [81316] J Gen Virol. 1979 Jan;42(1):1-26 [215703] Nature. 1979 Apr 26;278(5707):857-9 [220540] J Biol Chem. 1981 Apr 10;256(7):3405-14 [6259165] J Virol. 1982 Jan;41(1):163-71 [6283110] Annu Rev Biochem. 1982;51:429-57 [6214209] Proc Natl Acad Sci U S A. 1983 Jan;80(2):487-91 [6300848] Biochemistry. 1983 May 10;22(10):2378-84 [6344919] Nucleic Acids Res. 1983 Sep 10;11(17):5953-67 [6310522] Proc Natl Acad Sci U S A. 1984 Mar;81(5):1494-8 [6369329] J Biol Chem. 1984 Jul 25;259(14):9314-9 [6235226] J Biol Chem. 1985 May 10;260(9):5787-96 [3988773] J Virol. 1985 Nov;56(2):589-99 [2414465] J Biol Chem. 1986 Jan 5;261(1):160-6 [3941068] Nature. 1970 Jun 27;226(5252):1209-11 [4316300] Ann N Y Acad Sci. 1980;354:410-25 [6261656] Science. 1981 Aug 14;213(4509):765-7 [6454965] J Biol Chem. 1981 Oct 10;256(19):9883-9 [6456268] Proc Natl Acad Sci U S A. 1981 Nov;78(11):6734-8 [6458818] Proc Natl Acad Sci U S A. 1982 Feb;79(4):1230-4 [6951170] Proc Natl Acad Sci U S A. 1986 Mar;83(6):1867-71 [2937062] Science. 1986 Jun 20;232(4757):1548-53 [3012778] Cell. 1986 Jul 4;46(1):1-4 [3013415] Proc Natl Acad Sci U S A. 1987 Jul;84(14):4865-9 [3474631] J Biol Chem. 1987 Aug 5;262(22):10824-30 [3038898] J Gen Virol. 1987 Nov;68 ( Pt 11):2729-40 [3316486] J Biol Chem. 1988 Mar 25;263(9):4450-9 [2831231] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1777-81 [2450347] Genetics. 1988 Feb;118(2):181-91 [3282984] Proc Natl Acad Sci U S A. 1988 Jun;85(11):3918-22 [2453880] Science. 1988 Jun 10;240(4858):1427-35 [3287617] J Virol. 1988 Aug;62(8):2817-22 [2839703] Proc Natl Acad Sci U S A. 1988 Oct;85(19):7064-8 [3174620] Biochim Biophys Acta. 1988 Nov 10;951(1):1-15 [2847793] J Biol Chem. 1972 May 25;247(10):3139-46 [4554914] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transforming growth factor alpha: an aromatic side chain at position 38 is essential for biological activity. AN - 78919099; 2710128 AB - Site-directed mutagenesis has been performed in the human transforming growth factor alpha gene. When tyrosine 38 is mutated into phenylalanine or tryptophane, biological activity is retained. In contrast, other alterations between cysteine 34 and cysteine 43 and disruption of disulfide bonds 8 to 21 and 34 to 43 resulted in loss of activities. The presence of an aromatic side chain at position 38 of transforming growth factor alpha seems to be essential for its activity. JF - Molecular and cellular biology AU - Lazar, E AU - Vicenzi, E AU - Van Obberghen-Schilling, E AU - Wolff, B AU - Dalton, S AU - Watanabe, S AU - Sporn, M B AD - Laboratory of Chemoprevention, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 860 EP - 864 VL - 9 IS - 2 SN - 0270-7306, 0270-7306 KW - Transforming Growth Factors KW - 76057-06-2 KW - Index Medicus KW - Animals KW - Biological Evolution KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Species Specificity KW - Mutation KW - Structure-Activity Relationship KW - Cloning, Molecular KW - Transforming Growth Factors -- physiology KW - Transforming Growth Factors -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78919099?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-26 N1 - Date created - 1989-05-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1973 Nov 25;248(22):7669-72 [4750422] Mol Cell Biol. 1988 Mar;8(3):1247-52 [3285178] Anal Biochem. 1976 May 7;72:248-54 [942051] Genetics. 1977 Jan;85(1):23-33 [320092] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Proc Natl Acad Sci U S A. 1978 Aug;75(8):4001-5 [211512] Proc Natl Acad Sci U S A. 1983 Oct;80(20):6264-8 [6604914] J Biol Chem. 1983 Nov 25;258(22):13614-20 [6315706] Science. 1984 Mar 9;223(4640):1079-82 [6320373] Cell. 1984 Aug;38(1):287-97 [6088071] Proc Natl Acad Sci U S A. 1984 Dec;81(23):7363-7 [6334307] Science. 1985 May 24;228(4702):1007-9 [3859011] Cell. 1985 Dec;43(3 Pt 2):567-81 [3935325] Cell. 1985 Dec;43(3 Pt 2):583-90 [3000611] Eur J Biochem. 1985 Dec 16;153(3):629-37 [3000782] Science. 1986 Jun 6;232(4755):1250-3 [2422759] Cell. 1986 Jul 18;46(2):301-9 [3459590] Mol Cell Biol. 1985 Dec;5(12):3644-6 [3870134] J Biol Chem. 1986 Nov 5;261(31):14408-13 [3464597] Proc Natl Acad Sci U S A. 1986 Nov;83(22):8594-8 [3490668] Mol Cell Biol. 1986 Sep;6(9):3094-108 [3097517] Nucleic Acids Res. 1986 Nov 11;14(21):8427-46 [3491360] Science. 1987 Jan 16;235(4786):350-2 [3492044] Cancer Res. 1987 Feb 1;47(3):707-12 [3467839] Cell. 1987 Feb 13;48(3):429-40 [3467848] J Virol. 1987 Apr;61(4):1271-5 [3029424] Proc Natl Acad Sci U S A. 1987 Mar;84(5):1258-62 [3469667] Mol Cell Biol. 1987 Jan;7(1):535-40 [3031480] Nature. 1987 May 28-Jun 3;327(6120):339-41 [3495735] Proc Natl Acad Sci U S A. 1987 Aug;84(15):5226-30 [3496602] Cell. 1987 Sep 25;50(7):1131-7 [3497724] Nature. 1987 Aug 27-Sep 2;328(6133):817-20 [2442615] Nature. 1975 Sep 25;257(5524):325-7 [1161035] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ifosfamide--pharmacologic overview. AN - 78897189; 2649983 AB - Ifosfamide and its structural analogue cyclophosphamide are oxazaphosphorine nitrogen mustards, a group of compounds synthesized in West Germany more than 20 years ago. Whereas both chloroethyl groups of cyclophosphamide are attached to the same exocyclic nitrogen, one of ifosfamide's chloroethyl groups is attached to an endocyclic nitrogen. This minor structural change may account for the different pharmacologic behavior of these two compounds as well as their different spectrums of clinical activity and toxicity. Initial clinical trials of ifosfamide explored the use of a single intravenous dose. Hemorrhagic cystitis appeared to be dose-dependent and limited the use of this agent. However, the development of a systemic thiol uroprotector, such as mesna, has overcome this toxicity, permitting higher ifosfamide doses to be administered. Currently, ifosfamide is usually administered daily for five days in combination with mesna. The pharmacology and metabolism of ifosfamide may explain the toxicities associated with this compound and should be considered when designing schedules of administration. JF - Seminars in oncology AU - Sarosy, G AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 2 EP - 8 VL - 16 IS - 1 Suppl 3 SN - 0093-7754, 0093-7754 KW - Ifosfamide KW - UM20QQM95Y KW - Index Medicus KW - Drug Evaluation KW - Animals KW - Humans KW - Ifosfamide -- pharmacokinetics KW - Ifosfamide -- adverse effects KW - Ifosfamide -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78897189?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-15 N1 - Date created - 1989-05-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Halogenated pyrimidines as radiosensitizers for high-LET radiation. AN - 78892417; 2922478 AB - The incorporation of iododeoxyuridine (IdUrd) into Chinese hamster cells was examined as a possible radiosensitizer for fission spectrum neutrons. Dose-response curves comparing both X rays and neutrons in the same cell line with the same IdUrd replacement showed a similar radiation enhancement for IdUrd incorporation. Enhancement ratios at the 1% survival level were 1.8 for X rays and 1.5 for fission spectrum neutrons. While the mechanism of this enhancement in the response for fission neutron radiation is unclear, these positive data should support further exploration to determine if halogenated pyrimidine incorporation results in sensitization for neutron energies employed in therapy. JF - Radiation research AU - Atcher, R W AU - Russo, A AU - DeGraff, W G AU - Moore, M AU - Grdina, D J AU - Mitchell, J B AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 351 EP - 355 VL - 117 IS - 2 SN - 0033-7587, 0033-7587 KW - Radiation-Sensitizing Agents KW - 0 KW - Idoxuridine KW - LGP81V5245 KW - Index Medicus KW - Space life sciences KW - Animals KW - Dose-Response Relationship, Radiation KW - Cell Line KW - Neutrons KW - Idoxuridine -- pharmacology KW - Cell Survival -- drug effects KW - Radiation-Sensitizing Agents -- pharmacology KW - Cell Survival -- radiation effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78892417?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-17 N1 - Date created - 1989-04-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of FSH-stimulated cAMP accumulation by mono(2-ethylhexyl) phthalate in primary rat Sertoli cell cultures. AN - 78888407; 2538009 AB - High doses of phthalate esters in vivo cause testicular lesions. One initial target for these effects is the sustentacular Sertoli cell. Sertoli cells are unique in that they have surface membrane receptors for follicle-stimulating hormone (FSH), which couple to adenylate cyclase. As a means of investigating why phthalates appear specific for Sertoli cells, we evaluated possible effects of an active monoester [mono(2-ethylhexyl) phthalate, MEHP] on the ability of FSH to elevate intracellular levels of cAMP. MEHP reduced FSH-induced elevation of cAMP levels by approximately 40%. This inhibition by MEHP required a lag period of 6 hr and did not affect the dose of FSH which gave half-maximal stimulation, suggesting that MEHP does not compete with FSH for binding to its receptor. The MEHP inhibition was not affected by incubation in the presence of methylisobutylxanthine, a phosphodiesterase inhibitor, suggesting that MEHP does not stimulate the breakdown of cAMP. The MEHP-induced inhibition is specific for FSH; it does not affect the ability of forskolin, cholera toxin, isoproterenol, or prostaglandin E1 to stimulate Sertoli cell cAMP. Furthermore, inhibition occurs in the presence of pertussis toxin suggesting that MEHP action is independent of the inhibitory adenylate cyclase pathway. Further experiments will be necessary to define the specific mechanism of action of phthalates on Sertoli cells; however, these experiments do describe a specific site of action of MEHP in vitro which may be related to the in vivo testicular toxicity of phthalate esters. JF - Toxicology and applied pharmacology AU - Heindel, J J AU - Chapin, R E AD - Developmental and Reproductive Toxicology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 377 EP - 385 VL - 97 IS - 2 SN - 0041-008X, 0041-008X KW - Phthalic Acids KW - 0 KW - di-n-pentyl phthalate KW - 131-18-0 KW - Colforsin KW - 1F7A44V6OU 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 - Colforsin -- pharmacology KW - Cells, Cultured KW - Male KW - Sertoli Cells -- drug effects KW - Cyclic AMP -- biosynthesis KW - Sertoli Cells -- metabolism KW - Diethylhexyl Phthalate -- toxicity KW - Follicle Stimulating Hormone -- pharmacology KW - Diethylhexyl Phthalate -- analogs & derivatives KW - Phthalic Acids -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78888407?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-07 N1 - Date created - 1989-04-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparative metabolism and disposition of ethyl carbamate (urethane) in male Fischer 344 rats and male B6C3F1 mice. AN - 78888315; 2493688 AB - The metabolism, disposition, and excretion of ethyl carbamate (EC) was investigated following oral or iv administration of a wide range of doses to male rats and mice. At a low dose, 4.75 mg/kg, administered iv, approximately 98% was exhaled as CO2 within 8 or 12 hr by mice or rats, respectively. However, as the dose increased, the percentage of dose eliminated as CO2 decreased in a dose-dependent manner which was much more pronounced in rats than mice. At all doses studied, mice eliminated EC as CO2 (as % dose) more rapidly than rats. Evidence of saturation of metabolism and elimination was observed at doses greater than 4.75 mg/kg in rats and greater than 47.5 mg/kg in mice. Following iv administration of 47.5 or 475 mg/kg, EC was initially evenly distributed in all tissues of each species except fat. After the initial time point (15 min), rat tissues contained higher concentrations of 14C compared to tissues of mice receiving the same dose. The disappearance of 14C from blood and various tissues followed monoexponential kinetics with rates dependent upon the species and the dose but independent of the tissue. Following oral administration, EC was completely absorbed from the gastrointestinal tracts of rats and mice at all doses studied. Approximately 5, 0.7, and 1% of the doses were excreted in urine, in feces, and as volatile organics, respectively. EC was neither an inducer nor an inhibitor of its own metabolism to CO2 following daily treatment of rats with oral doses of 47.5 mg/kg for 9 days. Only the parent compound was present in blood, lungs, skin, liver, kidney, muscle, and bile of treated rats. The urinary metabolic profile of EC was not affected by the route of administration in either species; however, in the rat but not in the mouse it was influenced by dose. Pretreatment of rats with piperonyl butoxide or SKF 525A (cytochrome P-450 inhibitors) or tri-o-cresyl phosphate (TOCP) or paraoxon (carboxylesterase inhibitors) or methyl carbamate (competitive substrate) did not greatly alter the metabolism of EC to CO2. The in vitro metabolism of EC to CO2 was not highly localized in any particular tissue or subcellular fraction of liver and was not affected by NADPH, GSH, NADH, or combinations of these cofactors. This work indicates that a number of studies of EC carcinogenicity have used doses that exceed the capacity of rats and mice to metabolize this chemical in a linear fashion. JF - Toxicology and applied pharmacology AU - Nomeir, A A AU - Ioannou, Y M AU - Sanders, J M AU - Matthews, H B AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 203 EP - 215 VL - 97 IS - 2 SN - 0041-008X, 0041-008X KW - Carcinogens, Environmental KW - 0 KW - Tritolyl Phosphates KW - Carbon Dioxide KW - 142M471B3J KW - Urethane KW - 3IN71E75Z5 KW - tri-o-cresyl phosphate KW - X8II18JD0A KW - Index Medicus KW - Rats KW - Mice, Inbred Strains KW - Animals KW - Rats, Inbred F344 KW - Tritolyl Phosphates -- pharmacology KW - Mice KW - Tissue Distribution KW - Carcinogens, Environmental -- toxicity KW - Carbon Dioxide -- metabolism KW - Species Specificity KW - Male KW - Urethane -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78888315?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-07 N1 - Date created - 1989-04-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interaction of peptides related to VIP and secretin with guinea pig pancreatic acini. AN - 78886320; 2465694 AB - The abilities of human and rat growth hormone-releasing factors (hGHRF, rGHRF), peptide histidine isoleucine or methionine (PHI, PHM) and the Gila monster venom peptides (helospectin I, helospectin II, and helodermin) to interact with guinea pig pancreatic acini were characterized and compared with vasoactive intestinal peptide (VIP) and secretin. Each peptide caused a sevenfold stimulation of amylase release, and the relative potencies were: VIP greater than helospectin I = helospectin II = helodermin = rGHRF greater than PHI = PHM greater than hGHRF greater than secretin. Each peptide inhibited 125I-labeled VIP binding, and the relative potencies agreed closely with those for stimulating enzyme secretion. Each peptide inhibited 125I-labeled secretin binding with the potencies: secretin greater than helospectin I = helospectin II = helodermin greater than rGHRF = PHI = VIP greater than PHM greater than hGHRF. Each peptide caused a 78-fold increase in adenosine 3',5'-cyclic monophosphate cAMP. VIP or rGHRF and PHI or PHM demonstrated high and low selectivity, respectively, for VIP receptors, secretin high selectivity for the secretin receptor, and helospectin I or II and helodermin a relatively high affinity for both VIP and secretin receptors. Correlation of the ability of each peptide to increase cAMP or amylase release and inhibit binding of 125I-VIP or 125I-secretin suggested all the actions of these peptides could be explained by the occupation of VIP or secretin receptors. To investigate this further, 125I-labeled helodermin was prepared, and binding was saturable, specific, and could be accounted for by the binding to VIP or secretin receptors.(ABSTRACT TRUNCATED AT 250 WORDS) JF - The American journal of physiology AU - Zhou, Z C AU - Gardner, J D AU - Jensen, R T AD - Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - G283 EP - G290 VL - 256 IS - 2 Pt 1 SN - 0002-9513, 0002-9513 KW - Peptide PHI KW - 0 KW - Receptors, Gastrointestinal Hormone KW - Receptors, Vasoactive Intestinal Peptide KW - Recombinant Proteins KW - Venoms KW - Secretin KW - 1393-25-5 KW - Vasoactive Intestinal Peptide KW - 37221-79-7 KW - Growth Hormone-Releasing Hormone KW - 9034-39-3 KW - Amylases KW - EC 3.2.1.- KW - Index Medicus KW - Animals KW - Growth Hormone-Releasing Hormone -- pharmacology KW - Recombinant Proteins -- pharmacology KW - Guinea Pigs KW - Lizards KW - Amino Acid Sequence KW - Peptide PHI -- pharmacology KW - Structure-Activity Relationship KW - Receptors, Gastrointestinal Hormone -- drug effects KW - Molecular Sequence Data KW - Receptors, Gastrointestinal Hormone -- metabolism KW - Venoms -- pharmacology KW - Vasoactive Intestinal Peptide -- pharmacology KW - Pancreas -- cytology KW - Vasoactive Intestinal Peptide -- metabolism KW - Vasoactive Intestinal Peptide -- analogs & derivatives KW - Secretin -- pharmacology KW - Pancreas -- enzymology KW - Amylases -- secretion KW - Pancreas -- drug effects KW - Secretin -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78886320?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-29 N1 - Date created - 1989-03-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Glucose utilization in the rat brain during chronic morphine treatment and naloxone-precipitated morphine withdrawal. AN - 78877388; 2918470 AB - Rates of local cerebral glucose utilization (LCGU) were measured in morphine-dependent and morphine-abstinent rats. Morphine pellets were implanted s.c. (one pellet 7 days before glucose utilization measurement and two pellets 4 days before the measurement) to produce opioid dependence. LCGU rates in 85 brain regions of placebo- and morphine-pelleted rats were similar. In contrast, LCGU rates, 5 hr after implantation of one morphine pellet, were decreased significantly in six areas. The lack of a chronic morphine effect on LCGU suggests tolerance to morphine. Additional support for this view was that an additional dose of morphine (8 mg/kg s.c.) in morphine-dependent rats was also ineffective in altering LCGU and in an antinociception (hot plate) test. Furthermore, plasma morphine levels in chronically treated animals were greater than those in acutely treated animals. Naloxone-precipitated morphine withdrawal enhanced LCGU, most notably in thalamic and limbic areas, but also in some hypothalamic and hindbrain regions. The findings identify brain areas that may be important in the opioid abstinence syndrome. Furthermore they suggest that adaptations in the brain produce tolerance to morphine, reflected in LCGU rates and latencies in the hot-plate test. JF - The Journal of pharmacology and experimental therapeutics AU - Kimes, A S AU - London, E D AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 538 EP - 545 VL - 248 IS - 2 SN - 0022-3565, 0022-3565 KW - Naloxone KW - 36B82AMQ7N KW - Testosterone KW - 3XMK78S47O KW - Morphine KW - 76I7G6D29C KW - Glucose KW - IY9XDZ35W2 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Morphine Dependence -- metabolism KW - Testosterone -- blood KW - Male KW - Naloxone -- pharmacology KW - Substance Withdrawal Syndrome -- metabolism KW - Morphine -- blood KW - Glucose -- metabolism KW - Brain -- drug effects KW - Brain -- metabolism KW - Morphine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78877388?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-03 N1 - Date created - 1989-04-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of the uptake and metabolism of retinol delivered to primary mouse keratinocytes either free or bound to rat serum retinol-binding protein. AN - 78871412; 2465355 AB - Serum retinol-binding protein (RBP) is believed to be responsible for the transport of retinol from its storage site in the liver to vitamin A requiring target cells such as keratinocytes. We have used primary mouse keratinocytes as a model system to compare the uptake and metabolism of [3H] retinol delivered to them either free in solution or bound to RBP. RBP was purified from rat serum, loaded with [3H]retinol, and the [3H]retinol-RBP complex purified by affinity chromatography on human transthyretin-Sepharose. Keratinocytes incubated with either free [3H]retinol or [3H]retinol-RBP complex accumulated [3H]retinol in a time and temperature dependent manner. However, cells incubated with free [3H]retinol acquired 15- to 20-fold more ligand than if the retinol was delivered via RBP. The uptake of free [3H]retinol or [3H]retinol from RBP was not inhibited by excess unlabeled free retinol. The uptake of [3H]retinol from RBP was inhibited by high concentrations of holo-RBP, with half maximal inhibition occurring at 3 microM holo-RBP. However, no specific binding of 125I-labeled RBP to monolayers of keratinocytes or membranes prepared from them was found indicating the absence of a high affinity RBP receptor on keratinocytes. Surprisingly, 50% of the [3H]retinol delivered to the keratinocytes during a 30-min uptake period was released from them within 30-min irrespective of whether or not it was initially delivered to them as free [3H]retinol or bound to RBP. The remaining 50% was lost at a much slower rate, but only 20% remained 24-h after delivery. Studies on retinol metabolism demonstrated that 7%-12% of the total cell-associated [3H]retinol delivered during a 90-min uptake period was esterified (mostly as retinyl palmitate) whether or not it was given free in solution or bound to RBP. Additionally, [3H]retinol taken up by the keratinocytes during the initial 90-min incubation was not chased into a stable retinyl ester pool in a subsequent 9.5-h incubation, but instead, retinyl ester was lost from the cells with kinetics similar to those of total cell-associated radioactivity. These results suggest that a function of RBP is to protect cells from a rapid accumulation of the vitamin which occurs when it is delivered free in solution. However, the cellular fate and metabolism of retinol appears to be the same whether the vitamin is delivered free in solution or bound to RBP. JF - The Journal of investigative dermatology AU - Creek, K E AU - Silverman-Jones, C S AU - De Luca, L M AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 283 EP - 289 VL - 92 IS - 2 SN - 0022-202X, 0022-202X KW - Retinol-Binding Proteins KW - 0 KW - Solutions KW - Vitamin A KW - 11103-57-4 KW - Keratins KW - 68238-35-7 KW - Index Medicus KW - Animals KW - Rats -- blood KW - Mice KW - Mice, Inbred BALB C KW - Vitamin A -- blood KW - Vitamin A -- pharmacokinetics KW - Epidermis -- cytology KW - Epidermis -- metabolism KW - Retinol-Binding Proteins -- metabolism KW - Retinol-Binding Proteins -- blood KW - Vitamin A -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78871412?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-24 N1 - Date created - 1989-03-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibitory effects of the antiprogestin, RU 486, on progesterone actions and luteinizing hormone secretion in pituitary gonadotrophs. AN - 78869780; 2646475 AB - The effects of RU 486 on the modulation of LH release by progesterone were investigated in cultured anterior pituitary cells from ovariectomized adult female rats. The inhibitory effect of progesterone on LH secretion was demonstrable in estrogen-treated pituitary cells, in which addition of 10(-6) M progesterone to cells cultured in the presence of 10(-9) M estradiol for 52 h reduced the LH response to GnRH (10(-11) to 10(-7) M). When RU 486 was superimposed upon such combined treatment with estradiol and progesterone, the suppressive effect of progesterone on GnRH-induced LH release was completely abolished. The converse (facilitatory) effect of progesterone on LH secretion was observed in pituitary cells pretreated with 10(-9) M estradiol for 48 h and then with 10(-6) M progesterone for 4 h. When RU 486 was added together with progesterone during the 4 h treatment period, the facilitatory effect of progesterone was blocked and LH release fell to below the corresponding control value. The direct effect of RU 486 on LH secretion in the absence of exogenous progesterone was evaluated in cells cultured in the absence or presence of 10(-9) M estradiol and then treated for 4 to 24 h with increasing concentrations of RU 486 (10(-12) to 10(-5) M) and stimulated with GnRH (10(-9) M) during the last 3 h of incubation. In estrogen-deficient cultures, 4 h exposure to RU 486 concentrations of 10(-6) M and above decreased the LH response to GnRH by up to 50%. In cultures pretreated with 10(-9) M estradiol, GnRH-stimulated LH responses was inhibited by much lower RU 486 concentrations, of 10(-9) M and above. After 24 h of incubation the effects of RU 486 were similar in control and estradiol-pretreated pituitary cell cultures. Thus, RU 486 alone has a significant inhibitory effect on LH secretion that is enhanced in the presence of estrogen. The antiprogestin is also a potent antagonist of both the inhibitory and the facilitatory actions of progesterone upon pituitary gonadotropin release in vitro. JF - Journal of steroid biochemistry AU - Ortmann, O AU - Emons, G AU - Knuppen, R AU - Catt, K J AD - Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 291 EP - 297 VL - 32 IS - 2 SN - 0022-4731, 0022-4731 KW - Estrenes KW - 0 KW - Mifepristone KW - 320T6RNW1F KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 KW - Progesterone KW - 4G7DS2Q64Y KW - Estradiol KW - 4TI98Z838E KW - Luteinizing Hormone KW - 9002-67-9 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Estradiol -- pharmacology KW - Drug Synergism KW - Gonadotropin-Releasing Hormone -- pharmacology KW - Female KW - Luteinizing Hormone -- secretion KW - Pituitary Gland, Anterior -- drug effects KW - Pituitary Gland, Anterior -- secretion KW - Progesterone -- pharmacology KW - Estrenes -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78869780?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-07 N1 - Date created - 1989-04-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Are complications in intraoperative radiation therapy more frequent than in conventional treatment? AN - 78868812; 2644922 AB - To evaluate whether intraoperative radiation therapy (IORT) results in higher complication rates than conventional radiotherapy, 119 patients were studied who entered four prospectively randomized clinical trials that compared IORT with conventional therapy. Malignant neoplasms included 33 gastric carcinomas, 35 retroperitoneal sarcomas, 22 resectable pancreatic cancers, and 29 unresectable pancreatic cancers. One hundred thirty-six complications developed among 66 patients who received conventional therapy, and 108 complications developed among 53 patients who received IORT. There was no statistical significance between treatment groups with respect to the overall incidence of complications. Analysis of types of complications by tumor type using Fisher's exact test revealed only one significant complication: an increased rate of sepsis among the patients with retroperitoneal sarcoma who received conventional therapy compared with their IORT cohorts. The overall complication rate associated with IORT was equivalent to conventional radiotherapy in the treatment of these malignant neoplasms and supported the use of IORT where clinically indicated. JF - Archives of surgery (Chicago, Ill. : 1960) AU - Cromack, D T AU - Maher, M M AU - Hoekstra, H AU - Kinsella, T J AU - Sindelar, W F AD - Surgery Branche, National Cancer Institute, Bethesda, Md 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 229 EP - 234 VL - 124 IS - 2 SN - 0004-0010, 0004-0010 KW - Abridged Index Medicus KW - Index Medicus KW - Random Allocation KW - Combined Modality Therapy KW - Stomach Neoplasms -- surgery KW - Humans KW - Clinical Trials as Topic KW - Aged KW - Retroperitoneal Neoplasms -- radiotherapy KW - Pancreatic Neoplasms -- radiotherapy KW - Prospective Studies KW - Stomach Neoplasms -- radiotherapy KW - Adult KW - Middle Aged KW - Intraoperative Period KW - Retroperitoneal Neoplasms -- surgery KW - Female KW - Male KW - Pancreatic Neoplasms -- surgery KW - Postoperative Complications KW - Abdominal Neoplasms -- surgery KW - Radiotherapy -- adverse effects KW - Abdominal Neoplasms -- radiotherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78868812?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-14 N1 - Date created - 1989-03-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Quantitative methods for assessing a synergistic or potentiated genotoxic response. AN - 78865415; 2918861 AB - The problem of assessing chemical interactions in studies of genotoxicity is discussed. Attention is focused on assessing possible synergism or potentiation when the observed genotoxic response is binary (yes-no). Different forms of enhancement are distinguished based upon different assumptions on the genotoxic activity of the experimental treatments. A generalized linear statistical model is considered that links the probability of the binary response to the doses, and data-analytic strategies are described for detecting synergy and potentiation in factorially designed experiments. This approach is illustrated with a series of analyses of various genotoxicity data-sets. JF - Mutation research AU - Piegorsch, W W AU - Margolin, B H AD - Statistics and Biomathematics Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 1 EP - 8 VL - 216 IS - 1 SN - 0027-5107, 0027-5107 KW - Chromates KW - 0 KW - Potassium Compounds KW - Caffeine KW - 3G6A5W338E KW - potassium chromate(VI) KW - 5P0R38CN2X KW - Aminacrine KW - 78OY3Z0P7Z KW - Hydroxyurea KW - X6Q56QN5QC KW - Index Medicus KW - X-Rays KW - Caffeine -- toxicity KW - Chromates -- toxicity KW - Aminacrine -- toxicity KW - Statistics as Topic KW - Models, Biological KW - Hydroxyurea -- toxicity KW - Mutagenicity Tests -- standards KW - Drug Synergism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78865415?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-29 N1 - Date created - 1989-03-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mortality and career radiation doses for workers at a commercial nuclear power plant: feasibility study. AN - 78863121; 2917842 AB - Career radiation doses for 8,961 male workers at the Calvert Cliffs Nuclear Power Plant (CCNPP) were determined for both utility (n = 4,960) and contractor (n = 4,001) employees. Workers were followed from the time of first employment at CCNPP (including plant construction) to the end of 1984 (mean follow-up = 5.4 y). Plant operation began in 1975. The mean duration of employment was 1.9 y at CCNPP and 3.1 y in the nuclear industry. Career radiation doses were determined from dosimetry records kept by the utility company and the U.S. Nuclear Regulatory Commission (NRC). For all exposed workers, the average career dose was 21 mSv and was higher for contractor (30 mSv) than utility (13 mSv) workers. Career doses were also higher among those employed in the nuclear industry for greater than or equal to 15 y (111 mSv) and among workers classified as health physicists (56 mSv). Cumulative doses of greater than or equal to 50 mSv were received by 12% of the workers; the maximum career dose reported was 470 mSv. The availability of social security numbers for practically all employees facilitated record-linkage methods to determine mortality; 161 deaths were identified. On average the workers experienced mortality from all causes that was 15% less than that of the general population of the U.S., probably due to healthier members of the population being selected for employment. Our investigation demonstrates that historical information is available from which career doses could be constructed and that, in principle, it is feasible to conduct epidemiologic studies of nuclear power plant workers in the U.S. Although difficult, the approach taken could prove useful until such time as a comprehensive registry of U.S. radiation workers is established. JF - Health physics AU - Goldsmith, R AU - Boice, J D AU - Hrubec, Z AU - Hurwitz, P E AU - Goff, T E AU - Wilson, J AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 139 EP - 150 VL - 56 IS - 2 SN - 0017-9078, 0017-9078 KW - Index Medicus KW - United States KW - Power Plants KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Cause of Death KW - Radiation Dosage KW - Mortality KW - Occupational Medicine KW - Nuclear Energy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78863121?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-03 N1 - Date created - 1989-04-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genetic characterization of FLA, the cat major histocompatibility complex. AN - 78861568; 2492667 AB - The major histocompatibility complex (MHC) of the domestic cat (termed FLA) has been refractile to genetic and serological definition largely because of repeated failure to detect cytotoxic antibodies in multiparous cats or to elicit antibody following allogeneic lymphocyte immunization. We have developed a protocol for producing cytotoxic alloantisera in the cat following rejection of multiple surgical skin grafts. Of 59 cats subjected to grafting, 13 produced lymphocytotoxic antisera which had varying specificities among a panel of outbred cat cells. A population cluster analysis of the 13 alloantisera permitted the identification of six clusters of overlapping FLA specificities. Serological analysis of cells from 12 cat kindreds led to the definition of 24 allogeneic haplotypes, which segregate as a single Mendelian complex. Feline FLA antisera were characterized as class I or class II specific by immunoprecipitation of FLA gene products on lymphocyte cell surfaces. Abundant antigenic polymorphisms for both class I and class II MHC determinants were discovered, a result consistent with precedence in other species and the common expectation of the adaptive value of MHC variation. Development of feline MHC typing reagents and the definition of haplotypes for the cat hold promise for experimental analysis of valuable feline models for virus-induced immune deficiencies. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Winkler, C AU - Schultz, A AU - Cevario, S AU - O'Brien, S AD - Laboratory of Viral Carcinogenesis, National Cancer Institute-Frederick Cancer Research Facility, MD 21701. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 943 EP - 947 VL - 86 IS - 3 SN - 0027-8424, 0027-8424 KW - Immune Sera KW - 0 KW - Index Medicus KW - Cytotoxicity, Immunologic KW - Animals KW - Haplotypes KW - Polymorphism, Genetic KW - Transplantation, Homologous KW - Male KW - Female KW - Genes, MHC Class II KW - Genes, MHC Class I KW - Cats -- genetics KW - Skin Transplantation KW - Cats -- immunology KW - Major Histocompatibility Complex UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78861568?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-16 N1 - Date created - 1989-03-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Scand J Immunol. 1974;3(2):161-72 [4595707] Proc Natl Acad Sci U S A. 1974 Jan;71(1):35-9 [4129801] J Immunol. 1976 Jul;117(1):136-42 [58931] J Immunol. 1979 Jul;123(1):342-9 [87477] Chem Biol Interact. 1979 Dec;28(2-3):181-99 [162045] Cell. 1981 May;24(2):287-99 [7016338] J Biol Chem. 1982 Mar 10;257(5):2619-26 [6174509] Immunogenetics. 1982;16(4):339-47 [7174000] J Virol. 1983 May;46(2):355-61 [6302307] Immunology. 1983 Dec;50(4):613-24 [6197354] Transplantation. 1983 Dec;36(6):712-8 [6581642] Transplantation. 1984 May;37(5):509-13 [6233766] Transplantation. 1984 Jun;37(6):634-6 [6375021] Vet Immunol Immunopathol. 1984 May;6(1-2):107-65 [6204435] Vet Immunol Immunopathol. 1984 Aug;7(1):1-9 [6237486] Nature. 1984 Nov 29-Dec 5;312(5993):467-9 [6438532] Science. 1985 Mar 22;227(4693):1428-34 [2983425] Hum Immunol. 1985 Mar;12(3):143-64 [3156824] Immunogenetics. 1985;21(6):569-79 [2989165] Annu Rev Immunol. 1985;3:237-61 [2415139] Immunogenetics. 1986;23(5):341-7 [3458670] Science. 1987 Feb 13;235(4790):790-3 [3643650] Lancet. 1987 Aug 1;2(8553):245-9 [2886718] Nature. 1987 Oct 8-14;329(6139):506-12 [3309677] Science. 1988 Feb 19;239(4842):906-10 [2893454] Immunogenetics. 1988;27(6):414-25 [2897330] Proc Natl Acad Sci U S A. 1988 Jun;85(11):4005-9 [3375250] Transplantation. 1967 Sep 5;5(5):1323-33 [6056944] J Natl Cancer Inst. 1972 Nov;49(5):1357-65 [4346537] J Exp Med. 1975 Jun 1;141(6):1427-36 [47901] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Derivation of a T cell line that is highly responsive to IL-4 and IL-2 (CT.4R) and of an IL-2 hyporesponsive mutant of that line (CT.4S). AN - 78856755; 2783601 AB - The derivation of subline of CTLL cells that grow in IL-4/B cell stimulatory factor-1 is described. These cells, designated CT.4R cells, were obtained by extended culture of the CTLL line CT.EV in IL-4. CT.4R cells are highly responsive to both IL-4 and IL-2. Mutagenesis of CT.4R cells with ethylmethane sulfonate and selection for lack of expression of the p55 chain of the IL-2R was carried out and a clone was selected that was hyporesponsive to IL-2 but retained full sensitivity to IL-4. These cells, designated CT.4S cells, develop a very meager response to IL-2 at concentrations of 100 U/ml or less although that display vigorous responses to higher IL-2 concentrations. CT.4S cells give measurable responses to 3-10 U/ml (approximately 15-50 pg/ml) of IL-4. CT.4R and CT.4S cells fail to respond to IL-1, IL-3, IL-6, granulocyte-macrophage-CSF, granulocyte-CSF, CSF-1 or IFN-gamma. Thus, CT.4S cells can be used as a sensitive and specific bioassay for IL-4. ID CT.4R cells can be grown in either IL-4 or IL-2. When grown in IL-4, CT.4R cells express small amounts of the p55 chain of the IL-2R but rapidly upregulate their level of expression of p55 when IL-2 is added and rapidly diminish p55 expression when IL-2 is removed. Thus, although IL-2 and IL-4 both stimulate vigorous growth responses by CT.4R cells, they differ in their capacity to induce the expression of the p55 chain implying that their mechanisms of T cell stimulation are not identical. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Hu-Li, J AU - Ohara, J AU - Watson, C AU - Tsang, W AU - Paul, W E AD - Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1989/02/01/ PY - 1989 DA - 1989 Feb 01 SP - 800 EP - 807 VL - 142 IS - 3 SN - 0022-1767, 0022-1767 KW - Interleukin-2 KW - 0 KW - Interleukins KW - Receptors, Interleukin-2 KW - Interleukin-4 KW - 207137-56-2 KW - Abridged Index Medicus KW - Index Medicus KW - Receptors, Interleukin-2 -- metabolism KW - Humans KW - Dose-Response Relationship, Immunologic KW - Drug Synergism KW - Receptors, Interleukin-2 -- immunology KW - Cell Line KW - Receptors, Interleukin-2 -- drug effects KW - Lymphocyte Activation -- drug effects KW - Interleukin-2 -- pharmacology KW - Interleukins -- pharmacology KW - Interleukin-2 -- metabolism KW - Interleukins -- metabolism KW - T-Lymphocytes, Cytotoxic -- immunology KW - T-Lymphocytes, Cytotoxic -- metabolism KW - Mutation KW - T-Lymphocytes, Cytotoxic -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78856755?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-01 N1 - Date created - 1989-03-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cardiac allograft survival in mice treated with IL-2-PE40. AN - 78855784; 2644640 AB - IL-2-PE40 is a chimeric protein composed of human interleukin 2 (IL-2) genetically fused to the amino terminus of a modified form of Pseudomonas exotoxin lacking its cell recognition domain. IL-2-PE40, which is extremely cytotoxic to IL-2 receptor-positive cells, was examined for its ability to prevent graft rejection in mice in which activation of T cells is prominent. We demonstrate that intraperitoneally administered IL-2-PE40 specifically and significantly prolongs the survival of vascularized heart allografts in mice. The chimeric toxin, IL-2-PE40, offers an alternative approach to the treatment of autoimmune diseases and transplant rejection in humans. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Lorberboum-Galski, H AU - Barrett, L V AU - Kirkman, R L AU - Ogata, M AU - Willingham, M C AU - FitzGerald, D J AU - Pastan, I AD - Laboratory of Molecular Biology, National Institutes of Health, Bethesda, MD 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 1008 EP - 1012 VL - 86 IS - 3 SN - 0027-8424, 0027-8424 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - IL-2-PE40 chimeric protein, recombinant KW - Immunotoxins KW - Interleukin-2 KW - Recombinant Fusion Proteins KW - Recombinant Proteins KW - Virulence Factors KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Aspartate Aminotransferases KW - EC 2.6.1.1 KW - Alanine Transaminase KW - EC 2.6.1.2 KW - Index Medicus KW - Animals KW - Liver -- enzymology KW - Liver -- pathology KW - Heart -- drug effects KW - Mice KW - Transplantation, Homologous KW - Mice, Inbred BALB C KW - Mice, Inbred Strains KW - Aspartate Aminotransferases -- blood KW - Alanine Transaminase -- blood KW - Liver -- drug effects KW - L-Lactate Dehydrogenase -- blood KW - Mice, Inbred C57BL KW - Recombinant Fusion Proteins -- pharmacology KW - Female KW - Male KW - Exotoxins -- genetics KW - Interleukin-2 -- pharmacology KW - Exotoxins -- pharmacology KW - Heart Transplantation KW - Interleukin-2 -- genetics KW - Interleukin-2 -- toxicity KW - Graft Survival -- drug effects KW - Exotoxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78855784?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-16 N1 - Date created - 1989-03-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Transplant Proc. 1987 Feb;19(1 Pt 1):594-8 [3103282] Proc Natl Acad Sci U S A. 1986 Nov;83(21):8258-62 [3095831] Diabetologia. 1987 Jan;30(1):44-6 [3106125] Proc Natl Acad Sci U S A. 1987 Jul;84(13):4538-42 [3299371] Science. 1987 Jul 17;237(4812):278-80 [2955518] J Bacteriol. 1987 Nov;169(11):4967-71 [2889718] Transplant Proc. 1987 Oct;19(5):4231-3 [3118538] J Exp Med. 1988 Feb 1;167(2):612-22 [3126255] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1922-6 [3126499] Transplant Proc. 1988 Apr;20(2 Suppl 2):207-16 [3129841] Proc Natl Acad Sci U S A. 1988 Jun;85(11):3980-4 [3131768] J Biol Chem. 1988 Sep 15;263(26):13203-7 [2901411] Nature. 1988 Sep 22;335(6188):369-72 [2843774] Proc Natl Acad Sci U S A. 1989 Jan;86(1):287-91 [2492102] Protein Eng. 1987 Dec;1(6):493-8 [3334101] Biotechniques. 1988 Apr;6(4):299-303 [3273853] Transplant Proc. 1987 Feb;19(1 Pt 1):618-9 [3274828] Transplantation. 1973 Oct;16(4):343-50 [4583148] J Immunol. 1979 Dec;123(6):2704-8 [315430] Ann N Y Acad Sci. 1979;332:423-32 [316981] J Immunol. 1981 Apr;126(4):1323-6 [6451643] Immunol Rev. 1982;63:129-66 [7042543] J Clin Endocrinol Metab. 1983 Jan;56(1):164-9 [6600169] J Exp Med. 1983 Feb 1;157(2):461-72 [6296263] Gut. 1984 Jan;25(1):32-40 [6228498] J Immunol. 1984 May;132(5):2330-7 [6325537] J Immunol. 1984 Aug;133(2):582-8 [6234351] Science. 1985 Jan 25;227(4685):415-7 [3155574] J Exp Med. 1985 Feb 1;161(2):378-91 [3919141] J Exp Med. 1985 Jul 1;162(1):358-62 [3925068] N Engl J Med. 1985 Aug 8;313(6):353-60 [3159965] J Exp Med. 1985 Sep 1;162(3):1105-10 [3928802] Proc Natl Acad Sci U S A. 1986 Apr;83(8):2624-7 [2939456] Clin Exp Immunol. 1986 Apr;64(1):71-9 [3089651] Eur J Immunol. 1987 Mar;17(3):335-41 [3106058] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Opioids induce convulsions and wet dog shakes in rats: mediation by hippocampal mu, but not delta or kappa opioid receptors. AN - 78855290; 2537392 AB - The opioid receptor subtypes and brain regions involved in eliciting convulsions and wet dog shakes (WDS) were studied by testing different opioid receptor selective agonists in unanesthetized rats. Selective mu agonists, [NMe-Phe3-D-Pro4]-morphiceptin (PL017) and [D-Ala2-N-methyl-Phe3-Gly5-ol]-enkephalin, induced convulsions and WDS when unilaterally injected into the ventral hippocampus. [D-Ala2,D-Leu5]-enkephalin (DADLE), a mixed mu and delta agonist, also elicited such behavioral changes, but its effect was less potent than the selective mu agonists. DADLE-induced WDS were dose dependent, and both convulsions and WDS were antagonized by the irreversible mu receptor antagonist, beta-funaltrexamine, but not by the selective delta receptor antagonist, ICI-174,864. Treatment with the selective delta agonist [D-Pen2,5]-enkephalin or the selective kappa agonists U-50,488H, dynorphin-A amide, or dynorphin-A(1-8) did not produce convulsions or WDS. The injection of a high dose of PL017 intraventricularly or into other brain regions such as the dorsal hippocampus, frontal cortex, striatum, and amygdala did not produce convulsions or WDS, therefore suggesting the ventral hippocampus is an important site for the expression of opioid-induced convulsions and WDS. These results suggest that opioid-induced convulsions and WDS are mediated exclusively by mu but not delta or kappa opioid receptors in the ventral hippocampus. JF - The Journal of neuroscience : the official journal of the Society for Neuroscience AU - Lee, P H AU - Obie, J AU - Hong, J S AD - Neuropharmacology Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 692 EP - 697 VL - 9 IS - 2 SN - 0270-6474, 0270-6474 KW - Narcotics KW - 0 KW - Receptors, Opioid KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Dose-Response Relationship, Drug KW - Male KW - Seizures -- chemically induced KW - Behavior, Animal -- drug effects KW - Hippocampus -- metabolism KW - Narcotics -- pharmacology KW - Receptors, Opioid -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78855290?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-03 N1 - Date created - 1989-04-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - NIMH report. Carbamazepine: treatment option for bipolar patients. AN - 78854283; 2914664 JF - Hospital & community psychiatry AU - Wise, S S AD - Office of Scientific Communications, National Institute of Mental Health, Rockville, Maryland 20857. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 123 EP - 124 VL - 40 IS - 2 SN - 0022-1597, 0022-1597 KW - Carbamazepine KW - 33CM23913M KW - Lithium KW - 9FN79X2M3F KW - Index Medicus KW - Drug Interactions KW - Humans KW - Lithium -- therapeutic use KW - Lithium -- adverse effects KW - Carbamazepine -- adverse effects KW - Bipolar Disorder -- drug therapy KW - Carbamazepine -- administration & dosage KW - Carbamazepine -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78854283?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-17 N1 - Date created - 1989-03-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mixed chimerism and permanent specific transplantation tolerance induced by a nonlethal preparative regimen. AN - 78850115; 2562984 AB - The use of allogeneic bone marrow transplantation as a means of inducing donor-specific tolerance across MHC barriers could provide an immunologically specific conditioning regimen for organ transplantation. However, a major limitation to this approach is the toxicity of whole body irradiation as currently used to abrogate host resistance and permit marrow engraftment. The present study describes methodology for abrogating host resistance and permitting marrow engraftment without lethal irradiation. Our preparative protocol involves administration of anti-CD4 and anti-CD8 mAbs in vivo, 300-rad WBI, 700-rad thymic irradiation, and unmanipulated fully MHC-disparate bone marrow. B10 mice prepared by this regimen developed stable mixed lymphohematopoetic chimerism without any clinical evidence of graft-vs.-host disease. Engraftment was accompanied by induction of specific tolerance to donor skin grafts (B10.D2), while third-party skin grafts (B10.BR) were promptly rejected. Mice treated with the complete regimen without bone marrow transplantation appeared healthy and enjoyed long-term survival. This study therefore demonstrates that stable mixed chimerism with donor-specific tolerance can be induced across an MHC barrier after a nonlethal preparative regimen, without clinical GVHD and without the risk of aplasia. JF - The Journal of experimental medicine AU - Sharabi, Y AU - Sachs, D H AD - Transplantation Biology Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/02/01/ PY - 1989 DA - 1989 Feb 01 SP - 493 EP - 502 VL - 169 IS - 2 SN - 0022-1007, 0022-1007 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Surface KW - Antigens, Thy-1 KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Mice KW - Flow Cytometry KW - Dose-Response Relationship, Radiation KW - Time Factors KW - Antigens, Surface -- analysis KW - Thymus Gland -- immunology KW - Thymus Gland -- radiation effects KW - Immunosuppression -- methods KW - T-Lymphocytes -- immunology KW - Radiation Chimera KW - Bone Marrow Transplantation KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78850115?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-21 N1 - Date created - 1989-02-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Exp Med. 1978 Apr 1;147(4):963-72 [25942] J Immunol. 1980 Dec;125(6):2665-72 [6159417] J Exp Med. 1981 May 1;153(5):1286-301 [6166716] Transplantation. 1982 Mar;33(3):269-73 [6121406] Transplantation. 1982 Sep;34(3):113-20 [7135466] J Immunol. 1983 Nov;131(5):2445-51 [6415170] Nature. 1984 Jan 12-18;307(5947):168-70 [6361574] J Exp Med. 1985 Jul 1;162(1):231-44 [3159825] J Immunol. 1985 Sep;135(3):1698-701 [3160776] Transplantation. 1985 Aug;40(2):201-10 [3161225] J Exp Med. 1986 Jun 1;163(6):1376-90 [3086480] Nature. 1986 Sep 11-17;323(6084):164-6 [3528866] Immunol Today. 1988 Jan;9(1):23-7 [3076756] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A phase I clinical trial of recombinant interleukin-2 by periodic 24-hour intravenous infusions. AN - 78849605; 2783732 AB - Recombinant interleukin-2 (rIL-2) (NSC# 600664; Hoffmann-La Roche, Inc., Nutley, NJ) was studied in a phase I clinical trial in 33 patients with advanced, measureable cancer of the colon or malignant melanoma, Eastern Cooperative Oncology Group (ECOG) performance status O-1, and no prior chemotherapy or radiotherapy. The goal of the study was to identify a dose and schedule of IL-2 to generate maximal immune modulation with tolerable toxicity. Such a regimen might allow the addition of other treatment modalities and/or prolonged treatment duration in later trials. Each patient received IL-2 as a continuous 24-hour infusion once weekly for 4 weeks and then twice weekly for 4 weeks. Five treatment groups received from 10(3) U/m2 to 3 x 10(7) U/m2 per 24-hour infusion. The maximal tolerated dose was 3 x 10(7) U/m2/d twice weekly. Patients treated twice weekly at 1 x 10(7) and 3 x 10(7) U/m2/d had immune modulation in terms of lymphocytosis, eosinophilia, increased natural killer (NK) activity, and elevated numbers of peripheral blood mononuclear cells expressing CD16, OKT10/Leu-17, and Leu-19 surface markers. Endogenous generation of peripheral blood lymphokine-activated killer (LAK) activity was demonstrated by lysis of NK-resistant Daudi targets, in patients treated at 3 x 10(7) U/m2/d. Biochemical and hematological abnormalities were moderate and reversible. Clinical toxicity included hypotension, myalgia, arthralgia, stomatitis, fever, fatigue, nausea, headache, chills, diarrhea, and oliguria at high doses. Cardiovascular toxicity was tolerable for most patients and reversed after IL-2 was stopped. Two of six melanoma patients at 3 x 10(7) U/m2/d achieved partial responses by the end of the eighth week. This IL-2 schedule appears to produce potentially clinically useful immune enhancement with tolerable toxicity. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Creekmore, S P AU - Harris, J E AU - Ellis, T M AU - Braun, D P AU - Cohen, I I AU - Bhoopalam, N AU - Jassak, P F AU - Cahill, M A AU - Canzoneri, C L AU - Fisher, R I AD - Biological Resources Branch, NCI, Frederick, MD 21701-1013. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 276 EP - 284 VL - 7 IS - 2 SN - 0732-183X, 0732-183X KW - Interleukin-2 KW - 0 KW - Index Medicus KW - Drug Administration Schedule KW - Infusions, Intravenous KW - Humans KW - Adrenal Gland Neoplasms -- secondary KW - Skin Neoplasms -- therapy KW - Aged KW - Killer Cells, Natural -- drug effects KW - Drug Evaluation KW - Leukocyte Count -- drug effects KW - Colonic Neoplasms -- therapy KW - Adult KW - Middle Aged KW - Lymphocytes -- classification KW - Melanoma -- therapy KW - Adolescent KW - Lymphocytes -- drug effects KW - Adrenal Gland Neoplasms -- therapy KW - Interleukin-2 -- adverse effects KW - Interleukin-2 -- administration & dosage KW - Neoplasms -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78849605?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-16 N1 - Date created - 1989-03-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Homologous desensitization of muscarinic cholinergic, histaminergic, adrenergic, and serotonergic receptors coupled to phospholipase C in cerebellar granule cells. AN - 78849070; 2536077 AB - Cultured cerebellar granule cells express phospholipase C-coupled muscarinic cholinergic, histaminergic, alpha 1-adrenergic, and serotonergic receptors. In an attempt to study desensitization of these neurotransmitter receptors, cells were prestimulated with saturating concentrations of carbachol, histamine, norepinephrine, or serotonin during the labeling of cells with myo-[3H]inositol and then rechallenged with various receptor agonists for their ability to elicit accumulation of [3H]inositol monophosphate in the presence of lithium. Prestimulation with each of these receptor agonists was found to cause a time-dependent desensitization to subsequent stimulation with the desensitizing agonist. Thus, prestimulation for 0.5, 4, and 18 h decreased carbachol response to 87 +/- 4, 52 +/- 2, and 40 +/- 1% of the control, respectively; histamine response to 37 +/- 2, 24 +/- 2, and 18 +/- 2%, respectively; norepinephrine response to 55 +/- 5, 14 +/- 1, and 10 +/- 1%, respectively; and serotonin response to 36 +/- 1, 18 +/- 1, and 9 +/- 2%, respectively. In all cases, the responses mediated by receptors which were not prestimulated remained virtually unchanged, thus indicating homologous desensitization. Dose-response studies indicate that the desensitization was associated with a major reduction in the maximal extent of agonist-induced responses. The basal accumulation was markedly enhanced following 0.5- and 4-h prestimulation, but returned to near normal after 18-h pretreatment. Biologically active phorbol ester, 4 beta-phorbol 12-myristate 13-acetate, rapidly attenuated basal phospholipase C activity, as well as the responses mediated by carbachol, histamine, norepinephrine, and serotonin, suggesting that activation and translocation of protein kinase C might play a role in the desensitization of phospholipase C-coupled receptors.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Journal of neurochemistry AU - Dillon-Carter, O AU - Chuang, D M AD - Laboratory of Preclinical Pharmacology, National Institute of Mental Health, St. Elizabeths Hospital, Washington, DC 20032. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 598 EP - 603 VL - 52 IS - 2 SN - 0022-3042, 0022-3042 KW - Inositol Phosphates KW - 0 KW - Phosphatidylinositols KW - Receptors, Adrenergic, alpha KW - Receptors, Histamine KW - Receptors, Muscarinic KW - Receptors, Serotonin KW - Serotonin KW - 333DO1RDJY KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Histamine KW - 820484N8I3 KW - Carbachol KW - 8Y164V895Y KW - Type C Phospholipases KW - EC 3.1.4.- KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Serotonin -- pharmacology KW - Phosphatidylinositols -- metabolism KW - Animals KW - Cytoplasmic Granules KW - Histamine -- pharmacology KW - Norepinephrine -- pharmacology KW - Inositol Phosphates -- metabolism KW - Cells, Cultured KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Carbachol -- pharmacology KW - Phorbol 12,13-Dibutyrate -- pharmacology KW - Receptors, Serotonin -- drug effects KW - Cerebellum -- cytology KW - Receptors, Histamine -- drug effects KW - Receptors, Muscarinic -- drug effects KW - Receptors, Adrenergic, alpha -- metabolism KW - Receptors, Adrenergic, alpha -- drug effects KW - Receptors, Histamine -- metabolism KW - Receptors, Serotonin -- metabolism KW - Type C Phospholipases -- metabolism KW - Receptors, Muscarinic -- metabolism KW - Cerebellum -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78849070?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-23 N1 - Date created - 1989-02-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cardiovascular responses to cocaine placebo in humans: a preliminary report. AN - 78848447; 2914153 AB - Cardiovascular responses after placebo-cocaine injections were in the same direction as the effect of cocaine iv in 22 male volunteers. Subjects received iv placebo in a room where they had been given repeated doses of iv cocaine. The placebo response consisted of an increase from baseline values of systolic and diastolic blood pressure and pulse rate. The control group, 8 subjects, which was not exposed to a conditioning phase, showed a smaller increase in the pulse rate and systolic blood pressure after the placebo injection. The results, in accordance with animal literature, suggest the existence of cocaine-conditioned effects in humans. JF - Biological psychiatry AU - Cascella, N AU - Muntaner, C AU - Kumor, K M AU - Nagoshi, C T AU - Jaffe, J H AU - Sherer, M A AD - National Institute on Drug-Abuse, Addiction Research Center, Baltimore, MD 21224. Y1 - 1989/02/01/ PY - 1989 DA - 1989 Feb 01 SP - 285 EP - 295 VL - 25 IS - 3 SN - 0006-3223, 0006-3223 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Set (Psychology) KW - Heart Rate -- drug effects KW - Injections, Intravenous KW - Humans KW - Adult KW - Blood Pressure -- drug effects KW - Substance-Related Disorders -- psychology KW - Male KW - Arousal -- drug effects KW - Conditioning, Classical -- drug effects KW - Cocaine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78848447?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-15 N1 - Date created - 1989-03-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antitumor activity of murine neutrophils demonstrated by cytometric analysis. AN - 78845272; 2910472 AB - The cytostatic and cytolytic activities of activated polymorphonuclear neutrophils (PMNs) against YAC-1 lymphoma target cells were examined using multiparameter flow cytometric analysis. PMNs were resolved from tumor cells by 90 degrees light scatter. The number of surviving tumor cells was determined by adding a known concentration of fluorescent latex particles to the fixed cell suspension immediately prior to analysis and counting the particles simultaneously with the cells. Cell cycle progression of the YAC-1 target was studied by dual parameter analysis of DNA content and bromodeoxyuridine incorporation into tumor cell DNA either prior to or following addition of PMNs. The results indicate that activated PMNs effectively kill tumor cells within the first 24 h of coculture. However, between 24 and 48 h, tumor cells which escape destruction resume growth and eventually reach a growth rate greater than control cells. JF - Cancer research AU - Ackermann, M F AU - Lamm, K R AU - Wiegand, G W AU - Luster, M I AD - Immunotoxicology Group, National Institute of Environmental Health Sciences/National Toxicology Program, Triangle Park, North Carolina 27709. Y1 - 1989/02/01/ PY - 1989 DA - 1989 Feb 01 SP - 528 EP - 532 VL - 49 IS - 3 SN - 0008-5472, 0008-5472 KW - DNA, Neoplasm KW - 0 KW - Bromodeoxyuridine KW - G34N38R2N1 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Scattering, Radiation KW - Bromodeoxyuridine -- pharmacokinetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - Light KW - Flow Cytometry KW - DNA, Neoplasm -- analysis KW - Female KW - Neutrophils -- immunology KW - Lymphoma -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78845272?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-23 N1 - Date created - 1989-02-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Deaths from all causes in non-smokers who lived with smokers. AN - 78843423; 2913834 AB - Mortality associated with passive smoking was evaluated in a 12-year study of 27,891 White adult smokers and 19,035 never smokers identified in 1963. Death rates were calculated using an estimate of the person-years at risk. Adjusted for age, marital status, education, and quality of housing, the estimated relative risks of death from all causes were 1.17 (approximate 95% confidence interval 1.01, 1.36) for men and 1.15 (1.06, 1.24) for women with passive exposure. These relative risks were similar to those for ex-smokers and for pipe or cigar smokers. Risks increased slightly with level of exposure. The relative risk from passive smoking was greatest for men under age 50 (RR = 2.09, 1.31-3.34). Risks from passive smoking were slightly elevated for several causes among men and women, and may be broader than those previously reported. On the other hand, these small nonspecific increases in death rates may reflect other characteristics of passive smokers that increase mortality. JF - American journal of public health AU - Sandler, D P AU - Comstock, G W AU - Helsing, K J AU - Shore, D L AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 163 EP - 167 VL - 79 IS - 2 SN - 0090-0036, 0090-0036 KW - Tobacco Smoke Pollution KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Coronary Artery Disease -- etiology KW - Neoplasms -- mortality KW - Humans KW - Cerebrovascular Disorders -- mortality KW - Adult KW - Cerebrovascular Disorders -- etiology KW - Aged KW - Middle Aged KW - Male KW - Female KW - Coronary Artery Disease -- mortality KW - Tobacco Smoke Pollution -- adverse effects KW - Cause of Death UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78843423?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-02 N1 - Date created - 1989-03-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Public Health. 1983 Apr;73(4):401-5 [6829823] Clin Pharmacol Ther. 1981 Nov;30(5):687-92 [7297026] Lancet. 1984 Jan 28;1(8370):230-1 [6141373] Eur J Respir Dis Suppl. 1984;133:121-6 [6586460] Br Med J (Clin Res Ed). 1984 Jun 16;288(6433):1801-2 [6428550] J Epidemiol Community Health. 1984 Dec;38(4):335-9 [6512488] Am J Epidemiol. 1985 Feb;121(2):309-23 [3839345] Am J Epidemiol. 1985 May;121(5):645-50 [4014156] Prev Med. 1984 Nov;13(6):680-90 [6536942] Tokai J Exp Clin Med. 1985 Aug;10(4):287-93 [3836507] Br J Cancer. 1986 Jul;54(1):97-105 [3730259] N Engl J Med. 1986 Sep 18;315(12):717-20 [3748080] Environ Mutagen. 1986;8(5):693-704 [3533527] Am J Epidemiol. 1987 Nov;126(5):783-95 [3661526] Lancet. 1987 Dec 5;2(8571):1325-6 [2890917] N Engl J Med. 1988 Apr 14;318(15):937-41 [3352685] Am Rev Respir Dis. 1981 Aug;124(2):143-8 [7258826] J Health Soc Behav. 1978 Mar;18(1):54-61 [641331] Am J Epidemiol. 1988 May;127(5):915-22 [3358412] Cancer Lett. 1983 May;19(1):85-90 [6850572] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phase I and pharmacokinetic evaluation of thiotepa in the cerebrospinal fluid and plasma of pediatric patients: evidence for dose-dependent plasma clearance of thiotepa. AN - 78841930; 2491958 AB - A Phase I trial of thiotepa (TT) administered as an i.v. bolus was performed in 19 children with refractory malignancies. The starting dose was 25 mg/m2 with escalations to 50, 65, and 75 mg/m2. Seven additional patients were treated with 8-h infusions at 50 or 65 mg/m2. The maximum tolerated bolus dose was 65 mg/m2. Reversible myelosuppression was the dose-limiting toxicity. The plasma and cerebrospinal fluid (CSF) pharmacokinetic parameters of TT and its major active metabolite tepa (TP) were also evaluated. When the bolus or infusion methods of TT administration were compared, there was little difference observed in any pharmacokinetic parameter for either TT or TP. The plasma disappearance of TT was rapid and biphasic with half-lives of 0.14 to 0.32 and 1.34 to 2.0 h. Dose-dependent pharmacokinetics was demonstrated by steadily declining plasma clearance with increasing TT dose. Clearance values declined from 28.6 liters/m2/h at the 25-mg/m2 dose to 11.9 liters/m2/h at the 75-mg/m2 dose. The half-life of TP was longer than that of TT and ranged between 4.3 and 5.6 h. There was evidence of the saturation of TP production. TT and TP both exhibited excellent penetration into the CSF, producing lumbar and ventricular concentrations which were nearly identical to simultaneous plasma concentrations. In one patient with a Rickham reservoir, the CSF:plasma area under the (concentration x time) curve ratios for TT and TP were 1.01 and 0.95, respectively. The above data indicate that TT can be safely administered to pediatric patients at doses higher than conventionally used. The favorable CSF penetration of TT and TP suggests that Phase II studies of TT be considered in patients with central nervous system tumors. JF - Cancer research AU - Heideman, R L AU - Cole, D E AU - Balis, F AU - Sato, J AU - Reaman, G H AU - Packer, R J AU - Singher, L J AU - Ettinger, L J AU - Gillespie, A AU - Sam, J AD - Pediatric Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/02/01/ PY - 1989 DA - 1989 Feb 01 SP - 736 EP - 741 VL - 49 IS - 3 SN - 0008-5472, 0008-5472 KW - Thiotepa KW - 905Z5W3GKH KW - Index Medicus KW - Infant KW - Drug Evaluation KW - Dose-Response Relationship, Drug KW - Humans KW - Adult KW - Child KW - Adolescent KW - Male KW - Female KW - Child, Preschool KW - Neoplasms -- drug therapy KW - Neoplasms -- cerebrospinal fluid KW - Neoplasms -- blood KW - Thiotepa -- pharmacokinetics KW - Thiotepa -- cerebrospinal fluid KW - Thiotepa -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78841930?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-23 N1 - Date created - 1989-02-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lactate and hyperventilation substantially attenuate vagal tone in normal volunteers. A possible mechanism of panic provocation? AN - 78841547; 2913973 AB - Many aspects of panic attacks, eg, palpitations, tremor, sweating, and an emotional sense of "fear," have been theorized to arise from sympathetic nervous system activation. However, most studies have not demonstrated clearly increased levels of catecholamines during an attack, which is contrary to this hypothesis. To explore another possible cause for the physiological changes known to occur during a panic attack, we assessed parasympathetic nervous system activity by measuring vagal tone during treatments known to produce panic symptoms: sodium lactate administration and hyperventilation. Our findings showed a marked reduction in vagal tone during both procedures. We postulate that withdrawal of parasympathetic activity may explain some of the physiological changes occurring in panic attacks and be contributing to the origin of panic. JF - Archives of general psychiatry AU - George, D T AU - Nutt, D J AU - Walker, W V AU - Porges, S W AU - Adinoff, B AU - Linnoila, M AD - National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Md 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 153 EP - 156 VL - 46 IS - 2 SN - 0003-990X, 0003-990X KW - Lactates KW - 0 KW - Lactic Acid KW - 33X04XA5AT KW - Abridged Index Medicus KW - Index Medicus KW - Heart -- innervation KW - Arrhythmia, Sinus -- physiopathology KW - Respiration KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Female KW - Hyperventilation -- physiopathology KW - Lactates -- pharmacology KW - Hyperventilation -- complications KW - Anxiety Disorders -- etiology KW - Vagus Nerve -- physiology KW - Panic -- physiology KW - Lactates -- administration & dosage KW - Fear -- physiology KW - Anxiety Disorders -- chemically induced KW - Anxiety Disorders -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78841547?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-07 N1 - Date created - 1989-03-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synergistic killing of virus-transformed human cells with interferon and N-methyl-N'-nitro-N-nitrosoguanidine. AN - 78839395; 2463881 AB - Interferons potentiate the cytotoxic effects of certain antineoplastic drugs on human tumor cells both in vitro and in vivo, although the mechanism of interferon's synergistic action is unknown. Interferon may act by modulating the expression of DNA repair activity in cells. To test this hypothesis, we maintained parallel cultures of normal O6-methylguanine repair-proficient human fibroblasts and tumor cells, or RSV-and SV40-transformed repair-deficient Mer- human fibroblasts in medium containing 0, 100, 500 or 680 U/ml human interferon alpha or beta; after 1-10 weeks, cultures were challenged with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG, CAS: 70-25-7) and assayed for colony-forming ability. Based on the dose at 99% lethality, MNNG cytotoxicity was potentiated from 1.3- to 9-fold in interferon-treated cultures, compared with control cultures (no interferon). A significant potentiation was observed both with Mer+ normal fibroblasts (KD strain) and tumor cells (HOS) and with Mer- SV40-transformed fibroblasts (IMR90-830 and GM638) as well as with RSV-transformed cells (RHOS). However, the degree of potentiation was greater in Mer- virus-transformed cells than in Mer+ cells. The greatest effects were observed with Mer- IMR90-830 cells (5- to 9-fold reduction of dose at 99% lethality). Therefore, because the Mer+ phenotype is not required in order for HuIFNs to sensitize cells to killing by MNNG, interferon does not act by modulating O6-methylguanine repair. However, the effect of interferon on O6-methylguanine-DNA methyltransferase levels and on DNA excision repair should be examined in future experiments. JF - Carcinogenesis AU - Babich, M A AU - Day, R S AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 265 EP - 268 VL - 10 IS - 2 SN - 0143-3334, 0143-3334 KW - Methylnitronitrosoguanidine KW - 12H3O2UGSF KW - Interferons KW - 9008-11-1 KW - Index Medicus KW - Cell Survival -- drug effects KW - Humans KW - Drug Synergism KW - Colony-Forming Units Assay KW - Fibroblasts KW - DNA Repair KW - Methylnitronitrosoguanidine -- pharmacology KW - Interferons -- pharmacology KW - Cell Transformation, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78839395?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-07 N1 - Date created - 1989-03-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Factors associated with past household exposure to tobacco smoke. AN - 78838632; 2912047 AB - With data that were obtained in a private census in Washington County, Maryland, in 1963, the prevalence of household exposure to tobacco smoke was determined, and factors associated with passive smoke exposure were identified among 48,342 white adults. In 1963, 52% of men and 72% of women were exposed to smoke from others at home. Smokers of both sexes were more likely to live with other smokers than were nonsmokers. However, 30% of men who never smoked and 64% of women who never smoked lived with smokers. Marriage was a primary determinant of exposure for women but not for men, with 75% of married women who did not smoke exposed but only 38% of unmarried women who did not smoke exposed. Conversely, among men who did not smoke, exposure was more common among those who were not married than among those who were married. After control for other factors associated with exposure, exposure prevalence increased with years of school among men who did not smoke but decreased with years of school among women who did not smoke. Exposure prevalence also varied slightly with housing quality and location of residence. Smoking by spouse was an accurate reflection of household exposure for women but not for men; 88% of the exposure among women who did not smoke was contributed by the spouse, whereas only 62% of exposure among men who did not smoke was from the spouse. JF - American journal of epidemiology AU - Sandler, D P AU - Helsing, K J AU - Comstock, G W AU - Shore, D L AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 380 EP - 387 VL - 129 IS - 2 SN - 0002-9262, 0002-9262 KW - Tobacco Smoke Pollution KW - 0 KW - Index Medicus KW - Family Characteristics KW - Age Factors KW - Housing KW - Sex Factors KW - Humans KW - Marriage KW - Smoking -- epidemiology KW - Risk Factors KW - Adult KW - Middle Aged KW - Maryland KW - Female KW - Male KW - Tobacco Smoke Pollution -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78838632?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-14 N1 - Date created - 1989-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Translation and processing of Bacillus amyloliquefaciens extracellular RNase. AN - 78836293; 2914867 AB - Bacillus amyloliquefaciens extracellular RNase has been previously cloned and expressed in Bacillus subtilis. Site-specific mutagenesis experiments have identified codon -39 as the start site of translation. We have determined the primary signal peptide cleavage site of preprobarnase and propose a pathway for the conversion of probarnase to mature barnase. JF - Journal of bacteriology AU - Paddon, C J AU - Vasantha, N AU - Hartley, R W AD - Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 1185 EP - 1187 VL - 171 IS - 2 SN - 0021-9193, 0021-9193 KW - Codon KW - 0 KW - Protein Sorting Signals KW - Ribonucleases KW - EC 3.1.- KW - Index Medicus KW - Base Sequence KW - Codon -- genetics KW - Protein Sorting Signals -- genetics KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Mutation KW - Protein Biosynthesis KW - Bacillus -- enzymology KW - Genes, Bacterial KW - Genes KW - Protein Processing, Post-Translational KW - Ribonucleases -- genetics KW - Bacillus -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78836293?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-16 N1 - Date created - 1989-03-16 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M14442; GENBANK N1 - SuppNotes - Cited By: Anal Biochem. 1981 Apr;112(2):195-203 [6266278] J Mol Biol. 1988 Aug 20;202(4):913-5 [3050134] Gene. 1985;40(2-3):231-9 [3007290] Plasmid. 1986 Jul;16(1):45-51 [3016781] J Mol Biol. 1980 Oct 25;143(2):161-78 [6260957] Gene. 1987;53(1):11-9 [3297926] Nature. 1985 Jan 10-18;313(5998):152-4 [2981414] Nat New Biol. 1972 Jan 5;235(53):15-6 [4553460] Prep Biochem. 1972;2(3):243-50 [5031050] Gene. 1986;49(1):23-8 [3106154] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Protective monoclonal antibodies to Chlamydia trachomatis serovar- and serogroup-specific major outer membrane protein determinants. AN - 78834449; 2463971 AB - Monoclonal antibodies exhibiting Chlamydia trachomatis serovar specificity (serovar A, B-Ba, or C) and serogroup specificity (B, intermediate, or C serogroup) were produced and characterized. These antibodies reacted with the major outer membrane protein, recognized epitopes located at the chlamydial cell surface, and passively neutralized chlamydial toxicity for mice. The antibodies should be useful reagents for defining the molecular structure of these protective epitopes, a necessary step toward the development of a subunit or recombinant C. trachomatis vaccine. JF - Infection and immunity AU - Zhang, Y X AU - Stewart, S J AU - Caldwell, H D AD - Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 59840. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 636 EP - 638 VL - 57 IS - 2 SN - 0019-9567, 0019-9567 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Bacterial KW - Bacterial Outer Membrane Proteins KW - Epitopes KW - Index Medicus KW - Antigen-Antibody Reactions KW - Animals KW - Immunization, Passive KW - Serotyping KW - Mice KW - Chlamydia trachomatis -- classification KW - Bacterial Outer Membrane Proteins -- immunology KW - Chlamydia Infections -- immunology KW - Antigens, Bacterial -- immunology KW - Epitopes -- immunology KW - Chlamydia trachomatis -- immunology KW - Chlamydia Infections -- prevention & control KW - Antibodies, Monoclonal -- therapeutic use KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78834449?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-01 N1 - Date created - 1989-03-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Clin Microbiol. 1986 Feb;23(2):333-8 [2422202] J Immunol. 1987 Jan 15;138(2):575-81 [3540122] JAMA. 1987 Apr 17;257(15):2070-2 [3560383] JAMA. 1965 Nov 8;194(6):620-32 [5319187] Appl Microbiol. 1974 Jan;27(1):102-6 [4855645] J Infect Dis. 1975 Jul;132(1):87-105 [1097546] Infect Immun. 1981 Mar;31(3):1161-76 [7228399] J Immunol. 1982 Mar;128(3):1083-9 [7035557] Infect Immun. 1982 Mar;35(3):1024-31 [7068209] Infect Immun. 1984 May;44(2):306-14 [6425219] J Infect Dis. 1985 Oct;152(4):791-800 [4045232] Rev Infect Dis. 1985 Nov-Dec;7(6):713-6 [3840910] Rev Infect Dis. 1985 Nov-Dec;7(6):717-25 [4070905] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Potentiation of doxorubicin cytotoxicity by buthionine sulfoximine in multidrug-resistant human breast tumor cells. AN - 78833727; 2535960 AB - Resistance to antineoplastic drugs is a major problem in the clinical management of cancer. Previous studies have demonstrated that the cytotoxicity of certain anticancer drugs is increased by lowering the glutathione (GSH) levels with buthionine sulfoximine (BSO), a specific inhibitor of gamma-glutamylcysteine synthetase. In this study we report that the resistance to doxorubicin, an anthracycline antibiotic and the most active agent in the treatment of breast cancer, can be partially reversed by exposing MCF-7 doxorubicin-resistant breast tumor cells (MCF-7/ADRR) to minimally cytotoxic doses of BSO. We found that the BSO treatment (50 microM, 48 h) of MCF-7/ADRR cells resulted in 80 to 90% depletion in total GSH concentrations. The toxicity of doxorubicin, as determined by growth inhibition and clonogenic assays, was significantly potentiated in the BSO-treated GSH-depleted cells relative to control breast tumor cells, and a dose-modifying factor of 5 to 7 was observed. Since the cytotoxicity of doxorubicin has been associated with its ability to undergo enzymatic activation and to form hydroxyl (OH) radicals in this cell line, we also quantitated the OH formation in the BSO-treated and untreated MCF-7/ADRR cells using electron spin resonance spintrapping techniques. These results show that doxorubicin stimulated at least 2-fold more OH formation in the tumor cells after GSH levels were decreased by 90%. These results indicate that GSH plays an important role in modulating doxorubicin-induced OH formation via the scavenging of hydrogen peroxide by glutathione peroxidase and thus partially protects MCF-7/ADRR cells from the cytotoxic effect of doxorubicin. JF - Cancer research AU - Dusre, L AU - Mimnaugh, E G AU - Myers, C E AU - Sinha, B K AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/02/01/ PY - 1989 DA - 1989 Feb 01 SP - 511 EP - 515 VL - 49 IS - 3 SN - 0008-5472, 0008-5472 KW - Free Radicals KW - 0 KW - Methionine Sulfoximine KW - 1982-67-8 KW - Buthionine Sulfoximine KW - 5072-26-4 KW - Doxorubicin KW - 80168379AG KW - Hydrogen Peroxide KW - BBX060AN9V KW - Glutathione Peroxidase KW - EC 1.11.1.9 KW - Index Medicus KW - Glutathione Peroxidase -- metabolism KW - Cell Survival -- drug effects KW - Hydrogen Peroxide -- metabolism KW - Humans KW - Electron Spin Resonance Spectroscopy KW - Cell Line -- drug effects KW - Drug Resistance KW - Drug Synergism KW - Doxorubicin -- pharmacology KW - Breast Neoplasms -- pathology KW - Methionine Sulfoximine -- pharmacology KW - Methionine Sulfoximine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78833727?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-23 N1 - Date created - 1989-02-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fluorescence and mass spectral evidence for the formation of benzo[a]pyrene anti-diol-epoxide-DNA and -hemoglobin adducts in humans. AN - 78832206; 2912575 AB - Highly specific methods are required to detect and quantitate carcinogen-macromolecular adducts in humans who are exposed to complex mixtures of chemical carcinogens. High performance liquid chromatography and fluorescence spectroscopy have been used successfully to detect and identify residues of benzo[a]pyrene-7,10/8,9-tetrahydrotetrol (BP-7,10/8,9-tetrol) that were released upon mild acid hydrolysis of human DNA or hemoglobin. Synchronous fluorescence spectroscopy data indicate that levels of benzo[a]pyrene-diol-epoxide-DNA (BPDE-DNA) adducts as high as 1.54 fmol BPDE/micrograms DNA are formed (1 adduct in 5 million nucleotides) in peripheral blood lymphocytes of coke-oven workers; these data were subsequently corroborated by gas chromatography/mass spectroscopy single ion monitoring analysis (m/z 404+). Additionally, among lung cancer patients, 5 samples of tumor DNA were found to be negative and 1 of 4 samples of corresponding lung tissue was found to be positive. Extraction and purification of BP-7,10/8,9-tetrol from the hemoglobin of smokers suggested levels of bound carcinogen in excess of 1 ng BPDE/gm of hemoglobin. High performance liquid chromatography combined with synchronous fluorescence spectroscopy provides a highly specific method for the detection of covalently bound BP residues in both human hemoglobin and DNA. JF - Carcinogenesis AU - Weston, A AU - Rowe, M L AU - Manchester, D K AU - Farmer, P B AU - Mann, D L AU - Harris, C C AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 251 EP - 257 VL - 10 IS - 2 SN - 0143-3334, 0143-3334 KW - DNA Adducts KW - 0 KW - benzo(a)pyrene-DNA adduct KW - Benzo(a)pyrene KW - 3417WMA06D KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Mass Spectrometry KW - Chromatography, Gas KW - Humans KW - Lymphocytes -- analysis KW - Spectrometry, Fluorescence KW - DNA -- blood KW - Benzo(a)pyrene -- blood KW - Chromatography, High Pressure Liquid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78832206?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-07 N1 - Date created - 1989-03-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Glutathione deficiency in the epithelial lining fluid of the lower respiratory tract in idiopathic pulmonary fibrosis. AN - 78831827; 2913886 AB - Glutathione (L-gamma-glutamyl-L-cysteinyl-glycine, GSH), a sulfhydryl-containing tripeptide produced by most mammalian cells, is an efficient scavenger of toxic oxidants, including hydrogen peroxide, an oxidant that plays a major role in the oxidant burden placed on the epithelial surface of the lower respiratory tract in chronic inflammatory states. GSH is present in the epithelial lining fluid of the normal lower respiratory tract, where it is thought to play a major role in providing antioxidant protection to the epithelial cells. In this regard, we hypothesized that the lower respiratory tract of patients with IPF may be chronically depleted of this antioxidant, thus leading to an increased susceptibility of lung epithelial cells to oxidant injury. To evaluate this concept, the concentration of glutathione was determined in the epithelial lining fluid of the lower respiratory tract of 15 patients with IPF and compared to that of 19 normal subjects. Strikingly, whereas ELF glutathione concentrations were high in normal subjects (429 +/- 34 microM), a fourfold decrease was found in patients with IPF (97 +/- 18 microM, p less than 0.001). In the context of the known oxidant burden present in the lower respiratory tract of patients with IPF, these observations of a "GSH deficiency" in IPF ELF suggest that there is a marked oxidant-antioxidant imbalance at the alveolar surface of these persons, thus increasing the susceptibility to the severe epithelial cell damage characteristic of this disease. JF - The American review of respiratory disease AU - Cantin, A M AU - Hubbard, R C AU - Crystal, R G AD - Pulmonary Branch, National Heart, Lung and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 370 EP - 372 VL - 139 IS - 2 SN - 0003-0805, 0003-0805 KW - Antioxidants KW - 0 KW - Glutathione KW - GAN16C9B8O KW - Abridged Index Medicus KW - Index Medicus KW - Oxidation-Reduction KW - Cell Count KW - Humans KW - Adult KW - Middle Aged KW - Epithelium -- metabolism KW - Epithelium -- pathology KW - Male KW - Female KW - Pulmonary Alveoli -- pathology KW - Pulmonary Alveoli -- metabolism KW - Bronchoalveolar Lavage Fluid -- analysis KW - Pulmonary Fibrosis -- pathology KW - Glutathione -- analysis KW - Glutathione -- deficiency KW - Bronchoalveolar Lavage Fluid -- cytology KW - Pulmonary Fibrosis -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78831827?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-09 N1 - Date created - 1989-03-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reduced DNA repair in cultured melanocytes and nevus cells from a patient with xeroderma pigmentosum. AN - 78829726; 2913963 AB - Patients with xeroderma pigmentosum (XP) have more than a 1000-fold increased risk of cutaneous melanoma. To determine if the XP DNA repair defect is present in cutaneous pigmentary cells, nevus cells and melanocytes from four large, pigmented nevi were cultured from a 12-year-old girl with XP. Cultured melanocytes showed dendritic morphologic features, contained mature melanosomes, and reacted with monoclonal antibody to tyrosinase. Nevus cells were spindle shaped and expressed nevus cell-associated antigens. Melanocytes, nevus cells, and dermal fibroblasts from the patient with XP all had a similar reduction in DNA repair: unscheduled DNA synthesis was 30% to 50% of that in normal fibroblasts following a 30 J/m2 ultraviolet dose. After a 6 J/m2 ultraviolet dose, the proliferative ability of XP nevus cells and fibroblasts was reduced to 10% of that of normal fibroblasts. This study indicates that cultured melanocytes and nevus cells express the characteristic XP DNA repair defect. JF - Archives of dermatology AU - Kraemer, K H AU - Herlyn, M AU - Yuspa, S H AU - Clark, W H AU - Townsend, G K AU - Neises, G R AU - Hearing, V J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 263 EP - 268 VL - 125 IS - 2 SN - 0003-987X, 0003-987X KW - Abridged Index Medicus KW - Index Medicus KW - Tumor Cells, Cultured KW - Humans KW - Fibroblasts -- ultrastructure KW - Microscopy, Electron -- methods KW - Child KW - Female KW - Cell Survival KW - DNA Repair KW - Melanocytes -- ultrastructure KW - Nevus -- ultrastructure KW - Xeroderma Pigmentosum -- genetics KW - Nevus -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78829726?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-09 N1 - Date created - 1989-03-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cardiac-compressing intrapericardial teratoma at birth. AN - 78829414; 2913750 JF - The American journal of cardiology AU - Brabham, K R AU - Roberts, W C AD - Pathology Branch, National Heart, Lung and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989/02/01/ PY - 1989 DA - 1989 Feb 01 SP - 386 EP - 387 VL - 63 IS - 5 SN - 0002-9149, 0002-9149 KW - Abridged Index Medicus KW - Index Medicus KW - Delivery, Obstetric KW - Humans KW - Infant, Newborn KW - Pressure KW - Male KW - Heart Neoplasms -- complications KW - Teratoma -- complications KW - Teratoma -- pathology KW - Heart Neoplasms -- pathology KW - Heart Diseases -- mortality KW - Pericardium KW - Heart Diseases -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78829414?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-06 N1 - Date created - 1989-03-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reorganization and stabilization of acetylcholine receptor aggregates on rat myotubes. AN - 78828496; 2912807 AB - Aggregation of acetylcholine receptors (AChRs) is an important early feature of the postsynaptic development of the vertebrae neuromuscular junction. At later stages of differentiation, aggregates are remodeled and stabilized. Aggregation of AChRs can be induced on rat myotubes in culture within 4 hr by treatment with embryonic pig brain extract (EBX). In this study, further sequential changes in the distribution of AChRs were followed by video-intensified fluorescence microscopy. These studies have revealed that groups of AChR aggregates that have formed after 4 hr in EBX are reorganized during the exposure to EBX for 20 additional hr to form a smaller number of larger, oval-shaped aggregates. We have named these two types of aggregates "4-hr aggregates" and "24-hr aggregates". This reorganization occurs by the expansion and merging of individual aggregates within a group, and by the incorporation of newly inserted AChRs. The 24-hr aggregates are an average of 15 times greater in area than 4-hr aggregates, and contain regions with an apparent AChR site density (fluorescence intensity) that is more than twice that of 4-hr aggregates. Electron microscopy of mapped 24-hr aggregates revealed that folded plasma membrane is associated with these regions, probably accounting for the elevated fluorescence. The 24-hr aggregates are more stable than 4-hr aggregates, as determined by their significantly slower disassembly after removal of EBX, elevation of temperature (38 degrees C), reduction of extracellular calcium levels (0.1 mM), or the addition of sodium azide (7 mM). This was determined by following disassembly both statistically (using fixed cultures) and by direct observations of living myotubes. These findings were confirmed by measuring the sequential changes in relative AChR site density over time in individual living myotubes. Thus, 24-hr aggregates form by the reorganization of 4-hr aggregates; exhibit a more regular, compact shape; and are more stable than 4-hr aggregates. These changes in AChR organization and aggregate stability resemble the changes occurring after the initial formation of junctional AChR aggregates during embryonic development, demonstrating additional similarities between this model system and the developing neuromuscular junction. JF - Developmental biology AU - Krikorian, J G AU - Daniels, M P AD - Laboratory of Biochemical Genetics, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 524 EP - 538 VL - 131 IS - 2 SN - 0012-1606, 0012-1606 KW - Azides KW - 0 KW - Receptors, Cholinergic KW - Tissue Extracts KW - Sodium Azide KW - 968JJ8C9DV KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Swine KW - Animals KW - Temperature KW - Tissue Extracts -- pharmacology KW - Brain -- physiology KW - Microscopy, Fluorescence KW - Rats KW - Rats, Inbred Strains KW - Azides -- pharmacology KW - Brain -- embryology KW - Calcium -- physiology KW - Microscopy, Electron KW - Cell Membrane -- metabolism KW - Neuromuscular Junction -- embryology KW - Receptors, Cholinergic -- drug effects KW - Muscles -- metabolism KW - Neuromuscular Junction -- metabolism KW - Muscles -- embryology KW - Receptors, Cholinergic -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78828496?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-03 N1 - Date created - 1989-03-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The relation of polychlorinated biphenyls to birth weight and gestational age in the offspring of occupationally exposed mothers. AN - 78827278; 2492144 AB - The authors studied the relation of polychlorinated biphenyls (PCBs) to birth weight and gestational age among the live offspring of women occupationally exposed to PCBs during the manufacture of capacitors in Upstate New York. Interviews were conducted in 1982 with 200 women who had held jobs with direct exposure and 205 women who had never held a direct-exposure job in order to ascertain information on reproductive history and other factors influencing reproductive outcome. Exposure was assessed as high-homolog PCB (Aroclor 1254), a continuous exposure variable estimated from an independently derived prediction model. After adjustment for variables other than gestational age known to influence birth weight, a significant effect of high-homolog exposure is seen for birth weight (slope of the regression beta = -33 g/unit change in natural logarithm (In) estimated serum PCB; 90% confidence interval (CI) -59 to -7; p(1) = 0.02). For gestational age, a small but significant decrease is also observed with an increase in estimated exposure (beta = -1.1 days/unit change in In estimated serum PCB; 90% CI -2.0 to -0.1; p(1) = 0.03). When gestational age is accounted for in addition to other variables related to birth weight, estimated serum PCB is no longer a significant predictor of birth weight (beta = -24 g/unit change in In estimated serum PCB; 90% CI -49 to 2; p(1) = 0.06). The authors conclude that these data indicate that there is a significant relation between increased estimated serum PCB level and decreased birth weight and gestational age, and that the decrease in birth weight is at least partially related to shortened gestational age. The magnitude of these effects was quite small compared with those of other known determinants of gestational age and birth weight, and the biologic importance of these effects is likely to be negligible except among already low birth weight or short gestation infants. JF - American journal of epidemiology AU - Taylor, P R AU - Stelma, J M AU - Lawrence, C E AD - Cancer Prevention Studies Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 395 EP - 406 VL - 129 IS - 2 SN - 0002-9262, 0002-9262 KW - Polychlorinated Biphenyls KW - DFC2HB4I0K KW - Index Medicus KW - Infant, Low Birth Weight KW - Humans KW - Cohort Studies KW - Infant, Newborn KW - Environmental Exposure KW - Female KW - Pregnancy KW - Polychlorinated Biphenyls -- pharmacology KW - Polychlorinated Biphenyls -- blood KW - Gestational Age KW - Birth Weight -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78827278?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-14 N1 - Date created - 1989-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lactotransferrin gene expression in the mouse uterus and mammary gland. AN - 78822949; 2463910 AB - The mouse mammary gland and uterus expressed the gene for the secretory protein lactotransferrin under various physiological conditions. Lactotransferrin, however, was induced by estrogen in a time- and dose-dependent fashion in the uterus of the immature mouse, but was not affected by estrogen in the mammary gland. Differences were also found in the expression of lactotransferrin in mammary glands and uteri of adult females during lactation. A high level of the protein was detected by immunocytochemistry in uterine epithelial cells 1 day after parturition, but immunoreactivity disappeared quickly thereafter. Lactotransferrin message was, however, relatively abundant in the mammary gland at the end of the lactation period. The presence of lactotransferrin in various tissues also was investigated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot analysis. Two forms of immunoreactive material was detected by this method; a 70K band was found in uterine luminal fluid from the estrogen-stimulated immature mouse and in homogenates of lung, vagina, mammary gland, oviduct, spleen, lymph node, and uterus of the adult female mouse, and a 65K band was detected in submaxillary gland, kidney, ovary, and all of the above tissues. Brain and duodenum had no detectable immunoreactive material. A transient appearance of lactotransferrin was observed in the uterine luminal fluid of pseudopregnant mice. These changes in the level of lactotransferrin in the uterus and mammary gland under various physiological conditions suggest that the regulation of this protein's expression is tissue specific. JF - Endocrinology AU - Teng, C T AU - Pentecost, B T AU - Chen, Y H AU - Newbold, R R AU - Eddy, E M AU - McLachlan, J A AD - Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/02// PY - 1989 DA - February 1989 SP - 992 EP - 999 VL - 124 IS - 2 SN - 0013-7227, 0013-7227 KW - Lactoglobulins KW - 0 KW - RNA KW - 63231-63-0 KW - Diethylstilbestrol KW - 731DCA35BT KW - Lactoferrin KW - EC 3.4.21.- KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Blotting, Western KW - RNA -- isolation & purification KW - Diethylstilbestrol -- pharmacology KW - Mice KW - Female KW - Sexual Maturation KW - Pseudopregnancy KW - Pregnancy KW - Lactation KW - Uterus -- metabolism KW - Uterus -- growth & development KW - Lactoferrin -- genetics KW - Genes KW - Lactoferrin -- biosynthesis KW - Mammary Glands, Animal -- metabolism KW - Mammary Glands, Animal -- growth & development KW - Lactoglobulins -- genetics KW - Transcription, Genetic KW - Uterus -- drug effects KW - Lactoferrin -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78822949?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-07 N1 - Date created - 1989-03-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selective mutagenic activation by cytochrome P3-450 of carcinogenic arylamines found in foods. AN - 78821618; 2911085 AB - Heterocyclic arylamines found in cooked foods including fish and beef are potent mutagens and carcinogens. The purpose of this investigation was to determine the specificity of cytochromes P1-450 and P3-450 toward the metabolic activation of these arylamines. We used a novel mutagenicity test system which combined human cells expressing either recombinant cytochrome P1-450 or P3-450 with Salmonella typhimurium to score mutants. Cytochrome P3-450, a single isoform of the cytochrome P-450 supergene family, bioactivated these food mutagens. Cytochrome P1-450 showed little or no activation of these arylamines but was the isoform predominantly responsible for the activation of the aromatic hydrocarbon benzo[a]pyrene-7,8-diol. This assay system should serve to define the specificities of individual cytochromes P-450 in the metabolic activation of carcinogens. JF - Journal of the National Cancer Institute AU - Snyderwine, E G AU - Battula, N AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/02/01/ PY - 1989 DA - 1989 Feb 01 SP - 223 EP - 227 VL - 81 IS - 3 SN - 0027-8874, 0027-8874 KW - Amines KW - 0 KW - Antibodies, Monoclonal KW - Imidazoles KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Antigen-Antibody Reactions KW - Mutagenicity Tests KW - HeLa Cells KW - Biotransformation KW - Humans KW - Food Analysis KW - In Vitro Techniques KW - Antibodies, Monoclonal -- immunology KW - Imidazoles -- metabolism KW - Amines -- metabolism KW - Cytochrome P-450 Enzyme System -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78821618?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-16 N1 - Date created - 1989-02-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Age-related changes in the iron spin state of testosterone-binding rat liver microsomal cytochromes P-450. AN - 78870353; 2537074 AB - The aging process is accompanied by decreased drug metabolism as well as lower levels of sex hormones such as testosterone. We examined the age-dependence of liver microsomal cytochromes P-450 from young (3 months) and old (24 months) male rats by absorption and ESR spectroscopy. Spectral perturbations by testosterone were used to identify testosterone-specific P-450 forms. Absorption difference spectra indicated that testosterone induced a greater conversion of P-450 to the high spin form in young rats than in old rats. ESR signals corresponding to total low spin P-450 were of higher intensity in the young rats and were increased by testosterone. Testosterone also interconverted one low spin P-450 species to another. These results demonstrate age-related differences in the types and amounts of testosterone-specific P-450's in rats. JF - Biochemical and biophysical research communications AU - Friedman, F K AU - Robinson, R C AU - Rifkind, J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/01/31/ PY - 1989 DA - 1989 Jan 31 SP - 480 EP - 484 VL - 158 IS - 2 SN - 0006-291X, 0006-291X KW - Testosterone KW - 3XMK78S47O KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Iron KW - E1UOL152H7 KW - Index Medicus KW - Rats KW - Animals KW - Spectrum Analysis KW - Electron Spin Resonance Spectroscopy KW - Male KW - Testosterone -- metabolism KW - Microsomes, Liver -- enzymology KW - Aging KW - Cytochrome P-450 Enzyme System -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78870353?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-16 N1 - Date created - 1989-03-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Maitotoxin, a potent, general activator of phosphoinositide breakdown. AN - 78856124; 2537233 AB - Maitotoxin (MTX), a potent marine toxin, elicits a calcium-dependent activation of cells that can be inhibited by calcium channel blockers like nifedipine. MTX also stimulates phosphoinositide breakdown in smooth muscle cells, NCB-20 cells and PC12 cells through a nifedipine-insensitive mechanism. We now report that MTX stimulates phosphoinositide breakdown in a wide variety of cells, and appears to represent the first general activator of this second messenger-generating system. MTX-induced stimulation of phosphoinositide breakdown is dependent in every cell line on the presence of extracellular calcium. In differentiated HL60 cells, in which a chemotactic peptide (fMLP) activates phosphoinositide breakdown via a pertussis toxin-sensitive mechanism, MTX-induced stimulation is not affected by pertussis toxin treatment. A phorbol ester has no effect on the response to MTX. Thus, MTX stimulates phosphoinositide breakdown through a calcium-dependent mechanism that at least in three cell lines (PC12, NCB20 and HL60) is not mediated by a pathway that involves a pertussis toxin-sensitive guanine nucleotide-binding protein. JF - FEBS letters AU - Gusovsky, F AU - Yasumoto, T AU - Daly, J W AD - Laboratory of Bioorganic Chemistry, NIDDK, National Institutes of Health, Bethesda, MD 20892. Y1 - 1989/01/30/ PY - 1989 DA - 1989 Jan 30 SP - 307 EP - 312 VL - 243 IS - 2 SN - 0014-5793, 0014-5793 KW - Marine Toxins KW - 0 KW - Oxocins KW - Phosphatidylinositols KW - maitotoxin KW - 9P59GES78D KW - Type C Phospholipases KW - EC 3.1.4.- KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Humans KW - Calcium -- physiology KW - Brain -- metabolism KW - Type C Phospholipases -- physiology KW - Synaptosomes -- metabolism KW - Cell Line KW - Marine Toxins -- pharmacology KW - Phosphatidylinositols -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78856124?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-03 N1 - Date created - 1989-04-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phorbol ester stimulates the hydrolysis of phosphatidylethanolamine in leukemic HL-60, NIH 3T3, and baby hamster kidney cells. AN - 78832297; 2912968 AB - Treatment of leukemic HL-60, NIH 3T3, and baby hamster kidney (BHK-21) cells, prelabeled with [2-14C]ethanolamine, with 12-O-tetradecanoylphorbol-13-acetate (TPA), a potent activator of protein kinase C, resulted in increased degradation of both 14C-labeled phosphatidylethanolamine and its alkenyl (plasmalogen) derivate. A half-maximal and a maximal (approximately 3.4-fold) stimulation of ethanolamine phospholipid degradation required 3 and 10-20 nM TPA, respectively. TPA had a similar concentration-dependent stimulatory effect on the hydrolysis of phosphatidylcholine in cells previously prelabeled with [methyl-14C]choline. Increased phospholipid degradation was not accompanied by the formation of lysophosphatidylethanolamine, indicating that a phospholipase A-type enzyme was not involved. About 80% of total water-soluble degradation products was ethanolamine, suggesting that phospholipid hydrolysis was catalyzed by a phospholipase D-type enzyme. Increased formation of ethanolamine with exposure of cells to TPA was observed only after a 10-min lag period. Mezerein, bryostatin, sn-1-oleoyl-2-acetylglycerol, and polymyxin B, all of which mimic the action of TPA on protein phosphorylation in vivo, also stimulated the hydrolysis of ethanolamine phospholipids in HL-60 cells, suggesting that the TPA effect was mediated by protein kinase C. JF - The Journal of biological chemistry AU - Kiss, Z AU - Anderson, W B AD - Division of Cancer Biology and Diagnosis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/01/25/ PY - 1989 DA - 1989 Jan 25 SP - 1483 EP - 1487 VL - 264 IS - 3 SN - 0021-9258, 0021-9258 KW - Phorbol Esters KW - 0 KW - Phosphatidylcholines KW - Phosphatidylethanolamines KW - Protein Kinase C KW - EC 2.7.11.13 KW - Index Medicus KW - Protein Kinase C -- metabolism KW - Animals KW - Dose-Response Relationship, Drug KW - Phosphatidylcholines -- metabolism KW - Hydrolysis KW - Cell Line KW - Cricetinae KW - Phorbol Esters -- pharmacology KW - Kidney -- metabolism KW - Phosphatidylethanolamines -- metabolism KW - Leukemia, Myeloid, Acute -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78832297?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-03 N1 - Date created - 1989-03-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Excess information at bacteriophage T7 genomic promoters detected by a random cloning technique. AN - 19796690; 8740242 AB - In our previous analysis of the information at binding sites on nucleic acids, we found that most of the sites examined contain the amount of information expected from their frequency in the genome. The sequences at bacteriophage T7 promoters are an exception, because they are far more conserved (35 bits of information content) than should be necessary to distinguish them from the background of the Escherichia coli genome (17 bits). To determine the information actually used by the T7 RNA polymerase, promoters were chemically synthesized with many variations and those that function well in an in vivo assay were sequenced. Our analysis shows that the polymerase uses 18 bits of information, so the sequences at phage genomic promoters have significantly more information than the polymerase needs. The excess may represent the binding site of another protein. JF - Nucleic Acids Research AU - Schneider, T D AU - Stormo, G D AD - National Cancer Institute, Laboratory of Mathematical Biology, Frederick, MD 21701. Y1 - 1989/01/25/ PY - 1989 DA - 1989 Jan 25 SP - 659 EP - 674 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 17 IS - 2 SN - 0305-1048, 0305-1048 KW - Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - Phages KW - Genomes KW - Promoters KW - DNA-directed RNA polymerase KW - nucleic acids KW - Escherichia coli KW - genomics KW - J 02310:Genetics & Taxonomy KW - A 01490:Miscellaneous KW - V 22320:Replication KW - N 14830:RNA KW - G 07760:Viruses & Phages UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19796690?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2008-12-01 N1 - Last updated - 2015-03-27 N1 - SubjectsTermNotLitGenreText - Genomes; Phages; Promoters; DNA-directed RNA polymerase; nucleic acids; genomics; Escherichia coli ER - TY - JOUR T1 - Chronic morphine increases mu-opiate receptor binding in rat brain: a quantitative autoradiographic study. AN - 78916504; 2539233 AB - Quantitative autoradiography was used to show the locations of mu-opiate receptor binding sites which are upregulated following chronic morphine treatment in rats. A saturating concentration of the mu-specific ligand [3H]D-ala2-N-methyl-Phe4,Gly-ol5-enkephalin was used to label sites in slide-mounted sections through one level of the thalamus in rats implanted subcutaneously with morphine pellets for 5 days. In vitro binding and autoradiography showed the largest increase in binding in the hypothalamus, especially the ventromedial nucleus (155%), with smaller increases in the basolateral and medial amygdaloid nuclei and the striatum. The set of structures showing the upregulation appears to be a subset of those upregulated by opiate antagonists, but there appears to be no correlation of the mu-sites showing upregulation with other anatomical features of the brain opiate system. The physiological significance of the upregulation is not known at present. JF - Brain research AU - Brady, L S AU - Herkenham, M AU - Long, J B AU - Rothman, R B AD - Unit on Functional Neuroanatomy, NIMH, Bethesda, MD 20892. Y1 - 1989/01/16/ PY - 1989 DA - 1989 Jan 16 SP - 382 EP - 386 VL - 477 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Drug Implants KW - 0 KW - Receptors, Opioid KW - Receptors, Opioid, mu KW - Tritium KW - 10028-17-8 KW - Morphine KW - 76I7G6D29C KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Reference Values KW - Morphine Dependence -- metabolism KW - Organ Specificity KW - Autoradiography KW - Male KW - Receptors, Opioid -- metabolism KW - Receptors, Opioid -- drug effects KW - Brain -- drug effects KW - Brain -- metabolism KW - Morphine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78916504?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-19 N1 - Date created - 1989-05-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment with recombinant IFN-gamma decreases cell surface CD4 levels on peripheral blood monocytes and on myelomonocyte cell lines. AN - 78840793; 2492048 AB - The human cell surface protein CD4 is not only an important accessory molecule in the activation of MHC class-II-restricted T cells, but has also been implicated to be a receptor for the human immunodeficiency virus HIV-I on lymphoid and monocytic cells. We have found that a 24-h treatment of the promonocytic leukemia cell line U937 with rIFN-gamma decreases the expression of the CD4 Ag by 50% as measured by cytofluorographic analysis. The decrease in CD4 expression was dependent on the concentration of rIFN-gamma, with maximal effects occurring at 20 to 200 U/ml. The decrease appeared to be due to actual loss of the CD4 molecule from the cell surface rather than masking of a particular epitope, inasmuch as similar results were obtained with the OKT4 and OKT4A antibodies. The effect of rIFN-gamma to decrease CD4 expression was not due to a general loss of cell surface Ag, because the binding of OKM1 and anti-HLe-1 increased after rIFN-gamma treatment. Treatment of rIFN-gamma also decreased cell surface CD4 expression on the promyelocytic leukemia cell line HL-60, and on the monocytic cell line THP-1, although the extent of the decrease was less than on U937 cells. Freshly isolated normal peripheral blood monocytes treated for 48 h with rIFN-gamma bound much less OKT4 or OKT4A antibody than cells incubated in the absence of rIFN-gamma. Moreover, treatment with rIFN-gamma reduced the percentage of peripheral blood monocytes that were positive for the CD4 Ag. In contrast with the decrease in CD4 levels on rIFN-gamma-treated monocytes, treatment with rIFN-gamma had no effect on CD4 levels on peripheral blood T lymphocytes or T cell lines. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Faltynek, C R AU - Finch, L R AU - Miller, P AU - Overton, W R AD - Biological Carcinogenesis Development Program, National Cancer Institute, Frederick, MD 21701. Y1 - 1989/01/15/ PY - 1989 DA - 1989 Jan 15 SP - 500 EP - 508 VL - 142 IS - 2 SN - 0022-1767, 0022-1767 KW - Culture Media KW - 0 KW - Growth Substances KW - Lymphokines KW - Receptors, HIV KW - Receptors, Virus KW - Recombinant Proteins KW - Interferon-gamma KW - 82115-62-6 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Humans KW - Growth Substances -- pharmacology KW - Lymphokines -- pharmacology KW - Leukemia, Promyelocytic, Acute -- metabolism KW - T-Lymphocytes -- drug effects KW - Cell Differentiation -- drug effects KW - T-Lymphocytes -- immunology KW - Leukemia, Monocytic, Acute -- metabolism KW - Cell Line KW - Neoplastic Stem Cells -- physiology KW - Monocytes -- physiology KW - Monocytes -- metabolism KW - Monocytes -- drug effects KW - Interferon-gamma -- pharmacology KW - Receptors, Virus -- metabolism KW - Neoplastic Stem Cells -- metabolism KW - Neoplastic Stem Cells -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78840793?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-14 N1 - Date created - 1989-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - IL-4 regulation of murine lymphokine-activated killer activity in vitro. Effects on the IL-2-induced expansion, cytotoxicity, and phenotype of lymphokine-activated killer effectors. AN - 78823076; 2783444 AB - The in vitro incubation of B6 splenocytes with purified, mouse rIL-4 for 4 to 5 days was sufficient to generate lymphokine-activated killer (LAK) activity. In addition, rIL-4 augmented LAK cytotoxic activity when combined with rIL-2, as measured in a 4 h 51Cr-release assay against fresh, syngeneic MCA-sarcoma (MCA-102 and MCA-105) cells. Interestingly, this augmentation was not observed against the cultured YAC-1 target. LAK generation and augmentation of cytotoxicity by rIL-4 was species-specific, because human rIL-4 (up to 20,000 U/ml) failed to elicit these effects in the mouse splenocyte cultures. When 5-day B6 LAK cells (splenocytes incubated in rIL-2 at 1000 U/ml for 5 days) were split and recultured in the combination of rIL-2 plus rIL-4 for 4 additional days at least a twofold greater expansion in cell number resulted compared to similar cells cultured in either rIL-2 or rIL-4 alone. Moreover, LAK cells expanded in rIL-2 plus rIL-4 exhibited substantial increases in in vitro cytolytic activity (on a per cell basis) against MCA-102 and MCA-105 sarcoma cells, but not against YAC-1 targets. FACS analysis or negative selection using Lyt-2 or NK-1.1 mAb plus C revealed no differences in effector phenotype(s) of LAK cells expanded in rIL-2 alone compared to rIL-2 plus rIL-4 to account for the differences observed in both expansion and cytolytic activity by rIL-4. The majority of cells was Thy-1+, Lyt-2+, T3+, and ASGM-1+. However, a marked increase in the granule-associated serine esterase, BLT-E, was found only in LAK cells expanded in the combination of both lymphokines. Collectively, these studies show that rIL-4 has potent regulatory activities on splenic LAK generation, expansion, and cytotoxic function in the mouse. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Mulé, J J AU - Krosnick, J A AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/01/15/ PY - 1989 DA - 1989 Jan 15 SP - 726 EP - 733 VL - 142 IS - 2 SN - 0022-1767, 0022-1767 KW - Adjuvants, Immunologic KW - 0 KW - Antibodies, Monoclonal KW - Antigens, Ly KW - Antigens, Surface KW - Drug Combinations KW - Interleukin-2 KW - Interleukins KW - Recombinant Proteins KW - Interleukin-4 KW - 207137-56-2 KW - Granzymes KW - EC 3.4.21.- KW - Serine Endopeptidases KW - GZMA protein, human KW - EC 3.4.21.78 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Recombinant Proteins -- pharmacology KW - Antigens, Ly -- immunology KW - Mice KW - Antigens, Surface -- immunology KW - Phenotype KW - Serine Endopeptidases -- metabolism KW - Mice, Inbred C57BL KW - Cytotoxicity Tests, Immunologic KW - Adjuvants, Immunologic -- pharmacology KW - Species Specificity KW - Antigens, Surface -- analysis KW - Female KW - Lymphocyte Activation KW - Killer Cells, Natural -- classification KW - Interleukin-2 -- pharmacology KW - Interleukins -- pharmacology KW - Cytotoxicity, Immunologic -- drug effects KW - Killer Cells, Natural -- immunology KW - Killer Cells, Natural -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78823076?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-14 N1 - Date created - 1989-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cyclic GMP does not inhibit protein kinase C-mediated enzyme secretion in rat pancreatic acini. AN - 78814815; 2463255 AB - In pancreatic acini, cGMP can be increased by secretagogues such as cholecystokinin (CCK), cholinergic agents, and bombesin, whose actions on enzyme secretion are believed to be mediated by protein kinase C. However, the role of cGMP in acinar cell function has been unclear. A recent paper by Rogers et al. (Rogers, J., Hughes, R.G., and Matthews, E. K. (1988) J. Biol. Chem. 263, 3713-3719) reported that two analogues of cGMP, N2,O2-dibutyl guanosine 3':5'-monophosphate (Bt2cGMP) and 8-bromoguanosine 3':5'-monophosphate (8Br-cGMP), at concentrations in the nanomolar range, inhibited the stimulation of amylase secretion caused by CCK-8, bethanechol, bombesin, and 12-O-tetradecanoylphorbol-13-acetate (TPA). Rogers et al. also reported that sodium nitroprusside inhibited the stimulation of enzyme secretion caused by CCK-8 or TPA. These authors concluded that cGMP inhibits protein kinase C-mediated secretion in pancreatic acini. In the present study we attempted to confirm the findings of Rogers et al., We found, however, that Bt2cGMP inhibited CCK-8-stimulated amylase release only at concentrations of the nucleotide above 10 microM. Moreover, there was a close correlation between the ability of Bt2cGMP to inhibit CCK-8-stimulated amylase release and its ability to inhibit binding of 125I-CCK-8. Bt2cGMP, at concentrations as high as 3 mM, did not alter the stimulation of amylase release caused by carbachol, bombesin, TPA, or A23187. 8Br-cGMP, at concentrations up to 1 mM, did not inhibit the stimulation of amylase release caused by CCK-8 or TPA. At concentrations above 0.1 mM, 8Br-cGMP augmented the stimulation of amylase release caused by CCK-8, carbachol, bombesin, or TPA. Sodium nitroprusside, at a concentration that causes a 60-fold increase in cGMP, did not inhibit the stimulation of amylase release caused by CCK-8, carbachol, bombesin, or TPA. Our results do not confirm the findings of Rogers et al. and indicate that cGMP does not inhibit protein kinase C-mediated secretion in pancreatic acini. JF - The Journal of biological chemistry AU - Menozzi, D AU - Sato, S AU - Jensen, R T AU - Gardner, J D AD - Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1989/01/15/ PY - 1989 DA - 1989 Jan 15 SP - 995 EP - 999 VL - 264 IS - 2 SN - 0021-9258, 0021-9258 KW - Nitroprusside KW - 169D1260KM KW - 8-bromocyclic GMP KW - 31356-94-2 KW - Dibutyryl Cyclic GMP KW - 32266-35-6 KW - Vasoactive Intestinal Peptide KW - 37221-79-7 KW - Calcimycin KW - 37H9VM9WZL KW - Carbachol KW - 8Y164V895Y KW - Protein Kinases KW - EC 2.7.- KW - Amylases KW - EC 3.2.1.- KW - Cyclic GMP KW - H2D2X058MU KW - Sincalide KW - M03GIQ7Z6P KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Bombesin KW - PX9AZU7QPK KW - Index Medicus KW - Vasoactive Intestinal Peptide -- pharmacology KW - Animals KW - Reference Values KW - Calcimycin -- pharmacology KW - Sincalide -- pharmacology KW - Dibutyryl Cyclic GMP -- pharmacology KW - Rats KW - Rats, Inbred Strains KW - Kinetics KW - In Vitro Techniques KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Bombesin -- pharmacology KW - Nitroprusside -- pharmacology KW - Carbachol -- pharmacology KW - Male KW - Protein Kinases -- physiology KW - Pancreas -- cytology KW - Cyclic GMP -- pharmacology KW - Cyclic GMP -- physiology KW - Pancreas -- enzymology KW - Amylases -- secretion KW - Pancreas -- drug effects KW - Cyclic GMP -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78814815?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-17 N1 - Date created - 1989-02-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Shiga toxin, Shiga-like toxin II variant, and ricin are all single-site RNA N-glycosidases of 28 S RNA when microinjected into Xenopus oocytes. AN - 78828893; 2642481 AB - Ricin, Shiga toxin, and Shiga-like toxin II (SLT-II, Vero toxin 2) exhibit an RNA N-glycosidase activity which specifically removes a single base near the 3' end of 28 S rRNA in isolated rat liver ribosomes and deproteinized 28 S rRNA (Endo Y., Mitsui, K., Motizuki, M., & Tsurugi, K. (1987) J. Biol. Chem. 262, 5908-5912; Endo Y. & Tsurugi, K. (1987) J. Biol. Chem. 262, 8128-8130, Endo, Y., Tsurugi, K., Yutsudo, T., Takeda, Y., Ogasawara, K. & Igarashi, K. (1988) Eur. J. Biochem. 171, 45-50). These workers identified the single base removed, A-4324, by examining a 28 S rRNA degradation product which was generated by contaminating ribonucleases associated with the ribosomes. To determine whether this N-glycosidase activity applies in living cells, we microinjected ricin into Xenopus oocytes. We also microinjected Shiga toxin and a variant of Shiga-like toxin II (SLT-IIv). All three toxins specifically removed A-3732, located 378 nucleotides from the 3' end of 28 S rRNA. This base is analogous to the site observed in rat 28 S rRNA for ricin, Shiga toxin, and SLT-II. Purified, glycosylated, ricin A chain contains this RNA N-glycosidase activity in oocytes. We also demonstrated that the nonglycosylated A subunit of recombinant ricin exhibits this RNA N-glycosidase activity when injected into Xenopus oocytes. Ricin, Shiga toxin, and SLT-IIv also caused a rapid decline in oocyte protein synthesis for nonsecretory proteins. JF - The Journal of biological chemistry AU - Saxena, S K AU - O'Brien, A D AU - Ackerman, E J AD - Genetics and Biochemistry Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1989/01/05/ PY - 1989 DA - 1989 Jan 05 SP - 596 EP - 601 VL - 264 IS - 1 SN - 0021-9258, 0021-9258 KW - Bacterial Toxins KW - 0 KW - Cytotoxins KW - RNA, Ribosomal KW - RNA, Ribosomal, 28S KW - Shiga Toxin 2 KW - Shiga Toxins KW - Ricin KW - 9009-86-3 KW - N-Glycosyl Hydrolases KW - EC 3.2.2.- KW - Ribosome Inactivating Proteins KW - EC 3.2.2.22 KW - Index Medicus KW - Animals KW - Base Sequence KW - Xenopus KW - Escherichia coli -- enzymology KW - Substrate Specificity KW - Microinjections KW - Female KW - RNA, Ribosomal -- metabolism KW - Cytotoxins -- metabolism KW - Bacterial Toxins -- metabolism KW - Oocytes -- metabolism KW - Ricin -- metabolism KW - Ricin -- administration & dosage KW - N-Glycosyl Hydrolases -- metabolism KW - RNA, Ribosomal, 28S -- metabolism KW - Bacterial Toxins -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78828893?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-07 N1 - Date created - 1989-02-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparative anxiogenic, neuroendocrine, and other physiologic effects of m-chlorophenylpiperazine given intravenously or orally to healthy volunteers. AN - 85258821; pmid-2502799 AB - The serotonin agonist m-chlorophenylpiperazine (m-CPP) had greater anxiogenic and other mood and cognitive effects when administered intravenously (0.1 mg/kg) rather than orally (0.5 mg/kg) to healthy subjects. Nonetheless, similar elevations in peak plasma cortisol and prolactin concentrations were obtained with the two dosage regimens, and temperature elevations were greater after oral m-CPP. Plateau phase plasma concentrations of m-CPP at the times of the maximum neuroendocrine responses to intravenous and oral m-CPP were similar. Since all rodent and nonhuman primate studies have used parenterally administered m-CPP, and previous clinical investigations using intravenous rather than oral m-CPP have yielded somewhat discrepant results, our normative data should be useful for comparing results across different human studies and across species. JF - Psychopharmacology AU - Murphy, D L AU - Mueller, E A AU - Hill, J L AU - Tolliver, T J AU - Jacobsen, F M AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD 20892. PY - 1989 SP - 275 EP - 282 VL - 98 IS - 2 SN - 0033-3158, 0033-3158 KW - Administration, Oral KW - Emotions KW - Hydrocortisone KW - Sex Factors KW - Anxiety KW - Double-Blind Method KW - Injections, Intravenous KW - Random Allocation KW - Human KW - Prolactin KW - Piperazines KW - Comparative Study KW - Body Temperature KW - Behavior KW - Adult KW - Affect KW - Neurosecretory Systems KW - Female KW - Male UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85258821?accountid=14244 LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Stop consonant production in isolated and repeated syllables in Parkinson's disease. AN - 85233226; pmid-2755591 AB - To determine if Parkinson's disease (PD) patients have increasing difficulty as speech tasks become longer or more complex, the timing and accuracy of isolated syllables and repeated sequences of syllables were studied. Acoustic measures of PD patient's syllables were similarly impaired relative to normal controls for both isolated and repeated syllable sequences. Listeners' identification scores were equally high for both types of productions. Unlike previous studies of other types of movements in PD, speech accuracy and timing does not deteriorate as items become longer or more complex. JF - Neuropsychologia AU - Connor, N P AU - Ludlow, C L AU - Schulz, G M AD - Speech and Voice Unit, National Institute on Deafness and Other Communication Disorders, Bethesda, Maryland. PY - 1989 SP - 829 EP - 838 VL - 27 IS - 6 SN - 0028-3932, 0028-3932 KW - Speech Disorders KW - Parkinson Disease KW - Dysarthria KW - Human KW - Speech Intelligibility KW - Sound Spectrography KW - Aged KW - Middle Age KW - Female KW - Male KW - Speech Production Measurement KW - Phonetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85233226?accountid=14244 LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Gastrin-releasing peptide (GRP, mammalian bombesin) in the pathogenesis of lung cancer. AN - 79581712; 2491257 AB - Established human lung cancer exhibits a complex pattern of genetic changes as well as several distinct autocrine growth factor loops for regulatory peptides. The best studied example is that of gastrin-releasing peptide (GRP), the mammalian homolog of the amphibian bombesin. It is produced by up to 70% of small cell lung cancers and 10-20% of non-small cell lung cancers. GRP stimulates the growth of normal bronchial epithelium as well as that of small cell lung cancer, and its blockade with the use of antibodies or synthetic antagonists inhibits the growth of these tumors. Study of its molecular biology has revealed a complex pattern of mRNA processing which has lead to the recent isolation of a novel family of peptides termed gastrin-releasing peptide gene-associated peptides (GGAPs), present in normal and malignant human tissues. Additional efforts have been directed at characterizing the GRP receptor as well as its intracellular signaling pathways which have been reported both as G protein phospholipase C coupled events as well as activation of a membrane associated tyrosine kinase. In view of its expression in normal bronchial epithelium and its mitogenic effects on this tissue, GRP appears to play a central role in the early events of pulmonary carcinogenesis. JF - Progress in growth factor research AU - Viallet, J AU - Minna, J D AD - NCI-Navy Medical Oncology Branch, National Cancer Institute and Uniformed Services, University of the Health Sciences, Bethesda, MD 20814. Y1 - 1989 PY - 1989 DA - 1989 SP - 89 EP - 97 VL - 1 IS - 2 SN - 0955-2235, 0955-2235 KW - Peptides KW - 0 KW - Gastrin-Releasing Peptide KW - 80043-53-4 KW - Bombesin KW - PX9AZU7QPK KW - Index Medicus KW - Animals KW - Humans KW - Lung Neoplasms -- etiology KW - Bombesin -- genetics KW - Peptides -- genetics KW - Peptides -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79581712?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-01 N1 - Date created - 1991-10-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effects of drug abuse on glucose metabolism. AN - 79581341; 2535418 JF - The Journal of neuropsychiatry and clinical neurosciences AU - London, E D AD - Neuropharmacology Laboratory, National Institute on Drug Abuse, Baltimore, Maryland 21224. Y1 - 1989 PY - 1989 DA - 1989 SP - S30 EP - S36 VL - 1 IS - 1 SN - 0895-0172, 0895-0172 KW - Narcotics KW - 0 KW - Placebos KW - Fluorodeoxyglucose F18 KW - 0Z5B2CJX4D KW - Morphine KW - 76I7G6D29C KW - Deoxyglucose KW - 9G2MP84A8W KW - Glucose KW - IY9XDZ35W2 KW - Index Medicus KW - Morphine -- adverse effects KW - Humans KW - Electroencephalography KW - Narcotics -- adverse effects KW - Mental Disorders -- etiology KW - Morphine -- metabolism KW - Mental Disorders -- metabolism KW - Mental Disorders -- diagnosis KW - Narcotics -- metabolism KW - Deoxyglucose -- analogs & derivatives KW - Female KW - Male KW - Deoxyglucose -- metabolism KW - Substance-Related Disorders -- blood KW - Glucose -- metabolism KW - Tomography, Emission-Computed KW - Brain -- metabolism KW - Substance-Related Disorders -- metabolism KW - Brain -- diagnostic imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79581341?accountid=14244 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 - Potential therapeutic value of muramyl peptides for modulating human immunologic responses. AN - 79577878; 2562645 AB - The clinical potential and the limitations of synthetic muramyl peptides have been suggested through extensive work describing their immunomodulating properties and toxicology. The intent of this paper is to offer the clinician a summary of these studies and to introduce the reader to the biological effects associated with administration of muramyl peptides. JF - Biotechnology therapeutics AU - Fogler, W E AD - Biologics Evaluation Section, National Cancer Institute, Bethesda, Maryland 20892. PY - 1989 SP - 69 EP - 83 VL - 1 IS - 1 SN - 0898-2848, 0898-2848 KW - Vaccines KW - 0 KW - Acetylmuramyl-Alanyl-Isoglutamine KW - 53678-77-6 KW - Index Medicus KW - Vaccines -- immunology KW - Animals KW - Immunity, Innate -- drug effects KW - Humans KW - Communicable Diseases -- immunology KW - Phagocytes -- drug effects KW - Acetylmuramyl-Alanyl-Isoglutamine -- metabolism KW - Acetylmuramyl-Alanyl-Isoglutamine -- adverse effects KW - Acetylmuramyl-Alanyl-Isoglutamine -- pharmacology KW - Acetylmuramyl-Alanyl-Isoglutamine -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79577878?accountid=14244 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 - Antigen presentation to specific T cells by Ia molecules selectively altered by site-directed mutagenesis. AN - 79574621; 2518656 AB - A functional analysis of mutant class II molecules was conducted to identify regions important for antigen-specific T cell activation. Site-directed mutagenesis was used to construct a panel of mutant A beta k genes containing either single or multiple d allele substitutions in the beta 1 domain. The product of each of these genes was expressed with either the A alpha d or A alpha k polypeptide in the Ia-negative B cell lymphoma M12.C3. These mutant class II molecule-bearing cells were tested for their ability to present antigen to a panel of Ak-restricted T cell clones specific for various epitopes of myoglobin. Results from this analysis demonstrate that T helper clones recognized complex determinants interacting with multiple residues on the beta 1 domain and also requiring the haplotype-matched alpha 1 domain. This is in contrast to monoclonal antibodies that recognize a domain-specific, immunodominant region involving residues 40, 63, and 65-67. Every T helper clone was found to interact with a distinct pattern of residues, even among clones recognizing the same combination of peptide and major histocompatibility complex (MHC) molecule. The 3 for 1 residue substitution between k and d alleles at residues 65-67 was one of the most important, because it resulted in loss of ability to present antigen to 7 of 7 I-Ak-restricted T cell clones. These residues have been shown previously to comprise the immunodominant allo-specific serological determinants and to stimulate some alloreactive T cell clones. Substitution at residues 12 and 13 also abrogated antigen presentation to all the T cell clones, but this may be a consequence of a conformational change due to altered alpha beta chain pairing. Substitution at position 9, which is predicted to be located in the floor of the peptide-binding groove where it should not interact directly with the T cell receptor, enhanced presentation of the antigenic site 102-118 to some T cells and diminished it to others. This finding suggests a most interesting conclusion that the same antigenic site may bind in different conformations or orientations to the same MHC molecule, although an indirect effect on the conformation of the MHC molecule itself cannot be excluded. Substitutions at residues 85, 86 and 88 also abrogated the response of one T cell clone but not others specific for the same peptide with the same Ia molecule.(ABSTRACT TRUNCATED AT 400 WORDS) JF - International immunology AU - Brett, S J AU - McKean, D AU - York-Jolley, J AU - Berzofsky, J A AD - Molecular Immunogenetics and Vaccine Research Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 130 EP - 140 VL - 1 IS - 2 SN - 0953-8178, 0953-8178 KW - Histocompatibility Antigens Class II KW - 0 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Lymphocyte Activation KW - Animals KW - Haplotypes KW - Models, Molecular KW - Molecular Sequence Data KW - Mice KW - Amino Acid Sequence KW - Genes, MHC Class II KW - Clone Cells -- immunology KW - Histocompatibility Antigens Class II -- genetics KW - Histocompatibility Antigens Class II -- chemistry KW - Antigen-Presenting Cells -- immunology KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79574621?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-22 N1 - Date created - 1991-03-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular mechanisms of malignant conversion in skin carcinogenesis. AN - 79572976; 2518687 AB - The elucidation of the cellular and molecular events involved in progressive stages of malignant transformation has been enhanced by the development of new in vitro and in vivo model systems. In the model of chemically induced mouse skin tumors, multiple benign squamous papillomas precede the development of an occasional squamous cell carcinoma. The incidence of carcinomas can be substantially enhanced by treating papilloma-bearing mice with mutagens such as urethane, nitroquinoline-N-oxide, or cisplatinum suggesting that a distinct genetic event is responsible for malignant conversion. The malignant phenotype is characterized by a marked reduction in the transcription of specific epidermal differentiation markers, a pattern which is useful for the early diagnosis of malignant conversion. Cells expressing a benign phenotype can be obtained by introducing the v-ras oncogene into primary epidermal cells or by culturing cells from benign tumors induced by chemical carcinogens in vivo. Benign epidermal tumor cells in culture are good recipients for exogenous DNA and can be used to detect genes involved in malignant conversion. Transfection studies reveal that transforming constructs of the fos oncogene induce malignant conversion, whereas myc and adenovirus E1A oncogenes do not. Malignant tumors induced by fos transfection do not express differentiation-specific epidermal markers and secrete transin and urokinase, proteases characteristic of malignant skin tumors. Introduction of v-ras and v-fos oncogenes into cultured normal epidermal cells is sufficient to produce the malignant phenotype. Alone the v-fos oncogene does not detectably alter the normal phenotype of recipient cells. These studies imply that a limited number of genetic changes is sufficient to produce squamous malignancies.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Princess Takamatsu symposia AU - Yuspa, S H AU - Greenhalgh, D A AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 281 EP - 288 VL - 20 KW - Antigens, Differentiation KW - 0 KW - Carcinogens KW - Mutagens KW - Oncogene Proteins v-fos KW - Oncogene Proteins, Viral KW - Endopeptidases KW - EC 3.4.- KW - Oncogene Protein p21(ras) KW - EC 3.6.5.2 KW - Index Medicus KW - Animals KW - Carcinogens -- pharmacology KW - Tumor Cells, Cultured -- drug effects KW - Epidermis -- metabolism KW - Antigens, Differentiation -- biosynthesis KW - Tumor Cells, Cultured -- transplantation KW - Oncogene Proteins, Viral -- physiology KW - Mice KW - Mutagens -- pharmacology KW - Endopeptidases -- physiology KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Phenotype KW - Epidermis -- drug effects KW - Oncogenes KW - Transfection KW - Cell Transformation, Neoplastic -- chemically induced KW - Oncogene Protein p21(ras) -- physiology KW - Cell Transformation, Neoplastic -- genetics KW - Neoplasms, Multiple Primary -- etiology KW - Carcinoma, Squamous Cell -- etiology KW - Carcinoma -- etiology KW - Cocarcinogenesis KW - Neoplasms, Multiple Primary -- pathology KW - Papilloma -- pathology KW - Skin Neoplasms -- etiology KW - Skin Neoplasms -- pathology KW - Skin Neoplasms -- genetics KW - Carcinoma -- pathology KW - Papilloma -- etiology KW - Carcinoma, Squamous Cell -- pathology KW - Carcinoma, Squamous Cell -- genetics KW - Neoplasms, Multiple Primary -- genetics KW - Carcinoma -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79572976?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-22 N1 - Date created - 1991-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transforming growth factor-beta and suppression of carcinogenesis. AN - 79571911; 2562184 AB - Transforming growth factor-beta (TGF-beta) plays an important role in controlling proliferation or differentiation in almost all epithelial tissues. The pathophysiology of TGF-beta during carcinogenesis is now an important area of investigation, since it appears that as the process of carcinogenesis progresses, epithelial cells often become refractory to the growth-regulatory actions of TGF-beta. In this article we consider the possible cellular and molecular bases for this phenomenon, and then discuss some pharmacological approaches to enhancing the synthesis or activity of TGF-beta. These approaches may provide new modalities for prevention of carcinogenesis, if they can be applied during the early stages of the disease process, before cells become refractory. We give particular attention to tamoxifen and retinoic acid, since it has been shown that these agents, which are of known efficacy for prevention of cancer, can markedly enhance the secretion of specific isotypes of TGF-beta by several types of cells. JF - Princess Takamatsu symposia AU - Sporn, M B AU - Roberts, A B AU - Wakefield, L M AU - Glick, A B AU - Danielpour, D AD - Laboratory of Chemoprevention, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 259 EP - 266 VL - 20 KW - Growth Inhibitors KW - 0 KW - Receptors, Cell Surface KW - Receptors, Transforming Growth Factor beta KW - Transforming Growth Factor beta KW - Tamoxifen KW - 094ZI81Y45 KW - Tretinoin KW - 5688UTC01R KW - Index Medicus KW - Tretinoin -- pharmacology KW - Tamoxifen -- pharmacology KW - Animals KW - Tumor Cells, Cultured -- secretion KW - Tumor Cells, Cultured -- drug effects KW - Sequence Homology, Nucleic Acid KW - Humans KW - Cell Division -- drug effects KW - Amino Acid Sequence KW - Epithelium -- drug effects KW - Receptors, Cell Surface -- metabolism KW - Rats KW - Receptors, Cell Surface -- deficiency KW - Cells, Cultured KW - Blood Platelets -- secretion KW - Epithelium -- physiology KW - Molecular Sequence Data KW - Cell Differentiation -- drug effects KW - Species Specificity KW - Growth Inhibitors -- physiology KW - Transforming Growth Factor beta -- pharmacology KW - Transforming Growth Factor beta -- physiology KW - Cell Transformation, Neoplastic -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79571911?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-22 N1 - Date created - 1991-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activated killer monocytes: preclinical model systems. AN - 79571690; 2488316 JF - Immunology series AU - Shinomiya, H AU - Shinomiya, M AU - Stevenson, G W AU - Stevenson, H C AD - National Cancer Institute, Frederick, Maryland. Y1 - 1989 PY - 1989 DA - 1989 SP - 101 EP - 126 VL - 48 SN - 0092-6019, 0092-6019 KW - Index Medicus KW - Macrophages -- immunology KW - Humans KW - Cytotoxicity Tests, Immunologic KW - Cell Separation -- methods KW - Monocytes -- immunology KW - Immunotherapy, Adoptive KW - Neoplasms -- therapy KW - Killer Cells, Natural -- immunology KW - Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79571690?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-30 N1 - Date created - 1991-04-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Strategies and techniques for testing the precision, reliability and reproducibility of computerized two-dimensional gel electrophoresis analysis systems. AN - 79571683; 2488595 AB - A set of test procedures is described for evaluating the reliability, precision and reproducibility of computer systems designed to analyze two-dimensional gel electrophoretograms. The Elsie 4 gel analysis system (Analyt. Biochem., 169, 49-70 (1988) is used to demonstrate the use of these tests. Three major groups of tests are described: analysis of the scanner; analysis of mathematically constructed model gels; and analysis of real gel images. Scanner tests involve evaluating the stability and reproducibility of the scanner. The tests consist primarily of measuring the output of the scanner over a time period to determine its stability, and evaluating the consistency of the scanner at different points in the scanning field. Commonly encountered real gel situations are simulated and analyzed by arranging computer-generated 'ideal spots' in different ways. With such gels we can determine such things as the ability of the computer system to separate closely resolved and/or shoulder spots; whether or not streaks and/or smears are handled correctly; how random noise affects measurements; and, in idealized situation, the accuracy of the quantitation. The idealized spots are generated using the two-dimensional Gaussian as a model of density distribution; other spot models can be used. The Elsie 4 system is capable of finding virtually any spot (if detection parameters are set low enough), and of resolving different-sized spots whose peaks are separated by one and one-half their mean half width). The most significant tests are done on a set of actual gels.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Applied and theoretical electrophoresis : the official journal of the International Electrophoresis Society AU - Miller, M J AU - Merril, C AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 127 EP - 135 VL - 1 IS - 3 SN - 0954-6642, 0954-6642 KW - Index Medicus KW - Computer Simulation KW - Models, Molecular KW - Autoradiography KW - Reproducibility of Results KW - Electrophoresis, Gel, Two-Dimensional KW - Automatic Data Processing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79571683?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-06 N1 - Date created - 1991-05-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Implication for research of the 1988 Anti-Drug Abuse Act. AN - 79553305; 2640964 JF - NIDA research monograph AU - Schuster, C R AD - National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1989 PY - 1989 DA - 1989 SP - 16 EP - 22 VL - 95 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - AIDS/HIV KW - United States KW - Acquired Immunodeficiency Syndrome -- prevention & control KW - Humans KW - Financing, Government -- legislation & jurisprudence KW - Health Priorities -- legislation & jurisprudence KW - Substance Abuse, Intravenous -- prevention & control KW - Drug and Narcotic Control -- legislation & jurisprudence KW - Health Policy -- legislation & jurisprudence KW - Substance-Related Disorders -- rehabilitation KW - Substance-Related Disorders -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79553305?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-09-20 N1 - Date created - 1990-09-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of amantadine and desipramine combined with psychotherapy for treatment of cocaine dependence. AN - 79552610; 2701321 JF - NIDA research monograph AU - Weddington, W W AU - Brown, B S AU - Haertzen, C A AU - Hess, J M AU - Kolar, A F AU - Mahaffey, J R AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland. Y1 - 1989 PY - 1989 DA - 1989 SP - 483 EP - 484 VL - 95 SN - 1046-9516, 1046-9516 KW - Amantadine KW - BF4C9Z1J53 KW - Cocaine KW - I5Y540LHVR KW - Desipramine KW - TG537D343B KW - Index Medicus KW - Single-Blind Method KW - Personality Tests KW - Combined Modality Therapy KW - Humans KW - Clinical Trials as Topic KW - Follow-Up Studies KW - Amantadine -- administration & dosage KW - Psychotherapy KW - Desipramine -- administration & dosage KW - Substance-Related Disorders -- rehabilitation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79552610?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-09-20 N1 - Date created - 1990-09-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Major initiatives in alcoholism research: current questions, future answers. AN - 79552038; 2640969 JF - NIDA research monograph AU - Gordis, E AD - Federal National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland. Y1 - 1989 PY - 1989 DA - 1989 SP - 23 EP - 33 VL - 95 SN - 1046-9516, 1046-9516 KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - United States KW - Ethanol -- adverse effects KW - Risk Factors KW - Humans KW - Brain -- drug effects KW - Substance-Related Disorders -- etiology KW - Alcohol Drinking -- psychology KW - Research KW - Social Environment KW - Alcoholism -- rehabilitation KW - Alcoholism -- etiology KW - Alcoholism -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79552038?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-09-20 N1 - Date created - 1990-09-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Structural and conformational aspects of the binding of aryl-alkyl amines to the phencyclidine binding site. AN - 79551505; 2561843 JF - NIDA research monograph AU - Thurkauf, A AU - Monn, J AU - Mattson, M V AU - Jacobson, A E AU - Rice, K C AD - Laboratory of Medicinal Chemistry, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 51 EP - 56 VL - 95 SN - 1046-9516, 1046-9516 KW - Anticonvulsants KW - 0 KW - Dibenzocycloheptenes KW - Receptors, Neurotransmitter KW - Receptors, Phencyclidine KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - Phencyclidine KW - J1DOI7UV76 KW - Index Medicus KW - Animals KW - Chemistry KW - Humans KW - Chemical Phenomena KW - Molecular Conformation KW - Structure-Activity Relationship KW - Dibenzocycloheptenes -- pharmacokinetics KW - Phencyclidine -- pharmacokinetics KW - Phencyclidine Abuse -- etiology KW - Dibenzocycloheptenes -- chemical synthesis KW - Brain -- drug effects KW - Receptors, Neurotransmitter -- drug effects KW - Phencyclidine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79551505?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-09-20 N1 - Date created - 1990-09-20 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. XIII. Drug Testing Program of the Committee on Problems of Drug Dependence, Inc. AN - 79551252; 2641053 JF - NIDA research monograph AU - Jacobson, A E AD - Laboratory of Medicinal Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 556 EP - 577 VL - 95 SN - 1046-9516, 1046-9516 KW - Narcotics KW - 0 KW - Psychotropic Drugs KW - Street Drugs KW - Index Medicus KW - Animals KW - Chemistry KW - Chemical Phenomena KW - Mice KW - Opioid-Related Disorders -- etiology KW - Drug Evaluation, Preclinical -- methods KW - Structure-Activity Relationship KW - Substance-Related Disorders -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79551252?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-09-20 N1 - Date created - 1990-09-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - NIDA's Medication Development Program--1989. AN - 79551214; 2641056 JF - NIDA research monograph AU - Schuster, C R AU - Snyder, M AD - National Institute on Drug Abuse, Rockville, Maryland 20857. Y1 - 1989 PY - 1989 DA - 1989 SP - 64 EP - 73 VL - 95 SN - 1046-9516, 1046-9516 KW - Psychotropic Drugs KW - 0 KW - Naltrexone KW - 5S6W795CQM KW - Cocaine KW - I5Y540LHVR KW - Methadyl Acetate KW - L59OC40KWJ KW - Methadone KW - UC6VBE7V1Z KW - Index Medicus KW - AIDS/HIV KW - Methadone -- therapeutic use KW - Substance Abuse, Intravenous -- rehabilitation KW - Brain -- drug effects KW - Humans KW - Infant, Newborn KW - Research Support as Topic -- legislation & jurisprudence KW - Naltrexone -- therapeutic use KW - Pregnancy KW - Acquired Immunodeficiency Syndrome -- prevention & control KW - Risk Factors KW - Drug and Narcotic Control -- legislation & jurisprudence KW - Heroin Dependence -- rehabilitation KW - Methadyl Acetate -- therapeutic use KW - Female KW - Psychotropic Drugs -- therapeutic use KW - Substance-Related Disorders -- rehabilitation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79551214?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-09-20 N1 - Date created - 1990-09-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of microinjected catalytic fragment of protein kinase C on morphological change in Swiss 3T3 cells. AN - 79545850; 2700912 AB - Although phorbol esters can enhance formation of an active, catalytic domain of protein kinase C (PKC) in intact cells, little is known about the actual importance of the proteolytic pathway in mediating cellular responses to the phorbol esters or other PKC activators. To explore this issue, we examined the effect of microinjected catalytic fragment of PKC on Swiss 3T3 cell morphology. In contrast to the dramatic, rapid response upon phorbol ester treatment, catalytic fragment microinjected in the presence of bovine serum albumin or normal goat immunoglobulin G as carrier protein had no effect. A morphological response similar but not identical to the effect of phorbol ester treatment was obtained, however, if catalytic fragment was microinjected in the presence of normal rabbit immunoglobulin G rather than the usual carrier proteins. The normal rabbit immunoglobulin by itself was inactive. Although the mechanism remains undefined, normal rabbit immunoglobulin but not other carrier proteins modulated PKC activity in vitro. We conclude that the generation of free catalytic fragment of PKC cannot account for the morphological response of Swiss 3T3 cells to the phorbol esters; secondary factors may, however, potentiate its action. JF - Cancer communications AU - Nakakuma, H AU - Willingham, M C AU - Blumberg, P M AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 127 EP - 132 VL - 1 IS - 2 SN - 0955-3541, 0955-3541 KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Index Medicus KW - Brain -- enzymology KW - Animals KW - Cells, Cultured KW - Mice KW - Microinjections KW - Fluorescent Antibody Technique KW - Protein Kinase C -- metabolism KW - Protein Kinase C -- administration & dosage KW - Protein Kinase C -- isolation & purification KW - Cell Transformation, Neoplastic KW - Phorbol 12,13-Dibutyrate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79545850?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-08-23 N1 - Date created - 1990-08-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of receptors for insulin and insulin-like growth factor-1 on FRTL-5 thyroid cells. AN - 79519519; 2561505 AB - FRTL-5 rat thyroid cells have receptors for both insulin and IGF-I which can be distinguished in binding studies. The ability of TSH to regulate each in an antiparallel manner is atypical. If these receptors are shown to have independent as well as coordinate activities, studies of the mechanisms of their receptor cross-talk in these cells will be relevant to understanding IGF-I and insulin receptors in other tissues. JF - Advances in experimental medicine and biology AU - Perrotti, N AU - Rotella, C M AU - Alvarez, F V AU - Kohn, L D AU - Taylor, S AD - Diabetes Branch, NIDDK, National Institutes of Health, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 105 EP - 119 VL - 261 SN - 0065-2598, 0065-2598 KW - Cross-Linking Reagents KW - 0 KW - Insulin KW - Receptors, Cell Surface KW - Receptors, Somatomedin KW - Somatomedins KW - Insulin-Like Growth Factor I KW - 67763-96-6 KW - Thyrotropin KW - 9002-71-5 KW - Receptor, Insulin KW - EC 2.7.10.1 KW - Index Medicus KW - Rats KW - Animals KW - Drug Interactions KW - Thyrotropin -- pharmacology KW - Cross-Linking Reagents -- pharmacology KW - Binding, Competitive KW - Cell Division -- drug effects KW - Protein Binding KW - Cell Line KW - Binding Sites KW - Receptors, Cell Surface -- metabolism KW - Insulin-Like Growth Factor I -- metabolism KW - Insulin -- metabolism KW - Insulin -- pharmacology KW - Somatomedins -- metabolism KW - Insulin-Like Growth Factor I -- pharmacology KW - Thyroid Gland -- cytology KW - Thyroid Gland -- metabolism KW - Receptor, Insulin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79519519?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-06-26 N1 - Date created - 1990-06-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of interleukin-6 on the growth of normal and transformed rat liver cells in culture. AN - 79514691; 2635056 AB - Recombinant human interleukin-6 produced a dose-dependent inhibition of DNA synthesis in both growing and mitogen-stimulated cultures of normal rat liver epithelial cells and also in primary rat hepatocytes. A significant inhibition of DNA synthesis (P less than 0.001) was obtained with 1 ng/ml (10 Units/ml) interleukin-6 in normal rat liver epithelial cells. The ID50 for inhibition of DNA synthesis in primary rat hepatocytes was 1 ng/ml. In contrast to the effects of transforming growth factor beta (Type I), where an almost complete inhibition of DNA synthesis could be achieved with either cell type, the maximal inhibition observed with interleukin-6 for both of these cell types was about 45%. Thus distinct mechanisms are involved in the inhibition of liver cell growth by these growth modulators. Transformed liver-derived cell lines were relatively resistant to the growth inhibitory effects of both interleukin-6 and TGF-beta 1 compared with the normal cells. However, human Hep G2 cells, which were completely resistant to the growth inhibitory effects of TGF-beta 1, were moderately inhibited by interleukin-6, indicating that the mechanisms responsible for the acquired resistance to growth inhibition is different for these growth inhibitors. The ability of interleukin-6 to function as a growth inhibitor in vitro was confirmed using normal rat liver epithelial cells. Interleukin-6 at a concentration of 10 ng/ml produced a significant decrease (P less than 0.05) in the proliferation of these cells. These data demonstrate that interleukin-6 may have the capability of functioning as a growth regulatory polypeptide for liver cells in vivo.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Growth factors (Chur, Switzerland) AU - Huggett, A C AU - Ford, C P AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 83 EP - 89 VL - 2 IS - 1 SN - 0897-7194, 0897-7194 KW - Growth Substances KW - 0 KW - Interleukin-6 KW - Transforming Growth Factors KW - 76057-06-2 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Rats KW - Animals KW - Cells, Cultured KW - Cell Division -- drug effects KW - Transforming Growth Factors -- pharmacology KW - Cell Line, Transformed KW - Growth Substances -- physiology KW - DNA -- biosynthesis KW - Liver -- cytology KW - Interleukin-6 -- physiology KW - Liver -- drug effects KW - Liver -- metabolism KW - Interleukin-6 -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79514691?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-06-11 N1 - Date created - 1990-06-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The biology and exploitation of the retrotransposon Ty in Saccharomyces cerevisiae. AN - 79505656; 2561112 AB - Retrotransposons are a widely distributed group of eukaryotic mobile genetic elements that transpose through an RNA intermediate. The element is transcribed into RNA, and this RNA is reverse transcribed into a DNA copy capable of insertion into many different chromosomal locations. Maturation of proteins and reverse transcription take place within noninfectious intracellular viruslike particles. We have studied the element Ty, which is found dispersed in the genome of the yeast Saccharomyces cerevisiae. The frequency of Ty element transposition is normally quite low but can be greatly increased by expressing an element from a strong promoter. We have used the ability to control the level of Ty transposition to investigate the functions of Ty proteins, the regulation of Ty transposition, and the exploitation of Ty elements as insertional mutagens in yeast. The information gained from these experiments should be applicable to the study of retrotransposons found in multicellular organisms. JF - Genome AU - Garfinkel, D J AU - Curcio, M J AU - Youngren, S D AU - Sanders, N J AD - Bionetics Research Inc., National Cancer Institute, Frederick Cancer Research Facility, MD 21701. Y1 - 1989 PY - 1989 DA - 1989 SP - 909 EP - 919 VL - 31 IS - 2 SN - 0831-2796, 0831-2796 KW - DNA Transposable Elements KW - 0 KW - DNA, Fungal KW - RNA, Fungal KW - Index Medicus KW - Gene Expression Regulation, Fungal KW - RNA, Fungal -- genetics KW - Recombination, Genetic KW - Transcription, Genetic KW - DNA, Fungal -- genetics KW - Plasmids KW - Cloning, Molecular KW - Saccharomyces cerevisiae -- genetics KW - Genes, Fungal UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79505656?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-05-17 N1 - Date created - 1990-05-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The human endonexin II (ENX2) gene is located at 4q28----q32. AN - 79495011; 2534288 AB - A relatively recently identified family of structurally similar Ca2(+)-dependent phospholipid binding proteins is called the annexin gene family. At least seven genes are known, although their exact functions are unclear. The endonexin II gene (ENX2), one member of the gene family, is assigned to 4q28----q32 using both Southern transfer analysis of human x rodent somatic cell hybrid DNAs and in situ chromosome hybridization. One of the lipocortin II genes, another annexin, had previously been assigned to the long arm of chromosome 4. JF - Cytogenetics and cell genetics AU - Modi, W S AU - Seuànez, H N AU - Jaye, M AU - Haigler, H J AU - Kaplan, R AU - O'Brien, S J AD - Biological Carcinogenesis and Development Program, Program Resources Inc., NCI-Frederick Cancer Research Facility, MD 21701. Y1 - 1989 PY - 1989 DA - 1989 SP - 167 EP - 169 VL - 52 IS - 3-4 SN - 0301-0171, 0301-0171 KW - Annexin A5 KW - 0 KW - Calcium-Binding Proteins KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Hybrid Cells -- ultrastructure KW - Cricetulus KW - Humans KW - Chick Embryo KW - DNA -- genetics KW - DNA -- analysis KW - Mice KW - Nucleic Acid Hybridization KW - Cricetinae KW - Chromosomes, Human, Pair 4 -- analysis KW - Chromosomes, Human, Pair 4 -- ultrastructure KW - Calcium-Binding Proteins -- genetics KW - Chromosome Mapping KW - Genes -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79495011?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-04-30 N1 - Date created - 1990-04-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Neurotoxicity at the N-methyl-D-aspartate receptor in energy-compromised neurons. An hypothesis for cell death in aging and disease. AN - 79492744; 2576506 AB - Our results demonstrated that the neurotoxicity of glutamate and closely related agonists was mediated by the NMDA receptor in rat cerebellar granule cells. Evidence was presented to support our hypothesis that the pivotal event in the transition of these EAAs from neurotransmitters to neurotoxins is relief of the voltage-dependent Mg++ block of the NMDA channel due to changes in membrane potential which can be caused by depletion of highly phosphorylated nucleotides or by other depolarizing stimuli. Persistent stimulation of NMDA receptors whose channels are unblocked by Mg++ can permit excessive influx of Na+ and Ca++ and neuronal death can follow by a mechanism not yet understood. Glutamate is not toxic at kainate receptors although they are present on these cells. These findings underline the potential importance of perturbations in energy metabolism in a variety of neurodegenerative disorders and in the normal process of aging which share the common feature of the loss of neurons. JF - Annals of the New York Academy of Sciences AU - Henneberry, R C AU - Novelli, A AU - Cox, J A AU - Lysko, P G AD - Molecular Neurobiology Section, National Institute of Neurological and Communicative, Disorders & Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 225 EP - 233 VL - 568 SN - 0077-8923, 0077-8923 KW - Glutamates KW - 0 KW - Receptors, N-Methyl-D-Aspartate KW - Receptors, Neurotransmitter KW - Glutamic Acid KW - 3KX376GY7L KW - Magnesium KW - I38ZP9992A KW - Glucose KW - IY9XDZ35W2 KW - Index Medicus KW - Rats KW - Animals KW - Glucose -- pharmacology KW - Cells, Cultured KW - Neurons -- drug effects KW - Magnesium -- pharmacology KW - Aging -- physiology KW - Cell Survival -- drug effects KW - Cerebellum -- drug effects KW - Receptors, Neurotransmitter -- drug effects KW - Glutamates -- toxicity KW - Energy Metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79492744?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-04-19 N1 - Date created - 1990-04-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Quantitative analysis of alveolar type II cell tumors in mice by whole lung serial and step sections. AN - 79491685; 2483278 AB - Alveolar type II cell tumors were induced transplacentally by intraperitoneal injection of pregnant C3H/HeNCr MTV- or Swiss Webster mice with N-nitrosoethylurea at a dose of 0.5 mmol/kg and 0.74 mmol/kg. At different time points after birth (1-32 weeks), the entire lungs from 40 of the male offspring were inflated with Bouin's fixative, separated into lobes, and sectioned at 5 microns serially to detect every microscopic lesion. Results were compared with those obtained from examining only every 10th, 20th, or a single midlevel section from the same material. On average, 150 serial sections were prepared per mouse lung. Initially, only purely solid/alveolar or purely tubulopapillary types were observed but with tumor progression, papillary structures developed within solid tumors resulting in mixed neoplasms. Analyzing mouse lungs in step sections of every 10th section (50-60 microns), 5/238 (2%) of the tumors were missed, in step sections of every 20th section (100-120 microns), 16/238 (7%) of the tumors were not detected and usually less than half of the tumors were seen in the single mid-level section. The approximate size of the neoplasms is indicated by the total number of sections per tumor. The dimensions of tumors evaluated with step sections of 10 or 20 were comparable to the size observed with serial sections. It is concluded that the evaluation of mouse lung tumors in steps of approximately 50 microns is basically equivalent to the study of serial sections and appears to be a feasible method to assess the complete incidence, histological type, and size of all proliferative processes throughout the entire lung. JF - Toxicologic pathology AU - Rehm, S AU - Ward, J M AD - Tumor Pathology and Pathogenesis Section, National Cancer Institute, Frederick, Maryland 21701. Y1 - 1989 PY - 1989 DA - 1989 SP - 737 EP - 742 VL - 17 IS - 4 Pt 2 SN - 0192-6233, 0192-6233 KW - Ethylnitrosourea KW - P8M1T4190R KW - Index Medicus KW - Animals KW - Ethylnitrosourea -- toxicity KW - Mice, Inbred C3H KW - Mice KW - Staining and Labeling KW - Female KW - Pregnancy KW - Lung Neoplasms -- chemically induced KW - Lung -- pathology KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79491685?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-04-10 N1 - Date created - 1990-04-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A screening method using tissue culture for evaluation of potential retinal adhesives. AN - 79487147; 2629047 AB - Several adhesives have been tested for their potentially toxic effects on embryonic retinal tissue. The authors have characterized the effects of the adhesives on neurofilament extension and also on surgical-wound "re-knitting." While none of the adhesives in the sample (including those in current surgical use) seem to be ideal, the model advanced has application for the continuing development of better 'bio-adhesives'. The most immediate application is within the field of vitreoretinal surgery in situations where conventional procedures currently seem inadequate. JF - Retina (Philadelphia, Pa.) AU - Jaffe, M J AU - Oliver, A P AU - Von Fricken, M A AU - Silberstein, L AU - Wyatt, R J AD - Neuropsychiatry Branch, National Institute of Mental Health, Washington, DC. Y1 - 1989 PY - 1989 DA - 1989 SP - 328 EP - 333 VL - 9 IS - 4 SN - 0275-004X, 0275-004X KW - Cell-Tak KW - 0 KW - Drug Combinations KW - Laminin KW - Membrane Proteins KW - Proteoglycans KW - Tissue Adhesives KW - matrigel KW - 119978-18-6 KW - Fibrinogen KW - 9001-32-5 KW - Collagen KW - 9007-34-5 KW - Enbucrilate KW - F8CEP82QNP KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Collagen -- toxicity KW - Animals KW - Culture Techniques KW - Fibrinogen -- toxicity KW - Methods KW - Enbucrilate -- toxicity KW - Drug Combinations -- toxicity KW - Proteoglycans -- toxicity KW - Laminin -- toxicity KW - Membrane Proteins -- toxicity KW - Tissue Adhesives -- toxicity KW - Retina -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79487147?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-04-20 N1 - Date created - 1990-04-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of rat liver altered focus models for testing chemicals that have completed two-year carcinogenicity studies. AN - 79485474; 2629100 AB - Partial hepatectomy (PH) and neonatal rat short-term liver focus models were used to examine the effects of selected chemicals that had been previously tested in the National Toxicology Program (NTP) 2-yr carcinogenicity studies. C.I. Solvent Yellow 14, monuron, chlorendic acid, and 4-hydroxyacetanilide were tested for initiating and promoting activity in the PH model. Chlorendic acid, 4,4'-oxydianiline, 1-amino-2,4-dibromoanthraquinone (ADBAQ), and 4-hydroxyacetanilide were similarly tested in a neonatal rat liver focus model. With the exception of 4-hydroxyacetanilide which was not carcinogenic in the NTP studies, all chemicals tested showed clear evidence of hepatocarcinogenicity. While none of the chemicals showed initiating activity in either the PH or neonatal models, promoting activity, as indicated by increased number, size, or volume fraction of histochemically detected hepatic foci of cellular alteration, was evident for all chemicals with previously demonstrated hepatocarcinogenicity. Liver tumor incidence was documented at 14 months in the PH model and at 300 days in the neonatal model. On the basis of the results obtained from these few chemicals, it is suggested that the use of short-term rat liver focus models may represent a reliable means for identifying chemicals with hepatocarcinogenic potential. JF - Toxicologic pathology AU - Maronpot, R R AU - Pitot, H C AU - Peraino, C AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989 PY - 1989 DA - 1989 SP - 651 EP - 662 VL - 17 IS - 4 Pt 1 SN - 0192-6233, 0192-6233 KW - Carcinogens KW - 0 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Hydrogen-Ion Concentration KW - Hepatectomy KW - Carcinogenicity Tests KW - Models, Biological KW - Male KW - Female KW - Liver -- ultrastructure KW - Liver -- pathology KW - Liver Neoplasms, Experimental -- pathology KW - Liver Neoplasms, Experimental -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79485474?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-04-13 N1 - Date created - 1990-04-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment of chronic type B hepatitis. AN - 79463373; 2620310 AB - Therapy for chronic hepatitis B virus (HBV) infection is primarily directed at those patients with evidence of replicative infection because they are most at risk for developing chronic hepatitis, cirrhosis, and possibly hepatocellular carcinoma (HCC). Although a number of agents or therapeutic approaches have been tested against HBV infection, only a few have been subjected to controlled clinical trial. Corticosteroid therapy, particularly if prolonged, may be harmful and should be avoided. Adenine arabinoside monophosphate (Ara-AMP) has potent inhibitory effects on HBV replication, but its use is limited by severe neurotoxicity. At present, prolonged treatment with alpha interferon offers the most promise as a beneficial therapy for chronic type B hepatitis. Alpha interferon consistently induces permanent clearance of hepatitis B e antigen (HBeAg) and HBV DNA from serum more often than in untreated patients. Present efforts are directed at determining the factors predictive of a favorable response to interferon, and attempting to increase the response rate by using alpha interferon in combination with other antiviral or immunomodulatory agents. JF - Cancer detection and prevention AU - Di Bisceglie, A M AU - Hoofnagle, J H AD - Liver Diseases Section, National Institutes of Health, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 291 EP - 293 VL - 14 IS - 2 SN - 0361-090X, 0361-090X KW - Interferon Type I KW - 0 KW - Index Medicus KW - Humans KW - Interferon Type I -- therapeutic use KW - Meta-Analysis as Topic KW - Hepatitis B -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79463373?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-22 N1 - Date created - 1990-03-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of hepatocellular carcinoma in nonhuman primates by chemical carcinogens. AN - 79461940; 2559797 AB - Several compounds were evaluated in nonhuman primates for their potential to induce neoplasms, especially hepatocellular carcinoma (HCC). The compounds can be classified into three groups: food contaminants, model rodent carcinogens, and nitrosamines. All three compounds in the food contaminants group, namely, aflatoxin B1, sterigmatocystin, and methylazoxymethanol acetate, induced HCC. None of the model rodent carcinogens tested consistently induced HCC in rhesus and cynomolgus monkeys. Three of four nitrosamines evaluated induced HCC in rhesus and cynomolgus monkeys. One nitrosamine, diethylnitrosamine, is a predictable and potent inducer of HCC and is useful for establishment of a nonhuman primate model for numerous oncologic studies. JF - Cancer detection and prevention AU - Adamson, R H AD - Division of Cancer Etiology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 215 EP - 219 VL - 14 IS - 2 SN - 0361-090X, 0361-090X KW - Aflatoxins KW - 0 KW - Carcinogens, Environmental KW - Environmental Pollutants KW - Food Additives KW - Nitrosamines KW - Sterigmatocystin KW - 10048-13-2 KW - Urethane KW - 3IN71E75Z5 KW - Methyldimethylaminoazobenzene KW - 55-80-1 KW - Methylazoxymethanol Acetate KW - 592-62-1 KW - 2-Acetylaminofluorene KW - 9M98QLJ2DL KW - p-Dimethylaminoazobenzene KW - A49L8E13FD KW - Index Medicus KW - Animals KW - Macaca fascicularis KW - Carcinogens, Environmental -- adverse effects KW - Cercopithecus aethiops KW - Food Additives -- adverse effects KW - Macaca mulatta KW - Environmental Pollutants -- adverse effects KW - Female KW - Male KW - Liver Neoplasms -- chemically induced KW - Carcinoma, Hepatocellular -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79461940?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-22 N1 - Date created - 1990-03-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Polybrominated naphthalene and diiodobenzene interactions with specific binding sites for 2,3,7,8-tetrachlorodibenzo-p-dioxin in rat liver cytosol. AN - 79448088; 2559323 AB - We provide evidence for two new classes of halogenated aromatic hydrocarbon ligands for the 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or Ah) receptor: brominated naphthalenes and iodobenzenes. Polybrominated naphthalenes with four or more bromine atoms concentrated in lateral positions were shown to bind specifically and with high affinity (Kd approximately 10(-8) M) to the Ah receptor in rat liver cytosol preparations. The hexabrominated naphthalene isomers bind with high and nearly equal affinities but have been previously shown to have different toxicological properties. Possible explanations for these differences include differences in metabolism, antagonist versus agonist Ah receptor binding of some isomers, and the involvement of other binding sites in vivo that require different structural requirements. The moderate binding activity of the diiodobenzenes suggests that thyroid hormones should receive further study as possible endogenous ligands for the Ah receptor. It is difficult to explain the binding results with these two classes of compounds using previously developed molecular concepts for Ah receptor interactions based primarily on molecular size considerations. JF - Molecular toxicology AU - Cheung, E N AU - McKinney, J D AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989 PY - 1989 DA - 1989 SP - 39 EP - 52 VL - 2 IS - 1 SN - 0883-9492, 0883-9492 KW - Hydrocarbons, Brominated KW - 0 KW - Iodobenzenes KW - Naphthalenes KW - Polychlorinated Dibenzodioxins KW - Receptors, Aryl Hydrocarbon KW - Receptors, Drug KW - Index Medicus KW - Rats KW - Centrifugation, Density Gradient KW - Cytosol -- metabolism KW - Animals KW - In Vitro Techniques KW - Binding, Competitive KW - Radioligand Assay KW - Polychlorinated Dibenzodioxins -- metabolism KW - Male KW - Naphthalenes -- metabolism KW - Hydrocarbons, Brominated -- metabolism KW - Receptors, Drug -- metabolism KW - Liver -- metabolism KW - Iodobenzenes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79448088?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-23 N1 - Date created - 1990-02-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Neurocirculatory regulation in cortisol-induced hypertension. AN - 79432402; 2558818 AB - Effects of chronic glucocorticoid treatment on arterial baroreflex function and on cardiac beta- and vascular alpha-adrenoceptor-mediated responses were assessed in conscious, unrestrained Wistar-Kyoto rats. Cortisol (25 mg/kg/day) was administered for seven days using a subcutaneous reservoir pump. Arterial baroreflex-cardiac sensitivity was assessed by examining the relationship of the cardiac interbeat interval to the mean arterial blood pressure during phenylephrine or nitroprusside challenge; baroreflex-sympathoneural sensitivity was assessed from the ratio of the increase in the arterial norepinephrine concentration to the decrease in mean arterial pressure at 15 min during intravenous infusion of nitroprusside; cardiac beta-adrenoceptor-mediated responsiveness was estimated from heart rate responses to bolus-injected isoproterenol; and vascular alpha-adrenoceptor-mediated responsiveness was estimated from peak mean arterial pressure responses to bolus-injected phenylephrine. Cortisol treatment increased mean arterial pressure, decreased heart rate, and increased heart rate responses to isoproterenol, whereas baroreflex-vagal sensitivity, baroreflex-sympathoneural sensitivity, and pressor responses to phenylephrine were unaffected. The results indicate that hypertension due to chronic cortisol administration is not associated with decreased sensitivity of the baroreceptor-cardiac reflex. Baroreflex-sympathoneural sensitivity and alpha 1-adrenoceptor responsiveness also remain normal, whereas beta-adrenoceptor responsiveness is increased. The findings suggest that the pattern of neurocirculatory adjustment in glucocorticoid hypertension differs from that seen in other forms of hypertension. JF - Clinical and experimental hypertension. Part A, Theory and practice AU - Szemeredi, K AU - Bagdy, G AU - Kopin, I J AU - Goldstein, D S AD - Clinical Neurosciences Branch, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 1425 EP - 1439 VL - 11 IS - 8 SN - 0730-0077, 0730-0077 KW - Catecholamines KW - 0 KW - Receptors, Adrenergic, beta KW - Nitroprusside KW - 169D1260KM KW - Phenylephrine KW - 1WS297W6MV KW - Methoxyhydroxyphenylglycol KW - 534-82-7 KW - dihydroxyphenylethylene glycol KW - CF5G2G268A KW - Hydrocortisone KW - WI4X0X7BPJ KW - Index Medicus KW - Rats KW - Animals KW - Heart Rate KW - Catecholamines -- blood KW - Rats, Inbred WKY KW - Blood Pressure KW - Methoxyhydroxyphenylglycol -- blood KW - Receptors, Adrenergic, beta -- physiology KW - Methoxyhydroxyphenylglycol -- analogs & derivatives KW - Nitroprusside -- pharmacology KW - Male KW - Phenylephrine -- pharmacology KW - Hydrocortisone -- pharmacology KW - Hypertension -- chemically induced KW - Hypertension -- physiopathology KW - Hypertension -- blood KW - Nervous System -- physiopathology KW - Blood Circulation -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79432402?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-07 N1 - Date created - 1990-03-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Efficacy of intracavitary administration of cyclophosphamide, interleukin-2 and lymphokine activated killer cells against established intraperitoneal tumor. AN - 79428131; 2609913 AB - In an established intraperitoneal tumor modell combination of chemo- and immunotherapy was tested in mice and shown to be superior to either treatment modell alone. This combination treatment is shown to prolong survival significantly in animals massively inoculated with tumor cells. JF - Acta medica Austriaca AU - Eggermont, A M AU - Sugarbaker, P H AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, Maryland. Y1 - 1989 PY - 1989 DA - 1989 SP - 47 EP - 50 VL - 16 IS - 3-4 SN - 0303-8173, 0303-8173 KW - Interleukin-2 KW - 0 KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - Neoplasm Transplantation KW - Injections, Intraperitoneal KW - Animals KW - Dose-Response Relationship, Drug KW - Combined Modality Therapy KW - Mice, Inbred C57BL KW - Mice KW - Female KW - Cyclophosphamide -- administration & dosage KW - Interleukin-2 -- administration & dosage KW - Sarcoma, Experimental -- therapy KW - Immunization, Passive -- methods KW - Peritoneal Neoplasms -- therapy KW - Killer Cells, Lymphokine-Activated -- transplantation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79428131?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-15 N1 - Date created - 1990-02-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The role of immunomodulators in the treatment of patients with AIDS. AN - 79422620; 2514735 AB - In the last several years, the biologic modification of the immune system has become one of the therapeutic alternatives in medicine. The use of interferon alpha has resulted in both antineoplastic and antiviral effects in patients with AIDS-associated Kaposi's sarcoma. Trials currently underway will determine whether or not this drug, either alone or in combination with zidovudine, is of overall value to patients with early stages of HIV-1 infection. Hematopoietic growth factors, GM-CSF and erythropoietin in particular, offer new hope that the bone marrow suppressing toxicities of certain therapeutic agents such as zidovudine and ganciclovir can be ameliorated, thus allowing the more aggressive use of these important medications. Although a variety of non-biologic immunomodulators have been evaluated in patients with HIV-1 infection, none thus far has shown the clear clinical advantage that has been demonstrated for zidovudine and a variety of clinical trials continue in this area. The area of immunologic reconstitution, although promising in concept, has been disappointing in practice, even in combination with zidovudine. Recent approaches to immunomodulation have included active immunotherapy involving immunization of HIV-1 infected individuals with either inactivated virus or recombinant HIV-1 proteins. Continued investigation of the role of immunomodulation in the therapy of patients with HIV-1 infection should be of value, not only in developing better therapies for patients with HIV-infection, but also in helping develop a better understanding of the nature of the immunologic defects seen in the context of this infection. JF - AIDS (London, England) AU - Lane, H C AD - Clinical and Molecular Retrovirology Section, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - S181 EP - S185 VL - 3 Suppl 1 SN - 0269-9370, 0269-9370 KW - Immunologic Factors KW - 0 KW - Recombinant Proteins KW - Index Medicus KW - AIDS/HIV KW - Lymphocytes -- immunology KW - Bone Marrow Transplantation -- immunology KW - Humans KW - Immunization, Passive KW - Recombinant Proteins -- therapeutic use KW - Acquired Immunodeficiency Syndrome -- therapy KW - Immunologic Factors -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79422620?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-03-05 N1 - Date created - 1990-03-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of brain interactions with methylenedioxyamphetamine and methylenedioxymethamphetamine. AN - 79420382; 2575226 AB - Brain recognition sites have been identified for [3H]MDA and [3H]MDMA. The dissociation constants of MDA and MDMA for these sites are similar to the concentrations needed to affect several brain neurochemical parameters and are in keeping with concentrations of MDA in brain (165 microM) following administration of behaviorally active doses (20 mg/kg) of the drug. While the characteristics of these binding sites suggest a possible hydrophobic interaction with brain membranes, this interaction is not without specificity, since it has a unique pharmacology and a heterogeneous distribution in brain. Similarities have been found between [3H]MDA binding studied in the present report and that of apparent [3H](+)amphetamine binding studied by Hauger et al. (1984). Both have extremely high Bmax values, are optimal in p2 preparations, are stabilized by sucrose, and share similar patterns of regional distribution. Measuring the specific binding of [3H]amphetamine, [3H]fenfluramine, [3H]MDA, and related compounds under identical conditions will be required to determine the possible relationships among the interactions of these compounds with brain membranes. Further study is also needed to determine the possible importance such interactions of amphetamine and its substituted analogs may have with brain membranes in relation to the pharmacology of these substances. JF - NIDA research monograph AU - Zaczek, R AU - Hurt, S AU - Culp, S AU - De Souza, E B AD - Neurobiology Laboratory, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1989 PY - 1989 DA - 1989 SP - 223 EP - 239 VL - 94 SN - 1046-9516, 1046-9516 KW - Amphetamines KW - 0 KW - 3,4-Methylenedioxyamphetamine KW - 4764-17-4 KW - N-Methyl-3,4-methylenedioxyamphetamine KW - KE1SEN21RM KW - Index Medicus KW - Animals KW - Humans KW - Brain Chemistry -- drug effects KW - Brain -- drug effects KW - 3,4-Methylenedioxyamphetamine -- analogs & derivatives KW - Brain -- metabolism KW - 3,4-Methylenedioxyamphetamine -- metabolism KW - 3,4-Methylenedioxyamphetamine -- toxicity KW - Amphetamines -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79420382?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-21 N1 - Date created - 1990-02-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of the lethal effects of cocaine by cholinomimetics. AN - 79401794; 2601580 AB - In view of the toxicity of cocaine and recent reports on the antimuscarinic properties of cocaine, the present study evaluated the effects of manipulations in cholinergic neurotransmission on the lethal effects of cocaine. Physostigmine pretreatment significantly altered the lethality of cocaine, increasing the LD 50 from 82.5 mg/kg to 96.9 mg/kg in male F344 rats. Atropine alone did not alter the lethal effects of cocaine at doses that are effective in preventing parasympathetic effects and lethality of oxotremorine. The prophylactic effect of physostigmine was not prevented by atropine. Neostigmine did not significantly affect the cocaine lethality dose-effect function. Both oxotremorine and (-)-nicotine were also devoid of protective actions. At higher doses, all of the cholinomimetics potentiated the lethal effects of cocaine. These results suggest that whereas cocaine lethality may be enhanced by stimulation of muscarinic receptors, low doses of physostigmine protect against lethality through actions at noncholinergic sites. JF - Life sciences AU - Witkin, J M AU - Goldberg, S R AU - Katz, J L AU - Kuhar, M J AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1989 PY - 1989 DA - 1989 SP - 2295 EP - 2301 VL - 45 IS - 24 SN - 0024-3205, 0024-3205 KW - Parasympathomimetics KW - 0 KW - Atropine KW - 7C0697DR9I KW - Physostigmine KW - 9U1VM840SP KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Physostigmine -- pharmacology KW - Lethal Dose 50 KW - Atropine -- pharmacology KW - Male KW - Parasympathomimetics -- pharmacology KW - Cocaine -- toxicity KW - Cocaine -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79401794?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-08 N1 - Date created - 1990-02-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Energy-related neurotoxicity at the NMDA receptor: a possible role in Alzheimer's disease and related disorders. AN - 79398092; 2481321 AB - Using rat cerebellar granule cells in primary culture as our model system, we have shown that excitatory amino acids (EAAs) become neurotoxic via the NMDA (N-methyl-D-aspartate) receptor when neuronal energy levels are compromised. Omission of glucose, exclusion of oxygen, or inclusion of inhibitors of oxidative phosphorylation or of Na+/K+-ATPases enables NMDA receptor agonists to express their neurotoxic potential. Both competitive and noncompetitive NMDA receptor antagonists are potent blockers of EAA neurotoxicity, with MK-801 fully effective at 20 nM. We interpret these results as indicating that glucose metabolism, ATP production, and functioning ion pumps are necessary to generate a resting potential sufficient to maintain the voltage-dependent Mg++ block of the NMDA receptor channel; relief of the block enables EAAs to act persistently at the NMDA receptor causing an excessive ion influx which leads to neuronal death by a mechanism not yet understood. These findings are discussed in the context of the potential role for NMDA receptor-mediated neurotoxicity in Alzheimer's disease and related disorders. JF - Progress in clinical and biological research AU - Henneberry, R C AU - Novelli, A AU - Vigano, M A AU - Reilly, J A AU - Cox, J A AU - Lysko, P G AD - Laboratory of Molecular Biology NINDS, NIH, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 143 EP - 156 VL - 317 SN - 0361-7742, 0361-7742 KW - Glutamates KW - 0 KW - Ion Channels KW - Pyruvates KW - Receptors, N-Methyl-D-Aspartate KW - Receptors, Neurotransmitter KW - Magnesium KW - I38ZP9992A KW - Glucose KW - IY9XDZ35W2 KW - Index Medicus KW - Rats KW - Animals KW - Glucose -- pharmacology KW - Magnesium -- physiology KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - Pyruvates -- pharmacology KW - Ion Channels -- metabolism KW - Neurons -- metabolism KW - Receptors, Neurotransmitter -- metabolism KW - Glutamates -- metabolism KW - Alzheimer Disease -- metabolism KW - Glutamates -- toxicity KW - Alzheimer Disease -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79398092?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-31 N1 - Date created - 1990-01-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Correlates of self-reported early childhood aggression in subjects volunteering for drug studies. AN - 79394384; 2596443 AB - The construct validity of a retrospective self-report measure of early childhood aggression, the Early Experience Questionnaire (EEQ), was assessed in a sample of substance abusing volunteers for drug studies at a research center in Baltimore. In contrast to the diagnosis of Antisocial Personality Disorder (APD), EEQ scores were not only associated with adult aggression, criminality, and substance abuse, but were also highly correlated with a cluster of measures reflecting emotionally reactive impulsivity. Correlations of the EEQ with the Minnesota Multiphasic Personality Inventory confirmed earlier findings obtained on a sample of alcoholics. Over and above the predictive influence of APD, early childhood aggression had some predictive influence on the incidence and severity of substance abuse but a substantial influence on the prediction of criminality. JF - The American journal of drug and alcohol abuse AU - Muntaner, C AU - Nagoshi, C AU - Jaffe, J H AU - Walter, D AU - Haertzen, C AU - Fishbein, D AD - National Institute on Drug Abuse Addiction Research Center, Baltimore, Maryland 21224. Y1 - 1989 PY - 1989 DA - 1989 SP - 383 EP - 402 VL - 15 IS - 4 SN - 0095-2990, 0095-2990 KW - Index Medicus KW - Attention Deficit Disorder with Hyperactivity -- psychology KW - Psychiatric Status Rating Scales KW - Personality Tests KW - Risk Factors KW - Humans KW - Adult KW - Retrospective Studies KW - Psychometrics KW - Aggression -- psychology KW - Personality Development KW - Antisocial Personality Disorder -- psychology KW - Substance-Related Disorders -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79394384?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-22 N1 - Date created - 1990-01-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lung cancer in motor exhaust-related occupations. AN - 79391765; 2480711 AB - The association between employment in motor exhaust-related occupations and the risk for lung cancer was examined in 2,291 male cases of lung cancer and 2,570 controls in data pooled from three U.S. case control studies carried out by the National Cancer Institute between 1976 and 1983. Most analyses were limited to subjects providing direct, in-person interviews, including 1,444 cases and 1,893 controls. For those providing direct interviews and employed 10 years or more in motor exhaust-related (MER) occupations, the age, smoking, and study area adjusted odds ratio (OR) for lung cancer was 1.5 (95% CI = 1.2-1.9). Risk was elevated for truck drivers (OR = 1.5; 95% CI = 1.1-1.9) and for other MER occupations (OR = 1.4; 95% CI = 1.1-2.0). The odds ratios associated with MER employment of 10+ years were 1.6 (95% CI = 1.2-2.1) for whites and 1.4 (95% CI = 0.9-2.1) for nonwhites; 1.2 (95% CI = 0.7-2.0) [corrected] for those with possible exposure to other recognized or reported lung carcinogens; and 1.6 (95% CI 1.2-2.1) for those without such exposure. The 50% excess risk for lung cancer associated with employment in motor exhaust-related occupations could not be explained by greater use of cigarettes or by other occupational exposures among these workers. JF - American journal of industrial medicine AU - Hayes, R B AU - Thomas, T AU - Silverman, D T AU - Vineis, P AU - Blot, W J AU - Mason, T J AU - Pickle, L W AU - Correa, P AU - Fontham, E T AU - Schoenberg, J B AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 685 EP - 695 VL - 16 IS - 6 SN - 0271-3586, 0271-3586 KW - Vehicle Emissions KW - 0 KW - Index Medicus KW - United States KW - Logistic Models KW - Risk Factors KW - Humans KW - Case-Control Studies KW - Smoking -- adverse effects KW - Interviews as Topic KW - Aged KW - Middle Aged KW - Male KW - Lung Neoplasms -- etiology KW - Occupational Diseases -- etiology KW - Vehicle Emissions -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79391765?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-12 N1 - Date created - 1990-01-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Am J Ind Med 1991 Jan;19(1):135 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nephrotoxicity of 5-(N-phenylcarboxamido)-2-thiobarbituric acid in the Fischer 344 rat. AN - 79387228; 2598397 AB - In the present investigation, administration of a single i.p. dose of the anticancer drug merbarone [5-(N-phenylcarboxamido)-2-thiobarbituric acid] produced an acute and reversible decrease in renal function in female but not male Fischer 344 rats. The renal lesion in female rats was biochemically characterized as a decrease in p-aminohippuric acid accumulation by renal slices along with polyuria, glucosuria, proteinuria, and enzymuria. These functional changes were accompanied by histopathologic changes of focal tubular necrosis that was confined to the deep cortex and outer stripe of the outer medulla. The changes in these parameters were dose-dependent and were observed at doses as low as 0.2 x MELD(10) (12 mg/kg). This low merbarone dose increased urinary glucose and protein excretion by 26- and 9-fold, respectively, in the initial 16-h urine collection in female rats. This increase was accompanied by a 2- to 15-fold increase in the excretion of N-acetyl-beta-D-glucosaminidase (NAG), gamma-glutamyl transpeptidase (gamma-GTP), and lactate dehydrogenase (LDH) activities. No significant changes in renal function were observed in male rats apart from mild enzymuria after a high dose of merbarone (36 mg/kg). The drug did not increase urea nitrogen levels in male or female rats, reflecting the focal nature of this tubular lesion. Merbarone produced small elevations in serum transaminase activities [i.e., glutamic-oxalacetic transaminase (GOT), glutamic-pyruvic transaminase (GPT)] at doses that produced marked alterations in renal function in female rats, suggesting only mild hepatotoxicity. The present study establishes the kidney as a possible dose-limiting target organ for merbarone toxicity. JF - Cancer chemotherapy and pharmacology AU - Nakagawa, Y AU - Kramer, R A AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 109 EP - 113 VL - 25 IS - 2 SN - 0344-5704, 0344-5704 KW - Antineoplastic Agents KW - 0 KW - Thiobarbiturates KW - merbarone KW - 97534-21-9 KW - Aspartate Aminotransferases KW - EC 2.6.1.1 KW - Alanine Transaminase KW - EC 2.6.1.2 KW - Index Medicus KW - Rats KW - Aspartate Aminotransferases -- blood KW - Animals KW - Rats, Inbred F344 KW - Alanine Transaminase -- blood KW - Sex Characteristics KW - Dose-Response Relationship, Drug KW - Blood Urea Nitrogen KW - Urine -- analysis KW - Male KW - Female KW - Kidney -- metabolism KW - Kidney -- pathology KW - Thiobarbiturates -- toxicity KW - Kidney -- drug effects KW - Antineoplastic Agents -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79387228?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-29 N1 - Date created - 1990-01-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Studies of the mechanisms of toxicity of the administration of recombinant tumor necrosis factor alpha in normal and tumor-bearing mice. AN - 79387090; 2598182 AB - Tumor-bearing mice have a greater sensitivity to the acute lethal effects of the administration of high-dose recombinant human tumor necrosis factor alpha (rhTNF-alpha) compared to normal, non-tumor-bearing mice. We studied whether or not the presence of tumor per se was responsible for the enhanced rhTNF-alpha toxicity. Tumor-bearing mice underwent tumor excision or sham operation before the systemic administration of rhTNF alpha at staged times (0.5-24 h) following surgery. There was little survival difference between sham-operated tumor-bearing mice and tumor-bearing mice undergoing tumor excision (at 24 h, treatment with 12 micrograms rhTNF-alpha, survival:sham-operated tumor bearers = 0/12, excised tumor-bearers = 0/12; p2 less than 0.01 compared to non-tumor-bearers). Mice without tumors receiving sham operation, had minimal toxicity (10 of 12 mice surviving). The injection of 3 ml Ringer's lactate i.p. before i.v. rhTNF-alpha therapy increased survival in tumor-bearing animals; following pretreatment with Ringer's lactate 30/42 mice survived 12 micrograms rhTNF-alpha compared to 6/42 surviving a similar rhTNF-alpha dose without hydration (P2 less than 0.001). Since the production of oxygen free-radical metabolites has been postulated to play a role in the acute toxicity of rhTNF-alpha, bismuth subnitrate was used to induce the enzyme metallothionein to act as a natural scavenger for these metabolites. Daily oral bismuth subnitrate treatments improved survival of mice with MCA-106 or MCA-102 sarcoma and of mice without tumors, with higher rhTNF-alpha doses (12-20 micrograms), without reducing the therapeutic effect of rhTNF-alpha against the weakly immunogenic MCA-106 sarcoma. These studies suggest methods for reducing the toxicity of rhTNF-alpha administration in clinical trials. JF - Cancer immunology, immunotherapy : CII AU - Krosnick, J A AU - McIntosh, J K AU - Mulé, J J AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 133 EP - 138 VL - 30 IS - 3 SN - 0340-7004, 0340-7004 KW - Recombinant Proteins KW - 0 KW - Tumor Necrosis Factor-alpha KW - bismuth subnitrate KW - H19J064BA5 KW - Bismuth KW - U015TT5I8H KW - Index Medicus KW - Recombinant Proteins -- toxicity KW - Bismuth -- pharmacology KW - Animals KW - Fluid Therapy KW - Mice, Inbred C57BL KW - Mice KW - Recombinant Proteins -- therapeutic use KW - Female KW - Tumor Necrosis Factor-alpha -- toxicity KW - Neoplasms, Experimental -- surgery KW - Neoplasms, Experimental -- drug therapy KW - Tumor Necrosis Factor-alpha -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79387090?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-30 N1 - Date created - 1990-01-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Glial uptake of excitatory amino acids influences neuronal survival in cultures of mouse hippocampus. AN - 79384442; 2574833 AB - Several reports have described apparently normal survival and development of hippocampal and spinal cord culture preparations grown in Ham's F-12 medium, which contains 100 microM each of L-glutamate and L-aspartate. As at this concentration these amino acids are neurotoxic, some adaptive mechanism must occur to allow neuronal survival. We have investigated the mechanism underlying such adaptation. Dissociated cultures of mouse hippocampal neurons were grown in either Eagle's minimum essential medium or Ham's F-12 medium, supplemented with 5% horse serum. Analysis of neuronal density in cultures stained for neuron-specific enolase showed that although large numbers of neurons were present in mature cultures grown in either medium, neuronal survival in cultures grown continuously in F-12 was reduced to 41% compared to controls grown in Eagle's minimum essential medium. Physiological studies showed that those neurons which survived in F-12 did not lose their sensitivity to excitatory amino acids. In addition, the acute application of fresh, serum-free F-12 to 10-14-day-old cultures grown in either minimum essential medium or F-12 was highly neurotoxic. Three lines of evidence suggest that glial uptake of amino acids, and reduction of the extracellular concentration of glutamate and aspartate below neurotoxic levels, rather than receptor desensitization underlies the adaptive mechanism allowing neuronal survival. First, application of fresh F-12 produced large depolarizations, and profound neuronal swelling in cultures grown in F-12; however, after several hours swelling reversed suggesting a slow onset of the adaptive process. Second, pressure application of conditioned F-12 obtained from sister cultures also elicited depolarizations in neurons grown in F-12, but the amplitude of the underlying inward current was 25-30% of that produced by fresh F-12, suggesting a loss of potency of F-12 exposed to prolonged contact with hippocampal cultures. Third, measurement by high performance liquid chromatography showed reduction of aspartate concentrations to around 10% of those present in fresh F-12, within 24 h after exposing glial cell cultures to fresh F-12. It is concluded that cellular uptake mechanisms for amino acids have a strong impact on excitotoxicity in vitro, and most likely play an important role in protecting neurons from the potentially damaging action of high concentrations of excitatory transmitters in vivo. In addition our experiments help to explain the mechanisms permitting neuronal survival in cultures grown in Ham's F-12 medium, which when applied acutely to mature cultures is strikingly neurotoxic. JF - Neuroscience AU - Sugiyama, K AU - Brunori, A AU - Mayer, M L AD - Unit of Neurophysiology and Biophysics, LDN, NICHD, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 779 EP - 791 VL - 32 IS - 3 SN - 0306-4522, 0306-4522 KW - Culture Media KW - 0 KW - Glutamates KW - Receptors, Amino Acid KW - Receptors, Cell Surface KW - Aspartic Acid KW - 30KYC7MIAI KW - Glutamic Acid KW - 3KX376GY7L KW - N-Methylaspartate KW - 6384-92-5 KW - Phosphopyruvate Hydratase KW - EC 4.2.1.11 KW - Kainic Acid KW - SIV03811UC KW - Index Medicus KW - Animals KW - Phosphopyruvate Hydratase -- metabolism KW - Cell Survival -- drug effects KW - Cells, Cultured KW - Mice, Inbred C57BL KW - Mice KW - Action Potentials -- drug effects KW - Kainic Acid -- toxicity KW - Aspartic Acid -- toxicity KW - Neuroglia -- cytology KW - Glutamates -- pharmacokinetics KW - Hippocampus -- metabolism KW - Neuroglia -- drug effects KW - Culture Media -- pharmacology KW - Hippocampus -- drug effects KW - Receptors, Cell Surface -- metabolism KW - Aspartic Acid -- pharmacokinetics KW - Neuroglia -- metabolism KW - Aspartic Acid -- analogs & derivatives KW - Hippocampus -- cytology KW - Glutamates -- toxicity KW - Receptors, Cell Surface -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79384442?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-02-01 N1 - Date created - 1990-02-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evolution of metaplastic squamous cells of alveolar walls in pulmonary fibrosis produced by paraquat. An ultrastructural and immunohistochemical study. AN - 79383825; 2480685 AB - Sequential histologic, ultrastructural, immunohistochemical and morphometric studies were made of the evolutional changes of metaplastic and regenerating alveolar epithelial cells in monkeys from 3 days to 8 weeks after paraquat administration. In the early proliferative phase, many alveoli were lined by single-layered and stratified squamous epithelium and bronchiolized epithelium (i.e., presumably derived from bronchi and bronchioles). The regenerating epithelial cells had well developed bundles of actin-like filaments, which were arranged parallel to the basal surfaces of the cells and were associated with zonulae adherentes; these cells also had intermediate filaments and some desmosomes, but lacked basement membranes, hemidesmosomes and anchoring fibrils. They covered either denuded, wavy and disrupted original epithelial basement membranes or areas of developing intraalveolar fibrosis. In zones of squamous epithelial cell metaplasia associated with intraalveolar fibrosis, fibronexus-like structures appeared to be responsible for the initial adhesion of the cells to the underlying connective tissue. In later phases, single-layered and stratified squamous epithelial cells disappeared, and only bronchiolized epithelial cells, with hemidesmosomes and anchoring fibrils on their basal surfaces, were found in fibrotic alveoli. Although bronchiolized and squamous metaplastic epithelial cells are generally thought to be formed as late events in pulmonary damage, such cells play an important role in early, temporary repair of damaged alveoli. JF - Virchows Archiv. B, Cell pathology including molecular pathology AU - Fukuda, Y AU - Takemura, T AU - Ferrans, V J AD - Pathology Branch, National Heart, Lung and Blood Institute, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 27 EP - 43 VL - 58 IS - 1 SN - 0340-6075, 0340-6075 KW - Keratins KW - 68238-35-7 KW - Paraquat KW - PLG39H7695 KW - Index Medicus KW - Keratins -- metabolism KW - Animals KW - Macaca fascicularis KW - Metaplasia -- pathology KW - Microscopy, Electron KW - Epithelium -- metabolism KW - Epithelium -- pathology KW - Time Factors KW - Immunohistochemistry KW - Pulmonary Alveoli -- pathology KW - Pulmonary Alveoli -- metabolism KW - Pulmonary Fibrosis -- pathology KW - Pulmonary Fibrosis -- chemically induced KW - Pulmonary Fibrosis -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79383825?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-12 N1 - Date created - 1990-01-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A comparison of calcium antagonists and diazepam in reducing ethanol withdrawal tremors. AN - 79372362; 2594904 AB - The calcium antagonists nimodipine and dantrolene were compared with diazepam in an animal model of tolerance and physical dependence upon ethanol. Nimodipine and dantrolene were both effective in suppressing withdrawal tremors but diazepam was clearly superior to both agents. These results suggest that the ethanol withdrawal syndrome is only partially mediated by increased calcium flux. JF - Psychopharmacology AU - Bone, G H AU - Majchrowicz, E AU - Martin, P R AU - Linnoila, M AU - Nutt, D J AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 386 EP - 388 VL - 99 IS - 3 SN - 0033-3158, 0033-3158 KW - Calcium Channel Blockers KW - 0 KW - Ethanol KW - 3K9958V90M KW - Nimodipine KW - 57WA9QZ5WH KW - Dantrolene KW - F64QU97QCR KW - Diazepam KW - Q3JTX2Q7TU KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Nimodipine -- pharmacokinetics KW - Animals KW - Nimodipine -- administration & dosage KW - Dantrolene -- pharmacology KW - Brain Chemistry -- drug effects KW - Nimodipine -- pharmacology KW - Male KW - Tremor -- physiopathology KW - Substance Withdrawal Syndrome -- physiopathology KW - Tremor -- drug therapy KW - Calcium Channel Blockers -- pharmacology KW - Ethanol -- pharmacology KW - Diazepam -- pharmacology KW - Substance Withdrawal Syndrome -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79372362?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-25 N1 - Date created - 1990-01-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Testing and abuse liability of drugs in humans. AN - 79372123; 2512489 AB - In summary, there are a number of factors to be considered in abuse liability testing such as the purpose of the testing and its potential applications that determine which subject population we should employ. Furthermore, we should not expect to see a perfect correlation between abuse liability testing and the actual abuse of these drugs because there are many factors that will modulate or modify whether or not abuse liability becomes activated and the abuse of any specific drug becomes a social problem. JF - NIDA research monograph AU - Schuster, C R AD - National Institute on Drug Abuse, Rockville, Maryland 20857. Y1 - 1989 PY - 1989 DA - 1989 SP - 1 EP - 6 VL - 92 SN - 1046-9516, 1046-9516 KW - Amphetamines KW - 0 KW - Street Drugs KW - Benzodiazepines KW - 12794-10-4 KW - Index Medicus KW - Drug Evaluation KW - Humans KW - Substance-Related Disorders -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79372123?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-23 N1 - Date created - 1990-01-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The formation of 2-aminofluorene-DNA adducts in vivo: evidence for peroxidase-mediated activation. AN - 79371639; 2593130 AB - Formation of DNA adducts in various tissues of dogs fed a single dose of the carcinogen 2-aminofluorene was investigated. Adduct analysis was performed using a technique that allows measurement of both N-(deoxyguanosin-8-yl)-2-amino-2-aminofluorene-DNA adduct formed by reaction of N-hydroxy-2-aminofluorene with DNA, as well as the polar 2-aminofluorene-DNA adducts formed when 2-aminofluorene is activated by prostaglandin H synthase-peroxidase in vitro. Two male beagle (A and B) dogs were examined and a different DNA adduct profile was observed with each dog. For the dog A, N-(deoxyguanosin-8-yl)-2-aminofluorene was the major adduct found in hepatic DNA; no peroxidase-derived adducts were detected in this tissue. In contrast, adducts eluting similarly to peroxidase-derived adducts were found in urinary tract tissues of this dog with the relative abundance of these adducts in the order urothelium greater than renal medulla greater than renal cortex, which correlates with the respective tissues' prostaglandin H synthase activity. N-(Deoxyguanosin-8-yl)-2-aminofluorene was detected in the renal tissues, but not in urothelium. For dog B, only the N-(deoxyguanosin-8-yl)-2-aminofluorene adduct was observed in all tissues examined, including the urothelium. However, total binding to liver, kidney, and bladder were two-, two-, and four-fold lower, respectively, than dog A. These data indicate that both prostaglandin H synthase-mediated activation and N-hydroxylation of 2-aminofluorene occur in vivo and may be subjected to pharmacodynamic considerations. Furthermore, the tissue distribution of the peroxidase-mediated 2-aminofluorene adducts suggests this process may also be of importance in the bladder-specific carcinogenicity of aromatic amines. JF - Journal of biochemical toxicology AU - Krauss, R S AU - Angerman-Stewart, J AU - Eling, T E AU - Dooley, K L AU - Kadlubar, F F AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989 PY - 1989 DA - 1989 SP - 111 EP - 117 VL - 4 IS - 2 SN - 0887-2082, 0887-2082 KW - 2-aminofluorene-DNA complex KW - 0 KW - DNA Adducts KW - Fluorenes KW - Mutagens KW - 2-aminofluorene KW - 3A69OS195N KW - DNA KW - 9007-49-2 KW - Mixed Function Oxygenases KW - EC 1.- KW - Peroxidases KW - EC 1.11.1.- KW - Index Medicus KW - Urinary Bladder -- metabolism KW - Animals KW - Kidney -- metabolism KW - Mixed Function Oxygenases -- metabolism KW - Enzyme Activation KW - Microsomes, Liver -- enzymology KW - Microsomes, Liver -- drug effects KW - Kidney -- drug effects KW - Dogs KW - Epithelium -- metabolism KW - Male KW - Epithelium -- drug effects KW - Chromatography, High Pressure Liquid KW - Urinary Bladder -- drug effects KW - Fluorenes -- toxicity KW - Fluorenes -- analysis KW - Fluorenes -- metabolism KW - DNA Damage KW - Mutagens -- metabolism KW - DNA -- analysis KW - Mutagens -- toxicity KW - Peroxidases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79371639?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-25 N1 - Date created - 1990-01-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Historical perspectives on the use of subjective effects measures in assessing the abuse potential of drugs. AN - 79367170; 2512502 JF - NIDA research monograph AU - Jaffe, J H AU - Jaffe, F K AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland 21224. Y1 - 1989 PY - 1989 DA - 1989 SP - 43 EP - 72 VL - 92 SN - 1046-9516, 1046-9516 KW - Street Drugs KW - 0 KW - Index Medicus KW - History of medicine KW - Drug Evaluation KW - History, 20th Century KW - Humans KW - History, 18th Century KW - History, Ancient KW - History, 19th Century KW - History, 17th Century KW - History, Medieval KW - History, 16th Century KW - Substance-Related Disorders -- history KW - Street Drugs -- history UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79367170?accountid=14244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-23 N1 - Date created - 1990-01-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 6-18F-L-dopa imaging of the dopamine neostriatal system in normal and clinically normal MPTP-treated rhesus monkeys. AN - 79361900; 2512179 AB - Positron emission tomography following intravenous administration of 6-[18F]-L-fluorodopa was used to investigate the usefulness of PET for the assessment of normal and abnormal dopaminergic function. For this purpose, the incracerebral distribution of 6-[18F]-L-fluorodopa and its metabolites was evaluated in normal control and asymptomatic MPTP-treated rhesus monkeys. MPTP is a neurotoxic compound which destroys selectively the dapaminergic neurons of the nigrostriatal pathways in primates. The 18F accumulation was found to be significantly reduced in the striatum, putamen more than caudate, of the MPTP-treated animals compared to the normal controls. The 18F accumulation in dopamine-poor areas did not differ between the two groups. The ratios of striatum to dopamine-poor brain area were highly correlated to the concentrations of the dopamine metabolite, homovanillic acid, in the cerebrospinal fluid of the same animals. The findings are consistent with the hypothesis that "silent damage" to the dopaminergic nigral neurons may precede the onset of parkinsonism by many years and that PET scanner examination using 6-[18F]-L-fluorodopa may be useful in the detection of subtle dopaminergic dysfunctions as may exist in DA-related motor syndromes and neuropsychiatric disorders. JF - Experimental brain research AU - Doudet, D J AU - Miyake, H AU - Finn, R T AU - McLellan, C A AU - Aigner, T G AU - Wan, R Q AU - Adams, H R AU - Cohen, R M AD - Section on Clinical Brain Imaging, NIMH, Bethesda, Md 20892-1000. Y1 - 1989 PY - 1989 DA - 1989 SP - 69 EP - 80 VL - 78 IS - 1 SN - 0014-4819, 0014-4819 KW - fluorodopa F 18 KW - 2C598205QX KW - Dihydroxyphenylalanine KW - 63-84-3 KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Animals KW - Cerebral Cortex -- metabolism KW - Tomography, Emission-Computed KW - Cerebral Cortex -- diagnostic imaging KW - Male KW - Female KW - Corpus Striatum -- diagnostic imaging KW - MPTP Poisoning KW - Corpus Striatum -- metabolism KW - Macaca mulatta -- metabolism KW - Macaca -- metabolism KW - Dopamine -- physiology KW - Dopamine -- metabolism KW - Dihydroxyphenylalanine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79361900?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+brain+research&rft.atitle=6-18F-L-dopa+imaging+of+the+dopamine+neostriatal+system+in+normal+and+clinically+normal+MPTP-treated+rhesus+monkeys.&rft.au=Doudet%2C+D+J%3BMiyake%2C+H%3BFinn%2C+R+T%3BMcLellan%2C+C+A%3BAigner%2C+T+G%3BWan%2C+R+Q%3BAdams%2C+H+R%3BCohen%2C+R+M&rft.aulast=Doudet&rft.aufirst=D&rft.date=1989-01-01&rft.volume=78&rft.issue=1&rft.spage=69&rft.isbn=&rft.btitle=&rft.title=Experimental+brain+research&rft.issn=00144819&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-22 N1 - Date created - 1990-01-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Relationship of mortality, occupation, and pulmonary diffusing capacity to pleural thickening in the First National Health and Nutrition Examination Survey. AN - 79356468; 2589326 AB - We studied the relationship of pleural thickening consistent with asbestos exposure to mortality, career employment in asbestos-related jobs, and pulmonary diffusing capacity among participants in the first National Health and Nutrition Examination Survey. Three "B" readers examined chest X-rays to identify 59 individuals with such pleural abnormalities. From 1975 to 1984, the all-cause mortality rate ratio (RR) comparing males with and without occupational pleural thickening was 1.3 (95% C.I. 0.8-2.2). For lung cancer, the mortality RR for males was 3.0 (95% C.I. 1.0-9.1). Career asbestos work was not associated with occupational pleural thickening among men, probably because some with the condition had only short-term exposure to asbestos. Pulmonary diffusing capacity was lower in those with occupational pleural thickening, taking smoking into account. These results suggest that individuals in the general population who have occupational pleural thickening are at risk for some of the health consequences of asbestos work, including lung cancer, even if they were not career asbestos workers. JF - American journal of industrial medicine AU - Loomis, D P AU - Collman, G W AU - Rogan, W J AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989 PY - 1989 DA - 1989 SP - 477 EP - 484 VL - 16 IS - 5 SN - 0271-3586, 0271-3586 KW - Asbestos KW - 1332-21-4 KW - Index Medicus KW - United States KW - Odds Ratio KW - Pneumoconiosis -- mortality KW - Pneumoconiosis -- etiology KW - Humans KW - Smoking -- adverse effects KW - Aged KW - Lung Neoplasms -- etiology KW - Adult KW - Asbestos -- adverse effects KW - Lung Neoplasms -- mortality KW - Middle Aged KW - Pneumoconiosis -- physiopathology KW - Adolescent KW - Lung Neoplasms -- physiopathology KW - Female KW - Male KW - Pleural Diseases -- mortality KW - Pleural Diseases -- etiology KW - Health Surveys KW - Pulmonary Diffusing Capacity -- physiology KW - Occupations -- statistics & numerical data KW - Pleural Diseases -- physiopathology KW - Pleural Diseases -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79356468?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Relationship+of+mortality%2C+occupation%2C+and+pulmonary+diffusing+capacity+to+pleural+thickening+in+the+First+National+Health+and+Nutrition+Examination+Survey.&rft.au=Loomis%2C+D+P%3BCollman%2C+G+W%3BRogan%2C+W+J&rft.aulast=Loomis&rft.aufirst=D&rft.date=1989-01-01&rft.volume=16&rft.issue=5&rft.spage=477&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 - 1990-01-03 N1 - Date created - 1990-01-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human liver cytochrome P-450 related to a rat acetone-inducible, nitrosamine-metabolizing cytochrome P-450: identification and isolation. AN - 79347816; 2587619 AB - A monoclonal antibody (MAb) to a rat acetone-inducible and nitrosamine-metabolizing form of microsomal cytochrome P-450, P-450ac, detected a related P-450 in human liver microsomes by both immunoblot and competitive radioimmunoassay. This MAb was also used to immunopurify microsomal cytochromes P-450 from both human liver and acetone-treated rats; these were electrophoretically homogeneous with apparent molecular weights of 56,200 and 53,000 daltons, respectively. The structures of the cytochromes P-450 were compared by peptide mapping and amino-terminal sequence analyses. They differed in their peptide maps but displayed amino-terminal sequence similarity in their first 19 residues. This report thus demonstrates the utility of MAbs to rat cytochromes P-450 for detection, identification and structural characterization of human P-450s. JF - Pharmacology AU - Robinson, R C AU - Shorr, R G AU - Varrichio, A AU - Park, S S AU - Gelboin, H V AU - Miller, H AU - Friedman, F K AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Md. Y1 - 1989 PY - 1989 DA - 1989 SP - 137 EP - 144 VL - 39 IS - 3 SN - 0031-7012, 0031-7012 KW - Antibodies, Monoclonal KW - 0 KW - Nitrosamines KW - Acetone KW - 1364PS73AF KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Animals KW - Immunoblotting KW - Microsomes, Liver -- analysis KW - Peptide Mapping KW - Humans KW - Nitrosamines -- metabolism KW - Acetone -- pharmacology KW - Amino Acid Sequence KW - Radioimmunoassay KW - Antibodies, Monoclonal -- immunology KW - Rats, Inbred Strains KW - Rats KW - Molecular Sequence Data KW - Male KW - Cytochrome P-450 Enzyme System -- isolation & purification KW - Liver -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79347816?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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&rft.atitle=Human+liver+cytochrome+P-450+related+to+a+rat+acetone-inducible%2C+nitrosamine-metabolizing+cytochrome+P-450%3A+identification+and+isolation.&rft.au=Robinson%2C+R+C%3BShorr%2C+R+G%3BVarrichio%2C+A%3BPark%2C+S+S%3BGelboin%2C+H+V%3BMiller%2C+H%3BFriedman%2C+F+K&rft.aulast=Robinson&rft.aufirst=R&rft.date=1989-01-01&rft.volume=39&rft.issue=3&rft.spage=137&rft.isbn=&rft.btitle=&rft.title=Pharmacology&rft.issn=00317012&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-05 N1 - Date created - 1990-01-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Introduction of HIV infection among intravenous drug abusers in low prevalence areas. AN - 79343363; 2585246 AB - To explore the introduction of human immunodeficiency virus (HIV) infection into intravenous drug abusing populations, risk behaviors of 1,154 intravenous drug abusers (IVDAs) in four U.S. cities with low prevalence of IVDA/HIV infection (0.9-13.0%) were examined. Seropositive subjects (N = 54) were compared with demographically matched seronegative controls regarding drug use practices, homosexual contact, blood transfusions, risk behaviors while traveling or living in high prevalence areas, and acquaintance with persons with AIDS. With the exception of needle sharing with homosexual/bisexual males, no differences in risk behaviors were found between seropositive subjects and matched seronegatives. Seropositives were substantially more likely than matched seronegatives to report having shared a needle with a homosexual or bisexual male, suggesting that needle sharing between homosexual/bisexual IVDAs and heterosexual IVDAs may be an important means by which HIV is introduced among heterosexual IVDAs in low prevalence areas. JF - Journal of acquired immune deficiency syndromes AU - Battjes, R J AU - Pickens, R W AU - Amsel, Z AD - National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1989 PY - 1989 DA - 1989 SP - 533 EP - 539 VL - 2 IS - 6 SN - 0894-9255, 0894-9255 KW - Index Medicus KW - AIDS/HIV KW - Illinois KW - Injections, Intravenous KW - Humans KW - Continental Population Groups KW - Texas KW - Homosexuality KW - California KW - HIV Seropositivity KW - HIV Seroprevalence KW - Bisexuality KW - Adult KW - Blood Transfusion KW - New Jersey KW - Male KW - Female KW - HIV Infections -- etiology KW - Substance Abuse, Intravenous -- complications KW - HIV Infections -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79343363?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Introduction+of+HIV+infection+among+intravenous+drug+abusers+in+low+prevalence+areas.&rft.au=Battjes%2C+R+J%3BPickens%2C+R+W%3BAmsel%2C+Z&rft.aulast=Battjes&rft.aufirst=R&rft.date=1989-01-01&rft.volume=2&rft.issue=6&rft.spage=533&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 - 1989-12-26 N1 - Date created - 1989-12-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Blockade of N-methyl-D-aspartate induced convulsions by 1-aminocyclopropanecarboxylates. AN - 79342044; 2685487 AB - 1-Aminocyclopropanecarboxylic acid is a potent and selective ligand for the glycine modulatory site on the N-methyl-D-aspartate receptor complex. This compound blocks (ED50 234 mg/kg) the convulsions and deaths produced by N-methyl-D-aspartate (125 mg/kg) in a dose dependent fashion. In contrast, 1-aminocyclopropanecarboxylic acid does not protect mice against convulsions induced by pentylenetetrazole (80 mg/kg), strychnine (2 mg/kg), bicuculline (6 mg/kg), or maximal electroshock (50 mA, 0.2 s), and does not impair motor performance on either a rotarod or horizontal wire at doses of up to 2 g/kg. The methyl- and ethyl- esters of 1-aminocyclopropanecarboxylic acid are 5- and 2.3-fold more potent, respectively, than the parent compound in blocking the convulsant and lethal effects of N-methyl-D-aspartate. However, these esters are several orders of magnitude less potent (IC50 greater than 40 microM) than 1-aminocyclopropanecarboxylic acid as inhibitors of strychnine-insensitive [3H] glycine binding, indicating that conversion to the parent compound may be required to elicit an anticonvulsant action. These findings suggest that 1-aminocyclopropanecarboxylates may be useful in the treatment of neuropathologies associated with excessive activation of N-methyl-D-aspartate receptor coupled cation channels. JF - Life sciences AU - Skolnick, P AU - Marvizón, J C AU - Jackson, B W AU - Monn, J A AU - Rice, K C AU - Lewin, A H AD - Laboratory of Neuroscience, NIDDK, National Institutes of Health, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 1647 EP - 1655 VL - 45 IS - 18 SN - 0024-3205, 0024-3205 KW - Amino Acids KW - 0 KW - Amino Acids, Cyclic KW - Anticonvulsants KW - Aspartic Acid KW - 30KYC7MIAI KW - 1-aminocyclopropane-1-carboxylic acid KW - 3K9EJ633GL KW - N-Methylaspartate KW - 6384-92-5 KW - Strychnine KW - H9Y79VD43J KW - Pentylenetetrazole KW - WM5Z385K7T KW - Bicuculline KW - Y37615DVKC KW - Index Medicus KW - Aspartic Acid -- toxicity KW - Animals KW - Pentylenetetrazole -- metabolism KW - Dose-Response Relationship, Drug KW - Strychnine -- metabolism KW - Mice KW - Synaptic Membranes -- metabolism KW - Rats, Inbred Strains KW - Rats KW - Bicuculline -- metabolism KW - Bicuculline -- toxicity KW - Pentylenetetrazole -- toxicity KW - Strychnine -- toxicity KW - Electroshock KW - Synaptic Membranes -- drug effects KW - Aspartic Acid -- antagonists & inhibitors KW - Male KW - Amino Acids -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79342044?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=unknown&rft.jtitle=Film+Index+International&rft.atitle=Un+T%C3%89MOIN+DANS+LA+VILLE&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1959-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-01-02 N1 - Date created - 1990-01-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Clozapine in China: a review and preview of US/PRC collaboration. AN - 79306706; 2682733 JF - Psychopharmacology AU - Potter, W Z AU - Ko, G N AU - Zhang, L D AU - Yan, W W AD - Department of Health and Human Services, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - S87 EP - S91 VL - 99 Suppl SN - 0033-3158, 0033-3158 KW - Dibenzazepines KW - 0 KW - Clozapine KW - J60AR2IKIC KW - Chlorpromazine KW - U42B7VYA4P KW - Homovanillic Acid KW - X77S6GMS36 KW - Index Medicus KW - United States KW - Homovanillic Acid -- blood KW - Randomized Controlled Trials as Topic KW - Psychiatric Status Rating Scales KW - International Cooperation KW - Double-Blind Method KW - Humans KW - Adult KW - Chlorpromazine -- therapeutic use KW - Middle Aged KW - Male KW - Female KW - China KW - Clozapine -- therapeutic use KW - Schizophrenia -- drug therapy KW - Clozapine -- adverse effects KW - Dibenzazepines -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79306706?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Clozapine+in+China%3A+a+review+and+preview+of+US%2FPRC+collaboration.&rft.au=Potter%2C+W+Z%3BKo%2C+G+N%3BZhang%2C+L+D%3BYan%2C+W+W&rft.aulast=Potter&rft.aufirst=W&rft.date=1989-01-01&rft.volume=99+Suppl&rft.issue=&rft.spage=S87&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology&rft.issn=00333158&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-21 N1 - Date created - 1989-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparative transplacental carcinogenesis by directly acting and metabolism-dependent alkylating agents in rodents and nonhuman primates. AN - 79282584; 2553598 AB - Transplacental carcinogenesis by N-ethyl-N-nitrosourea (ENU) was studied in patas (Erythrocebus patas) and rhesus (Macaca mulatta) monkeys. Repeated intravenous injections throughout pregnancy caused gestational choriocarcinoma in female patas monkeys and a variety of non-trophoblastic neoplasms in their offspring. Latent periods for transplacentally induced tumours varied from less than one month to more than ten years. One case of congenital neoplasm was observed. Certain kinds of neoplasms were observed only in transplacentally exposed offspring, and not in monkeys given the same carcinogen during juvenile or adult life. These included a variety of embryonal tumours, especially nephroblastoma, and tumours of the brain, mostly gliomas. Schwannomas of the peripheral nervous system were not observed in patas monkeys given ENU. One embryonal tumour yielded DNA that transformed NIH 3T3 cells in a transfection assay. Similar protocols performed in rhesus monkeys also yielded a variety of tumours in the offspring, including brain tumours; but in this species the most common embryonal tumour was pulmonary blastoma, and no choriocarcinoma was seen in adult females given ENU during pregnancy. Administration of N-nitrosodiethylamine to patas monkeys during pregnancy at first appeared to have had no effect on the offspring, but administration of phenobarbital beginning at four years of age resulted in the rapid appearance of multiple hepatocellular tumours. With regard to potential human risk from prenatal exposure to carcinogens, three conclusions deserve special emphasis: (1) the extreme susceptibility of the fetal primate central nervous system to certain chemical carcinogens, which confirms and reinforces what was previously known from studies in rodents; (2) the prolonged latency of transplacentally initiated epithelial tumours and the importance of subsequent postnatal exposure to promoting agents; and (3) the concurrent risk of transplacental chemical carcinogenesis in offspring and gestational choriocarcinoma in the mother, suggesting that gestational choriocarcinoma with its short latent period may serve as an epidemiologically exploitable marker for human populations in which transplacental carcinogenesis is likely. JF - IARC scientific publications AU - Rice, J M AU - Rehm, S AU - Donovan, P J AU - Perantoni, A O AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research Facility, MD 21701-1013. Y1 - 1989 PY - 1989 DA - 1989 SP - 17 EP - 34 IS - 96 SN - 0300-5038, 0300-5038 KW - Alkylating Agents KW - 0 KW - Carcinogens KW - Diethylnitrosamine KW - 3IQ78TTX1A KW - Ethylnitrosourea KW - P8M1T4190R KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Animals KW - Uterine Neoplasms -- chemically induced KW - Neoplasms, Experimental -- congenital KW - Pregnancy KW - Brain Neoplasms -- chemically induced KW - Rats KW - Diethylnitrosamine -- toxicity KW - Phenobarbital -- pharmacology KW - Ethylnitrosourea -- toxicity KW - Neoplasms, Experimental -- chemically induced KW - Erythrocebus patas KW - Neoplasms, Germ Cell and Embryonal -- chemically induced KW - Choriocarcinoma -- chemically induced KW - Female KW - Male KW - Alkylating Agents -- metabolism KW - Alkylating Agents -- toxicity KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79282584?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparative+transplacental+carcinogenesis+by+directly+acting+and+metabolism-dependent+alkylating+agents+in+rodents+and+nonhuman+primates.&rft.au=Rice%2C+J+M%3BRehm%2C+S%3BDonovan%2C+P+J%3BPerantoni%2C+A+O&rft.aulast=Rice&rft.aufirst=J&rft.date=1989-01-01&rft.volume=&rft.issue=96&rft.spage=17&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 - 1989-12-12 N1 - Date created - 1989-12-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Structure and regulation of P-450s in the rat P450IIA gene subfamily. AN - 79282160; 2806080 AB - The rat P450IIA subfamily was characterized at the protein, cDNA, and gene level. The purified IIA1 and IIA2 P-450s displayed distinct positional specificities toward hydroxylation of the prototype substrate testosterone. The IIA1 and IIA2 genes were also regulated differently during development; IIA1 was expressed within 1 week after birth in both males and females, and was specifically suppressed in males at puberty, while IIA2 was not expressed in females and was activated at puberty in males. The cDNA-deduced amino acid sequences of these enzymes showed 88% similarity with interspersed regions of high and low similarity indicative of former gene conversion events. Both the IIA1 and IIA2 genes contained nine exons. JF - Drug metabolism reviews AU - Gonzalez, F J AU - Matsunaga, T AU - Nagata, K AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 827 EP - 837 VL - 20 IS - 2-4 SN - 0360-2532, 0360-2532 KW - Isoenzymes KW - 0 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Rats KW - Animals KW - Aging -- metabolism KW - Base Sequence KW - Liver -- growth & development KW - Microsomes, Liver -- enzymology KW - Molecular Sequence Data KW - DNA -- analysis KW - Amino Acid Sequence KW - Male KW - Female KW - Isoenzymes -- isolation & purification KW - Gene Expression Regulation, Enzymologic KW - Cytochrome P-450 Enzyme System -- genetics KW - Cytochrome P-450 Enzyme System -- isolation & purification KW - Isoenzymes -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79282160?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+reviews&rft.atitle=Structure+and+regulation+of+P-450s+in+the+rat+P450IIA+gene+subfamily.&rft.au=Gonzalez%2C+F+J%3BMatsunaga%2C+T%3BNagata%2C+K&rft.aulast=Gonzalez&rft.aufirst=F&rft.date=1989-01-01&rft.volume=20&rft.issue=2-4&rft.spage=827&rft.isbn=&rft.btitle=&rft.title=Drug+metabolism+reviews&rft.issn=03602532&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-19 N1 - Date created - 1989-12-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Neoantigens associated with halothane hepatitis. AN - 79280695; 2680380 JF - Drug metabolism reviews AU - Pohl, L R AU - Kenna, J G AU - Satoh, H AU - Christ, D AU - Martin, J L AD - Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 203 EP - 217 VL - 20 IS - 2-4 SN - 0360-2532, 0360-2532 KW - Antigens KW - 0 KW - Carrier Proteins KW - Trifluoroacetic Acid KW - E5R8Z4G708 KW - Halothane KW - UQT9G45D1P KW - Index Medicus KW - Animals KW - Trifluoroacetic Acid -- immunology KW - Humans KW - Halothane -- toxicity KW - Antigens -- immunology KW - Chemical and Drug Induced Liver Injury -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79280695?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+reviews&rft.atitle=Neoantigens+associated+with+halothane+hepatitis.&rft.au=Pohl%2C+L+R%3BKenna%2C+J+G%3BSatoh%2C+H%3BChrist%2C+D%3BMartin%2C+J+L&rft.aulast=Pohl&rft.aufirst=L&rft.date=1989-01-01&rft.volume=20&rft.issue=2-4&rft.spage=203&rft.isbn=&rft.btitle=&rft.title=Drug+metabolism+reviews&rft.issn=03602532&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-19 N1 - Date created - 1989-12-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Metabolism of transplacental carcinogens. AN - 79279458; 2680945 AB - Literature on fetal metabolism of carcinogens since 1980 has been systematically listed and selectively discussed. The published data continues to support the conclusion that animal and human fetal tissues have the capacity to metabolize carcinogens, but at a low rate compared to the adult. Metabolism of low-molecular-weight chemicals, including nitrosamines, appears only near term in the rodent and is poorly inducible transplacentally; these agents are correspondingly relatively ineffective as fetal carcinogens. Metabolism of aromatic carcinogens, by contrast, appears early in gestation and is highly inducible transplacentally in rodents by chemicals such as polycyclic aromatic hydrocarbons (PAH) and tetrachlorodibenzo-p-dioxin, resulting in dramatic percent increases in enzyme activity. Transplacental induction has not been unequivocally demonstrated for the human fetus. Phase II enzymes, metabolizing aromatic compounds to water-soluble forms, generally have higher constitutive activity but lower degree of inducibility in the fetus, compared with phase I (activating) enzymes, and appear to show quantitatively different patterns in the human compared with the rodent. Specific and sensitive new technologies, including 32P-postlabelling, immunodetection of specific proteins, and use of cDNA probes, are beginning to be applied to fetal systems and are providing a more definitive and detailed understanding of the ontogeny and modulation of fetal carcinogen metabolizing enzymes. Fetal and maternal metabolism of PAH, especially methylcholanthrene (MC), have been found to be important determinants in susceptibility of the fetus to tumorigenesis. In particular, we have utilized a mouse model system wherein a single dominant gene, Ah, confers responsiveness to induction of PAH metabolism by cytochrome Pl450 (IA1); the recessive allele, Ah, is associated with nonresponsiveness. In appropriate backcrosses between C57BL/6 (AhAh) and DBA/2 (AhAh) mice, responsive and nonresponsive fetuses were carried together in mothers who were, themselves, either responsive or nonresponsive. In both cases, responsive fetuses later developed more lung and liver tumours after transplacental MC, compared with nonresponsive littermates. Fetuses of responsive mothers, however, experienced a lower cancer risk than did those of nonresponsive mothers at a comparable MC dose. Pretreatment of the pregnant mice with the noncarcinogenic inducer, beta-naphthoflavone (BNF) had a uniform protective effect for all of the fetuses, especially the responsive ones, if the mother was responsive. For nonresponsive mothers, by contrast, BNF pretreatment led to an enhancement of tumorigenesis, in the responsive fetuses only, under certain conditions of dose and fetal sex.(ABSTRACT TRUNCATED AT 400 WORDS) JF - IARC scientific publications AU - Anderson, L M AU - Jones, A B AU - Miller, M S AU - Chauhan, D P AD - Division of Cancer Etiology National Cancer Institute, Frederick, MD. Y1 - 1989 PY - 1989 DA - 1989 SP - 155 EP - 188 IS - 96 SN - 0300-5038, 0300-5038 KW - Carcinogens KW - 0 KW - Isoenzymes KW - Polycyclic Compounds KW - Index Medicus KW - Gene Expression -- drug effects KW - Animals KW - Isoenzymes -- biosynthesis KW - Enzyme Induction KW - Polycyclic Compounds -- metabolism KW - Female KW - Pregnancy KW - Maternal-Fetal Exchange KW - Carcinogens -- pharmacology KW - Carcinogens -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79279458?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Metabolism+of+transplacental+carcinogens.&rft.au=Anderson%2C+L+M%3BJones%2C+A+B%3BMiller%2C+M+S%3BChauhan%2C+D+P&rft.aulast=Anderson&rft.aufirst=L&rft.date=1989-01-01&rft.volume=&rft.issue=96&rft.spage=155&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 - 1989-12-12 N1 - Date created - 1989-12-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chemical strategies for the inactivation of bay-region diol epoxides, ultimate carcinogens derived from polycyclic aromatic hydrocarbons. AN - 79277782; 2680377 JF - Drug metabolism reviews AU - Sayer, J M AU - Whalen, D L AU - Jerina, D M AD - Laboratory of Bioorganic Chemistry, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 155 EP - 182 VL - 20 IS - 2-4 SN - 0360-2532, 0360-2532 KW - Carcinogens KW - 0 KW - Epoxy Compounds KW - Ethers, Cyclic KW - Polycyclic Compounds KW - Ellagic Acid KW - 19YRN3ZS9P KW - Index Medicus KW - Animals KW - Humans KW - Ellagic Acid -- toxicity KW - Ellagic Acid -- metabolism KW - Polycyclic Compounds -- antagonists & inhibitors KW - Carcinogens -- metabolism KW - Epoxy Compounds -- antagonists & inhibitors KW - Polycyclic Compounds -- toxicity KW - Carcinogens -- toxicity KW - Ethers, Cyclic -- antagonists & inhibitors KW - Epoxy Compounds -- toxicity KW - Polycyclic Compounds -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79277782?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+reviews&rft.atitle=Chemical+strategies+for+the+inactivation+of+bay-region+diol+epoxides%2C+ultimate+carcinogens+derived+from+polycyclic+aromatic+hydrocarbons.&rft.au=Sayer%2C+J+M%3BWhalen%2C+D+L%3BJerina%2C+D+M&rft.aulast=Sayer&rft.aufirst=J&rft.date=1989-01-01&rft.volume=20&rft.issue=2-4&rft.spage=155&rft.isbn=&rft.btitle=&rft.title=Drug+metabolism+reviews&rft.issn=03602532&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-19 N1 - Date created - 1989-12-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human cDNA-expressed cytochrome P450 IA2: mutagen activation and substrate specificity. AN - 79269679; 2803520 AB - The vaccinia virus cDNA expression system was used to produce human cytochrome P450 IA2 in a hepatoma cell line that is devoid of significant basal levels of P450. The expressed enzyme yielded a reduced carbon monoxide-bound difference spectrum with a lambda max of 449 nm. Catalytic activities and mutagen activation ability of the human enzyme were assessed and directly compared with results obtained with the orthologous mouse IA2, which was also expressed using vaccinia virus. Both the human and mouse enzymes were able to catalyze efficiently the p-hydroxylation of aniline. Mouse IA2 also catalyzed ethoxyresorufin O-deethylation, and its activity was sevenfold greater than expressed human IA2. The mouse and human enzymes also activated several promutagens and procarcinogens. Mouse IA2 was five- to sevenfold more active than the human enzyme for activation of the procarcinogens 2-acetylaminofluorene and benzo[a]pyrene-trans-7,8-dihydrodiol and the promutagens Glu-P-2 and Trp-P-1. Comparable activities were observed with 2-aminoanthracene, 2-aminofluorene, and Glu-P-1. These data demonstrate the utility of cDNA expression for examining the activities of human P450s and further suggest potentially important differences in catalytic activities of orthologous P450s found in different species. JF - Molecular carcinogenesis AU - Aoyama, T AU - Gonzalez, F J AU - Gelboin, H V AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 192 EP - 198 VL - 2 IS - 4 SN - 0899-1987, 0899-1987 KW - Carcinogens KW - 0 KW - Mutagens KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Vaccinia virus -- genetics KW - Animals KW - Carcinogens -- metabolism KW - Tumor Cells, Cultured KW - Humans KW - Genetic Vectors KW - Mice KW - Substrate Specificity KW - Cloning, Molecular KW - Cytochrome P-450 Enzyme System -- genetics KW - Mutagens -- metabolism KW - Cytochrome P-450 Enzyme System -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79269679?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=unknown&rft.jtitle=Film+Index+International&rft.atitle=DEUX+HOMMES+DANS+MANHATTAN&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1959-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-12-13 N1 - Date created - 1989-12-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Spontaneous Ha-ras gene activation in cultured primary murine keratinocytes: consequences of Ha-ras gene activation in malignant conversion and malignant progression. AN - 79267167; 2679655 AB - The activation of the c-Ha-ras gene and its contribution to the tumorigenic phenotype were examined in cultured mouse keratinocytes and squamous tumors using transfection into NIH 3T3 cells and nucleic acid hybridization. When normal keratinocytes were cultured in medium with 0.05 mM Ca2+ (low Ca2+ medium), many cells died within 2-3 wk, while others formed rapidly growing foci that could be subcultured. These rapidly growing cells produced benign tumors when grafted to nude mice and possessed a heterozygous mutation in the c-Ha-ras gene with an A----T transversion in codon 61. Fibroblast-conditioned low Ca2+ medium prevented cell death, focus formation, c-Ha-ras gene mutation, and tumorigenicity. Thus, suboptimal culture conditions favored a spontaneous mutation in codon 61 of the c-Ha-ras gene of keratinocytes. When a v-Ha-ras gene was introduced into normal keratinocytes by a replication-defective retrovirus, the recipient cells produced papillomas in vivo, and after 2 mo, 60% of the tumors converted to squamos cell carcinomas. None of the 22 converted tumors had an endogenous c-Ha-ras gene mutation at codon 61. However, the A----T transversion mutation developed when these carcinoma cells were cultured in low Ca2+ medium but not in fibroblast-conditioned medium. Cells with both an exogenous v-Ha-ras and an activated c-Ha61-ras gene produced undifferentiated, rapidly lethal carcinomas, while cells with only v-Ha-ras maintained the squamous carcinoma phenotype. Undifferentiated carcinomas also developed when the v-Ha-ras gene was introduced into papilloma cells with a chemically induced endogenous c-Ha61-ras gene mutation. These results suggest that mutation in the c-Ha-ras gene can contribute to initiation, malignant conversion, and malignant progression in skin carcinogenesis, and gene dosage may determine the phenotype expressed. JF - Molecular carcinogenesis AU - Greenhalgh, D A AU - Welty, D J AU - Strickland, J E AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 199 EP - 207 VL - 2 IS - 4 SN - 0899-1987, 0899-1987 KW - Amino Acids KW - 0 KW - DNA KW - 9007-49-2 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Neoplasm Transplantation KW - DNA -- isolation & purification KW - Animals KW - Transfection KW - Cells, Cultured KW - DNA Mutational Analysis KW - Amino Acids -- analysis KW - Mice KW - Papilloma -- genetics KW - Mice, Inbred BALB C KW - Transcriptional Activation KW - Genes, ras KW - Keratinocytes -- metabolism KW - Gene Expression Regulation KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79267167?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Spontaneous+Ha-ras+gene+activation+in+cultured+primary+murine+keratinocytes%3A+consequences+of+Ha-ras+gene+activation+in+malignant+conversion+and+malignant+progression.&rft.au=Greenhalgh%2C+D+A%3BWelty%2C+D+J%3BStrickland%2C+J+E%3BYuspa%2C+S+H&rft.aulast=Greenhalgh&rft.aufirst=D&rft.date=1989-01-01&rft.volume=2&rft.issue=4&rft.spage=199&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 - 1989-12-13 N1 - Date created - 1989-12-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evolution of ciclosporin nephrotoxicity in patients treated for autoimmune uveitis. AN - 79263090; 2801787 AB - Among 73 patients treated with ciclosporin (CS) for autoimmune uveitis, a 50% elevation of serum creatinine was observed in 37% within 3 months of starting CS and in 25% after more than 6 months of relatively uncomplicated therapy. Sequential renal function and histologic evaluations were performed in 17 patients to further characterize the nephrotoxic effects of long-term CS therapy. Inulin clearance remained essentially unchanged in 12 patients despite CS dosage reductions in the majority. In 2 such patients, repeat renal biopsy specimens revealed evidence of progressive irreversible kidney injury even though renal function was stable. Inulin clearance decreased substantially in 3 patients; in 1 case a follow-up renal biopsy showed increased severity of chronic histologic change. For 2 patients, the inulin clearance more than doubled after CS dosage reduction; and in 1 of those cases, repeat renal biopsy showed no evidence of progressive renal scarring. Overall, the morphologic attributes of irreversible kidney injury (designated by a chronicity index including glomerular sclerosis, tubular atrophy and interstitial fibrosis) were increased in 3 of 6 follow-up renal biopsy specimens. Histologic alterations of renal arterioles, including hyaline change, were observed in all CS-treated patients. The hyaline change of arterioles was either extensive in the first renal biopsy specimen or became extensive in the second biopsy in the 3 cases manifesting an increased chronicity index on the follow-up renal biopsy. Thus, parenchymal injury can progress in some cases despite CS dosage reduction and stable renal function; renal arteriolar histologic change is a prominent finding in these patients. Patients that exhibit a substantial improvement in renal function after dosage reduction may experience a more favorable course. JF - American journal of nephrology AU - Austin, H A AU - Palestine, A G AU - Sabnis, S G AU - Balow, J E AU - Preuss, H G AU - Nussenblatt, R B AU - Antonovych, T T AD - Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Md. Y1 - 1989 PY - 1989 DA - 1989 SP - 392 EP - 402 VL - 9 IS - 5 SN - 0250-8095, 0250-8095 KW - Cyclosporins KW - 0 KW - Index Medicus KW - Kidney Function Tests KW - Humans KW - Kidney -- drug effects KW - Time Factors KW - Cyclosporins -- adverse effects KW - Cyclosporins -- therapeutic use KW - Autoimmune Diseases -- drug therapy KW - Kidney Failure, Chronic -- chemically induced KW - Uveitis -- drug therapy KW - Kidney Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79263090?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+nephrology&rft.atitle=Evolution+of+ciclosporin+nephrotoxicity+in+patients+treated+for+autoimmune+uveitis.&rft.au=Austin%2C+H+A%3BPalestine%2C+A+G%3BSabnis%2C+S+G%3BBalow%2C+J+E%3BPreuss%2C+H+G%3BNussenblatt%2C+R+B%3BAntonovych%2C+T+T&rft.aulast=Austin&rft.aufirst=H&rft.date=1989-01-01&rft.volume=9&rft.issue=5&rft.spage=392&rft.isbn=&rft.btitle=&rft.title=American+journal+of+nephrology&rft.issn=02508095&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-17 N1 - Date created - 1989-11-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Development and validation of a cellular transplant model for leukemia in Fischer rats: a short-term assay for potential anti-leukemic chemicals. AN - 79240817; 2796389 AB - The efficacy of a leukemia cell transplant model to measure potential chemotherapeutic activity was tested with five different chemicals that had previously been evaluated in 2-year studies. Leukemic spleen cells from Fischer rats were injected subcutaneously into syngeneic recipients and the effects of chemical treatment on tumor progression were evaluated at 70 days post-transplant. The data from the short-term assay were in all cases correlated with the trends reported for mononuclear cell leukemia in 2-year studies, where two chemicals were reported to decrease the incidence and three chemicals were reported to increase the incidence of leukemia. Short-term treatment with the two chemicals which caused negative trends for leukemia (2-ethoxyethanol or ethylene glycol monoethyl ether; 4-hexylresorcinol) delayed and/or reduced tumor growth in the transplant model in a dose-related fashion, as exhibited by reduction or elimination of splenomegaly and leukoblastosis, and a reversal in the depression of red blood cell indices or platelet counts. By contrast, the rate of tumor progression was increased in the short-term assay of the three chemicals which previously caused increased trends for leukemia in 2-year studies (pyridine; 2,4,6-trichlorophenol, dichlorvos). The severity of the mononuclear cell leukemia in the transplant recipients, as measured by histopathological examination of spleen and liver, was correlated with the changes in tumor growth rates. The in vivo leukemia transplant model is a short-term assay that could be used to screen a variety of potential chemotherapeutic agents, or to study structure-activity relationships within one class of chemicals. JF - Leukemia research AU - Dieter, M P AU - Jameson, C W AU - French, J E AU - Gangjee, S AU - Stefanski, S A AU - Chhabra, R S AU - Chan, P C AD - National Institutes of Health, National Toxicology Program, Research Triangle Park, NC 27709. Y1 - 1989 PY - 1989 DA - 1989 SP - 841 EP - 849 VL - 13 IS - 9 SN - 0145-2126, 0145-2126 KW - Antineoplastic Agents KW - 0 KW - Carcinogens KW - Chlorophenols KW - Ethylene Glycols KW - Pyridines KW - Resorcinols KW - Dichlorvos KW - 7U370BPS14 KW - 2-ethoxyethanol KW - IDK7C2HS09 KW - 2,4,6-trichlorophenol KW - MHS8C5BAUZ KW - pyridine KW - NH9L3PP67S KW - Index Medicus KW - Spleen -- anatomy & histology KW - Animals KW - Biological Assay KW - Neoplasm Transplantation KW - Rats KW - Rats, Inbred F344 KW - Organ Size -- drug effects KW - Leukemia, Experimental -- drug therapy KW - Leukemia, Experimental -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79240817?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Leukemia+research&rft.atitle=Development+and+validation+of+a+cellular+transplant+model+for+leukemia+in+Fischer+rats%3A+a+short-term+assay+for+potential+anti-leukemic+chemicals.&rft.au=Dieter%2C+M+P%3BJameson%2C+C+W%3BFrench%2C+J+E%3BGangjee%2C+S%3BStefanski%2C+S+A%3BChhabra%2C+R+S%3BChan%2C+P+C&rft.aulast=Dieter&rft.aufirst=M&rft.date=1989-01-01&rft.volume=13&rft.issue=9&rft.spage=841&rft.isbn=&rft.btitle=&rft.title=Leukemia+research&rft.issn=01452126&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-21 N1 - Date created - 1989-11-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Policy alternatives for alcohol-impaired driving. AN - 79231619; 2676914 AB - This article summarizes current scientific evidence about the impact of public policy measures on alcohol-related motor vehicle crashes. The public policy measures considered are (1) minimum drinking age laws, (2) taxation of alcoholic beverages, (3) drinking and driving laws, (4) laws and regulations governing the physical availability of alcoholic beverages, and (5) server intervention programs. It is concluded that certain public policy measures reduce alcohol-related crashes. These measures include higher taxes on alcoholic beverages and at least some laws and regulations governing the physical availability of alcohol (as well as the minimum drinking age). The article suggests that strengthening drinking and driving laws without also adopting these other measures may have less than optimum (and possibly disappointing) effects. JF - Health education quarterly AU - Farrell, S AD - National Institute on Alcohol Abuse and Alcoholism, Alcohol, Drug Abuse, and Mental Health Administration, Rockville, MD 20857. Y1 - 1989 PY - 1989 DA - 1989 SP - 413 EP - 427 VL - 16 IS - 3 SN - 0195-8402, 0195-8402 KW - Index Medicus KW - United States KW - Taxes KW - Age Factors KW - Humans KW - Alcoholic Beverages -- supply & distribution KW - Legislation as Topic KW - Alcoholic Intoxication KW - Health Policy KW - Alcohol Drinking KW - Automobile Driving UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79231619?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+education+quarterly&rft.atitle=Policy+alternatives+for+alcohol-impaired+driving.&rft.au=Farrell%2C+S&rft.aulast=Farrell&rft.aufirst=S&rft.date=1989-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-11-09 N1 - Date created - 1989-11-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutagen activation by cDNA-expressed P(1)450, P(3)450, and P450a. AN - 79218311; 2789689 AB - cDNAs for rodent P(1)450, P(3)450, and P450a were expressed in the modified vaccinia virus-T7 RNA polymerase system. Each P450 exhibited its appropriate molecular weight and characteristic enzyme activity. Aryl hydrocarbon hydroxylase activity was catalyzed by P(1)450, acetanilide hydroxylase by P(3)450, and testosterone 7 alpha-hydroxylase by P450a. Ethoxycoumarin deethylase was exhibited by both P(1)450 and P(3)450. Each expressed P450 was also analyzed for its ability to activate 19 carcinogens of diverse classes to their mutagenic forms. Most notable was the activation of several polycyclic aromatic hydrocarbons by P1 and the activation of acetylaminofluorene, 4-aminobiphenyl, and several heterocyclic amine food pyrolysate products by P(3)450. P450a, in contrast, showed slight mutagen activation only toward N-hydroxy-2-acetyl aminofluorene. The vaccinia virus-T7 RNA polymerase system described here can express cDNAs for diverse forms of P450, each of which can then be characterized for substrate and product specificity and for mutagen activation. JF - Molecular carcinogenesis AU - Aoyama, T AU - Gonzalez, F J AU - Gelboin, H V AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland. Y1 - 1989 PY - 1989 DA - 1989 SP - 253 EP - 259 VL - 1 IS - 4 SN - 0899-1987, 0899-1987 KW - Carcinogens KW - 0 KW - Mutagens KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Steroid Hydroxylases KW - EC 1.14.- KW - 7-Alkoxycoumarin O-Dealkylase KW - EC 1.14.13.- KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - acetanilide hydroxylase KW - testosterone 7-alpha-hydroxylase, hamster KW - DNA-Directed RNA Polymerases KW - EC 2.7.7.6 KW - Index Medicus KW - Vaccinia virus -- genetics KW - 7-Alkoxycoumarin O-Dealkylase -- genetics KW - Animals KW - 7-Alkoxycoumarin O-Dealkylase -- metabolism KW - Steroid Hydroxylases -- metabolism KW - T-Phages -- enzymology KW - Rats KW - Aryl Hydrocarbon Hydroxylases -- metabolism KW - Carcinogens -- metabolism KW - Biotransformation KW - DNA-Directed RNA Polymerases -- metabolism KW - Genetic Vectors KW - Steroid Hydroxylases -- genetics KW - Aryl Hydrocarbon Hydroxylases -- genetics KW - Cytochrome P-450 Enzyme System -- genetics KW - Mutagens -- metabolism KW - DNA -- genetics KW - Cytochrome P-450 Enzyme System -- metabolism KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79218311?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mutagen+activation+by+cDNA-expressed+P%281%29450%2C+P%283%29450%2C+and+P450a.&rft.au=Aoyama%2C+T%3BGonzalez%2C+F+J%3BGelboin%2C+H+V&rft.aulast=Aoyama&rft.aufirst=T&rft.date=1989-01-01&rft.volume=1&rft.issue=4&rft.spage=253&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 - 1989-10-30 N1 - Date created - 1989-10-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Mol Carcinog 1990;3(5):319 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanistic approaches in the study of testicular toxicity: toxicants that affect the endocrine regulation of the testis. AN - 79215185; 2675293 AB - This review will expand on the themes presented by Heindel and Treinen (1988). As a prelude to describing where selected compounds act on the endocrine regulation of the testis and the theories about their mechanisms, we will briefly review some of the central pathways that underlie this control. After reviewing some studies that define the site of action of lead on the reproductive system, we will discuss the "signature" lesion caused by androgen deficiency, and then move on to an evaluation of the effects of an antiandrogen (flutamide) on the male reproductive system. Finally, some consideration will be given to alterations in hepatic function which modify circulating levels of androgens. JF - Toxicologic pathology AU - Chapin, R E AU - Williams, J AD - Developmental and Reproductive Toxicology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989 PY - 1989 DA - 1989 SP - 446 EP - 451 VL - 17 IS - 2 SN - 0192-6233, 0192-6233 KW - Index Medicus KW - Animals KW - Humans KW - Male KW - Testis -- physiology KW - Testicular Diseases -- chemically induced KW - Endocrine Glands -- drug effects KW - Testicular Diseases -- physiopathology KW - Endocrine Glands -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79215185?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mechanistic+approaches+in+the+study+of+testicular+toxicity%3A+toxicants+that+affect+the+endocrine+regulation+of+the+testis.&rft.au=Chapin%2C+R+E%3BWilliams%2C+J&rft.aulast=Chapin&rft.aufirst=R&rft.date=1989-01-01&rft.volume=17&rft.issue=2&rft.spage=446&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 - 1989-10-17 N1 - Date created - 1989-10-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Physiology of the male reproductive system: endocrine, paracrine and autocrine regulation. AN - 79215133; 2675292 AB - This presentation reviews the male reproductive system, concentrating on newer advances in our knowledge of its physiology, biochemistry, and regulation, and introduces the topic of male reproductive toxicology. GnRH is the hypothalamic peptide responsible for the stimulation of LH and FSH release from the pituitary. It is synthesized as a pro-hormone, processed in the hypothalamus and released into the portal system in a pulsatile fashion. The timing of these pulses is critical to the release of LH and FSH into the general circulation. While LH and FSH are the main trophic hormones for the testis, we now realize the importance of not only endocrine control, but also of paracrine and autocrine regulation. Specifically, the local control of Leydig cells, Sertoli cells, and germ cells appears to be modulated by numerous growth factors and local regulators arising from within the testis. This point is emphasized both during a discussion of the interaction of the various cell types in the testis and during a discussion of spermatogenesis, where techniques which show stage-specific secretions are highlighted. Newest advances in the mechanism of action of steroidal and peptide hormones are also emphasized with special reference to the possible interaction between toxicants and endocrine control of the reproductive system. This update of the reproductive system "sets the stage" for an in-depth examination of the site and mechanism of action of reproductive toxicants. JF - Toxicologic pathology AU - Heindel, J J AU - Treinen, K A AD - Developmental and Reproductive Toxicology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989 PY - 1989 DA - 1989 SP - 411 EP - 445 VL - 17 IS - 2 SN - 0192-6233, 0192-6233 KW - Index Medicus KW - Animals KW - Infertility, Male -- physiopathology KW - Humans KW - Infertility, Male -- chemically induced KW - Male KW - Genitalia, Male -- physiology KW - Genitalia, Male -- drug effects KW - Endocrine Glands -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79215133?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Physiology+of+the+male+reproductive+system%3A+endocrine%2C+paracrine+and+autocrine+regulation.&rft.au=Heindel%2C+J+J%3BTreinen%2C+K+A&rft.aulast=Heindel&rft.aufirst=J&rft.date=1989-01-01&rft.volume=17&rft.issue=2&rft.spage=411&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 - 1989-10-17 N1 - Date created - 1989-10-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA damage, cytotoxicity and free radical formation by mitomycin C in human cells. AN - 79214286; 2550152 AB - Mitomycin C (MMC), a quinone-containing antitumor drug, has been shown to alkylate DNA and to form DNA cross-links. The ability of MMC to alkylate O6-guanine and to form interstrand cross-links (ISC) has been studied using Mer+ and Mer- human embryonic cells. Mer+ (IMR-90) cells have been reported to contain an O6-alkylguanine transferase enzyme and are, in general, more resistant to alkylating agents than the Mer- (VA-13) cell line, which is deficient in the repair of O6-lesions in DNA. Studies reported here show that MMC is more cytotoxic to VA-13 cells compared to IMR-90 cells. The alkaline elution technique was used to quantify MMC-induced ISC, and double strand breaks (DSB) in these cells. The drug-dependent formation of DSB was significantly lower in IMR-90 cells than in VA-13 cells. In contrast, no significant difference in cross-linking could be detected at the end of 2-h drug treatment. Although a small increase in cross-link frequency was observed in the VA-13 cell line relative to the IMR-90 cell line 6 h post drug treatment, it is not clear whether monoalkylated adducts at the O6-position are formed, and contribute to cross-link formation for differential cytotoxicity in VA-13 cells. Electron spin resonance and spin-trapping technique were used to detect the formation of hydroxyl radical from MMC-treated cells. Our studies show that MMC significantly stimulated the formation of hydroxyl radical in VA-13 cells, but not in the IMR-90 cells. The formation of the hydroxyl radical was inhibited by superoxide dismutase (SOD) and catalase. In addition, the presence of these enzymes partially protected VA-13 cells from MMC toxicity but not IMR-90 cells. Further studies indicated that the decreased free radical formation and resistance to MMC may be due to the increased activities of catalase and glutathione transferase in the IMR-90 cell line. These results suggest that MMC-dependent DNA damage (alkylation and DNA DSB) and the stimulation of oxy-radical formation may play critical roles in the determination of MMC-induced cell killing. JF - Chemico-biological interactions AU - Dusre, L AU - Covey, J M AU - Collins, C AU - Sinha, B K AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 63 EP - 78 VL - 71 IS - 1 SN - 0009-2797, 0009-2797 KW - Free Radicals KW - 0 KW - Mitomycins KW - Mitomycin KW - 50SG953SK6 KW - DNA KW - 9007-49-2 KW - Catalase KW - EC 1.11.1.6 KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Index Medicus KW - Superoxide Dismutase -- pharmacology KW - Kinetics KW - Humans KW - Electron Spin Resonance Spectroscopy KW - Cell Division -- drug effects KW - Catalase -- pharmacology KW - Cell Line KW - DNA -- drug effects KW - Mitomycins -- toxicity KW - Cell Survival -- drug effects KW - DNA Damage KW - Mitomycins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79214286?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=DNA+damage%2C+cytotoxicity+and+free+radical+formation+by+mitomycin+C+in+human+cells.&rft.au=Dusre%2C+L%3BCovey%2C+J+M%3BCollins%2C+C%3BSinha%2C+B+K&rft.aulast=Dusre&rft.aufirst=L&rft.date=1989-01-01&rft.volume=71&rft.issue=1&rft.spage=63&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 - 1989-10-23 N1 - Date created - 1989-10-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pulmonary toxicity of 4-ipomeanol. AN - 79209346; 2675137 JF - Pharmacology & therapeutics AU - Gram, T E AD - National Cancer Institute, Division of Cancer Treatment, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 291 EP - 297 VL - 43 IS - 2 SN - 0163-7258, 0163-7258 KW - Terpenes KW - 0 KW - 4-ipomeanol KW - 32954-58-8 KW - Index Medicus KW - Animals KW - Humans KW - Lung -- pathology KW - Terpenes -- toxicity KW - Lung Diseases -- chemically induced KW - Lung Diseases -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79209346?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pulmonary+toxicity+of+4-ipomeanol.&rft.au=Gram%2C+T+E&rft.aulast=Gram&rft.aufirst=T&rft.date=1989-01-01&rft.volume=43&rft.issue=2&rft.spage=291&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 - 1989-10-25 N1 - Date created - 1989-10-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Safety of fenofibrate--US and worldwide experience. AN - 79207457; 2673510 AB - Fenofibrate is a fibric acid derivative with enhanced potency and specificity of action on lipids. Preclinical toxicology reveals minimal toxic effects; dose-related changes occurred seldom, with only hepatic effects in rodents (mainly enzyme changes), some renal effects in dogs, and no reactions in monkeys. Teratogenicity tests were negative, and mutagenicity was not associated with fenofibrate. Carcinogenicity was evident in rodents with liver carcinoma at doses of 12 or 40 times the human dose, but cancer has not been associated with fenofibrate in over 10 years of clinical research and use. European experience with fenofibrate involved 7,145 patients in short- and long-term clinical trials, plus 10 years of marketing experience with a patient exposure of 6 million patient-years. Adverse effects were relatively low in frequency (6%) in the European clinical trials and manifested as gastrointestinal effects, muscle pain, skin problems, and sweating or dizziness. Short- and long-term fenofibrate studies revealed basically the same scope and frequency of adverse effects. Experience in US clinical trials mirrored the European experience; three types of adverse effects occurred more commonly in fenofibrate patients versus placebo: skin reactions, neurologic effects, and musculoskeletal reactions. Laboratory tests were mildly abnormal for liver function, leukocytes, and hemoglobin; these reactions were significant enough to be considered adverse drug experiences only occasionally. Hepatobiliary tests for lithogenicity showed an increase in cholesterol saturation, but gallstones seldom have been associated with fenofibrate. Postmarketing, open experiences in Europe over 10 years have been consistent with the study results. The rate of reactions has been low (about 115/year or a 0.3% incidence rate). The reactions noted in these spontaneous reports were hepatic, renal, gallstones, cutaneous, hematologic, sexual asthenia, and weight loss. In general, fenofibrate can be considered a safe and well-tolerated lipid-lowering drug that has been scrutinized extensively for safety in clinical research and during an already long marketing period in Europe. JF - Cardiology AU - Roberts, W C AD - Pathology Branch, National Heart, Lung, and Blood Institute, Bethesda, Md. Y1 - 1989 PY - 1989 DA - 1989 SP - 169 EP - 179 VL - 76 IS - 3 SN - 0008-6312, 0008-6312 KW - Propionates KW - 0 KW - Fenofibrate KW - U202363UOS KW - Index Medicus KW - United States KW - Humans KW - Hyperlipidemias -- drug therapy KW - Clinical Trials as Topic KW - Europe KW - Propionates -- toxicity KW - Fenofibrate -- therapeutic use KW - Fenofibrate -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79207457?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=unknown&rft.jtitle=Film+Index+International&rft.atitle=SOUPE+AU+LAIT&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1959-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-10-18 N1 - Date created - 1989-10-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cancer mortality among a cohort of chromium pigment workers. AN - 79202434; 2773944 AB - A study of mortality among 1,879 male workers employed in a New Jersey chromium pigment factory was carried out, with follow-up from 1940 to 1982. Vital status of 1,737 (92%) of the eligible cohort members was determined. For all malignant neoplasms, 101 deaths were observed while 108.8 were expected, SMR = 93 (standardized mortality ratio; n.s.). For the entire study group, no significant excess was observed for respiratory cancer or cancer at other sites. However, the total number of years of employment in the factory and the total number of years of exposure to chromate dusts were both statistically significantly (p less than .05, for trend) associated with an increased risk for lung cancer. The excess risk for lung cancer associated with duration of exposure to chromate dusts was, however, only clearly apparent for subjects followed for 30 years or more after initial employment. For this group, the SMRs were 81, 139, 201, and 321 for the subjects with 0 years, less than 1 year, 1-9 years, and 10+ years of exposure to chromate dusts (p less than .01, for trend), respectively. The risk for digestive cancer was only weakly associated with exposure to chromate dusts. JF - American journal of industrial medicine AU - Hayes, R B AU - Sheffet, A AU - Spirtas, R AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 127 EP - 133 VL - 16 IS - 2 SN - 0271-3586, 0271-3586 KW - Pigments, Biological KW - 0 KW - Chromium KW - 0R0008Q3JB KW - Index Medicus KW - Risk Factors KW - Humans KW - Cohort Studies KW - Follow-Up Studies KW - New Jersey KW - Time Factors KW - Male KW - Digestive System Neoplasms -- mortality KW - Lung Neoplasms -- mortality KW - Lung Neoplasms -- chemically induced KW - Occupational Diseases -- chemically induced KW - Occupational Diseases -- mortality KW - Digestive System Neoplasms -- chemically induced KW - Chromium -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79202434?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cancer+mortality+among+a+cohort+of+chromium+pigment+workers.&rft.au=Hayes%2C+R+B%3BSheffet%2C+A%3BSpirtas%2C+R&rft.aulast=Hayes&rft.aufirst=R&rft.date=1989-01-01&rft.volume=16&rft.issue=2&rft.spage=127&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 - 1989-09-27 N1 - Date created - 1989-09-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The role of arachidonic acid metabolites in mediating ethanol self-administration and intoxication. AN - 79198575; 2774408 AB - Prostaglandin synthesis inhibitors antagonize the effects of alcohols, indicating that some aspect of cyclooxygenase activity and arachidonic acid metabolism is involved in the mechanism of action of alcohols. In addition, ethanol increases in vivo brain PGE and PGF levels in a manner correlated across dose and time with the absorption phase of ethanol. These results have provided systematic evidence in support of the hypothesis that ethanol produces its intoxicating effects to a significant degree through a prostaglandin-mediated mechanism. This report has presented an overview of this work, as well as additional results from a series of recent studies that examined the effects of pretreatment with INDO, a potent PGSI, on ethanol self-administration. The results of these self-administration studies indicate that INDO can decrease responding for ethanol in a dose-related manner. The pattern of changes suggests that INDO decreases ethanol self-administration by decreasing the reinforcing effects of ethanol and not by producing a conditioned aversion to ethanol. In a subsequent study, INDO did not affect saccharin self-administration. These results suggest that there exists a common prostaglandin-related mechanism that is important in the mediation of both acute sensitivity to ethanol and the reinforcing properties of this drug. These findings may provide for the development of novel pharmaceutical treatments for acute alcohol overdose as well as for chronic alcohol abuse. JF - Annals of the New York Academy of Sciences AU - George, F R AD - National Institute on Drug Abuse, United States Department of Health and Human Services, Baltimore, Maryland 22124. Y1 - 1989 PY - 1989 DA - 1989 SP - 382 EP - 391 VL - 559 SN - 0077-8923, 0077-8923 KW - Arachidonic Acids KW - 0 KW - Ethanol KW - 3K9958V90M KW - Saccharin KW - FST467XS7D KW - Indomethacin KW - XXE1CET956 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Male KW - Ethanol -- blood KW - Self Administration KW - Alcoholic Intoxication KW - Ethanol -- administration & dosage KW - Arachidonic Acids -- physiology KW - Indomethacin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79198575?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+role+of+arachidonic+acid+metabolites+in+mediating+ethanol+self-administration+and+intoxication.&rft.au=George%2C+F+R&rft.aulast=George&rft.aufirst=F&rft.date=1989-01-01&rft.volume=559&rft.issue=&rft.spage=382&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 - 1989-10-03 N1 - Date created - 1989-10-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Potent convulsant actions of the adenosine receptor antagonist, xanthine amine congener (XAC). AN - 79198289; 2779359 AB - The convulsant properties of xanthine amine congener (XAC, 8-(4-(2-aminoethyl)-aminocarboxylmethyloxy)phenyl-1,3-dipropylxant hine) are compared to those of caffeine. Male Swiss albino mice were infused with convulsants through a lateral tail vein. Convulsion thresholds (i.e. the amount of convulsants required to elicit convulsions) of 39.8 +/- 2.0 mg/kg (n = 10) and 109.8 +/- 2.3 mg/kg (n = 10) were calculated for XAC and caffeine respectively. Pretreatment of animals with the adenosine receptor agonists 2-chloroadenosine, N6-cyclohexyladenosine or 5'-N-ethylcarboxamido-adenosine (1 mg/kg, i.p., 20 minutes prior to infusion) significantly decreased the seizure threshold of both XAC and caffeine. The adenosine uptake blockers, 6-nitrobenzylthioinosine or dipyridamole (0.25 mg/kg, i.p., 20 minutes prior to infusion) did not significantly affect the seizure threshold to either XAC or caffeine. The benzodiazepine agonist diazepam (5 mg/kg, i.p., 20 minutes prior to infusion) significantly increased the seizure threshold to both XAC (p less than 0.05) and caffeine (p less than 0.01), whereas the benzodiazepine antagonist Ro 15-1788 (10 mg/kg, i.p., 20 minutes prior to infusion) significantly increased the seizure threshold to caffeine (p less than 0.01), but not XAC. The results suggest that actions at benzodiazepine receptors may be a tenable hypothesis to explain the convulsant actions of caffeine, but not those of XAC. JF - Life sciences AU - Morgan, P F AU - Deckert, J AU - Jacobson, K A AU - Marangos, P J AU - Daly, J W AD - Biological Psychiatry Branch, N.I.M.H. Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 719 EP - 728 VL - 45 IS - 8 SN - 0024-3205, 0024-3205 KW - Convulsants KW - 0 KW - Purinergic Antagonists KW - Xanthines KW - Caffeine KW - 3G6A5W338E KW - Dipyridamole KW - 64ALC7F90C KW - 8-(4-((2-aminoethyl)aminocarbonylmethyloxy)phenyl)-1,3-dipropylxanthine KW - 96865-92-8 KW - Theophylline KW - C137DTR5RG KW - Diazepam KW - Q3JTX2Q7TU KW - Index Medicus KW - Animals KW - Random Allocation KW - Diazepam -- pharmacology KW - Theophylline -- toxicity KW - Dipyridamole -- toxicity KW - Mice KW - Male KW - Seizures -- chemically induced KW - Xanthines -- toxicity KW - Caffeine -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79198289?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Potent+convulsant+actions+of+the+adenosine+receptor+antagonist%2C+xanthine+amine+congener+%28XAC%29.&rft.au=Morgan%2C+P+F%3BDeckert%2C+J%3BJacobson%2C+K+A%3BMarangos%2C+P+J%3BDaly%2C+J+W&rft.aulast=Morgan&rft.aufirst=P&rft.date=1989-01-01&rft.volume=45&rft.issue=8&rft.spage=719&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 - 1989-10-17 N1 - Date created - 1989-10-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Arch Int Pharmacodyn Ther. 1980 Aug;246(2):205-14 [7436627] Proc Natl Acad Sci U S A. 1980 May;77(5):2551-4 [6248853] Psychopharmacology (Berl). 1981;72(3):269-73 [6784145] Neuroscience. 1981;6(4):523-55 [6113559] Proc Natl Acad Sci U S A. 1981 May;78(5):3260-4 [6265942] Br J Pharmacol. 1982 Nov;77(3):525-9 [6814559] Neurosci Lett. 1983 Oct 31;41(1-2):183-8 [6417576] Eur J Pharmacol. 1984 Jan 27;97(3-4):289-93 [6423394] Int Rev Neurobiol. 1985;27:63-139 [2867982] FEBS Lett. 1986 Apr 21;199(2):269-74 [3009222] Proc Natl Acad Sci U S A. 1986 Jun;83(11):4089-93 [3012550] Neurochem Res. 1986 May;11(5):637-46 [3014363] Prog Neurobiol. 1986;27(4):319-49 [3538187] J Pharmacol Exp Ther. 1987 Sep;242(3):882-7 [3656117] Br J Pharmacol. 1987 Sep;92(1):69-75 [3664093] Arch Int Pharmacodyn Ther. 1987 Dec;290(2):293-301 [3328570] Neurosci Lett. 1989 Mar 13;98(1):96-100 [2540461] Life Sci. 1981 Mar 2;28(9):1023-31 [6111732] Can J Physiol Pharmacol. 1979 Nov;57(11):1289-312 [93018] Life Sci. 1979 Feb 26;24(9):851-7 [449624] Trends Pharmacol Sci. 1988 Apr;9(4):130-4 [2907698] J Neurochem. 1979 Nov;33(5):999-1005 [228008] Life Sci. 1979 Sep 24;25(13):1093-102 [390284] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Regulation of phospholipase A2 and phospholipase C in rod outer segments of bovine retina involves a common GTP-binding protein but different mechanisms of action. AN - 79196564; 2505653 JF - Annals of the New York Academy of Sciences AU - Jelsema, C L AD - Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 158 EP - 177 VL - 559 SN - 0077-8923, 0077-8923 KW - Thionucleotides KW - 0 KW - Virulence Factors, Bordetella KW - Guanosine 5'-O-(3-Thiotriphosphate) KW - 37589-80-3 KW - Guanosine Triphosphate KW - 86-01-1 KW - Cholera Toxin KW - 9012-63-9 KW - Phospholipases KW - EC 3.1.- 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 - GTP-Binding Proteins KW - EC 3.6.1.- KW - Transducin KW - EC 3.6.5.1 KW - Index Medicus KW - Animals KW - Enzyme Activation KW - Cholera Toxin -- pharmacology KW - Thionucleotides -- metabolism KW - Homeostasis KW - Guanosine Triphosphate -- metabolism KW - Guanosine Triphosphate -- analogs & derivatives KW - Virulence Factors, Bordetella -- pharmacology KW - Cattle KW - Kinetics KW - Light KW - Transducin -- metabolism KW - Phospholipases -- metabolism KW - Rod Cell Outer Segment -- enzymology KW - GTP-Binding Proteins -- physiology KW - Photoreceptor Cells -- enzymology KW - Type C Phospholipases -- metabolism KW - Phospholipases A -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79196564?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Regulation+of+phospholipase+A2+and+phospholipase+C+in+rod+outer+segments+of+bovine+retina+involves+a+common+GTP-binding+protein+but+different+mechanisms+of+action.&rft.au=Jelsema%2C+C+L&rft.aulast=Jelsema&rft.aufirst=C&rft.date=1989-01-01&rft.volume=559&rft.issue=&rft.spage=158&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 - 1989-10-03 N1 - Date created - 1989-10-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interleukin-1 alpha gene intron containing variable repeat region coding for the SP1 transcription factor recognition sequence is polymorphic. AN - 79163188; 2569878 AB - Interleukin-1 alpha (IL-1 alpha) is a cytokine produced by a number of cell types including macrophages, fibroblasts, keratinocytes, and mesangial cells. We were interested in identifying a DNA restriction fragment length polymorphism (RFLP) for the IL-1 alpha gene for use in studies of genetic alteration in various human cancers. Human genomic DNA from 32 unrelated individuals was digested with various restriction enzymes, alone and in combination, and subjected to Southern blot analysis. Hybridization to 32P-labeled IL-1 alpha cDNA revealed an insertion-deletion-type polymorphic pattern. After digestion with RsaI, insertion-deletion-type polymorphic bands with sizes of 3.4 kb, 3.1 kb, and 2.8 kb and one invariant band of 0.8 kb were observed. These three alleles, designated A1, A2, and A3, had relative frequencies of 0.18, 0.06, and 0.78 with heterozygosity observed in 38% of the unrelated individuals studied. Evaluation of nine related individuals for this RsaI polymorphism was consistent with a Mendelian inheritance. Comparison of restriction patterns following Southern analysis of DNA digested with several different enzymes showed that the polymorphic region resides within the sixth intron. Furthermore, this RFLP results from a variable length region containing multiple copies of a recognition sequence for SP1, an imperfect copy of viral enhancer elements, and an inverse and complementary sequence of the glucocorticoid receptor binding site. The identified polymorphism may be of value in analyses of chromosome 2 and may help to elucidate mechanisms by which IL-1 alpha transcription is regulated. JF - Molecular carcinogenesis AU - Haugen, A AU - Mann, D AU - Murray, C AU - Weston, A AU - Willey, J C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, Maryland. Y1 - 1989 PY - 1989 DA - 1989 SP - 68 EP - 71 VL - 2 IS - 2 SN - 0899-1987, 0899-1987 KW - DNA Probes KW - 0 KW - DNA-Binding Proteins KW - Interleukin-1 KW - Sp1 Transcription Factor KW - Transcription Factors KW - Index Medicus KW - Pedigree KW - Gene Frequency KW - Polymorphism, Restriction Fragment Length KW - Humans KW - Binding Sites KW - Transcription Factors -- metabolism KW - Polymorphism, Genetic KW - Introns KW - Interleukin-1 -- genetics KW - Repetitive Sequences, Nucleic Acid KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79163188?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Interleukin-1+alpha+gene+intron+containing+variable+repeat+region+coding+for+the+SP1+transcription+factor+recognition+sequence+is+polymorphic.&rft.au=Haugen%2C+A%3BMann%2C+D%3BMurray%2C+C%3BWeston%2C+A%3BWilley%2C+J+C&rft.aulast=Haugen&rft.aufirst=A&rft.date=1989-01-01&rft.volume=2&rft.issue=2&rft.spage=68&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 - 1989-10-05 N1 - Date created - 1989-10-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of the characteristics and functioning of cocaine treatment and cocaine research subjects. AN - 79156966; 2763982 AB - Comparisons were made of the functioning and characteristics of cocaine-abusing volunteers to a research ward (N = 25) and to an outpatient treatment program (N = 33) at the same research facility. It was hypothesized that individuals volunteering for clinical studies and for treatment-related studies would represent different segments of the cocaine-abusing population, and that those differences could be significant to an understanding of study findings. Demographic/background variables were assessed through use of the Addiction Severity Index, risk-taking behaviors relative to HIV infection and AIDS through use of a structured interview schedule, intellectual functioning through use of the Shipley Institute for Living Scale, and psychiatric symptoms through use of the Hopkins Symptom Check List (SCL-90R). Significant differences were obtained for criminal activity, needle sharing, and selected psychiatric symptoms. Marital status was particularly important to an understanding of differences between research and treatment groups in that unmarried treatment subjects showed significantly greater psychopathology than research subjects on 3 of 11 symptom scores. Unmarried treatment subjects showed significantly greater deviance than married treatment subjects on 7 of 11 symptom scores. The findings suggest a relationship between marital status and the psychological functioning of treatment clients and indicates that different segments of the cocaine-abusing population volunteer for different types of research. JF - The American journal of drug and alcohol abuse AU - Rose, M R AU - Brown, B S AU - Haertzen, C A AD - Addiction Research Center/National Institute on Drug Abuse, Baltimore, Maryland 21224. Y1 - 1989 PY - 1989 DA - 1989 SP - 251 EP - 260 VL - 15 IS - 3 SN - 0095-2990, 0095-2990 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Psychiatric Status Rating Scales KW - Humans KW - Adult KW - Retrospective Studies KW - Research KW - Substance-Related Disorders -- rehabilitation KW - Substance-Related Disorders -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79156966?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparison+of+the+characteristics+and+functioning+of+cocaine+treatment+and+cocaine+research+subjects.&rft.au=Rose%2C+M+R%3BBrown%2C+B+S%3BHaertzen%2C+C+A&rft.aulast=Rose&rft.aufirst=M&rft.date=1989-01-01&rft.volume=15&rft.issue=3&rft.spage=251&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 - 1989-09-19 N1 - Date created - 1989-09-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular characterization and comparison of simian immunodeficiency virus isolates from macaques, mangabeys, and African green monkeys. AN - 79137348; 2547964 AB - Simian immunodeficiency virus (SIV)/Mne has been inoculated into three species of macaques and into baboons. Virus was isolated from all the macaques who subsequently died at 15 to 120 weeks (mean 80 weeks) with various manifestations of immune deficiency. Individual animals varied in their viral antibody profile as a function of time after infection. Independent SIV isolates obtained from African green monkeys and magabeys were compared to SIV/Mne for their ability to replicate in lymphocytes and macrophages and with respect to the immunological relatedness of their viral proteins. Antibodies present in human immunodeficiency virus-2 (HIV-2)-infected individuals were readily detected by the virus produced by a single-cell clone of SIV/Mne. JF - Journal of medical primatology AU - Benveniste, R E AU - Raben, D AU - Hill, R W AU - Knott, W B AU - Drummond, J E AU - Arthur, L O AU - Jahrling, P B AU - Morton, W R AU - Henderson, L E AU - Heidecker, G AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, MD. Y1 - 1989 PY - 1989 DA - 1989 SP - 287 EP - 303 VL - 18 IS - 3-4 SN - 0047-2565, 0047-2565 KW - Antibodies, Viral KW - 0 KW - HIV Antibodies KW - Retroviridae Proteins KW - Index Medicus KW - AIDS/HIV KW - Macaca -- microbiology KW - Animals KW - Immunoblotting KW - HIV-1 -- immunology KW - Retroviridae Proteins -- analysis KW - Humans KW - Lymphocytes -- microbiology KW - Cross Reactions KW - Retroviridae Proteins -- isolation & purification KW - HIV-2 -- immunology KW - Cercopithecus aethiops -- microbiology KW - HIV Antibodies -- analysis KW - Papio -- microbiology KW - Cell Line KW - Female KW - Simian Immunodeficiency Virus -- genetics KW - Simian Immunodeficiency Virus -- immunology KW - Retroviridae Infections -- veterinary KW - Retroviridae Infections -- immunology KW - Simian Immunodeficiency Virus -- isolation & purification KW - Monkey Diseases -- immunology KW - Cercopithecidae -- microbiology KW - Antibodies, Viral -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79137348?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+medical+primatology&rft.atitle=Molecular+characterization+and+comparison+of+simian+immunodeficiency+virus+isolates+from+macaques%2C+mangabeys%2C+and+African+green+monkeys.&rft.au=Benveniste%2C+R+E%3BRaben%2C+D%3BHill%2C+R+W%3BKnott%2C+W+B%3BDrummond%2C+J+E%3BArthur%2C+L+O%3BJahrling%2C+P+B%3BMorton%2C+W+R%3BHenderson%2C+L+E%3BHeidecker%2C+G&rft.aulast=Benveniste&rft.aufirst=R&rft.date=1989-01-01&rft.volume=18&rft.issue=3-4&rft.spage=287&rft.isbn=&rft.btitle=&rft.title=Journal+of+medical+primatology&rft.issn=00472565&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-08 N1 - Date created - 1989-09-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Complications of corticosteroid and immunosuppressive drugs. AN - 79127519; 2526794 JF - International ophthalmology clinics AU - Rubin, B AU - Palestine, A G AD - National Eye Institute, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 159 EP - 171 VL - 29 IS - 3 SN - 0020-8167, 0020-8167 KW - Adrenal Cortex Hormones KW - 0 KW - Alkylating Agents KW - Antimetabolites KW - Cyclosporins KW - Immunosuppressive Agents KW - Index Medicus KW - Intraocular Pressure -- drug effects KW - Administration, Oral KW - Cyclosporins -- adverse effects KW - Hypothalamo-Hypophyseal System -- drug effects KW - Drug Interactions KW - Drug Eruptions -- etiology KW - Injections, Intravenous KW - Wound Healing -- drug effects KW - Humans KW - Cataract -- chemically induced KW - Cyclosporins -- administration & dosage KW - Hypertension -- chemically induced KW - Antimetabolites -- adverse effects KW - Injections -- adverse effects KW - Corneal Injuries KW - Alkylating Agents -- adverse effects KW - Pituitary-Adrenal System -- drug effects KW - Osteoporosis -- chemically induced KW - Administration, Topical KW - Kidney Diseases -- chemically induced KW - Adrenal Cortex Hormones -- administration & dosage KW - Immunosuppressive Agents -- adverse effects KW - Adrenal Cortex Hormones -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79127519?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+ophthalmology+clinics&rft.atitle=Complications+of+corticosteroid+and+immunosuppressive+drugs.&rft.au=Rubin%2C+B%3BPalestine%2C+A+G&rft.aulast=Rubin&rft.aufirst=B&rft.date=1989-01-01&rft.volume=29&rft.issue=3&rft.spage=159&rft.isbn=&rft.btitle=&rft.title=International+ophthalmology+clinics&rft.issn=00208167&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-01 N1 - Date created - 1989-09-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanisms of alcohol tolerance. AN - 79124841; 2757699 AB - Functional tolerance to ethanol can be prolonged by administration of the neuropeptide arginine vasopressin (AVP), which acts at specific CNS receptors. AVP receptors in brain (lateral septum) have been shown to be localized, in part, presynaptically, and the mechanism of action of AVP may thus involve modulation of neurotransmitter release. AVP has also been found to increase the levels of mRNA for the cellular proto-oncogene, c-fos, in the septum and hippocampus. This response to AVP, which may be direct or indirect, may underlie the long-term neuroadaptive effects of the peptide. Studies with vasopressin antagonists have indicated a role for endogenous AVP in modulation of ethanol tolerance, and measurement of hypothalamic vasopressin mRNA by Northern blot analysis and in situ hybridization indicates that chronic ethanol ingestion may alter AVP synthesis. Tolerance to the aversive effects of ethanol has been postulated to influence alcohol drinking behavior in some individuals. Elucidation of the mechanism by which AVP affects ethanol tolerance may eventually lead to pharmacological means to modulate tolerance and, consequently, alcohol intake patterns. JF - Alcohol and alcoholism (Oxford, Oxfordshire) AU - Hoffman, P L AU - Tabakoff, B AD - Division of Intramural Clinical and Biological Research National Institute on Alcohol Abuse and Alcoholism Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 251 EP - 252 VL - 24 IS - 3 SN - 0735-0414, 0735-0414 KW - Receptors, Angiotensin KW - 0 KW - Receptors, Vasopressin KW - Arginine Vasopressin KW - 113-79-1 KW - Index Medicus KW - Drug Tolerance KW - Animals KW - Alcoholic Intoxication -- physiopathology KW - Humans KW - Hypothalamus -- physiopathology KW - Mice KW - Brain -- physiopathology KW - Receptors, Angiotensin -- physiology KW - Arginine Vasopressin -- physiology KW - Alcoholism -- physiopathology KW - Alcohol Drinking -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79124841?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+and+alcoholism+%28Oxford%2C+Oxfordshire%29&rft.atitle=Mechanisms+of+alcohol+tolerance.&rft.au=Hoffman%2C+P+L%3BTabakoff%2C+B&rft.aulast=Hoffman&rft.aufirst=P&rft.date=1989-01-01&rft.volume=24&rft.issue=3&rft.spage=251&rft.isbn=&rft.btitle=&rft.title=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29&rft.issn=07350414&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-09-08 N1 - Date created - 1989-09-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Association of sperm measures with reproductive outcome: National Toxicology Program studies in mice. AN - 79113772; 2755952 AB - In reproductive assessment by continuous breeding (RACB) studies, a crossover mating trial was conducted if an adverse effect on fertility was detectable over an 18-week cohabitation period during which Swiss (CD-1) mice were continuously treated. Results of 25 RACB crossover mating studies conducted to determine the affected sex were compared with results of sperm morphology and vaginal cytology examinations (SMVCE) performed at the conclusion of each mating trial. SMVCE endpoints included epididymal sperm concentration, motility, and morphology, vaginal cytology, and male reproductive organ weights. In most studies, multiple SMVCE endpoints were adversely affected. With this group of chemicals, epididymis weight was sensitive and specific to male reproductive toxicants and nontoxicants, respectively. Sperm motility and testis weight were also highly sensitive to male reproductive toxicants. The above endpoints demonstrated the greatest statistical significance relative to other SMVCE parameters, and were highly associated with fertility measurements from breeding experiments. These characteristics suggest that some SMVCE endpoints are more useful for screening chemicals for potential male reproductive toxicity than others. Caution must be exercised, however, because the compounds used in these studies are not representative of all classes of chemicals, and chemicals not tested here may produce adverse reproductive effects by different mechanisms of action. The dose-response effects of two glycol ethers evaluated in RACB, ethylene glycol monomethyl ether and ethylene glycol monoethyl ether, on reproductive outcome and SMVCE endpoints were examined in detail. Both caused adverse effects on testis weight and sperm head morphology, and these changes were associated with adverse effects on reproductive outcome. Until we have more experience with SMVCE and other screens, multiple endpoints should continue to be used for screening for reproductive toxicants. JF - Progress in clinical and biological research AU - Morrissey, R E AD - National Institute of Environmental Health Sciences, National Toxicology Program, Research Triangle Park, NC 27709. Y1 - 1989 PY - 1989 DA - 1989 SP - 229 EP - 47; discussion 248-50 VL - 302 SN - 0361-7742, 0361-7742 KW - Index Medicus KW - Animals KW - Mice KW - Male KW - Female KW - Spermatozoa -- drug effects KW - Fertility -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79113772?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Association+of+sperm+measures+with+reproductive+outcome%3A+National+Toxicology+Program+studies+in+mice.&rft.au=Morrissey%2C+R+E&rft.aulast=Morrissey&rft.aufirst=R&rft.date=1989-01-01&rft.volume=302&rft.issue=&rft.spage=229&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 - 1989-08-29 N1 - Date created - 1989-08-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human model systems for studies of skin cancer. AN - 79106060; 2748685 JF - Progress in clinical and biological research AU - Kraemer, K H AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 25 EP - 33 VL - 298 SN - 0361-7742, 0361-7742 KW - Index Medicus KW - Genes, Dominant KW - Humans KW - Dysplastic Nevus Syndrome -- genetics KW - Xeroderma Pigmentosum -- genetics KW - Basal Cell Nevus Syndrome -- genetics KW - Genes, Recessive KW - Skin Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79106060?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+model+systems+for+studies+of+skin+cancer.&rft.au=Kraemer%2C+K+H&rft.aulast=Kraemer&rft.aufirst=K&rft.date=1989-01-01&rft.volume=298&rft.issue=&rft.spage=25&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 - 1989-08-25 N1 - Date created - 1989-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The protein kinase C pathway in tumor promotion. AN - 79100222; 2748684 JF - Progress in clinical and biological research AU - Blumberg, P M AU - Pettit, G R AU - Warren, B S AU - Szallasi, A AU - Schuman, L D AU - Sharkey, N A AU - Nakakuma, H AU - Dell'Aquila, M L AU - de Vries, D J AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 201 EP - 212 VL - 298 SN - 0361-7742, 0361-7742 KW - Carcinogens KW - 0 KW - Phorbol Esters KW - Protein Kinase C KW - EC 2.7.11.13 KW - Index Medicus KW - Immunoblotting KW - Animals KW - Cells, Cultured KW - Kinetics KW - Epidermis -- cytology KW - Cell Communication KW - Mice KW - Phorbol Esters -- toxicity KW - Protein Kinase C -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79100222?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=unknown&rft.jtitle=Film+Index+International&rft.atitle=MAIGRET+ET+L%27AFFAIRE+SAINT-FIACRE&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1959-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-25 N1 - Date created - 1989-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pancreatic hepatocytes associated with chronic 2,6-dichloro-p-phenylenediamine administration in Fischer 344 rats. AN - 79095335; 2665028 AB - Pancreatic tissue (original and recut sections) from Fischer 344 rats fed 2,6-dichloro-p-phenylenediamine in a chronic (2-year) carcinogenesis bioassay was evaluated for presence of pancreatic hepatocytes (PH) by light microscopy. PH were found in dose groups as follows: males--0 ppm (controls)--0/50 (0%), 1,000 ppm--4/50 (8%), 2,000 ppm--9/50 (18%); females--0 ppm (controls)--1/50 (2%), 2,000 ppm-15/50 (30%), 6,000 ppm--15/49 (31%). This represented a significant dose-related increased incidence of PH in 2,000-ppm males, and 2,000- and 6,000-ppm females. A statistically significant increase (p less than 0.01) in pancreatic acinar atrophy and fibrosis was also seen in treated female rats, but the relationship of these lesions to the PH is unclear. JF - Toxicologic pathology AU - McDonald, M M AU - Boorman, G A AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989 PY - 1989 DA - 1989 SP - 1 EP - 6 VL - 17 IS - 1 Pt 1 SN - 0192-6233, 0192-6233 KW - Phenylenediamines KW - 0 KW - 2,6-dichloro-1,4-phenylenediamine KW - Z4QJ0R1U1Z KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Sex Factors KW - Fibrosis KW - Islets of Langerhans -- drug effects KW - Islets of Langerhans -- pathology KW - Male KW - Female KW - Pancreas -- pathology KW - Liver -- pathology KW - Phenylenediamines -- toxicity KW - Pancreas -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79095335?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=unknown&rft.jtitle=Film+Index+International&rft.atitle=TERRA+INCOGNITA&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1959-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-21 N1 - Date created - 1989-08-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Developing design standards for dermal initiation/promotion screening studies. AN - 79094098; 2501798 JF - Progress in clinical and biological research AU - Eastin, W C AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989 PY - 1989 DA - 1989 SP - 295 EP - 312 VL - 298 SN - 0361-7742, 0361-7742 KW - Methylnitronitrosoguanidine KW - 12H3O2UGSF KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Benzoyl Peroxide KW - W9WZN9A0GM KW - Index Medicus KW - Tetradecanoylphorbol Acetate -- toxicity KW - Mice, Inbred Strains KW - Animals KW - Skin -- drug effects KW - Methylnitronitrosoguanidine -- toxicity KW - 9,10-Dimethyl-1,2-benzanthracene -- toxicity KW - Benzoyl Peroxide -- toxicity KW - Mice KW - Research Design KW - Male KW - Female KW - Carcinogenicity Tests UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79094098?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Developing+design+standards+for+dermal+initiation%2Fpromotion+screening+studies.&rft.au=Eastin%2C+W+C&rft.aulast=Eastin&rft.aufirst=W&rft.date=1989-01-01&rft.volume=298&rft.issue=&rft.spage=295&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 - 1989-08-25 N1 - Date created - 1989-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Low-calcium, high-aluminum diet-induced motor neuron pathology in cynomolgus monkeys. AN - 79094034; 2750490 AB - Long-term epidemiological studies indicate that environmental factors play a causative role in high-incidence amyotrophic lateral sclerosis (ALS) and parkinsonism-dementia (PD) in the western Pacific. An increased risk for disease is acquired in youth and remains for life. The low concentrations of calcium and magnesium and high levels of aluminum in the soil and drinking water, along with the relative isolation of these populations, constitute an unusual environmental feature common to all three high-incidence foci. Studies of mineral deposition in brain tissue of Guamanian ALS and PD patients, as well as of neurologically normal Guamanians with neurofibrillary degeneration, demonstrate accumulations of calcium, aluminum and silicon in neurofibrillary tangle-bearing neurons. In an attempt to duplicate the low calcium and high aluminum and manganese in soil and drinking water in these foci, we maintained juvenile cynomolgus monkeys for 41 to 46 months on a low-calcium diet with or without supplemental aluminum and manganese. Experimental animals exhibited mild calcium and aluminum deposition and degenerative changes, compatible with those of early ALS and PD, in motor neurons of the spinal cord, brain stem, substantia nigra and cerebrum. Neuropathological findings included chromatolysis, aberrant perikaryal accumulation of phosphorylated neurofilament, neurofibrillary tangles, axonal spheroids, and basophilic and hyaline-like inclusions consisting of abnormal cytoskeletal elements by electron microscopy. The magnitude and extent of these lesions far exceeded those found in normal aged monkeys. JF - Acta neuropathologica AU - Garruto, R M AU - Shankar, S K AU - Yanagihara, R AU - Salazar, A M AU - Amyx, H L AU - Gajdusek, D C AD - Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 210 EP - 219 VL - 78 IS - 2 SN - 0001-6322, 0001-6322 KW - Calcium, Dietary KW - 0 KW - Aluminum KW - CPD4NFA903 KW - Index Medicus KW - Intermediate Filaments -- pathology KW - Intermediate Filaments -- metabolism KW - Animals KW - Manganese Poisoning KW - Diet KW - Macaca fascicularis -- metabolism KW - Motor Neurons -- pathology KW - Motor Neurons -- metabolism KW - Amyotrophic Lateral Sclerosis -- pathology KW - Brain Stem -- metabolism KW - Amyotrophic Lateral Sclerosis -- metabolism KW - Spinal Cord -- metabolism KW - Calcium, Dietary -- metabolism KW - Spinal Cord -- pathology KW - Brain Stem -- pathology KW - Aluminum -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79094034?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+neuropathologica&rft.atitle=Low-calcium%2C+high-aluminum+diet-induced+motor+neuron+pathology+in+cynomolgus+monkeys.&rft.au=Garruto%2C+R+M%3BShankar%2C+S+K%3BYanagihara%2C+R%3BSalazar%2C+A+M%3BAmyx%2C+H+L%3BGajdusek%2C+D+C&rft.aulast=Garruto&rft.aufirst=R&rft.date=1989-01-01&rft.volume=78&rft.issue=2&rft.spage=210&rft.isbn=&rft.btitle=&rft.title=Acta+neuropathologica&rft.issn=00016322&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-21 N1 - Date created - 1989-08-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Brief inhalation of chrysotile asbestos induces rapid proliferation of bronchiolar-alveolar epithelial and interstitial cells. AN - 79090057; 2545621 AB - Inhalation of asbestos fibres causes a progressive interstitial pulmonary fibrosis. To understand the basic cellular mechanisms which lead to this disease, we have studied the earliest proliferative events at the bronchiolar-alveolar regions of rats and mice exposed to chrysotile asbestos for 5 h. Animals were injected with tritiated thymidine 4 h prior to sacrifice at varying times ranging from immediately after cessation of exposure to one month post exposure. Light microscopic autoradiography showed that air-exposed control animals never had more than 1% of cells labelled. Rats and mice studied immediately after exposure also had normal numbers of labelled cells. However, between 12 and 48 h post exposure, asbestos-exposed animals exhibited up to 4-fold increases in the percentages of labelled epithelial and interstitial cells. Normal labelling returned by 8 days after exposure and was maintained through the one-month period studied. We conclude that inhalation of chrysotile asbestos induces rapid and highly significant increases in proliferation of epithelial and interstitial cells of the bronchiolar-alveolar regions where asbestos fibres were initially deposited. JF - IARC scientific publications AU - Brody, A R AU - McGavran, P D AU - Overby, L H AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, NC. Y1 - 1989 PY - 1989 DA - 1989 SP - 93 EP - 99 IS - 90 SN - 0300-5038, 0300-5038 KW - Asbestos, Serpentine KW - 0 KW - Asbestos KW - 1332-21-4 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Connective Tissue -- pathology KW - Mice KW - Epithelium -- pathology KW - Administration, Inhalation KW - Male KW - Pulmonary Alveoli -- pathology KW - Asbestos -- pharmacology KW - Bronchi -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79090057?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Brief+inhalation+of+chrysotile+asbestos+induces+rapid+proliferation+of+bronchiolar-alveolar+epithelial+and+interstitial+cells.&rft.au=Brody%2C+A+R%3BMcGavran%2C+P+D%3BOverby%2C+L+H&rft.aulast=Brody&rft.aufirst=A&rft.date=1989-01-01&rft.volume=&rft.issue=90&rft.spage=93&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 - 1989-08-25 N1 - Date created - 1989-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Malignant conversion: the first stage in progression from benign to malignant tumors. AN - 79086370; 2748689 JF - Progress in clinical and biological research AU - Hennings, H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 95 EP - 100 VL - 298 SN - 0361-7742, 0361-7742 KW - Fluocinolone Acetonide KW - 0CD5FD6S2M KW - Index Medicus KW - Animals KW - Mice KW - Cell Transformation, Neoplastic KW - Papilloma -- pathology KW - Carcinoma -- pathology KW - Skin Neoplasms -- chemically induced KW - Skin Neoplasms -- pathology KW - Papilloma -- chemically induced KW - Carcinoma -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79086370?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Malignant+conversion%3A+the+first+stage+in+progression+from+benign+to+malignant+tumors.&rft.au=Hennings%2C+H&rft.aulast=Hennings&rft.aufirst=H&rft.date=1989-01-01&rft.volume=298&rft.issue=&rft.spage=95&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 - 1989-08-25 N1 - Date created - 1989-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Study of lung cancer histologic types, occupation, and smoking in Missouri. AN - 79085793; 2741962 AB - A case-control study of lung cancer was conducted to evaluate the relationship between lung cancer histologic types and occupation, adjusted for smoking. A total of 4,431 white male cases and 11,326 cancer controls, diagnosed between 1980 and 1985, were identified through the Missouri Cancer Registry. For all histologic types combined, excess risk was observed among many a priori suspected high-risk occupations. Lung cancer was elevated among men employed as insulators (odds ratio [OR] = 6.0; 95% confidence interval [CI] = 0.7, 137.8), carpenters (OR = 1.3; 95% CI = 1.0, 1.7), painters, plasterers, and wallpaper hangers (OR = 2.0; 95% CI = 1.2,3.3), structural metal workers (OR = 1.9; 95% CI = 0.6,6.0), mechanics and repairers (OR = 1.3; 95% CI = 1.0,1.7), motor vehicle drivers (OR = 1.5; 95% CI = 1.2,1.8), police and firefighters (OR = 1.6; 95% CI = 1.1,2.3), and food service personnel (OR = 1.8; 95% CI = 1.0,3.5). A deficit of lung cancer was observed among farmers (OR = 0.9; 95% CI = 0.7,1.0). Adenocarcinoma of the lung was elevated among carpenters (OR = 1.6; 95% CI = 1.0,2.5) and cabinet and furniture makers (OR = 2.0; 95% CI = 0.4,8.1), which is interesting because of the previous reports of excess adenocarcinoma of the nasal cavity associated with wood dust exposure. Adenocarcinomas were also elevated among plumbers (OR = 2.0; 95% CI = 1.0,3.8) and printers (OR = 1.8; 95% CI = 0.7,4.2). Electricians were at slightly increased risk for adenocarcinoma (OR = 1.5; 95% CI = 0.7,2.8) and "other" or mixed cell types of lung cancer (OR = 1.5; 95% CI = 0.8,2.9) but at decreased risk for small cell (OR = 0.8; 95% CI = 0.3,2.0) and squamous cell (OR = 0.8; 95% CI = 0.4,1.6) tumors. Among welders, adenocarcinoma (OR = 1.7; 95% CI = 0.7,3.8) and squamous cell (OR = 1.7; 95% CI = 0.9,3.3) cancers were elevated, but small cell and "other" lung cancers were not. Despite the limitations of the Cancer Registry data, some interesting associations were observed that merit further study, particularly the association between lung adenocarcinoma and occupational exposure to wood and wood dust. JF - American journal of industrial medicine AU - Zahm, S H AU - Brownson, R C AU - Chang, J C AU - Davis, J R AD - Occupational Studies Section, National Cancer Institute, Rockville, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 565 EP - 578 VL - 15 IS - 5 SN - 0271-3586, 0271-3586 KW - Dust KW - 0 KW - Index Medicus KW - Registries KW - Risk Factors KW - Missouri KW - Humans KW - Environmental Exposure KW - Wood KW - Dust -- adverse effects KW - Male KW - Female KW - Adenocarcinoma -- pathology KW - Smoking -- adverse effects KW - Occupations KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79085793?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Study+of+lung+cancer+histologic+types%2C+occupation%2C+and+smoking+in+Missouri.&rft.au=Zahm%2C+S+H%3BBrownson%2C+R+C%3BChang%2C+J+C%3BDavis%2C+J+R&rft.aulast=Zahm&rft.aufirst=S&rft.date=1989-01-01&rft.volume=15&rft.issue=5&rft.spage=565&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 - 1989-08-09 N1 - Date created - 1989-08-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Benzene and lymphoma. AN - 79085719; 2741955 JF - American journal of industrial medicine AU - Young, N AD - Cell Biology Section, National Heart, Lung, and Blood Institute, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 495 EP - 498 VL - 15 IS - 5 SN - 0271-3586, 0271-3586 KW - Rubber KW - 9006-04-6 KW - Benzene KW - J64922108F KW - Index Medicus KW - Animals KW - Leukopenia -- chemically induced KW - Risk Factors KW - Humans KW - Leukemia, Lymphoid -- chemically induced KW - Cohort Studies KW - Rubber -- adverse effects KW - Benzene -- toxicity KW - Lymphoma -- chemically induced KW - Occupational Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79085719?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Benzene+and+lymphoma.&rft.au=Young%2C+N&rft.aulast=Young&rft.aufirst=N&rft.date=1989-01-01&rft.volume=15&rft.issue=5&rft.spage=495&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 - 1989-08-09 N1 - Date created - 1989-08-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Consequences of exposure to initiating levels of carcinogens in vitro and in vivo: altered differentiation and growth, mutations, and transformation. AN - 79085093; 2664806 JF - Progress in clinical and biological research AU - Yuspa, S H AU - Kilkenny, A E AU - Roop, D R AU - Strickland, J E AU - Tucker, R AU - Hennings, H AU - Jaken, S AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 127 EP - 135 VL - 298 SN - 0361-7742, 0361-7742 KW - Carcinogens KW - 0 KW - Index Medicus KW - Animals KW - Cell Differentiation KW - Mice KW - Cell Transformation, Neoplastic -- chemically induced KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79085093?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Consequences+of+exposure+to+initiating+levels+of+carcinogens+in+vitro+and+in+vivo%3A+altered+differentiation+and+growth%2C+mutations%2C+and+transformation.&rft.au=Yuspa%2C+S+H%3BKilkenny%2C+A+E%3BRoop%2C+D+R%3BStrickland%2C+J+E%3BTucker%2C+R%3BHennings%2C+H%3BJaken%2C+S&rft.aulast=Yuspa&rft.aufirst=S&rft.date=1989-01-01&rft.volume=298&rft.issue=&rft.spage=127&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 - 1989-08-25 N1 - Date created - 1989-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - CSF studies on alcoholism and related behaviours. AN - 79084768; 2473488 AB - 1. A defect in central serotonin metabolism may manifest itself in poor impulse control leading to attempts at suicide, violence towards others, and Type II alcohol abuse. 2. Studies reporting negative associations between low CSF levels of the serotonin metabolite 5-HIAA and personality traits of aggressiveness and hostility are reviewed. 3. We also studied pathological gamblers. They showed significantly increased central noradrenaline metabolism, perhaps related to sensation seeking. JF - Progress in neuro-psychopharmacology & biological psychiatry AU - Roy, A AU - Linnoila, M AD - Division of Intramural and Clinical Biological Research, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland. Y1 - 1989 PY - 1989 DA - 1989 SP - 505 EP - 511 VL - 13 IS - 3-4 SN - 0278-5846, 0278-5846 KW - Hydroxyindoleacetic Acid KW - 54-16-0 KW - Index Medicus KW - Reference Values KW - Gambling KW - Humans KW - Antisocial Personality Disorder -- cerebrospinal fluid KW - Personality KW - Alcoholism -- classification KW - Alcoholism -- cerebrospinal fluid KW - Suicide KW - Hydroxyindoleacetic Acid -- cerebrospinal fluid KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79084768?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+neuro-psychopharmacology+%26+biological+psychiatry&rft.atitle=CSF+studies+on+alcoholism+and+related+behaviours.&rft.au=Roy%2C+A%3BLinnoila%2C+M&rft.aulast=Roy&rft.aufirst=A&rft.date=1989-01-01&rft.volume=13&rft.issue=3-4&rft.spage=505&rft.isbn=&rft.btitle=&rft.title=Progress+in+neuro-psychopharmacology+%26+biological+psychiatry&rft.issn=02785846&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-21 N1 - Date created - 1989-08-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Resiniferatoxin, a phorbol-related diterpene, acts as an ultrapotent analog of capsaicin, the irritant constituent in red pepper. AN - 79081037; 2747924 AB - Resiniferatoxin is an extremely irritant diterpene present in the latex of several members of the genus Euphorbia. Its mechanism of action has been shown to be clearly distinct from that of the structurally related phorbol esters. Since resiniferatoxin possesses a 4-hydroxy-3-methoxyphenyl substituent, a key feature of capsaicin, the major pungent ingredient of plants of the genus Capsicum, we examined the ability of resiniferatoxin to induce typical capsaicin responses. We report here that treatment of rats with resiniferatoxin, like treatment with capsaicin, caused hypothermia, neurogenic inflammation, and pain. These responses were followed by loss of thermoregulation, by desensitization to neurogenic inflammation, and by chemical and thermal analgesia, with cross-tolerance between resiniferatoxin and capsaicin. Resiniferatoxin was 3 4 orders of magnitude more potent than capsaicin for the effects on thermoregulation and neurogenic inflammation. Resiniferatoxin was only comparable in potency to capsaicin, however, in the assay for induction of acute pain, and the desensitization to acute pain appeared to require less resiniferatoxin than did desensitization for the other responses. We conclude that resiniferatoxin acts as an ultrapotent capsaicin analog and hypothesize that it may distinguish between subclasses of capsaicin response. JF - Neuroscience AU - Szallasi, A AU - Blumberg, P M AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 515 EP - 520 VL - 30 IS - 2 SN - 0306-4522, 0306-4522 KW - Diterpenes KW - 0 KW - resiniferatoxin KW - A5O6P1UL4I KW - Capsaicin KW - S07O44R1ZM KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Female KW - Diterpenes -- pharmacology KW - Pain -- chemically induced KW - Inflammation -- chemically induced KW - Hypothermia -- chemically induced KW - Capsaicin -- analogs & derivatives KW - Capsaicin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79081037?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Resiniferatoxin%2C+a+phorbol-related+diterpene%2C+acts+as+an+ultrapotent+analog+of+capsaicin%2C+the+irritant+constituent+in+red+pepper.&rft.au=Szallasi%2C+A%3BBlumberg%2C+P+M&rft.aulast=Szallasi&rft.aufirst=A&rft.date=1989-01-01&rft.volume=30&rft.issue=2&rft.spage=515&rft.isbn=&rft.btitle=&rft.title=Neuroscience&rft.issn=03064522&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-21 N1 - Date created - 1989-08-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Public health policy: maternal substance use and child health. AN - 79079754; 2742282 AB - Maternal substance use and abuse is a public health issue. Much of what researchers have discovered in this field has been achieved through support of funds appropriated by Congress to the Public Health Service agencies and institutes whose mandates include stimulating and supporting this research in the scientific community. In this same vein the research institutes have a responsibility for disseminating new knowledge and encouraging its application in real-life settings. Individual freedom, social justice and public health relationships need to be carefully weighed by the architects of public policy. We elect those architects through our system of citizen participation in government. However, how to effectively incorporate the relevance of what has been learned about harmful effects of substance abuse into policy that will enable society to deal with emerging maternal and child health issues remains unresolved. Health-policy-relevant issues, as they impact the lives and well-being of our children, including the increasing number who are children of drug-abusing parents, are too important for politicians to ignore and too complex for health professionals to resolve alone. Participation by the research community in policy development is critical. It is clear that a policy of preventive intervention will need widespread public support. It will need to be feasible, effective and affordable in relation to other public demands. Society will ultimately need to make choices among those options that can be implemented and sustained in a political climate characterized by conflicting values. JF - Annals of the New York Academy of Sciences AU - Vanderveen, E AD - National Institute on Drug Abuse, Division of Clinical Research, Rockville, Maryland 20857. Y1 - 1989 PY - 1989 DA - 1989 SP - 255 EP - 259 VL - 562 SN - 0077-8923, 0077-8923 KW - Bioethics KW - Index Medicus KW - Genetics and Reproduction KW - United States KW - Humans KW - Child Advocacy KW - Child KW - Human Rights KW - Female KW - Pregnancy KW - Pregnant Women KW - Pregnancy Complications -- prevention & control KW - Health Policy KW - Substance-Related Disorders -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79079754?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Public+health+policy%3A+maternal+substance+use+and+child+health.&rft.au=Vanderveen%2C+E&rft.aulast=Vanderveen&rft.aufirst=E&rft.date=1989-01-01&rft.volume=562&rft.issue=&rft.spage=255&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 - 1989-07-28 N1 - Date created - 1989-07-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Epidemiology of substance abuse including alcohol and cigarette smoking. AN - 79077131; 2742271 JF - Annals of the New York Academy of Sciences AU - Adams, E H AU - Gfroerer, J C AU - Rouse, B A AD - National Institute on Drug Abuse, Division of Epidemiology and Statistical Analysis, Rockville, Maryland 20857. Y1 - 1989 PY - 1989 DA - 1989 SP - 14 EP - 20 VL - 562 SN - 0077-8923, 0077-8923 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - United States KW - Educational Status KW - Humans KW - Continental Population Groups KW - Adult KW - Marriage KW - Employment KW - Parents KW - Adolescent KW - Female KW - Alcohol Drinking -- statistics & numerical data KW - Substance-Related Disorders -- statistics & numerical data KW - Smoking -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79077131?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Epidemiology+of+substance+abuse+including+alcohol+and+cigarette+smoking.&rft.au=Adams%2C+E+H%3BGfroerer%2C+J+C%3BRouse%2C+B+A&rft.aulast=Adams&rft.aufirst=E&rft.date=1989-01-01&rft.volume=562&rft.issue=&rft.spage=14&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 - 1989-07-28 N1 - Date created - 1989-07-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immunohistochemical localization of cytochromes P450 with polyclonal and monoclonal antibodies. AN - 79068299; 2662165 JF - Pathology and immunopathology research AU - Anderson, L M AU - Ward, J M AU - Park, S S AU - Rice, J M AD - Laboratory of Comparative Carcinogenesis, Division of Cancer Etiology, National Cancer Institute, Frederick, Md. Y1 - 1989 PY - 1989 DA - 1989 SP - 61 EP - 94 VL - 8 IS - 2 SN - 0257-2761, 0257-2761 KW - Antibodies, Monoclonal KW - 0 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Rats KW - Animals KW - Humans KW - Rabbits KW - Cytochrome P-450 Enzyme System -- analysis KW - Immunohistochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79068299?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pathology+and+immunopathology+research&rft.atitle=Immunohistochemical+localization+of+cytochromes+P450+with+polyclonal+and+monoclonal+antibodies.&rft.au=Anderson%2C+L+M%3BWard%2C+J+M%3BPark%2C+S+S%3BRice%2C+J+M&rft.aulast=Anderson&rft.aufirst=L&rft.date=1989-01-01&rft.volume=8&rft.issue=2&rft.spage=61&rft.isbn=&rft.btitle=&rft.title=Pathology+and+immunopathology+research&rft.issn=02572761&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-03 N1 - Date created - 1989-08-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Developmental toxicity screen: results of rat studies with diethylhexyl phthalate and ethylene glycol monomethyl ether. AN - 79063738; 2568021 AB - The purpose of these investigations was to develop a protocol for an in vivo developmental toxicity screen (DETS) that would provide sufficient data to determine whether to 1) do a full developmental toxicity evaluation without additional range-finding studies, or, depending on the results, to 2) do no further testing of a chemical. In order to evaluate this screen, we compared results obtained by using the DETS protocol with results of previously conducted developmental toxicity evaluations of diethylhexyl phthalate (DEHP) and ethylene glycol monomethylether (EGME). Five groups (n greater than or equal to 17) of F344 rats were treated on days 6-15 of gestation by dosed feed (DEHP levels = 0, 0.5, 1.0, 1.5, 2.0%) or gavage (EGME doses = 0, 12.5, 25, 50, 100 mg/kg/day). One half of the rats in these studies were killed on day 16 of gestation, and the remaining animals were allowed to deliver litters which were killed on day 4. EGME caused only a small decrease in maternal weight gain during treatment (100 mg/kg group) that was accompanied by a decrease in gravid uterine weight. The percentage of resorptions was increased in the 50 and 100 mg/kg groups. The number of live pups was decreased in the 25, 50, and 100 mg/kg groups, and litter weight and postnatal survival were decreased in the 100 mg/kg group. These results are consistent with those reported in developmental toxicity studies on EGME conducted by the inhalation and dermal routes. With DEHP, there were treatment-related reductions in maternal body weight and weight gain. There was also a nonstatistical increase in percentage of resorptions per litter that was also observed, but at relatively high levels, in a definitive study in which F344 dams were treated on days 0-20 of gestation. The results of studies on these two chemicals compare well with published results and would have led to the selection of proper dose levels for subsequent FDA segment 2 studies. JF - Teratogenesis, carcinogenesis, and mutagenesis AU - Morrissey, R E AU - Harris, M W AU - Schwetz, B A AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina. Y1 - 1989 PY - 1989 DA - 1989 SP - 119 EP - 129 VL - 9 IS - 2 SN - 0270-3211, 0270-3211 KW - Ethylene Glycols KW - 0 KW - Phthalic Acids KW - Teratogens KW - Diethylhexyl Phthalate KW - C42K0PH13C KW - methyl cellosolve KW - EK1L6XWI56 KW - Index Medicus KW - Rats KW - Evaluation Studies as Topic KW - Body Weight KW - Animals KW - Random Allocation KW - Dose-Response Relationship, Drug KW - Gestational Age KW - Female KW - Pregnancy KW - Ethylene Glycols -- toxicity KW - Diethylhexyl Phthalate -- toxicity KW - Toxicology -- methods KW - Phthalic Acids -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79063738?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Developmental+toxicity+screen%3A+results+of+rat+studies+with+diethylhexyl+phthalate+and+ethylene+glycol+monomethyl+ether.&rft.au=Morrissey%2C+R+E%3BHarris%2C+M+W%3BSchwetz%2C+B+A&rft.aulast=Morrissey&rft.aufirst=R&rft.date=1989-01-01&rft.volume=9&rft.issue=2&rft.spage=119&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 - 1989-08-03 N1 - Date created - 1989-08-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Perspectives on the risks for occupational transmission of HIV-1 in the health-care workplace. AN - 79063632; 2662448 JF - Occupational medicine (Philadelphia, Pa.) AU - Henderson, D K AD - Warren G. Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 7 EP - 12 VL - 4 Suppl SN - 0885-114X, 0885-114X KW - Index Medicus KW - AIDS/HIV KW - Body Fluids KW - Risk Factors KW - Humans KW - Acquired Immunodeficiency Syndrome -- epidemiology KW - Occupational Diseases -- transmission KW - Acquired Immunodeficiency Syndrome -- transmission KW - Health Manpower UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79063632?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Occupational+medicine+%28Philadelphia%2C+Pa.%29&rft.atitle=Perspectives+on+the+risks+for+occupational+transmission+of+HIV-1+in+the+health-care+workplace.&rft.au=Henderson%2C+D+K&rft.aulast=Henderson&rft.aufirst=D&rft.date=1989-01-01&rft.volume=4+Suppl&rft.issue=&rft.spage=7&rft.isbn=&rft.btitle=&rft.title=Occupational+medicine+%28Philadelphia%2C+Pa.%29&rft.issn=0885114X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-02 N1 - Date created - 1989-08-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutagenicity of the human carcinogen treosulphan in Salmonella. AN - 79060032; 2544419 AB - The human carcinogen treosulphan was mutagenic in Salmonella typhimurium TA100 and TA1535, as was dl-1,2:3,4-diepoxybutane (DEB), a proposed hydrolysis product of treosulphan. Another proposed hydrolysis product, methane- sulfonic acid, was not mutagenic in these strains. The pattern of the mutagenic responses at pH 6,7, and 8 to treosulphan and DEB suggests that DEB formation may be responsible for the mutagenicity of treosulphan. JF - Environmental and molecular mutagenesis AU - Zeiger, E AU - Pagano, D A AD - Cellular and Genetic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989 PY - 1989 DA - 1989 SP - 343 EP - 346 VL - 13 IS - 4 SN - 0893-6692, 0893-6692 KW - Carcinogens KW - 0 KW - Epoxy Compounds KW - Mesylates KW - Mutagens KW - erythritol anhydride KW - 60OB65YNAB KW - treosulfan KW - CO61ER3EPI KW - Busulfan KW - G1LN9045DK KW - Index Medicus KW - Mutagenicity Tests KW - Epoxy Compounds -- toxicity KW - Mesylates -- toxicity KW - Hydrolysis KW - Busulfan -- analogs & derivatives KW - Busulfan -- toxicity KW - Salmonella typhimurium -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79060032?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mutagenicity+of+the+human+carcinogen+treosulphan+in+Salmonella.&rft.au=Zeiger%2C+E%3BPagano%2C+D+A&rft.aulast=Zeiger&rft.aufirst=E&rft.date=1989-01-01&rft.volume=13&rft.issue=4&rft.spage=343&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 - 1989-08-02 N1 - Date created - 1989-08-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment with polyamines can prevent monosodium glutamate neurotoxicity in the rat retina. AN - 79056657; 2739510 AB - It has been previously shown that treatment of newborn rats with the polyamines putrescine, spermidine and spermine can rescue sympathetic neurons from naturally occurring cell death and from induced death after axotomy or immunosympathectomy. The present study demonstrates that polyamine treatment can also prevent the neurodegenerative effects in the retina and the loss of body weight caused by monosodium glutamate. The findings indicate that polyamine treatment may have a rather general beneficial effect on neuron survival. JF - Life sciences AU - Gilad, G M AU - Gilad, V H AD - Neuropsychiatry Branch, NIMH Neurosciences Center at Saint Elizabeths, Washington, D.C. 20032. Y1 - 1989 PY - 1989 DA - 1989 SP - 1963 EP - 1969 VL - 44 IS - 25 SN - 0024-3205, 0024-3205 KW - Excitatory Amino Acid Antagonists KW - 0 KW - Polyamines KW - Sodium Glutamate KW - W81N5U6R6U KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Cell Survival -- drug effects KW - Neurons -- drug effects KW - Body Weight -- drug effects KW - Male KW - Nerve Degeneration -- drug effects KW - Sodium Glutamate -- antagonists & inhibitors KW - Polyamines -- pharmacology KW - Retina -- drug effects KW - Sodium Glutamate -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79056657?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Treatment+with+polyamines+can+prevent+monosodium+glutamate+neurotoxicity+in+the+rat+retina.&rft.au=Gilad%2C+G+M%3BGilad%2C+V+H&rft.aulast=Gilad&rft.aufirst=G&rft.date=1989-01-01&rft.volume=44&rft.issue=25&rft.spage=1963&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 - 1989-08-02 N1 - Date created - 1989-08-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Results of tests for micronuclei and chromosomal aberrations in mouse bone marrow cells with the human carcinogens 4-aminobiphenyl, treosulphan, and melphalan. AN - 79044249; 2737185 AB - Three human carcinogens, 4-aminobiphenyl, treosulphan, and melphalan, were tested for the induction of micronuclei or chromosomal aberrations in the bone marrow cells of male B6C3F1 mice. These studies were conducted to provide further information on the in vivo genetic toxicity of compounds known to cause cancer in humans. All three compounds gave positive results in the mouse bone marrow micronucleus test, and melphalan, the only compound tested for aberration induction, was positive in this assay. These results extend the evidence that nearly all known human carcinogens are detected in relatively simple and widely employed short-term in vivo tests. JF - Environmental and molecular mutagenesis AU - Shelby, M D AU - Gulati, D K AU - Tice, R R AU - Wojciechowski, J P AD - Cellular and Genetic Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989 PY - 1989 DA - 1989 SP - 339 EP - 342 VL - 13 IS - 4 SN - 0893-6692, 0893-6692 KW - Aminobiphenyl Compounds KW - 0 KW - Carcinogens KW - 4-biphenylamine KW - 16054949HJ KW - treosulfan KW - CO61ER3EPI KW - Busulfan KW - G1LN9045DK KW - Melphalan KW - Q41OR9510P KW - Index Medicus KW - Animals KW - Chemistry KW - Chemical Phenomena KW - Mice KW - Male KW - Chromosome Aberrations -- drug effects KW - Micronucleus Tests KW - Busulfan -- analogs & derivatives KW - Aminobiphenyl Compounds -- toxicity KW - Busulfan -- toxicity KW - Melphalan -- toxicity KW - Bone Marrow -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79044249?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Results+of+tests+for+micronuclei+and+chromosomal+aberrations+in+mouse+bone+marrow+cells+with+the+human+carcinogens+4-aminobiphenyl%2C+treosulphan%2C+and+melphalan.&rft.au=Shelby%2C+M+D%3BGulati%2C+D+K%3BTice%2C+R+R%3BWojciechowski%2C+J+P&rft.aulast=Shelby&rft.aufirst=M&rft.date=1989-01-01&rft.volume=13&rft.issue=4&rft.spage=339&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 - 1989-08-02 N1 - Date created - 1989-08-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Behavioral effects of alpha 2 adrenoceptor antagonists and their interactions with ethanol in tests of locomotion, exploration and anxiety in mice. AN - 79040420; 2567025 AB - The behavioral effects of two highly selective alpha 2-adrenoceptor antagonists, atipamezole and idazoxan, were investigated in mice using the plusmaze test of anxiety and the holeboard test of directed exploration and locomotor activity. No anxiogenic effect, as assessed by the tendency to enter the closed as opposed to open arms of the plusmaze, was noted for either drug at any dose tested. Neither were there any significant effects on locomotor activity or directed exploration (head-dipping) in the holeboard, or total plusmaze arm entries at any dose of either drug. The co-administration of either atipamezole or idazoxan had no effect on either the anxiolytic effect of ethanol (2 g/kg) or its locomotor stimulant effect in the holeboard. Atipamezole (1.0 and 3.0 mg/kg) significantly reversed the ethanol-induced reduction in exploratory head-dipping; a similar trend was seen for idazoxan. There was also a significant potentiation of the ethanol-induced increase in the number of total arm entries made on the plusmaze caused by 1.0 mg/kg (but not 3.0 mg/kg) atipamezole and both 0.3 and 1.0 mg/kg idazoxan. The results suggest that some of the behavioral effects of ethanol can be reversed by alpha 2-adrenoceptor antagonists whilst others are unchanged. JF - Psychopharmacology AU - Durcan, M J AU - Lister, R G AU - Linnoila, M AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 189 EP - 193 VL - 97 IS - 2 SN - 0033-3158, 0033-3158 KW - Adrenergic alpha-Antagonists KW - 0 KW - Dioxanes KW - Imidazoles KW - atipamezole KW - 03N9U5JAF6 KW - Ethanol KW - 3K9958V90M KW - Idazoxan KW - Y310PA316B KW - Index Medicus KW - Animals KW - Drug Interactions KW - Imidazoles -- pharmacology KW - Mice KW - Dioxanes -- pharmacology KW - Male KW - Anxiety -- psychology KW - Ethanol -- pharmacology KW - Exploratory Behavior -- drug effects KW - Motor Activity -- drug effects KW - Adrenergic alpha-Antagonists -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79040420?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Behavioral+effects+of+alpha+2+adrenoceptor+antagonists+and+their+interactions+with+ethanol+in+tests+of+locomotion%2C+exploration+and+anxiety+in+mice.&rft.au=Durcan%2C+M+J%3BLister%2C+R+G%3BLinnoila%2C+M&rft.aulast=Durcan&rft.aufirst=M&rft.date=1989-01-01&rft.volume=97&rft.issue=2&rft.spage=189&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology&rft.issn=00333158&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-03 N1 - Date created - 1989-07-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A view of the relation between carcinogenesis and mutagenesis. AN - 79040239; 2659336 AB - The somatic mutation theory of cancer causation gained the status of dogma following the demonstration in the 1970s that the majority of carcinogens were mutagens. However, more than a decade of "validation" and experimentation has failed to explain a notable group of noncongruent mutagens and carcinogens. Other evidence, including cases of nonparallel metabolic activation pathways for mutagenesis and carcinogenesis and patterns of organ-specific effects, does not support the somatic mutation theory. Therefore, the mutagenic reactions of carcinogens might be coincidental rather than causal; alternate mechanisms of carcinogenesis should be considered. JF - Environmental and molecular mutagenesis AU - Lijinsky, W AD - NCI-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1989 PY - 1989 DA - 1989 SP - 78 EP - 84 VL - 14 Suppl 16 SN - 0893-6692, 0893-6692 KW - Carcinogens, Environmental KW - 0 KW - Mutagens KW - Index Medicus KW - Animals KW - Mutagenicity Tests KW - Neoplasms, Experimental -- chemically induced KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79040239?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+view+of+the+relation+between+carcinogenesis+and+mutagenesis.&rft.au=Lijinsky%2C+W&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1989-01-01&rft.volume=14+Suppl+16&rft.issue=&rft.spage=78&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 - 1989-07-21 N1 - Date created - 1989-07-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Physostigmine-insensitive behavioral excitatory effects of atropine in squirrel monkeys. AN - 79034332; 2734342 AB - Lever press responses of squirrel monkeys were maintained under a multiple schedule in which the first response after 3 min produced either food or electric shock depending on the prevailing stimulus. Atropine sulfate (0.3-3 mg/kg, IM) given immediately before experimental sessions disrupted the temporal pattern of responding and produced dose-related decrease in rates of food- and shock-maintained responding. Increases in responding occurred when 1 mg/kg atropine was given 1 to 12 hr prior to experimental sessions. A maximal increase of 200% of control rates was seen following the 2-hr pretreatment. Qualitatively similar effects were obtained with scopolamine suggesting that the time-dependent increases may be a general consequence of muscarinic receptor blockade. Response patterning changes and response rate increases were also produced by coadministration of atropine and physostigmine both given immediately before the session. Increases in rates of responding have also been observed previously after administration of atropine with rate-decreasing doses of the direct-acting muscarinic agonist oxotremorine. Physostigmine did not reverse the rate increases or the alteration in temporal patterning produced by the 2-hr atropine pretreatment; rate decreases induced by immediate pretreatment with atropine were blocked by physostigmine. Thus, the response rate-decreasing effects of atropine were distinct from its rate-increasing effects. Whereas the rate-decreasing effects of atropine appear to involve muscarinic receptors, increases in responding may not. Such nonmuscarinic behavioral excitatory actions of atropine may be expressed when the muscarinic-related decreases are blocked by physostigmine or oxotremorine, or when the decreases are overridden by excessive nonmuscarinic stimulation, perhaps triggered by time-dependent changes in acetylcholine turnover associated with atropine. JF - Pharmacology, biochemistry, and behavior AU - Witkin, J M AU - Markowitz, R A AU - Barrett, J E AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 309 EP - 315 VL - 32 IS - 1 SN - 0091-3057, 0091-3057 KW - Scopolamine Hydrobromide KW - 451IFR0GXB KW - Atropine KW - 7C0697DR9I KW - Physostigmine KW - 9U1VM840SP KW - Index Medicus KW - Saimiri KW - Animals KW - Drug Interactions KW - Scopolamine Hydrobromide -- pharmacology KW - Reinforcement Schedule KW - Male KW - Behavior, Animal -- drug effects KW - Physostigmine -- pharmacology KW - Physostigmine -- administration & dosage KW - Atropine -- administration & dosage KW - Atropine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79034332?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Physostigmine-insensitive+behavioral+excitatory+effects+of+atropine+in+squirrel+monkeys.&rft.au=Witkin%2C+J+M%3BMarkowitz%2C+R+A%3BBarrett%2C+J+E&rft.aulast=Witkin&rft.aufirst=J&rft.date=1989-01-01&rft.volume=32&rft.issue=1&rft.spage=309&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 - 1989-07-17 N1 - Date created - 1989-07-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Long-term imipramine treatment potentiates m-chlorophenylpiperazine-induced changes in prolactin but not corticosterone or growth hormone levels in rats. AN - 79030825; 2734349 AB - Intravenous administration of m-chlorophenylpiperazine (m-CPP, a selective 5-HT agonist) to rats produced increases in plasma prolactin and corticosterone and a decrease in plasma growth hormone concentrations. Long-term but not short-term imipramine treatment potentiated m-CPP's effect on plasma prolactin, but not its effects on corticosterone or growth hormone. Short-term or long-term imipramine treatment did not produce significant changes in baseline levels of prolactin, corticosterone or growth hormone. These findings are compatible with development of functional supersensitivity of 5-HT receptors mediating prolactin release. Lack of potentiation of m-CPP's effects on corticosterone and growth hormone following long-term imipramine treatment suggests either differential regulation of these hormones by serotonergic and possibly other mechanisms, or different 5-HT receptor subtypes mediating the release of these hormones. Alternatively, adaptive changes in other aminergic neurotransmitter mechanisms such as the noradrenergic system may account for the differential effect of long-term imipramine treatment on m-CPP-induced neuroendocrine changes. JF - Pharmacology, biochemistry, and behavior AU - Aulakh, C S AU - Haass, M AU - Zohar, J AU - Wozniak, K M AU - Hill, J L AU - Murphy, D L AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 37 EP - 42 VL - 32 IS - 1 SN - 0091-3057, 0091-3057 KW - Piperazines KW - 0 KW - Prolactin KW - 9002-62-4 KW - Growth Hormone KW - 9002-72-6 KW - Imipramine KW - OGG85SX4E4 KW - 1-(3-chlorophenyl)piperazine KW - REY0CNO998 KW - Corticosterone KW - W980KJ009P KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Drug Synergism KW - Time Factors KW - Male KW - Prolactin -- blood KW - Corticosterone -- blood KW - Growth Hormone -- blood KW - Imipramine -- pharmacology KW - Piperazines -- pharmacology KW - Piperazines -- administration & dosage KW - Imipramine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79030825?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Long-term+imipramine+treatment+potentiates+m-chlorophenylpiperazine-induced+changes+in+prolactin+but+not+corticosterone+or+growth+hormone+levels+in+rats.&rft.au=Aulakh%2C+C+S%3BHaass%2C+M%3BZohar%2C+J%3BWozniak%2C+K+M%3BHill%2C+J+L%3BMurphy%2C+D+L&rft.aulast=Aulakh&rft.aufirst=C&rft.date=1989-01-01&rft.volume=32&rft.issue=1&rft.spage=37&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 - 1989-07-17 N1 - Date created - 1989-07-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vivo mammalian mutagenesis: in transition to DNA molecules. AN - 79019292; 2659337 AB - Approaches are presented for the detection of mutations in the mitochondrial and nuclear DNA of somatic and germinal cells in vivo in mammals. The difficulties in evaluating mitochondrial mutagenesis are stressed, and simulation experiments using oogonial transfer techniques with mitochondria from two closely subspecies, Mus musculus and Mus molossinus, are suggested. Arguments are presented for using transgenic animals in the study of mutagenesis in the nuclear genome instead of native DNA. Presently, the selection of vectors is limited to lambda and phi X174. The preferred mutation detection system should be independent of expression of the mutant phenotype in the mammalian cells. JF - Environmental and molecular mutagenesis AU - Burkhart, J G AU - Malling, H V AD - Laboratory of Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989 PY - 1989 DA - 1989 SP - 85 EP - 89 VL - 14 Suppl 16 SN - 0893-6692, 0893-6692 KW - DNA, Mitochondrial KW - 0 KW - Mutagens KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Mice KW - Mice, Transgenic KW - DNA, Mitochondrial -- drug effects KW - Base Sequence KW - DNA Mutational Analysis -- methods KW - Mutation KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79019292?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=In+vivo+mammalian+mutagenesis%3A+in+transition+to+DNA+molecules.&rft.au=Burkhart%2C+J+G%3BMalling%2C+H+V&rft.aulast=Burkhart&rft.aufirst=J&rft.date=1989-01-01&rft.volume=14+Suppl+16&rft.issue=&rft.spage=85&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 - 1989-07-21 N1 - Date created - 1989-07-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Structural models of alpha helical membrane peptides and the GABA receptor channel. AN - 79018026; 2471205 JF - Progress in clinical and biological research AU - Guy, H R AU - Raghunathan, G AD - Laboratory of Mathematical Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 231 EP - 243 VL - 289 SN - 0361-7742, 0361-7742 KW - Fish Venoms KW - 0 KW - Ion Channels KW - Membrane Proteins KW - Oligopeptides KW - Receptors, GABA-A KW - Receptors, Glycine KW - Receptors, Neurotransmitter KW - pardaxin KW - 67995-63-5 KW - Glycine KW - TE7660XO1C KW - Index Medicus KW - Models, Molecular KW - Protein Conformation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79018026?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Structural+models+of+alpha+helical+membrane+peptides+and+the+GABA+receptor+channel.&rft.au=Guy%2C+H+R%3BRaghunathan%2C+G&rft.aulast=Guy&rft.aufirst=H&rft.date=1989-01-01&rft.volume=289&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 - 1989-06-28 N1 - Date created - 1989-06-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genetic changes in the pathogenesis of lung cancer. AN - 79017558; 2658754 AB - Human lung cancer is a complex genetic disease resulting from a series of inherited and somatically occurring defects in a number of critical genes. These genetic events, produced in part by carcinogen exposure, include chromosomal deletion, rearrangement, and mutation, and lead to inactivation or activation of certain target genes. Recent data showed these genes to include both recessive oncogenes such as the retinoblastoma gene and dominantly acting oncogenes such as the myc and ras family members. JF - Annual review of medicine AU - Birrer, M J AU - Minna, J D AD - NCI-Navy Medical Oncology Branch, Naval Hospital, Bethesda, Maryland 20814. Y1 - 1989 PY - 1989 DA - 1989 SP - 305 EP - 317 VL - 40 SN - 0066-4219, 0066-4219 KW - Index Medicus KW - Chromosome Deletion KW - Disease Susceptibility KW - Risk Factors KW - Humans KW - Suppression, Genetic KW - Proto-Oncogenes KW - Gene Amplification KW - Precancerous Conditions -- genetics KW - Lung Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79017558?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+medicine&rft.atitle=Genetic+changes+in+the+pathogenesis+of+lung+cancer.&rft.au=Birrer%2C+M+J%3BMinna%2C+J+D&rft.aulast=Birrer&rft.aufirst=M&rft.date=1989-01-01&rft.volume=40&rft.issue=&rft.spage=305&rft.isbn=&rft.btitle=&rft.title=Annual+review+of+medicine&rft.issn=00664219&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-27 N1 - Date created - 1989-06-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanisms of mutagenesis. AN - 79017441; 2659325 AB - Our understanding of mechanisms of mutation, which has expanded greatly in the past few decades, served as the original impetus to the formation of the Environmental Mutagen Society. The advances in genetics and chemistry that have conditioned our present degree of knowledge are here catalogued and the future is predicted. JF - Environmental and molecular mutagenesis AU - Drake, J W AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989 PY - 1989 DA - 1989 SP - 11 EP - 15 VL - 14 Suppl 16 SN - 0893-6692, 0893-6692 KW - Carcinogens, Environmental KW - 0 KW - Mutagens KW - Index Medicus KW - History of medicine KW - United States KW - History, 20th Century KW - Humans KW - Europe KW - Genetics, Medical -- history KW - Mutation KW - Mutagenicity Tests -- history UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79017441?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mechanisms+of+mutagenesis.&rft.au=Drake%2C+J+W&rft.aulast=Drake&rft.aufirst=J&rft.date=1989-01-01&rft.volume=14+Suppl+16&rft.issue=&rft.spage=11&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 - 1989-07-21 N1 - Date created - 1989-07-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Two-stage models of tumor incidence for historical control animals in the National Toxicology Program's carcinogenicity experiments. AN - 79012041; 2724366 AB - The tumor incidence rate is modeled for various tumors in a database of control animals [Fischer 344 rats and (C57BL/6 x C3H)F1 mice] originally developed by the national Toxicology Program and recently augmented to include additional sacrifice data by Portier et al. (1986). These rates are assumed to follow a clonal two-stage model of carcinogenesis where cells in the various tissues are allowed to be in one of three states arbitrarily defined as a "normal" state, an "initiated" state, and a "tumor present" state. The parameters of this clonal two-stage model have a direct interpretation with regard to the mechanism of action and in some cases may suggest a common mechanism for various tumors in the different sex/species groups. Also, the risk of dying (from all causes) in tumor-bearing animals is compared to the risk of dying in non-tumor-bearing animals via estimates of relative risk. In general, it was found that the risk of dying was elevated for most tumors. The purpose of this analysis is to provide estimates of baseline tumor rates and relative risks, which are useful in the design and analysis of future carcinogenicity experiments. JF - Journal of toxicology and environmental health AU - Portier, C J AU - Bailer, A J AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989 PY - 1989 DA - 1989 SP - 21 EP - 45 VL - 27 IS - 1 SN - 0098-4108, 0098-4108 KW - Carcinogens KW - 0 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Carcinogenicity Tests KW - Mice KW - Neoplasms, Experimental -- epidemiology KW - Information Systems KW - Neoplasms, Experimental -- chemically induced KW - Neoplasms, Experimental -- mortality KW - Models, Biological UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79012041?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Two-stage+models+of+tumor+incidence+for+historical+control+animals+in+the+National+Toxicology+Program%27s+carcinogenicity+experiments.&rft.au=Portier%2C+C+J%3BBailer%2C+A+J&rft.aulast=Portier&rft.aufirst=C&rft.date=1989-01-01&rft.volume=27&rft.issue=1&rft.spage=21&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 - 1989-06-23 N1 - Date created - 1989-06-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The antioxidant butylated hydroxytoluene can retard cerebellar degeneration induced transplacentally by a single low dosage of N-methyl-N-nitrosourea. AN - 79000051; 2567066 AB - Late-onset cerebellar degeneration can be induced transplacentally in mice by a single low-dose (1 mg/kg) injection of the direct-acting DNA alkylating agent N-methyl-N-nitrosourea (MNU) on day 16 of pregnancy. The offspring develop a mild ataxia that manifests by 12-16 weeks of age postnatally when the animals are challenged with a motor coordination task. Morphological evidence of degeneration includes pyknosis of Purkinje cells and abnormal foliation patterns. Additionally, these animals demonstrate a progressive retinopathy characterized by thinning of the nuclear and plexiform layers of the retina. Efforts to retard the cerebellar degeneration were undertaken in the present study. MNU-exposed and control animals were fed a standard mouse chow diet supplemented with 0.75% butylated hydroxytoluene (BHT), an antioxidant. This supplementation commenced 24 h following exposure to the teratogen and continued throughout the life of the offspring. A second group of MNU-exposed and control mice were fed a non-BHT-supplemented, standard Purina mouse chow diet. Quantitative histological evaluation of cerebellar coronal sections indicated that by 4 weeks of age BHT-fed, MNU-exposed mice had significantly fewer pyknotic Purkinje cells than non-BHT-fed, MNU-exposed animals. This was true for the vermal, paravermal, and lateral areas of the cerebellum. The findings suggest the usefulness of teratogenic models of degenerative diseases for the testing of potential intervention strategies. JF - Teratogenesis, carcinogenesis, and mutagenesis AU - Smith, S B AU - Cooke, C B AU - Yielding, K L AD - National Eye Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1989 PY - 1989 DA - 1989 SP - 15 EP - 27 VL - 9 IS - 1 SN - 0270-3211, 0270-3211 KW - Antioxidants KW - 0 KW - Butylated Hydroxytoluene KW - 1P9D0Z171K KW - Methylnitrosourea KW - 684-93-5 KW - Index Medicus KW - Methylnitrosourea -- antagonists & inhibitors KW - Animals KW - Nerve Degeneration -- drug effects KW - Purkinje Cells -- pathology KW - Disease Models, Animal KW - Cerebellum -- pathology KW - Mice KW - Pregnancy KW - Purkinje Cells -- drug effects KW - Cerebellum -- drug effects KW - Diet KW - Female KW - Prenatal Exposure Delayed Effects KW - Cerebellar Diseases -- pathology KW - Cerebellar Diseases -- congenital KW - Antioxidants -- therapeutic use KW - Cerebellar Diseases -- embryology KW - Butylated Hydroxytoluene -- therapeutic use KW - Cerebellar Diseases -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/79000051?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+antioxidant+butylated+hydroxytoluene+can+retard+cerebellar+degeneration+induced+transplacentally+by+a+single+low+dosage+of+N-methyl-N-nitrosourea.&rft.au=Smith%2C+S+B%3BCooke%2C+C+B%3BYielding%2C+K+L&rft.aulast=Smith&rft.aufirst=S&rft.date=1989-01-01&rft.volume=9&rft.issue=1&rft.spage=15&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 - 1989-06-23 N1 - Date created - 1989-06-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intraperitoneal mesotheliomas induced in mice by a polycyclic aromatic hydrocarbon. AN - 78990185; 2724365 AB - Female mice of 6 strains (C3H/HeN, BALB/c, C57BL/6N, DBA/2, NIH Swiss, and AKR/N) were given the polycyclic aromatic hydrocarbon carcinogen 3-methylcholanthrene (MC) intragastrically in olive oil at a dose of 20 mg/kg, weekly for 12 wk. Half were pretreated 24 h before each MC administration with intraperitoneal beta-naphthoflavone (beta-NF, 150 mg/kg in olive oil), a noncarcinogenic inducer of certain cytochrome P-450 isozymes. Remaining mice were given olive oil prior to MC in the same fashion, or beta-NF in olive oil or olive oil alone without subsequent exposure to MC. All mice were killed when moribund or 13 mo after the start of treatment. Most of the mice, irrespective of treatment, exhibited signs of peritoneal injury, including inflammation, necrosis, granuloma formation, and mineralization. Mice of some of the strains also presented peritoneal mesotheliomas, in addition to a variety of other tumors. The incidence of unequivocal mesothelioma-bearing mice was 12/31 C3H/He and 9/32 BALB/c mice given only MC. Incidence was low in C57BL/6 (1/31) and DBA/2 (1/26), and no definite mesotheliomas were found in Swiss or AKR mice. There were in addition a number of cases of sarcoma (nine total in all strains) and of peritonitis (four total) that resembled mesothelioma to some degree and were initially diagnosed as much. beta-NF pretreatment reduced the frequency of mesotheliomas: there was only one definite mesothelioma in any of the beta-NF-MC groups, in a C3H/He mouse. Most of the mesotheliomas were mixed fibro-mesothelial type, sometimes with papillary epithelial excrescences. They typically grew in a botryoid pattern within the peritoneal cavity, coating the abdominal organs and sometimes actively invading these organs and the diaphragm. Some lesions exhibited pleomorphism, prominent giant cells, and frequent mitoses. In addition, several lesions consisting of severe mesothelial hyperplasia associated with tissue necrosis and inflammation were considered as possible early stages of mesothelioma development. It was postulated that peritoneal injury imposed by repeated intraperitoneal injection of oil acted as an enhancing factor for mesothelioma induction by MC. The pertinence of such a relationship to mechanisms in the etiology of human mesotheliomas is discussed. JF - Journal of toxicology and environmental health AU - Rice, J M AU - Kovatch, R M AU - Anderson, L M AD - Division of Cancer Etiology, National Cancer Institute, Frederick, Maryland 21701-1013. Y1 - 1989 PY - 1989 DA - 1989 SP - 153 EP - 160 VL - 27 IS - 1 SN - 0098-4108, 0098-4108 KW - Benzoflavones KW - 0 KW - Methylcholanthrene KW - 56-49-5 KW - beta-Naphthoflavone KW - 6051-87-2 KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Drug Interactions KW - Disease Models, Animal KW - Mice KW - Female KW - Peritoneal Neoplasms -- chemically induced KW - Mesothelioma -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78990185?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Intraperitoneal+mesotheliomas+induced+in+mice+by+a+polycyclic+aromatic+hydrocarbon.&rft.au=Rice%2C+J+M%3BKovatch%2C+R+M%3BAnderson%2C+L+M&rft.aulast=Rice&rft.aufirst=J&rft.date=1989-01-01&rft.volume=27&rft.issue=1&rft.spage=153&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 - 1989-06-23 N1 - Date created - 1989-06-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lethal effects of cocaine are reduced by the dopamine-1 receptor antagonist SCH 23390 but not by haloperidol. AN - 78989004; 2523996 AB - The prevalence of cocaine abuse has been associated with a host of medical complications and deaths. We investigated the effects of two dopamine antagonists with different affinities for dopamine-1 and dopamine-2 receptor subtypes on cocaine-induced lethality. Male Fischer-344 rats were given cocaine HCl (i.p.) and observed for lethality at 24 hrs. Cocaine was not lethal at 50 mg/kg and produced a steep dose-effect function from 60 to 100 mg/kg. Lethality was 88.9% at 100 mg/kg and the LD 50 was 79.7 mg/kg (95% CL: 74.8-84.9). Doses as high as 180 mg/kg failed to kill all rats. Lethality was often but not invariably associated with convulsions. Haloperidol (0.3-3 mg/kg i.p.) given 30 min prior to cocaine did not alter the lethal effects of cocaine but did reduce the lethality of methamphetamine. SCH 23390 (0.1-1 mg/kg i.p., 30 min prior) shifted the cocaine dose-effect function to the right at 0.3 mg/kg. Maximum protection was conferred by 0.3 mg/kg SCH 23390 where the LD 50 was increased to 100.1 mg/kg (95% CL: 91.5-109.5). Comparable protection was not observed if SCH 23390 was given 5 min after cocaine. These results suggest that dopamine receptors may play a role in the lethal effects of cocaine and that the D1 dopamine receptor subtype appears to be more relevant to lethality than the D2 subtype. JF - Life sciences AU - Witkin, J M AU - Goldberg, S R AU - Katz, J L AD - Preclinical Pharmacology Branch, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1989 PY - 1989 DA - 1989 SP - 1285 EP - 1291 VL - 44 IS - 18 SN - 0024-3205, 0024-3205 KW - Benzazepines KW - 0 KW - Dopamine Antagonists KW - Receptors, Dopamine KW - Receptors, Dopamine D1 KW - Cocaine KW - I5Y540LHVR KW - Haloperidol KW - J6292F8L3D KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Dose-Response Relationship, Drug KW - Male KW - Receptors, Dopamine -- drug effects KW - Receptors, Dopamine -- physiology KW - Benzazepines -- pharmacology KW - Haloperidol -- pharmacology KW - Cocaine -- toxicity KW - Cocaine -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78989004?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=unknown&rft.jtitle=Film+Index+International&rft.atitle=AU+BISEAU+DES+BAISERS&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1959-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-14 N1 - Date created - 1989-06-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lack of effect of selenium on induction of tumors of esophagus and bladder in rats by two nitrosamines. AN - 78984619; 2718186 AB - The effect of differences in level of dietary selenium on the induction of esophageal and bladder tumors in rats by two nitrosamines was investigated. Groups of 20 female F344 rats were given a synthetic diet containing less than 0.05 ppm Se to which selenium (as sodium selenite) was added at the concentration of 0.35, 0.7, 1.4 and 2.1 ppm selenium. These four groups, plus one without added Se, were treated with 20 ml per rat per day, 5 days a week, of a solution of nitrosomethylcyclohexylamine containing 5 mg/liter. A parallel five groups were treated in the same way with a solution of nitrosomethyl-3-carboxypropylamine in drinking water containing 600 mg per liter, as drinking water. Treatment lasted 28 weeks, at which time some animals had developed tumors. A group of 20 rats fed 0, 1.4 and 2.1 ppm Se was not treated with carcinogen. Rats consuming 1.4 ppm or 2.1 ppm Se gained weight more slowly than other groups. There was no significant difference in survival between the five groups treated with each carcinogen but receiving different dietary levels of selenium. Neither was there any significant difference between groups receiving each carcinogen in the incidence of tumors of the esophagus induced by nitrosomethylcyclohexylamine or of tumors of the urinary bladder induced by nitrosomethylcarboxypropylamine. Control rats on the synthetic diets did not survive as well as untreated rats eating regular chow diet. In these conditions there was no effect of dietary selenium levels on the induction of tumors in female rats by the two carcinogenic nitrosamines we used. JF - Toxicology and industrial health AU - Lijinsky, W AU - Milner, J A AU - Kovatch, R M AU - Thomas, B J AD - NCI-Frederick Cancer Research Facility, BRI-Basic Research Program, Frederick, Maryland. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 63 EP - 72 VL - 5 IS - 1 SN - 0748-2337, 0748-2337 KW - Carcinogens KW - 0 KW - Nitrosamines KW - 4-(N-nitroso-N-methylamino)butyric acid KW - 61445-55-4 KW - Selenium KW - H6241UJ22B KW - N-nitroso-N-methylcyclohexylamine KW - VVL0BT0AWL KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Drug Interactions KW - Dose-Response Relationship, Drug KW - Diet KW - Female KW - Nitrosamines -- administration & dosage KW - Esophageal Neoplasms -- chemically induced KW - Nitrosamines -- pharmacology KW - Carcinogens -- pharmacology KW - Selenium -- blood KW - Carcinogens -- administration & dosage KW - Selenium -- pharmacology KW - Selenium -- administration & dosage KW - Urinary Bladder Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78984619?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+industrial+health&rft.atitle=Lack+of+effect+of+selenium+on+induction+of+tumors+of+esophagus+and+bladder+in+rats+by+two+nitrosamines.&rft.au=Lijinsky%2C+W%3BMilner%2C+J+A%3BKovatch%2C+R+M%3BThomas%2C+B+J&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1989-01-01&rft.volume=5&rft.issue=1&rft.spage=63&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+industrial+health&rft.issn=07482337&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-22 N1 - Date created - 1989-06-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Therapeutic and toxic activity of tumor necrosis factor is synergistic with gamma interferon. AN - 78981878; 2497452 JF - Pathology and immunopathology research AU - Talmadge, J E AU - Bowersox, O AU - Tribble, H AU - Shepard, M AU - Liggitt, D AD - Program Resources, Inc., NCI-Frederick Cancer Research Facility, Md. Y1 - 1989 PY - 1989 DA - 1989 SP - 21 EP - 34 VL - 8 IS - 1 SN - 0257-2761, 0257-2761 KW - Recombinant Proteins KW - 0 KW - Tumor Necrosis Factor-alpha KW - Dexamethasone KW - 7S5I7G3JQL KW - Interferon-gamma KW - 82115-62-6 KW - Aspirin KW - R16CO5Y76E KW - Index Medicus KW - Injections, Intraperitoneal KW - Animals KW - Recombinant Proteins -- pharmacology KW - Dexamethasone -- therapeutic use KW - Injections, Intravenous KW - Immunotherapy KW - Lung Neoplasms -- therapy KW - Mice KW - Melanoma, Experimental -- therapy KW - Cells, Cultured KW - Aspirin -- therapeutic use KW - Mice, Inbred C57BL KW - Drug Synergism KW - Interferon-gamma -- pharmacology KW - Tumor Necrosis Factor-alpha -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78981878?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pathology+and+immunopathology+research&rft.atitle=Therapeutic+and+toxic+activity+of+tumor+necrosis+factor+is+synergistic+with+gamma+interferon.&rft.au=Talmadge%2C+J+E%3BBowersox%2C+O%3BTribble%2C+H%3BShepard%2C+M%3BLiggitt%2C+D&rft.aulast=Talmadge&rft.aufirst=J&rft.date=1989-01-01&rft.volume=8&rft.issue=1&rft.spage=21&rft.isbn=&rft.btitle=&rft.title=Pathology+and+immunopathology+research&rft.issn=02572761&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-12 N1 - Date created - 1989-06-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - High-dose mitomycin C: activity in hepatocellular carcinoma. AN - 78980381; 2541938 AB - Hepatocellular carcinoma is the most common cause of cancer death in Thai males. It is usually found to be inoperable, and the reported median survival for Thai patients is only 4.3 months. From October 1984 to December 1986, 30 cases of nonresectable hepatocellular carcinoma were treated at the National Cancer Institute, Bangkok, Thailand, with high-dose mitomycin C. Patients were given 20-25 m/m2 (median, 40 mg) by i.v. injection, followed by 10-12.5 mg/m2 (median, 20 mg) at 6-week intervals in responding patients until the disease progressed or toxicity was detected. In all, 23 patients were evaluable by WHO criteria. A partial response was achieved in 11 of 23 cases (48%); the median duration of this response was 7 months (range, 3-11 months). The median cumulative dose of mitomycin C was 80 mg (range, 40-120 mg). Toxicity was relatively well tolerated; only one patient developed an unusual erythematous, reticular skin rash that spontaneously disappeared within 1 month of injection of the drug. The median survival of responders was 12 months, and the longest survival was 18+ months. We conclude that high-dose mitomycin C given according to the present dose and schedule has antitumor activity in hepatocellular carcinoma in Thai patients. Although its response rate is as high as that produced by doxorubicin, with less toxicity, no complete response was achieved in this study. JF - Cancer chemotherapy and pharmacology AU - Cheirsilpa, A AU - Leelasethakul, S AU - Auethaveekiat, V AU - Maoleekulpriroj, S AU - Kangsumrit, N AU - Thanakaravit, P AU - Phanthumjida, P AD - Division of Medical Oncology, National Cancer Institute, Bangkok, Thailand. Y1 - 1989 PY - 1989 DA - 1989 SP - 50 EP - 53 VL - 24 IS - 1 SN - 0344-5704, 0344-5704 KW - Mitomycins KW - 0 KW - Mitomycin KW - 50SG953SK6 KW - Index Medicus KW - Drug Evaluation KW - Drug Administration Schedule KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Male KW - Female KW - Liver Neoplasms -- pathology KW - Mitomycins -- adverse effects KW - Carcinoma, Hepatocellular -- drug therapy KW - Mitomycins -- therapeutic use KW - Liver Neoplasms -- drug therapy KW - Mitomycins -- administration & dosage KW - Carcinoma, Hepatocellular -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78980381?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=High-dose+mitomycin+C%3A+activity+in+hepatocellular+carcinoma.&rft.au=Cheirsilpa%2C+A%3BLeelasethakul%2C+S%3BAuethaveekiat%2C+V%3BMaoleekulpriroj%2C+S%3BKangsumrit%2C+N%3BThanakaravit%2C+P%3BPhanthumjida%2C+P&rft.aulast=Cheirsilpa&rft.aufirst=A&rft.date=1989-01-01&rft.volume=24&rft.issue=1&rft.spage=50&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 - 1989-06-28 N1 - Date created - 1989-06-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nicotine and some related compounds: effects on schedule-controlled behaviour and discriminative properties in rats. AN - 78978134; 2497478 AB - Behavioural effects of d- and l-nicotine, d- and l-nornicotine and l-cotinine were studied in two paradigms. In experiment 1, rats responded under a multiple fixed-interval (FI) 5 min, fixed-ratio (FR) 20 schedule of food presentation. Aside from differences in potency and time course, l-nicotine and the stereoisomers of nornicotine produced qualitatively similar effects on rates of responding. With increasing doses of drugs, FI response rates first increased and then decreased, while FR response rates only decreased. In contrast, d-nicotine did not significantly increase FI response rates at lower doses, and only decreased FI and FR response rates at higher doses. At doses up to 100 mg/kg, cotinine produced only dose-dependent increases in FI response rates and had no effect on FR response rates. Rate-increasing effects of cotinine were not blocked by mecamylamine. In experiment 2, rats were trained to discriminate between l-nicotine (0.1 mg/kg SC) and saline (0.1 ml/kg SC) in a two-bar, operant conditioning procedure under a tandem variable-interval (VI) 1 min, FR 10 schedule of food presentation. Full generalization was obtained to d-nicotine and to l- and d-nornicotine. Generalization to cotinine occurred only with large doses that contained significant amounts of nicotine present as an impurity. There was no generalization to non-nicotinic drugs (morphine and clenbuterol), even at doses that reduced response rates.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Psychopharmacology AU - Goldberg, S R AU - Risner, M E AU - Stolerman, I P AU - Reavill, C AU - Garcha, H S AD - National Institute on Drug Abuse, Preclinical Pharmacology Branch, Baltimore, MD 21224. Y1 - 1989 PY - 1989 DA - 1989 SP - 295 EP - 302 VL - 97 IS - 3 SN - 0033-3158, 0033-3158 KW - Insecticides KW - 0 KW - Nicotine KW - 6M3C89ZY6R KW - nornicotine KW - 83H6L5QD8Z KW - Cotinine KW - K5161X06LL KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Reinforcement Schedule KW - Cotinine -- pharmacology KW - Dose-Response Relationship, Drug KW - Insecticides -- pharmacology KW - Male KW - Conditioning, Operant -- drug effects KW - Discrimination (Psychology) -- drug effects KW - Nicotine -- pharmacology KW - Nicotine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78978134?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Nicotine+and+some+related+compounds%3A+effects+on+schedule-controlled+behaviour+and+discriminative+properties+in+rats.&rft.au=Goldberg%2C+S+R%3BRisner%2C+M+E%3BStolerman%2C+I+P%3BReavill%2C+C%3BGarcha%2C+H+S&rft.aulast=Goldberg&rft.aufirst=S&rft.date=1989-01-01&rft.volume=97&rft.issue=3&rft.spage=295&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology&rft.issn=00333158&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-15 N1 - Date created - 1989-06-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Central nervous system pharmacology of antileukemic drugs. AN - 78965322; 2496615 AB - The blood-brain barrier provides a pharmacologic sanctuary for leukemic cells within the central nervous system (CNS), protecting them from the cytotoxic effects of systemic antileukemic therapy. Attempts to overcome this problem have included specific CNS-directed treatment in the form of direct intrathecal drug injection, cranial irradiation, and alteration in the dose and schedule of systemic agents to enhance their CNS penetration. Use of these treatments and strategies has led to the effective prevention and control of meningeal leukemia. Intrathecal therapy, primarily with methotrexate or cytosine arabinoside, is a form of regional chemotherapy that can achieve very high drug concentrations at the target site [i.e., in the meninges and cerebrospinal fluid (CSF)] with a low total dose. Therefore, there is minimal systemic toxicity. The dose and schedules, clinical pharmacology, and toxicities of the commonly used intrathecal agents are discussed in detail in this article. Another approach to overcoming the limited penetration of antileukemic drugs into the CNS has been the use of high-dose systemic therapy. Methotrexate and cytosine arabinoside in high doses have produced favorable clinical responses in patients with overt meningeal disease, and pharmacokinetic studies have documented cytotoxic concentrations of these drugs within the cerebrospinal fluid. A clear understanding of the CNS pharmacology of the antileukemic drugs is required in order to use these agents in the safest and most efficacious manner for the treatment of meningeal leukemia. JF - The American journal of pediatric hematology/oncology AU - Balis, F M AU - Poplack, D G AD - Pediatric Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 74 EP - 86 VL - 11 IS - 1 SN - 0192-8562, 0192-8562 KW - Antineoplastic Agents KW - 0 KW - Cytarabine KW - 04079A1RDZ KW - Thiotepa KW - 905Z5W3GKH KW - 6-Mercaptopurine KW - E7WED276I5 KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Methotrexate -- pharmacology KW - 6-Mercaptopurine -- therapeutic use KW - Humans KW - Thiotepa -- pharmacokinetics KW - 6-Mercaptopurine -- pharmacokinetics KW - Child KW - Cytarabine -- pharmacokinetics KW - Cytarabine -- pharmacology KW - Cytarabine -- therapeutic use KW - Thiotepa -- pharmacology KW - Thiotepa -- therapeutic use KW - Methotrexate -- pharmacokinetics KW - Methotrexate -- therapeutic use KW - 6-Mercaptopurine -- pharmacology KW - Leukemia -- drug therapy KW - Antineoplastic Agents -- pharmacokinetics KW - Central Nervous System -- drug effects KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78965322?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+pediatric+hematology%2Foncology&rft.atitle=Central+nervous+system+pharmacology+of+antileukemic+drugs.&rft.au=Balis%2C+F+M%3BPoplack%2C+D+G&rft.aulast=Balis&rft.aufirst=F&rft.date=1989-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-26 N1 - Date created - 1989-05-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The CRISP system: an untapped resource for biomedical research project information. AN - 78963769; 2720218 AB - CRISP (Computer Retrieval of Information on Scientific Projects) is a large database maintained and operated by the National Institutes of Health (NIH). It contains comprehensive scientific and selected administrative data on research carried out by the U.S. Public Health Service (PHS) or supported by PHS grants and contracts. Developed originally to meet the needs of NIH, it is an excellent, largely untapped resource for health information professionals at large, revealing new trends, methods, and techniques, often before they appear in the published literature. CRISP uses its own controlled vocabulary, developed to permit indexing of new and active research areas. Queries can combine subject headings with a great variety of administrative data elements (e.g., research category or principal investigator's name). Output is available in a variety of formats and media. While information professionals cannot directly access the CRISP system, abridged CRISP records are merged into the FEDRIP (Federal Research in Progress) database, and FEDRIP is publicly accessible through DIALOG. CRISP records in toxicology are also furnished to the National Library of Medicine's TOXLINE database. This paper discusses the indexing, information retrieval, publication products, and search services of the CRISP system, and how users of medical information can benefit from it. JF - Bulletin of the Medical Library Association AU - Collins, K A AD - Division of Research Grants, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 8 EP - 14 VL - 77 IS - 1 SN - 0025-7338, 0025-7338 KW - Index Medicus KW - United States KW - Humans KW - Abstracting and Indexing as Topic KW - Publishing KW - Information Systems KW - National Institutes of Health (U.S.) KW - Research UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78963769?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+of+the+Medical+Library+Association&rft.atitle=The+CRISP+system%3A+an+untapped+resource+for+biomedical+research+project+information.&rft.au=Collins%2C+K+A&rft.aulast=Collins&rft.aufirst=K&rft.date=1989-01-01&rft.volume=77&rft.issue=1&rft.spage=8&rft.isbn=&rft.btitle=&rft.title=Bulletin+of+the+Medical+Library+Association&rft.issn=00257338&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-29 N1 - Date created - 1989-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Epidemiologic studies of the molecular genetics of cancer. AN - 78962833; 2655742 JF - Birth defects original article series AU - Taylor, J A AD - Epidemiology Branch, NIEHS, Research Triangle Park, NC 27709. Y1 - 1989 PY - 1989 DA - 1989 SP - 83 EP - 93 VL - 25 IS - 2 SN - 0547-6844, 0547-6844 KW - Index Medicus KW - Disease Susceptibility KW - Epidemiologic Methods KW - Humans KW - Environmental Exposure KW - Oncogenes KW - Neoplasms -- epidemiology KW - Suppression, Genetic KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78962833?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Birth+defects+original+article+series&rft.atitle=Epidemiologic+studies+of+the+molecular+genetics+of+cancer.&rft.au=Taylor%2C+J+A&rft.aulast=Taylor&rft.aufirst=J&rft.date=1989-01-01&rft.volume=25&rft.issue=2&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=Birth+defects+original+article+series&rft.issn=05476844&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-07-11 N1 - Date created - 1989-07-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Epidemiology of smokeless tobacco use: a national study. AN - 78959400; 2785648 AB - The prevalence and patterns of smokeless tobacco use and its correlates were assessed in the National Institute on Drug Abuse National Household Survey of residents 12 years of age and older. Overall, 11% of the general population have "ever tried" chewing tobacco, snuff, or other smokeless tobacco. Of these, 5% were former users and 3% used smokeless tobacco almost daily in the past year. Rates of its use differed significantly by sex, age group, race, region, and metropolitan area size. Although females were far less likely to try it, those who did were as likely as males to be daily users. Smokeless tobacco users were also more likely to use alcohol, cigarettes, and marijuana. In general, those who used smokeless tobacco almost daily were more likely to report poor health and hospitalization for illness or injury in the past year, even when other substance use was controlled. Smokeless tobacco users also were more likely to report symptoms of depression. Finally, some substituted smokeless tobacco for cigarettes, but youths (12-17 yr old) were more likely than older tobacco users to use both forms of tobacco regularly. JF - NCI monographs : a publication of the National Cancer Institute AU - Rouse, B A AD - Epidemiology Research Branch, National Institute on Drug Abuse, Rockville, Maryland 20857. Y1 - 1989 PY - 1989 DA - 1989 SP - 29 EP - 33 IS - 8 SN - 0893-2751, 0893-2751 KW - Index Medicus KW - United States KW - Age Factors KW - Attitude to Health KW - Sex Factors KW - Humans KW - Child KW - Smoking -- epidemiology KW - Cross-Sectional Studies KW - Adult KW - Sampling Studies KW - Middle Aged KW - Adolescent KW - Female KW - Male KW - Plants, Toxic KW - Tobacco Use Disorder -- epidemiology KW - Tobacco KW - Tobacco, Smokeless UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78959400?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NCI+monographs+%3A+a+publication+of+the+National+Cancer+Institute&rft.atitle=Epidemiology+of+smokeless+tobacco+use%3A+a+national+study.&rft.au=Rouse%2C+B+A&rft.aulast=Rouse&rft.aufirst=B&rft.date=1989-01-01&rft.volume=&rft.issue=8&rft.spage=29&rft.isbn=&rft.btitle=&rft.title=NCI+monographs+%3A+a+publication+of+the+National+Cancer+Institute&rft.issn=08932751&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-12 N1 - Date created - 1989-06-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pharmacokinetic considerations on monoclonal antibodies. AN - 78956524; 2654958 JF - Progress in clinical and biological research AU - Dedrick, R L AU - Flessner, M F AD - Biomedical Engineering and Instrumentation Branch, National Institutes of Health, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 429 EP - 438 VL - 288 SN - 0361-7742, 0361-7742 KW - Antibodies, Monoclonal KW - 0 KW - Immunotoxins KW - Index Medicus KW - Injections, Intraperitoneal KW - Neoplasms -- drug therapy KW - Animals KW - Neoplasms, Experimental -- therapy KW - Humans KW - Biological Transport KW - Capillary Permeability KW - Neoplasms, Experimental -- metabolism KW - Mice KW - Tissue Distribution KW - Immunotoxins -- metabolism KW - Neoplasms -- therapy KW - Drug Administration Routes KW - Abdominal Neoplasms -- metabolism KW - Immunotoxins -- therapeutic use KW - Ascitic Fluid -- metabolism KW - Neoplasms -- metabolism KW - Abdominal Neoplasms -- therapy KW - Antibodies, Monoclonal -- analysis KW - Antibodies, Monoclonal -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78956524?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pharmacokinetic+considerations+on+monoclonal+antibodies.&rft.au=Dedrick%2C+R+L%3BFlessner%2C+M+F&rft.aulast=Dedrick&rft.aufirst=R&rft.date=1989-01-01&rft.volume=288&rft.issue=&rft.spage=429&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 - 1989-06-20 N1 - Date created - 1989-06-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immune reactions in a changing environment. USA initiatives. AN - 78956318; 2707890 AB - Environmental hazards occurring as an undesirable consequence of economic progress, urbanization and pollution have become a worldwide concern. In the US, this is evident from the campaign against smoking which has focused attention on the lung in part because the lung as a target organ is constantly exposed to many visible environmental hazards. On the other hand, environmental hazards which are not lethal, but cause their effects in an insidious fashion, may be difficult to study and identify. Among the disciplines available to assess adverse health consequences of xenobiotics ('strange' substances in our environment), application of modern immunological methods in concert with traditional toxicologic studies have to date demonstrated significant progress in drug allergy, food allergy, environmentally induced lung diseases and autoimmunity. These successes have come from the collaboration of immunologists, allergologists, pulmonologists, pharmacologists and toxicologists. In fact, a newer discipline of immunotoxicology has emerged in order to deal with these complex issues. The National Institutes of Health, through a series of workshops and research initiatives, and in collaboration with other US government agencies, including the Environmental Protection Agency, the National Institute of Environmental Health Sciences, and the National Academy of Sciences, is attempting to foster research aimed at enhancing progress in the field of immunotoxicology. The overall aim is to encourage the use of modern immunologic approaches to the study of the alleged harmful effects of xenobiotics on the immune system. Success will permit the development of improved diagnostic tools followed by initiatives concerned with prevention. Apart from their scientific implications the results are expected to have an impact on social, legal and economic issues within society. JF - International archives of allergy and applied immunology AU - Goldstein, R A AD - Clinical Immunology and Immunopathology Branch, National Institute of Allergy and Infectious Diseases, Bethesda, Md. Y1 - 1989 PY - 1989 DA - 1989 SP - 256 EP - 258 VL - 88 IS - 1-2 SN - 0020-5915, 0020-5915 KW - Index Medicus KW - United States KW - Humans KW - Environment KW - Hypersensitivity -- physiopathology KW - Immunity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78956318?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+archives+of+allergy+and+applied+immunology&rft.atitle=Immune+reactions+in+a+changing+environment.+USA+initiatives.&rft.au=Goldstein%2C+R+A&rft.aulast=Goldstein&rft.aufirst=R&rft.date=1989-01-01&rft.volume=88&rft.issue=1-2&rft.spage=256&rft.isbn=&rft.btitle=&rft.title=International+archives+of+allergy+and+applied+immunology&rft.issn=00205915&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-02 N1 - Date created - 1989-06-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cocaine-induced cocaine craving. AN - 78952787; 2496428 AB - In nine experienced users of cocaine, we examined the urge to use cocaine or other drugs following a 40 mg dose of intravenous (IV) cocaine with and without oral pretreatment with 2.5 mg bromocriptine. The urge to use cocaine was assessed with a questionnaire constructed to assess both "wanting" and "craving" for cocaine or other drugs. Fifteen minutes after the administration of cocaine (but not after placebo), subjects' ratings for both drug "wanting" and drug "craving" were significantly increased. Our results provide a laboratory demonstration of cocaine-induced increases in the urge to use drugs in humans. The findings, stressing the role of internal stimuli associated with drug administration, suggest the possibility of distinguishing among related, but perhaps distinct, components of the fluctuating levels of motivation to reuse drugs. JF - Psychopharmacology AU - Jaffe, J H AU - Cascella, N G AU - Kumor, K M AU - Sherer, M A AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1989 PY - 1989 DA - 1989 SP - 59 EP - 64 VL - 97 IS - 1 SN - 0033-3158, 0033-3158 KW - Bromocriptine KW - 3A64E3G5ZO KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Double-Blind Method KW - Humans KW - Adult KW - Bromocriptine -- pharmacology KW - Time Factors KW - Male KW - Substance-Related Disorders -- psychology KW - Cocaine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78952787?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cocaine-induced+cocaine+craving.&rft.au=Jaffe%2C+J+H%3BCascella%2C+N+G%3BKumor%2C+K+M%3BSherer%2C+M+A&rft.aulast=Jaffe&rft.aufirst=J&rft.date=1989-01-01&rft.volume=97&rft.issue=1&rft.spage=59&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology&rft.issn=00333158&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-30 N1 - Date created - 1989-05-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of bone marrow dosimetry and toxic effect of high dose 131I-labeled monoclonal antibodies administered to man. AN - 78952634; 2715010 AB - 131I-labeled monoclonal antibodies were used in therapeutic trials in two potentially useful clinical situations: disseminated melanoma (intravenously administered Fab fragments; 21 patients) and disseminated peritoneal adenocarcinomatosis (intraperitoneal injection of IgG; 5 patients). Acute toxicity observed is consistent with mild bone marrow suppression of acute radiation syndrome and the observed toxicity is dose related in a manner that conforms to the expected human response to total body irradiation. For single doses of both i.p. administered and intravenously administered 131I-labeled anti-tumor antibodies, 100 rad to red marrow, calculated by the absorbed dose fraction method (MIRD), appeared to be a threshold below which significant acute toxicity was unlikely. JF - International journal of radiation applications and instrumentation. Part B, Nuclear medicine and biology AU - Larson, S M AU - Raubitschek, A AU - Reynolds, J C AU - Neumann, R D AU - Hellstrom, K E AU - Hellstrom, I AU - Colcher, D AU - Schlom, J AU - Glatstein, E AU - Carrasquillo, J A AD - Department of Nuclear Medicine, National Institutes of Health, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 153 EP - 158 VL - 16 IS - 2 SN - 0883-2897, 0883-2897 KW - Antibodies, Monoclonal KW - 0 KW - Iodine Radioisotopes KW - Index Medicus KW - Peritoneal Neoplasms -- secondary KW - Humans KW - Adenocarcinoma -- secondary KW - Melanoma -- radiotherapy KW - Peritoneal Neoplasms -- radiotherapy KW - Adenocarcinoma -- radiotherapy KW - Iodine Radioisotopes -- therapeutic use KW - Neoplasms -- radiotherapy KW - Bone Marrow -- radiation effects KW - Radiotherapy -- adverse effects KW - Antibodies, Monoclonal -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78952634?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+applications+and+instrumentation.+Part+B%2C+Nuclear+medicine+and+biology&rft.atitle=Comparison+of+bone+marrow+dosimetry+and+toxic+effect+of+high+dose+131I-labeled+monoclonal+antibodies+administered+to+man.&rft.au=Larson%2C+S+M%3BRaubitschek%2C+A%3BReynolds%2C+J+C%3BNeumann%2C+R+D%3BHellstrom%2C+K+E%3BHellstrom%2C+I%3BColcher%2C+D%3BSchlom%2C+J%3BGlatstein%2C+E%3BCarrasquillo%2C+J+A&rft.aulast=Larson&rft.aufirst=S&rft.date=1989-01-01&rft.volume=16&rft.issue=2&rft.spage=153&rft.isbn=&rft.btitle=&rft.title=International+journal+of+radiation+applications+and+instrumentation.+Part+B%2C+Nuclear+medicine+and+biology&rft.issn=08832897&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-12 N1 - Date created - 1989-06-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The pulmonary toxicity of nitrosoureas. AN - 78951113; 2654964 AB - Drug-induced pulmonary fibrosis in cancer chemotherapy has become a more serious problem as treatment regimens are refined, larger total doses of cytotoxic drugs are administered and patient prognosis improves. The nitrosoureas are a class of chemotherapeutic agents whose clinical use is severely limited by drug-induced toxicities. The myelosuppression caused by nitrosourea administration can be managed clinically; however, the development of irreversible pulmonary fibrosis is a more serious clinical problem. Studies are needed to identify biochemical markers for early lung injury so that the amount of pulmonary tissue damage can be assessed and monitored. Additionally, considerable research is needed to understand the mechanisms by which these agents produce lung injury, so that therapeutic regimens can be developed to minimize or prevent lung toxicity. In understanding the mechanisms of toxicity, potentially the pulmonary injury caused by nitrosourea administration can be altered without affecting the clinical antitumor activity of this class of compounds. In the future, knowledge on mechanisms of drug-induced pulmonary injury can be used in the development of antineoplastic agents which are more disease specific and less pulmonary toxic. JF - Pharmacology & therapeutics AU - Smith, A C AD - Toxicology Branch, National Cancer Institute, Bethesda, Maryland. Y1 - 1989 PY - 1989 DA - 1989 SP - 443 EP - 460 VL - 41 IS - 3 SN - 0163-7258, 0163-7258 KW - Nitrosourea Compounds KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Lung Diseases -- chemically induced KW - Nitrosourea Compounds -- toxicity KW - Lung Diseases -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78951113?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+pulmonary+toxicity+of+nitrosoureas.&rft.au=Smith%2C+A+C&rft.aulast=Smith&rft.aufirst=A&rft.date=1989-01-01&rft.volume=41&rft.issue=3&rft.spage=443&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 - 1989-06-22 N1 - Date created - 1989-06-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cloned helper and cytotoxic T lymphocytes as effector cells in adoptive immunotherapy of murine leukemia. AN - 78950818; 2524069 JF - Progress in clinical and biological research AU - Bookman, M A AU - Horak, E AU - de Graaf, P W AD - Medicine Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 141 EP - 149 VL - 288 SN - 0361-7742, 0361-7742 KW - Recombinant Proteins KW - 0 KW - Interferon-gamma KW - 82115-62-6 KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - Animals KW - Cyclophosphamide -- therapeutic use KW - Interferon-gamma -- therapeutic use KW - Combined Modality Therapy KW - Lymphocyte Depletion KW - Mice, Inbred C57BL KW - Mice KW - Clone Cells -- transplantation KW - Recombinant Proteins -- therapeutic use KW - Hypersensitivity, Delayed -- immunology KW - Clone Cells -- immunology KW - T-Lymphocytes, Cytotoxic -- transplantation KW - Leukemia, Experimental -- immunology KW - Immunization, Passive KW - T-Lymphocytes, Cytotoxic -- immunology KW - T-Lymphocytes, Helper-Inducer -- transplantation KW - T-Lymphocytes, Helper-Inducer -- immunology KW - Leukemia, Experimental -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78950818?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cloned+helper+and+cytotoxic+T+lymphocytes+as+effector+cells+in+adoptive+immunotherapy+of+murine+leukemia.&rft.au=Bookman%2C+M+A%3BHorak%2C+E%3Bde+Graaf%2C+P+W&rft.aulast=Bookman&rft.aufirst=M&rft.date=1989-01-01&rft.volume=288&rft.issue=&rft.spage=141&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 - 1989-06-20 N1 - Date created - 1989-06-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Smokeless tobacco: association with increased cancer risk. AN - 78947468; 2654650 AB - Smokeless tobacco (chewing tobacco and snuff) contains known carcinogens shown to increase the risk for oral cancer. The effect of snuff has been more fully documented than other forms of smokeless tobacco, although the carcinogenic potential of all such products is acknowledged. Risk increases with increasing length of exposure, with risks greatest for anatomic sites where the product has been held in contact the longest time. In some studies, other organs, such as the esophagus, larynx, and stomach, have been shown to be at increased risk for cancer from the use of smokeless tobacco, although at present the data are insufficient to substantiate fully a causal association. Numerous reports have shown an association between snuff use and leukoplakia, with less evidence at present linking chewing tobacco use with leukoplakia. The documented early onset of the smokeless tobacco habit and reports of increases in certain oral cancers among young men raise serious concerns of an impending oral cancer epidemic in this population. In addition, synergistic interactions with other oral cancer risk factors, e.g., smoking and alcohol, and a high rate for second primaries observed for these cancers add to the concern. Unless the tide of its use is stemmed, long-term use can be expected to produce an increase in oral cancers, and perhaps cancers of other sites, as youthful users mature and accumulate exposure to this carcinogenic agent. JF - NCI monographs : a publication of the National Cancer Institute AU - Mattson, M E AU - Winn, D M AD - Division of Cancer Prevention and Control, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 13 EP - 16 IS - 8 SN - 0893-2751, 0893-2751 KW - Carcinogens KW - 0 KW - Index Medicus KW - Leukoplakia, Oral -- etiology KW - Carcinoma, Squamous Cell -- etiology KW - Risk Factors KW - Humans KW - Mouth Neoplasms -- etiology KW - Carcinogens -- analysis KW - Plants, Toxic KW - Tobacco -- analysis KW - Tobacco, Smokeless -- analysis KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78947468?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NCI+monographs+%3A+a+publication+of+the+National+Cancer+Institute&rft.atitle=Smokeless+tobacco%3A+association+with+increased+cancer+risk.&rft.au=Mattson%2C+M+E%3BWinn%2C+D+M&rft.aulast=Mattson&rft.aufirst=M&rft.date=1989-01-01&rft.volume=&rft.issue=8&rft.spage=13&rft.isbn=&rft.btitle=&rft.title=NCI+monographs+%3A+a+publication+of+the+National+Cancer+Institute&rft.issn=08932751&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-12 N1 - Date created - 1989-06-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Legionnaires' disease in a patient with rheumatoid arthritis treated with cyclosporine. AN - 78943106; 2715999 AB - We report a patient with long-standing rheumatoid arthritis (RA) treated with cyclosporine A; she developed a flare of her arthritis and evidence of vasculitis, cavitary pulmonary disease, nephritis and hepatitis, and was found to have Legionella pneumophila serotype I infection. Cyclosporine is a relatively new and investigational therapy in RA. Thus, it is important that any unusual complications in patients with RA treated with cyclosporine should be documented. JF - The Journal of rheumatology AU - Pillemer, S R AU - Webb, D AU - Yocum, D E AD - National Institutes of Health, Bethesda, MD 20892. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 117 EP - 120 VL - 16 IS - 1 SN - 0315-162X, 0315-162X KW - Cyclosporins KW - 0 KW - Index Medicus KW - Humans KW - Middle Aged KW - Female KW - Cyclosporins -- adverse effects KW - Arthritis, Rheumatoid -- drug therapy KW - Opportunistic Infections -- etiology KW - Legionnaires' Disease -- etiology KW - Arthritis, Rheumatoid -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78943106?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Legionnaires%27+disease+in+a+patient+with+rheumatoid+arthritis+treated+with+cyclosporine.&rft.au=Pillemer%2C+S+R%3BWebb%2C+D%3BYocum%2C+D+E&rft.aulast=Pillemer&rft.aufirst=S&rft.date=1989-01-01&rft.volume=16&rft.issue=1&rft.spage=117&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 - 1989-06-14 N1 - Date created - 1989-06-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Rheumatol. 1990 Jan;17(1):120-1 [2313665] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Radiation-damaged tyrosinase molecules are inactive. AN - 78942590; 2495032 AB - Target analysis of radiation inactivation of mushroom tyrosinase yields different target sizes for diphenoloxidase and monophenoloxidase activities, which correspond to the subunits H and HL2 (or HL), respectively. After gel electrophoresis of irradiated samples, all diphenoloxidase activity is observed at the same position as seen in the original material. Radiolytic fragments contain no detectable activity, consistent with a fundamental assumption of target theory. JF - Biophysical journal AU - Kempner, E S AU - Miller, J H AD - Laboratory of Physical Biology, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 159 EP - 162 VL - 55 IS - 1 SN - 0006-3495, 0006-3495 KW - Macromolecular Substances KW - 0 KW - Catechol Oxidase KW - EC 1.10.3.1 KW - Monophenol Monooxygenase KW - EC 1.14.18.1 KW - Index Medicus KW - Kinetics KW - Freezing KW - Dose-Response Relationship, Radiation KW - Agaricus -- enzymology KW - Molecular Weight KW - Catechol Oxidase -- radiation effects KW - Monophenol Monooxygenase -- radiation effects KW - Monophenol Monooxygenase -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78942590?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Radiation-damaged+tyrosinase+molecules+are+inactive.&rft.au=Kempner%2C+E+S%3BMiller%2C+J+H&rft.aulast=Kempner&rft.aufirst=E&rft.date=1989-01-01&rft.volume=55&rft.issue=1&rft.spage=159&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 - 1989-05-19 N1 - Date created - 1989-05-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1983 Nov 11;222(4624):586-9 [6635656] J Biol Chem. 1983 Oct 10;258(19):11997-2001 [6225783] J Biol Chem. 1963 Jul;238:2351-7 [13972077] Biochemistry. 1987 Jun 16;26(12):3340-7 [3307904] J Biol Chem. 1986 Dec 25;261(36):16963-8 [3782149] Methods Enzymol. 1985;117:65-94 [4079816] J Biol Chem. 1985 Sep 5;260(19):10551-6 [4040909] J Biol Chem. 1985 Jul 25;260(15):8726-30 [2862141] Biochem J. 1983 Aug 1;213(2):405-15 [6225423] J Biol Chem. 1983 Jan 25;258(2):953-9 [6822516] J Biol Chem. 1982 Aug 10;257(15):8919-21 [6212584] Biochemistry. 1981 Nov 10;20(23):6589-94 [6458330] J Biol Chem. 1981 Aug 10;256(15):7727-9 [6267022] J Biol Chem. 1981 Jun 10;256(11):5851-6 [6263891] J Biol Chem. 1980 Jul 25;255(14):6826-31 [6771277] J Biol Chem. 1977 Nov 10;252(21):7685-9 [334767] Biochem Biophys Res Commun. 1976 May 17;70(2):519-24 [820338] Radiat Res. 1972 Jul;51(1):56-71 [4338808] J Biol Chem. 1984 Apr 25;259(8):4890-5 [6232271] Biochim Biophys Acta. 1984 Oct 3;776(2):288-98 [6089887] J Biol Chem. 1984 Nov 25;259(22):13791-9 [6094530] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Trends in mortality from coronary heart disease and stroke among U.S. veterans; 1954-1979. AN - 78942176; 2709082 AB - A cohort of nearly 300,000 insured veterans (Dorn Cohort), experienced a much greater percent decline in CHD death rate over the period, 1954-1979, than the population of the U.S., while for stroke, the percent decline in death rate was virtually the same as the U.S. For CHD, greater percent declines were noted over the study period for non-smokers compared to cigarette smokers, for professionals compared to non-professionals and for persons with high socioeconomic scores (SES) compared to those with low scores. In each group, younger persons experienced greater percent declines than older persons. For stroke, non-smokers experienced a somewhat greater percent decline in rate than smokers but this did not hold true for all age groups. Unlike CHD, professionals experienced a smaller percent decline in their stroke death rate than non-professionals, as did persons with high SES compared to those with low SES. The contradictory patterns observed for the two diseases with respect to occupation and SES suggest that the risk factors for stroke and coronary heart disease are not exactly the same. Throughout, the findings were much more convincing for CHD than for stroke. JF - Journal of clinical epidemiology AU - Rogot, E AU - Hrubec, Z AD - Social and Environmental Epidemiology Branch, National Heart, Lung, and Blood Institute, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 245 EP - 256 VL - 42 IS - 3 SN - 0895-4356, 0895-4356 KW - Index Medicus KW - United States KW - Socioeconomic Factors KW - Smoking -- mortality KW - Smoking -- trends KW - Aged, 80 and over KW - Humans KW - Aged KW - Middle Aged KW - Time Factors KW - Male KW - Female KW - Occupational Diseases -- mortality KW - Coronary Disease -- mortality KW - Veterans -- statistics & numerical data KW - Cerebrovascular Disorders -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78942176?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+epidemiology&rft.atitle=Trends+in+mortality+from+coronary+heart+disease+and+stroke+among+U.S.+veterans%3B+1954-1979.&rft.au=Rogot%2C+E%3BHrubec%2C+Z&rft.aulast=Rogot&rft.aufirst=E&rft.date=1989-01-01&rft.volume=42&rft.issue=3&rft.spage=245&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+epidemiology&rft.issn=08954356&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-07 N1 - Date created - 1989-06-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Benzodiazepines in the treatment of alcoholism. AN - 78937462; 2564689 AB - This chapter comprises three sections that cover the main aspects of benzodiazepines and alcohol: (1) the basic pharmacology of benzodiazepines; (2) use of benzodiazepines in the treatment of withdrawal; and (3) the use of benzodiazepines in treating alcoholics. The basic studies suggest that a major site of action of alcohol may be the GABA/benzodiazepine receptor complex and that compensatory alterations in this complex may underly withdrawal. In the section on alcohol withdrawal, interactions between the GABA/benzodiazepine receptor complex, sympathetic nervous system, and hypothalamic-pituitary-adrenal axis are discussed. Use of benzodiazepines in the treatment of the alcohol withdrawal syndrome are reviewed, including the possibility that the benzodiazepines may prevent withdrawal-induced "kindling." Lastly, we review indications for, and efficacy of, benzodiazepines in long-term treatment of patients with alcoholism. Benzodiazepines are not indicated for the treatment of alcoholism. Furthermore, they have very few indications in alcoholics and their dependency-producing potency has to be appreciated when they are used in patients with alcoholism. 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 - Nutt, D AU - Adinoff, B AU - Linnoila, M AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 283 EP - 313 VL - 7 SN - 0738-422X, 0738-422X KW - Anti-Anxiety Agents KW - 0 KW - Receptors, GABA-A KW - Benzodiazepines KW - 12794-10-4 KW - Index Medicus KW - Alcohol Withdrawal Delirium -- rehabilitation KW - Humans KW - Brain -- drug effects KW - Alcohol Drinking -- drug effects KW - Receptors, GABA-A -- drug effects KW - Alcoholism -- rehabilitation KW - Anti-Anxiety Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78937462?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Benzodiazepines+in+the+treatment+of+alcoholism.&rft.au=Nutt%2C+D%3BAdinoff%2C+B%3BLinnoila%2C+M&rft.aulast=Nutt&rft.aufirst=D&rft.date=1989-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-11 N1 - Date created - 1989-05-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - T cell activation via cell-surface antigens other than the CD3/T cell receptor complex. AN - 78932460; 2467458 JF - The Year in immunology AU - Yokoyama, W M AU - Shevach, E M AD - Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, Md. Y1 - 1989 PY - 1989 DA - 1989 SP - 110 EP - 146 VL - 4 SN - 0256-2308, 0256-2308 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, CD28 KW - Antigens, CD58 KW - Antigens, Differentiation, T-Lymphocyte KW - Antigens, Ly KW - Antigens, Surface KW - Antigens, Thy-1 KW - Lymphokines KW - Membrane Glycoproteins KW - Receptors, Antigen, T-Cell KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Antigens, Ly -- immunology KW - Humans KW - Receptors, Antigen, T-Cell -- immunology KW - Mice KW - Antigens, Surface -- genetics KW - Antigens, Surface -- immunology KW - Antibodies, Monoclonal -- immunology KW - Antigens, Ly -- genetics KW - Rosette Formation KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Lymphokines -- secretion KW - Membrane Glycoproteins -- immunology KW - Lymphocyte Activation -- drug effects KW - Antigens, Differentiation, T-Lymphocyte -- immunology KW - T-Lymphocytes -- secretion KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78932460?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Year+in+immunology&rft.atitle=T+cell+activation+via+cell-surface+antigens+other+than+the+CD3%2FT+cell+receptor+complex.&rft.au=Yokoyama%2C+W+M%3BShevach%2C+E+M&rft.aulast=Yokoyama&rft.aufirst=W&rft.date=1989-01-01&rft.volume=4&rft.issue=&rft.spage=110&rft.isbn=&rft.btitle=&rft.title=The+Year+in+immunology&rft.issn=02562308&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-10 N1 - Date created - 1989-05-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of nicotine administration following 12 h of tobacco deprivation: assessment on computerized performance tasks. AN - 78930207; 2496420 AB - The purpose of this study was to assess the effects of acute nicotine administration, following a 12-h cigarette deprivation period, using a computerized performance assessment battery (PAB). The PAB was comprised of five tasks which were selected to reflect a variety of complex acquired behaviors, sometimes referred to as "cognitive performance". Subjects were six healthy, male, cigarette smokers who practiced on the approximately 15 min PAB until their performance was stable across trials. In the training and baseline phase, subjects were tested following 5-30 min deprivation of cigarettes. Subjects were then tested following 12 h cigarette deprivation; 20 min before these sessions, subjects were given one piece of gum to chew. The gum contained 0, 2, or 4 mg nicotine, and it was chewed for 10 min at a rate of one chew every 2 s. There were two main findings: (1) when placebo (0 mg) gum was given, the time taken to complete the PAB tasks was significantly elevated above values obtained in the baseline condition; (2) compared to placebo, nicotine administration produced a dose-related decrease in the time taken to complete the tasks such that with either 2 or 4 mg, performance time was similar to that which occurred in the baseline cigarette smoking condition. Performance accuracy was not reliably affected by the experimental manipulations. These data indicate that the performance decrements observed in the placebo condition were specific to deprivation of nicotine following 12 h tobacco abstinence and are treatable using nicotine gum as a replacement formulation. JF - Psychopharmacology AU - Snyder, F R AU - Henningfield, J E AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1989 PY - 1989 DA - 1989 SP - 17 EP - 22 VL - 97 IS - 1 SN - 0033-3158, 0033-3158 KW - Nicotine KW - 6M3C89ZY6R KW - Carbon Monoxide KW - 7U1EE4V452 KW - Index Medicus KW - Reaction Time -- drug effects KW - Memory -- drug effects KW - Humans KW - Adult KW - Middle Aged KW - Carbon Monoxide -- metabolism KW - Male KW - Psychomotor Performance -- drug effects KW - Nicotine -- pharmacology KW - Substance Withdrawal Syndrome -- psychology KW - Smoking -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78930207?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=unknown&rft.jtitle=Film+Index+International&rft.atitle=TU+ES+PIERRE&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1959-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-30 N1 - Date created - 1989-05-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genetic characterization of the mei-41 locus in Drosophila melanogaster. AN - 78927114; 2496295 AB - The mutagen-sensitive mutant mus(1) 104D1 of Drosophila melanogaster maps to a position on the X chromosome very close to the meiotic mutant mei-41D5. Both mutants have been characterized as mutagen-sensitive and defective in post-replication repair. In the present report we show by complementation studies that mus(1) 104 and mus(1) 103 are allelic with mei-41. In addition, two reported alleles of mus(1) 104 lie between the mei-41 alleles A10 and D5. The size of the mei-41 locus is estimated to be about 0.1 centimorgans (cM). Because several alleles of mei-41 have been shown to reduce recombination and increase meiotic chromosome loss and nondisjunction, mus(1) 104D1 females were examined for defects in meiosis. Although there was no evidence for reduced recombination on the second chromosome in homozygous mus(1) 104D1 females, heterozygous mus(1) 104D1/mei-41D5 and mus(1) 104D1/deficiency females showed reduced levels of recombination. However, there was no evidence of an increase in nondisjunction in these females. JF - Molecular & general genetics : MGG AU - Mason, J M AU - Scobie, N N AU - Yamamoto, A H AD - Cellular and Genetic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 190 EP - 199 VL - 215 IS - 2 SN - 0026-8925, 0026-8925 KW - Methyl Methanesulfonate KW - AT5C31J09G KW - Index Medicus KW - Genotype KW - Animals KW - Alleles KW - X Chromosome KW - Recombination, Genetic KW - Genetic Complementation Test KW - Male KW - Female KW - Methyl Methanesulfonate -- pharmacology KW - Drosophila melanogaster -- genetics KW - Drosophila melanogaster -- drug effects KW - Mutation KW - Chromosome Mapping UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78927114?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+%26+general+genetics+%3A+MGG&rft.atitle=Genetic+characterization+of+the+mei-41+locus+in+Drosophila+melanogaster.&rft.au=Mason%2C+J+M%3BScobie%2C+N+N%3BYamamoto%2C+A+H&rft.aulast=Mason&rft.aufirst=J&rft.date=1989-01-01&rft.volume=215&rft.issue=2&rft.spage=190&rft.isbn=&rft.btitle=&rft.title=Molecular+%26+general+genetics+%3A+MGG&rft.issn=00268925&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-08 N1 - Date created - 1989-06-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Spontaneous germ line virus infection and retroviral insertional mutagenesis in eighteen transgenic Srev lines of mice. AN - 78924546; 2927391 AB - SWR/J-RF/J hybrid mice spontaneously acquire new germ line ecotropic proviruses at high frequency. In the studies described here, we used these hybrids to produce 18 transgenic mouse lines, each carrying a single newly acquired Srev locus (SWR/J-RF/J ecotropic proviral locus). All of the newly acquired proviruses identified in mosaic founder SWR/J-RF/J mice that could be transmitted through the germ line were also present in somatic tissues, demonstrating that viral integration occurred before the germ line was set aside from the somatic lineages. Quantitative analysis of proviral DNA copy numbers in somatic and germinal tissues of mosaic founder parents combined with structural analysis of Srev loci indicated that these proviruses are acquired after multiple rounds of somatic viral reinfection and that most of these viral integration events occurred after DNA replication in the zygote and before DNA replication in the four-cell embryo. The frequency of provirus acquisition in Srev lines that expressed the infectious ecotropic virus was similar to that in SWR.RF mice carrying Emv-16 and Emv-17, suggesting that the chromosomal integration site of the parental locus is not an important determinant for high-frequency provirus acquisition. The frequency of recessive lethal mutations induced by spontaneous viral integration was 5%, which was similar to that induced by preimplantation embryo infection. This approach represents a simple and viable strategy for inducing and studying mutations that affect mammalian development. JF - Molecular and cellular biology AU - Spence, S E AU - Gilbert, D J AU - Swing, D A AU - Copeland, N G AU - Jenkins, N A AD - Mammalian Genetics Laboratory, NCI-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 177 EP - 184 VL - 9 IS - 1 SN - 0270-7306, 0270-7306 KW - DNA, Recombinant KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Phenotype KW - Genotype KW - DNA -- isolation & purification KW - Animals KW - Gene Frequency KW - Cells, Cultured KW - Restriction Mapping KW - Recombination, Genetic KW - Proviruses -- genetics KW - Mice KW - Mice, Transgenic KW - Proviruses -- growth & development KW - Transfection KW - DNA, Recombinant -- analysis KW - Retroviridae -- genetics KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78924546?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=unknown&rft.jtitle=Film+Index+International&rft.atitle=CHRONIQUE+PROVINCIALE&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1959-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-01 N1 - Date created - 1989-05-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1976 Apr;73(4):1260-4 [1063407] Cell. 1980 Jan;19(1):181-8 [7357600] J Embryol Exp Morphol. 1979 Aug;52:141-52 [521746] J Virol. 1980 May;34(2):373-82 [7373714] Cell. 1981 May;24(2):519-29 [7237558] Nature. 1981 Oct 1;293(5831):370-4 [6268990] J Embryol Exp Morphol. 1981 Aug;64:133-47 [7310300] Nucleic Acids Res. 1982 Jan 22;10(2):577-92 [6278422] Proc Natl Acad Sci U S A. 1981 Dec;78(12):7609-13 [6950402] J Virol. 1982 Jul;43(1):26-36 [6287001] Cell. 1983 Jan;32(1):209-16 [6825169] J Virol. 1983 Apr;46(1):70-82 [6298471] J Embryol Exp Morphol. 1983 Apr;74:207-20 [6886595] Annu Rev Genet. 1983;17:315-44 [6320712] Cell. 1985 Dec;43(3 Pt 2):811-9 [3000616] Cell. 1986 Jul 4;46(1):19-29 [3013418] Nature. 1986 Oct 2-8;323(6087):445-8 [3762693] J Virol. 1986 Nov;60(2):693-701 [3773055] Mol Cell Biol. 1986 Dec;6(12):4387-95 [3796606] Virology. 1970 Dec;42(4):1136-9 [4099080] J Biol Chem. 1974 Jul 10;249(13):4086-93 [4137275] Virology. 1975 May;65(1):128-34 [167514] Proc Natl Acad Sci U S A. 1975 Oct;72(10):4008-12 [1060083] J Virol. 1987 Feb;61(2):336-43 [3027365] Virology. 1987 Apr;157(2):543-7 [3029987] Genes Dev. 1987 Jun;1(4):366-75 [2824282] J Virol. 1988 Feb;62(2):479-87 [2826810] Proc Natl Acad Sci U S A. 1988 Feb;85(4):1156-60 [2829217] Science. 1988 Mar 4;239(4844):1121-8 [2830671] J Virol. 1988 Aug;62(8):2817-22 [2839703] J Exp Zool. 1957 Mar;134(2):207-37 [13428952] J Virol. 1978 Jan;25(1):104-4 [202729] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Kids and cocaine--a treatment dilemma. AN - 78923137; 2709470 AB - Despite aggressive efforts to recruit into treatment cocaine users 21 years and younger, we obtained only 12 such clients over a period of 9 months, while recruiting 122 adult cocaine clients during a comparable time frame. An examination of admissions data for the city, state, and nation indicated that our experience was typical. However, data from the most recent national household survey indicate that, to the extent need for treatment is determined by frequency of cocaine use, we should anticipate a much greater proportion of admissions to treatment to come from persons 21 years of age and younger. Yet, there appears to be an under-recruitment of youth into treatment, particularly evidenced by low rates of self-referral for juvenile as compared to older treatment admissions. Younger cocaine users may be less severely impaired and/or dependent, or may be more reluctant to use the treatment resources available. Whatever the barriers are to getting help, it becomes the special task of agencies and individuals in the community to help assure that younger cocaine users will obtain the assistance they need. Four community resources are seen as particularly relevant: family, schools, the medical community, and public agencies in the areas of health, social services, and criminal justice. The capacity of each to take action and possible impediments to that action are discussed. JF - Journal of substance abuse treatment AU - Brown, B S AU - Rose, M R AU - Weddington, W W AU - Jaffe, J H AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland 21224. Y1 - 1989 PY - 1989 DA - 1989 SP - 3 EP - 8 VL - 6 IS - 1 SN - 0740-5472, 0740-5472 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - United States KW - Patient Compliance KW - Humans KW - Hotlines -- trends KW - Adolescent KW - Community Mental Health Services -- trends KW - Referral and Consultation -- trends KW - Substance-Related Disorders -- rehabilitation KW - Substance-Related Disorders -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78923137?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Kids+and+cocaine--a+treatment+dilemma.&rft.au=Brown%2C+B+S%3BRose%2C+M+R%3BWeddington%2C+W+W%3BJaffe%2C+J+H&rft.aulast=Brown&rft.aufirst=B&rft.date=1989-01-01&rft.volume=6&rft.issue=1&rft.spage=3&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 - 1989-06-06 N1 - Date created - 1989-06-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Combined effects of interferon alpha and interleukin 2 on the induction of a vascular leak syndrome in mice. AN - 78914828; 2495179 AB - Immunotherapy with interleukin 2 (IL-2) alone or in combination with lymphokine-activated killer cells can mediate tumor regression in mice and in man. Further dose escalation of IL-2 along with lymphokine-activated killer cells has been prevented by the development of a vascular leak syndrome produced by IL-2. Because we have found that interferon alpha (IFN-alpha) or tumor necrosis factor (TNF-alpha) has synergistic antitumor effects when administered together with IL-2, we have tested the vascular leakage induced by these lymphokine combinations. We used a murine model to quantify vascular leakage by measuring the extravasation of 125I-albumin from the intravascular space as well as the wet and dry lung weights after treatment with different cytokines. Cytokines (or Hanks balanced salt solution) were administered to C57BL/6 mice and 4 h after the last injection the vascular leak was quantified. IFN-alpha alone did not cause extravasation of radiolabel or increase in wet lung weights, though when given in combination with IL-2, significantly greater extravasation (P less than 0.01) as well as increase in lung water weights (P less than 0.05) was observed compared to the response in mice treated with IL-2 alone. IFN-alpha in combination with IL-2 induced significant vascular leakage earlier than the response induced by IL-2 alone. For example treatment with IFN-alpha and IL-2 induced accumulation of 14,674 +/- 605 cpm in the lungs at day 1 while IL-2 alone induced 12,340 +/- 251 cpm. The degree of vascular leakage was highly related to the dose of IFN-alpha administered along with IL-2 and increased vascular leak syndrome was evident even at low doses (5000 units) of IFN-alpha. Immunosuppression of mice by pretreatment irradiation (500 rad) markedly decreased the development of vascular leak syndrome induced by IL-2 and IFN-alpha. Interestingly IFN-gamma and TNF-alpha did not induce vascular leakage in the lungs when given alone, and did not add or synergize with IL-2 in causing the syndrome. Thus the administration of IFN-alpha in combination with IL-2 produces a dose-limiting vascular leakage that is more severe than that caused by IL-2 alone, and may be mediated, directly or indirectly by host radiosensitive cells. JF - Cancer immunology, immunotherapy : CII AU - Puri, R K AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 267 EP - 274 VL - 28 IS - 4 SN - 0340-7004, 0340-7004 KW - Interferon Type I KW - 0 KW - Interleukin-2 KW - Recombinant Proteins KW - Serum Albumin, Radio-Iodinated KW - Tumor Necrosis Factor-alpha KW - Interferon-gamma KW - 82115-62-6 KW - Index Medicus KW - Animals KW - Drug Administration Schedule KW - Tumor Necrosis Factor-alpha -- administration & dosage KW - Humans KW - Mice KW - Kinetics KW - Syndrome KW - Mice, Inbred C57BL KW - Interferon-gamma -- administration & dosage KW - Drug Synergism KW - Female KW - Lung Diseases -- etiology KW - Lung Diseases -- physiopathology KW - Interferon Type I -- toxicity KW - Capillary Permeability -- drug effects KW - Interleukin-2 -- toxicity KW - Capillary Permeability -- radiation effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78914828?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+immunology%2C+immunotherapy+%3A+CII&rft.atitle=Combined+effects+of+interferon+alpha+and+interleukin+2+on+the+induction+of+a+vascular+leak+syndrome+in+mice.&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1959-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-12 N1 - Date created - 1989-05-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Enhancement of 5-fluorouracil's anticancer activity by dipyridamole. AN - 78892107; 2646650 AB - Although the interaction between FUra and DP in HCT 116 cells is fairly complex, data from other investigators indicate that in cell lines in which inhibition of TS is growth limiting at relatively low concentrations of fluoropyrimidines, DP appears to augment the cytotoxicity of FUra and FdUrd by blocking the salvage of dThd (Miller et al., 1987; Schwartz et al., 1987). The previous in vitro data regarding the ability of DP to modulate the toxicity of fluoropyrimidines was obtained in exponentially growing cells. An additional observation that warrants consideration is a report that the inhibition of nucleoside incorporation by DP changed as a function of time in culture (Zhen et al., 1986). Hepatoma 3924A cells in lag and log phase were highly sensitive to DP with IC50 values for dThd incorporation of 0.2 and 0.32 microM, respectively. In contrast, stationary phase cells were insensitive to DP (IC50 = 38.9 microM). Amphotericin B, an antifungal agent which perturbs cell membranes, restored the sensitivity to DP in stationary cells. Several investigators have presented information on the effect of DP on fluoropyrimidines in normal tissues. Lee and Park (1987) examined the effect of DP on FUra and MTX toxicity in a soft-agar cloning assay against two human cancer cell lines and on pooled normal human bone marrow (CFU-C). DP (1 microM) potentiated the action of both MTX (0.1 microM) and FUra (5 microM) on Hep-2 (epidermoid carcinoma), MCF-7 (breast carcinoma) and CFU-C in medium supplemented with either non-dialyzed or dialyzed serum. Woodcock et al. (1987) incubated gallbladder mucosa, obtained from patients undergoing elective surgery for cholelithiasis, with control medium or varying concentrations of DP for 1 hr, and then exposed the mucosal cells to 2.5 microCi [3H]-FdUrd (2.5 microM). After 1 hr, the uptake of FdUrd into the tissue was inhibited to 49% and 42% of control by 0.1 microM and 1 microM, respectively. JF - Pharmacology & therapeutics AU - Grem, J L AU - Fischer, P H AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, Maryland. Y1 - 1989 PY - 1989 DA - 1989 SP - 349 EP - 371 VL - 40 IS - 3 SN - 0163-7258, 0163-7258 KW - Pyrimidine Nucleosides KW - 0 KW - Dipyridamole KW - 64ALC7F90C KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - Drug Screening Assays, Antitumor KW - Animals KW - Pyrimidine Nucleosides -- metabolism KW - Humans KW - Cell Line, Transformed KW - Drug Synergism KW - Biological Transport -- drug effects KW - Fluorouracil -- therapeutic use KW - Neoplasms -- drug therapy KW - Dipyridamole -- therapeutic use KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78892107?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Enhancement+of+5-fluorouracil%27s+anticancer+activity+by+dipyridamole.&rft.au=Grem%2C+J+L%3BFischer%2C+P+H&rft.aulast=Grem&rft.aufirst=J&rft.date=1989-01-01&rft.volume=40&rft.issue=3&rft.spage=349&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 - 1989-04-13 N1 - Date created - 1989-04-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Glutathione and lipid peroxide levels in rat liver following administration of methapyrilene and analogs. AN - 78891769; 2564814 AB - The possibility was examined that the induction of tumors in rat liver by feeding methapyrilene, which is not mutagenic, is related to effects on glutathione levels and lipid peroxidation. Fischer 344 rats were given single-dose and multiple-dose treatments with the anti-histamine methapyrilene (MP), which is carcinogenic in rats, and with two non-carcinogenic analogs, methafurylene (MF) and thenyldiamine (TD) and the effects on malonaldehyde (MDA) formation and glutathione (GSH) levels in the liver were investigated. After a single dose, MDA levels were increased at 6 h by MF and TD and at 24 h by MP. MDA levels returned to normal after 30 h with MP and MF, but not with TD. Levels of MDA (and other TBA-reactive products) after four daily treatments were most elevated by TD, less elevated by MP, and were lowered by MF. Forty-two hours following treatment with both MP and MF, MDA levels had returned to normal, but in TD-treated animals MDA remained high. GSH levels were highest after MF and MP, and remained high at 42 h, but TD induced only a small increase. There appears to be increased lipid peroxidation in the liver as a result of treatment of rats with MP, MF and TD. The greater response induced by TD, as well as the increased liver GSH levels after repeated administration of all three drugs indicate that lipid peroxidation in rat liver is not a particular effect related to the liver carcinogen methapyrilene. JF - Chemico-biological interactions AU - Hernandez, L AU - Lijinsky, W AD - NCI-Frederick Cancer Research Facility, MD 21701. Y1 - 1989 PY - 1989 DA - 1989 SP - 217 EP - 224 VL - 69 IS - 2-3 SN - 0009-2797, 0009-2797 KW - Aminopyridines KW - 0 KW - Histamine H1 Antagonists KW - Lipid Peroxides KW - Pyridines KW - Malondialdehyde KW - 4Y8F71G49Q KW - Methapyrilene KW - A01LX40298 KW - thenyldiamine KW - E4U52363JE KW - Glutathione KW - GAN16C9B8O KW - methafurylene KW - HU5BZT118T KW - Index Medicus KW - Rats KW - Malondialdehyde -- metabolism KW - Animals KW - Reference Values KW - Rats, Inbred F344 KW - Kinetics KW - Histamine H1 Antagonists -- pharmacology KW - Pyridines -- pharmacology KW - Male KW - Methapyrilene -- pharmacology KW - Liver -- drug effects KW - Glutathione -- metabolism KW - Lipid Peroxidation -- drug effects KW - Aminopyridines -- pharmacology KW - Liver -- metabolism KW - Lipid Peroxides -- metabolism KW - Methapyrilene -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78891769?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Glutathione+and+lipid+peroxide+levels+in+rat+liver+following+administration+of+methapyrilene+and+analogs.&rft.au=Hernandez%2C+L%3BLijinsky%2C+W&rft.aulast=Hernandez&rft.aufirst=L&rft.date=1989-01-01&rft.volume=69&rft.issue=2-3&rft.spage=217&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 - 1989-05-12 N1 - Date created - 1989-05-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Thermoregulatory effects of resiniferatoxin in the mouse: comparison with capsaicin. AN - 78885248; 2927241 AB - Resiniferatoxin, an extremely irritant diterpene present in several members of the genus Euphorbia, produced an 8 C decrease in the rectal temperature of mice with an effective dose in the range of 2-20 micrograms/kg. The structurally related natural product capsaicin produced a similar magnitude of fall in body temperature, albeit with 1000-fold lower potency. Tolerance to the hypothermic effects of both compounds readily developed and cross-tolerance between the compounds was observed. The extreme potency of resiniferatoxin should facilitate biochemical analysis of the mechanism of action of this class of compounds. JF - Life sciences AU - de Vries, D J AU - Blumberg, P M AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 711 EP - 715 VL - 44 IS - 11 SN - 0024-3205, 0024-3205 KW - Diterpenes KW - 0 KW - resiniferatoxin KW - A5O6P1UL4I KW - Capsaicin KW - S07O44R1ZM KW - Index Medicus KW - Drug Tolerance KW - Animals KW - Dose-Response Relationship, Drug KW - Mice KW - Female KW - Diterpenes -- pharmacology KW - Diterpenes -- administration & dosage KW - Body Temperature -- drug effects KW - Capsaicin -- administration & dosage KW - Capsaicin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78885248?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Thermoregulatory+effects+of+resiniferatoxin+in+the+mouse%3A+comparison+with+capsaicin.&rft.au=de+Vries%2C+D+J%3BBlumberg%2C+P+M&rft.aulast=de+Vries&rft.aufirst=D&rft.date=1989-01-01&rft.volume=44&rft.issue=11&rft.spage=711&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 - 1989-05-05 N1 - Date created - 1989-05-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hypersensitivity reactions to deoxycoformycin. AN - 78877891; 2784360 AB - Deoxycoformycin (dCF) is a promising new antineoplastic agent in the treatment of lymphoid malignancies, particularly hairy cell leukemia (HCL). Skin toxicity in the form of a maculopapular eruption has previously been reported but has not clearly been associated with idiosyncratic reactions. We present five cases of dCF-related hypersensitivity reactions in which additional systemic manifestations indicated an allergic etiology. The value of dCF in treating lymphoid neoplasms suggests that further study of the treatment of these reactions is indicated. JF - Cancer chemotherapy and pharmacology AU - O'Dwyer, P J AU - King, S A AU - Eisenhauer, E AU - Grem, J L AU - Hoth, D F AD - Investigational Drug Branch, National Cancer Institute Bethesda, MD. Y1 - 1989 PY - 1989 DA - 1989 SP - 173 EP - 175 VL - 23 IS - 3 SN - 0344-5704, 0344-5704 KW - Antineoplastic Agents KW - 0 KW - Ribonucleosides KW - Coformycin KW - 11033-22-0 KW - Pentostatin KW - 395575MZO7 KW - Allopurinol KW - 63CZ7GJN5I KW - Index Medicus KW - Skin -- drug effects KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Allopurinol -- adverse effects KW - Male KW - Female KW - Ribonucleosides -- adverse effects KW - Drug Hypersensitivity -- etiology KW - Coformycin -- adverse effects KW - Coformycin -- analogs & derivatives KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78877891?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Hypersensitivity+reactions+to+deoxycoformycin.&rft.au=O%27Dwyer%2C+P+J%3BKing%2C+S+A%3BEisenhauer%2C+E%3BGrem%2C+J+L%3BHoth%2C+D+F&rft.aulast=O%27Dwyer&rft.aufirst=P&rft.date=1989-01-01&rft.volume=23&rft.issue=3&rft.spage=173&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 - 1989-05-09 N1 - Date created - 1989-05-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Keratin expression in mouse epidermal tumors. AN - 78871635; 2465821 JF - Carcinogenesis; a comprehensive survey AU - Roop, D R AU - Mehrel, T AU - Krieg, T M AU - Nakazawa, H AU - Cheng, C K AU - Yuspa, S H AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 257 EP - 271 VL - 11 SN - 0147-4006, 0147-4006 KW - DNA Probes KW - 0 KW - Keratins KW - 68238-35-7 KW - Index Medicus KW - Animals KW - Precancerous Conditions -- genetics KW - Cell Differentiation KW - Mice KW - Skin Neoplasms -- genetics KW - Keratins -- genetics KW - Papilloma -- analysis KW - Skin Neoplasms -- chemically induced KW - Skin Neoplasms -- analysis KW - Carcinoma -- analysis KW - Keratins -- analysis KW - Papilloma -- genetics KW - Carcinoma -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78871635?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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%3B+a+comprehensive+survey&rft.atitle=Keratin+expression+in+mouse+epidermal+tumors.&rft.au=Roop%2C+D+R%3BMehrel%2C+T%3BKrieg%2C+T+M%3BNakazawa%2C+H%3BCheng%2C+C+K%3BYuspa%2C+S+H&rft.aulast=Roop&rft.aufirst=D&rft.date=1989-01-01&rft.volume=11&rft.issue=&rft.spage=257&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis%3B+a+comprehensive+survey&rft.issn=01474006&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-17 N1 - Date created - 1989-04-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Validity testing of commercial urine cocaine metabolite assays: II. Sensitivity, specificity, accuracy, and confirmation by gas chromatography/mass spectrometry. AN - 78867067; 2918287 AB - A comprehensive validity assessment study was performed on eight commercial urine assays for detection of cocaine use. Sensitivity, specificity, and accuracy of each assay were evaluated by analyzing, in random order and under blind conditions, specimens spiked with known drug concentrations and clinical specimens obtained from human subjects after intravenous cocaine use. Commercial assay results were compared with gas chromatography/mass spectrometry (GC/MS) assay of the same specimens for benzoylecgonine. All of the assays examined were determined to have utility in screening for cocaine use, with the exception of the KDI Quik Test, which was not a reliable test for detection of cocaine use. Major differences in sensitivity, specificity, and confirmation rate by GC/MS were noted among the assays, differences which should be taken into consideration when implementing a urine screening test for cocaine use or interpreting test results involving use of these assays. JF - Journal of forensic sciences AU - Cone, E J AU - Mitchell, J AD - Laboratory of Chemistry and Drug Metabolism, National Institute on Drug Abuse, Baltimore, MD. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 32 EP - 45 VL - 34 IS - 1 SN - 0022-1198, 0022-1198 KW - benzoylecgonine KW - 5353I8I6YS KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Injections, Intravenous KW - Humans KW - Adult KW - Male KW - Cocaine -- analogs & derivatives KW - Gas Chromatography-Mass Spectrometry KW - Substance-Related Disorders -- urine KW - Cocaine -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78867067?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+forensic+sciences&rft.atitle=Validity+testing+of+commercial+urine+cocaine+metabolite+assays%3A+II.+Sensitivity%2C+specificity%2C+accuracy%2C+and+confirmation+by+gas+chromatography%2Fmass+spectrometry.&rft.au=Cone%2C+E+J%3BMitchell%2C+J&rft.aulast=Cone&rft.aufirst=E&rft.date=1989-01-01&rft.volume=34&rft.issue=1&rft.spage=32&rft.isbn=&rft.btitle=&rft.title=Journal+of+forensic+sciences&rft.issn=00221198&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-24 N1 - Date created - 1989-03-24 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Forensic Sci. 1990 Mar;35(2):230-2 [2329327] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Validity testing of commercial urine cocaine metabolite assays: I. Assay detection times, individual excretion patterns, and kinetics after cocaine administration to humans. AN - 78863185; 2918277 AB - A validity study of eight commercial urine assays for detection of cocaine metabolite was performed on clinical specimens collected from human subjects who received single 20-mg intravenous doses of cocaine hydrochloride. The specimens were collected under controlled conditions and analyzed in random order under blind conditions. Benzoylecgonine concentration in each specimen also was determined by gas chromatography/mass spectrometry (GC/MS). Mean times of detection of the last positive specimen (greater than or equal to 300 ng/mL of benzoylecgonine equivalents) after cocaine administration varied among seven of the commercial tests from 16.9 to 52.9 h in the following ascending order: Toxi-Lab less than TDx = EMIT dau = EMIT st less than Abuscreen less than Coat-A-Count = Double Antibody. In contrast, a commercial spot test (KDI Quik Test) which was evaluated for detection of cocaine metabolite produced both false positives and false negatives for benzoylecgonine and was not considered to be a valid test for detection of cocaine metabolite. Half-lives of excretion of benzoylecgonine among four subjects varied from 5.9 to 7.9 h, and overall recovery of benzoylecgonine varied from 15.0 to 34.3% of the administered dose of cocaine. JF - Journal of forensic sciences AU - Cone, E J AU - Menchen, S L AU - Paul, B D AU - Mell, L D AU - Mitchell, J AD - Laboratory of Chemistry and Drug Metabolism, National Institute on Drug Abuse, Baltimore, MD. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 15 EP - 31 VL - 34 IS - 1 SN - 0022-1198, 0022-1198 KW - benzoylecgonine KW - 5353I8I6YS KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Injections, Intravenous KW - Humans KW - Adult KW - Gas Chromatography-Mass Spectrometry KW - Radioimmunoassay KW - Male KW - Cocaine -- analogs & derivatives KW - Substance-Related Disorders -- urine KW - Cocaine -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78863185?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=unknown&rft.jtitle=Film+Index+International&rft.atitle=La+BO%C3%8ETE+%C3%81+MUSIQUE&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1959-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-24 N1 - Date created - 1989-03-24 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Forensic Sci. 1990 Mar;35(2):230-2 [2329327] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hepatocellular carcinoma: possible etiologies in patients without serologic evidence of hepatitis B virus infection. AN - 78862621; 2537873 AB - Although hepatitis B virus (HBV) has been closely associated with the development of hepatocellular carcinoma (HCC), no serologic markers of HBV can be found in up to 11% of HCC patients in developing countries and up to 68% of HCC patients in industrialized countries. Despite the absence of HBV serologic markers in these HCC patients, HBV DNA sequences have been found to be integrated into HCC DNA in 13-100% of these patients, indicating a possible role of HBV in the etiology of their HCC. Although six patients with chronic non-A, non-B hepatitis virus infection who were followed have been documented to develop HCC, it is not known whether the non-A, non-B hepatitis viruses cause or contribute to the development of HCC in some HCC patients without HBV serologic markers. Ethanol, cigarette smoking, oral contraceptives, and aflatoxin also have been suggested as possible etiologies and should be studied further. Suggested etiologies that are not supported by the published data include alpha-1-antitrypsin deficiency and schistosomiasis. JF - Journal of medical virology AU - Tabor, E AD - Biological Carcinogenesis Program, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 1 EP - 6 VL - 27 IS - 1 SN - 0146-6615, 0146-6615 KW - Aflatoxins KW - 0 KW - Contraceptives, Oral KW - Aflatoxin B1 KW - 9N2N2Y55MH KW - Index Medicus KW - Contraceptives, Oral -- adverse effects KW - Hepatitis B -- complications KW - Hepatitis C -- complications KW - alpha 1-Antitrypsin Deficiency KW - Humans KW - Schistosomiasis -- complications KW - Smoking -- adverse effects KW - Alcoholism -- complications KW - Aflatoxins -- adverse effects KW - Carcinoma, Hepatocellular -- etiology KW - Liver Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78862621?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+medical+virology&rft.atitle=Hepatocellular+carcinoma%3A+possible+etiologies+in+patients+without+serologic+evidence+of+hepatitis+B+virus+infection.&rft.au=Tabor%2C+E&rft.aulast=Tabor&rft.aufirst=E&rft.date=1989-01-01&rft.volume=27&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Journal+of+medical+virology&rft.issn=01466615&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-13 N1 - Date created - 1989-04-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immune response to intraocular injection of retinal S-antigen in adjuvant. AN - 78862391; 2784119 AB - It has been proposed that the introduction of foreign material into the eye at the moment of a penetrating trauma provides an adjuvant effect which, coupled with the release of antigen, might be responsible for sensitizing the immune system to produce a contralateral "sympathetic ophthalmia." We addressed that hypothesis by injecting S-antigen with complete Freund's adjuvant (CFA) into the anterior chamber (AC) of the eye of Lewis rats. The injection of an identical dose of antigen (30 micrograms S-Ag in CFA in a total volume of 10 microliters) via the foodpad (FP) or under the conjunctiva (SC) could induce typical experimental autoimmune uveitis (EAU). By immunizing via the AC route, we could demonstrate a positive sensitization of the immune system, manifested by serum antibody production against S-Ag and by the presence of S-Ag-specific, responsive T-lymphocytes in the spleen. However, immunization via the AC route did not induce contralateral uveitis, and the animals did not produce a DTH skin response when challenged intradermally with S-Ag as they did after FP immunization. In the light of these results, we evaluated the possibility that a DTH suppressive response was elicited by intracameral (IC) injection as seen in anterior chamber-associated immune deviation (ACAID): we tested the effect of splenectomy and cyclophosphamide pretreatment before IC immunization and the effect of secondary footpad immunization as well as T-helper cell transfer after IC immunization. The results given by these approaches argue against the induction of suppressor cells by IC immunization.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie AU - Roberge, F G AU - de Kozak, Y AU - Utsumi, T AU - Faure, J P AU - Nussenblatt, R B AD - National Eye Institute, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 67 EP - 71 VL - 227 IS - 1 SN - 0721-832X, 0721-832X KW - Antigens KW - 0 KW - Arrestin KW - Eye Proteins KW - Cyclophosphamide KW - 8N3DW7272P KW - Freund's Adjuvant KW - 9007-81-2 KW - Index Medicus KW - Animals KW - Rats, Inbred Lew KW - Splenectomy KW - Retina KW - Skin Tests KW - Antibody Formation KW - Immune Tolerance KW - Lymphocyte Activation KW - Rats KW - Immunization, Passive KW - Injections KW - Female KW - Anterior Chamber KW - Cyclophosphamide -- pharmacology KW - Eye Proteins -- immunology KW - Uveitis -- immunology KW - Uveitis -- etiology KW - Antigens -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78862391?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Graefe%27s+archive+for+clinical+and+experimental+ophthalmology+%3D+Albrecht+von+Graefes+Archiv+fur+klinische+und+experimentelle+Ophthalmologie&rft.atitle=Immune+response+to+intraocular+injection+of+retinal+S-antigen+in+adjuvant.&rft.au=Roberge%2C+F+G%3Bde+Kozak%2C+Y%3BUtsumi%2C+T%3BFaure%2C+J+P%3BNussenblatt%2C+R+B&rft.aulast=Roberge&rft.aufirst=F&rft.date=1989-01-01&rft.volume=227&rft.issue=1&rft.spage=67&rft.isbn=&rft.btitle=&rft.title=Graefe%27s+archive+for+clinical+and+experimental+ophthalmology+%3D+Albrecht+von+Graefes+Archiv+fur+klinische+und+experimentelle+Ophthalmologie&rft.issn=0721832X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-18 N1 - Date created - 1989-04-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Incorporation of tritiated thymidine by epithelial and interstitial cells in bronchiolar-alveolar regions of asbestos-exposed rats. AN - 78850143; 2913821 AB - Inhaled asbestos causes progressive interstitial lung disease. The authors have performed a series of studies to elucidate early pathogenetic events at sites of fiber deposition in asbestos-exposed rats. This study reports that a single 5-hour exposure to chrysotile asbestos induces significant increases in incorporation of tritiated thymidine (3HTdR) into nuclei of epithelial and interstitial cells of bronchiolar-alveolar regions. No cell populations in air-exposed or carbonyl iron-exposed control animals exhibited more than 1% labeling at any point in time. Immediately after the 5-hour asbestos exposure, incorporation was normal. By 19 hours after exposure there was a significant increase in incorporation of 3HTdR, particularly by Type II epithelial cells of the first alveolar duct bifurcations. The greatest increase in degree of incorporation (up to 18-fold) was observed 24 hours after exposure, and increased percentages of 3HTdR-labeled cells were maintained through the 48 hours postexposure period. Normal labeling was present by 8 days after exposure, and this level remained through the 1-month period studied. This apparent mitogenic response correlates with increased numbers of bronchiolar-alveolar epithelial and interstitial cells demonstrated by ultrastructural morphometry in correlative studies. The authors speculate that the incorporation of 3HTdR could be induced by the direct effects of inhaled fibers or by mitogenic factors released from macrophages attracted to the inhaled asbestos. JF - The American journal of pathology AU - Brody, A R AU - Overby, L H AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 133 EP - 140 VL - 134 IS - 1 SN - 0002-9440, 0002-9440 KW - Tritium KW - 10028-17-8 KW - Asbestos KW - 1332-21-4 KW - Iron KW - E1UOL152H7 KW - Thymidine KW - VC2W18DGKR KW - Abridged Index Medicus KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Iron -- pharmacology KW - Epithelium -- metabolism KW - Epithelium -- pathology KW - Time Factors KW - Male KW - Thymidine -- metabolism KW - Pulmonary Alveoli -- pathology KW - Pulmonary Alveoli -- metabolism KW - Pulmonary Alveoli -- drug effects KW - Asbestos -- pharmacology KW - Bronchi -- metabolism KW - Bronchi -- drug effects KW - Bronchi -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78850143?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Incorporation+of+tritiated+thymidine+by+epithelial+and+interstitial+cells+in+bronchiolar-alveolar+regions+of+asbestos-exposed+rats.&rft.au=Brody%2C+A+R%3BOverby%2C+L+H&rft.aulast=Brody&rft.aufirst=A&rft.date=1989-01-01&rft.volume=134&rft.issue=1&rft.spage=133&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 - 1989-03-06 N1 - Date created - 1989-03-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Pathol. 1984 Dec;117(3):484-98 [6095671] Environ Res. 1975 Oct;10(2):196-207 [1193032] Lab Invest. 1985 May;52(5):505-14 [3990243] Am Rev Respir Dis. 1985 Dec;132(6):1246-52 [4073665] Am J Pathol. 1986 Feb;122(2):261-7 [3004226] Am Rev Respir Dis. 1986 Jun;133(6):1055-9 [3087250] Cell. 1986 Jul 18;46(2):155-69 [3013421] Exp Mol Pathol. 1986 Jun;44(3):344-52 [3720923] Am Rev Respir Dis. 1986 Jul;134(1):128-33 [3729150] J Leukoc Biol. 1986 Oct;40(4):347-54 [3462284] Am Rev Respir Dis. 1987 Jan;135(1):78-82 [2948433] Lab Invest. 1987 Aug;57(2):219-29 [3613528] Proc Natl Acad Sci U S A. 1987 Sep;84(17):6020-4 [2888109] Cancer Res. 1988 Feb 1;48(3):709-14 [3335033] Exp Lung Res. 1988;14(1):51-66 [2830106] FASEB J. 1988 Apr;2(7):2272-7 [3280379] Cell. 1988 Apr 22;53(2):285-93 [3258795] Am Rev Respir Dis. 1969 Sep;100(3):372-8 [5810808] Exp Mol Pathol. 1975 Feb;22(1):142-50 [163758] Lab Invest. 1978 Jun;38(6):648-53 [661220] Br J Ind Med. 1980 Nov;37(4):337-62 [7004477] Int Rev Exp Pathol. 1980;22:131-91 [7005143] Am Rev Respir Dis. 1981 Jun;123(6):670-9 [6267971] J Clin Invest. 1982 Oct;70(4):806-22 [7119116] Am J Pathol. 1982 Oct;109(1):107-14 [7124904] Am Rev Respir Dis. 1982 Oct;126(4):708-11 [7125365] Am Rev Respir Dis. 1983 Oct;128(4):724-9 [6625350] Am Rev Respir Dis. 1984 Feb;129(2):301-10 [6696328] Rev Infect Dis. 1984 Jan-Feb;6(1):51-95 [6369481] J Toxicol Environ Health. 1984;13(2-3):301-21 [6737514] Br J Cancer. 1974 Mar;29(3):252-69 [4364384] Am J Pathol. 1973 Feb;70(2):199-208 [4566991] Exp Lung Res. 1984;7(2):133-47 [6098439] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vitro studies of the inhibition of protein kinase C from rat brain by di-(2-ethylhexyl)phthalate. AN - 78847679; 2914331 AB - The environmental contaminant di(2-ethylhexyl)phthalate (DEHP) has been shown to inhibit the phosphorylation of histone by purified protein kinase C (PK-C) from rat brain in a concentration-dependent manner. The inhibition does not involve making the substrate unavailable, although DEHP does bind to some extent to histone. DEHP displaces phorbol dibutyrate from PK-C, indicating that DEHP binds to the regulatory domain of the enzyme. Since DEHP does not affect the PK-C dependent phosphorylation of protamine, DEHP probably does not bind at the catalytic site. DEHP non-competitively blocked activation of PK-C by either phosphatidyl serine or calcium ion. Inhibition of histone phosphorylation by DEHP was enhanced if diglyceride was present, and the enhancement was stereoselective for the isomeric form of the diglyceride. The mechanism of the inhibition is thought to involve interference with the interaction between calcium ion and the regulatory domain of PK-C, and would have significance only for those PK-C substrates that require calcium activation of the enzyme. Thus the presence of DEHP in the high nanomolar concentration range alters the effective substrate specificity of PK-C. JF - Chemico-biological interactions AU - Shukla, R R AU - Albro, P W AU - Corbett, J T AU - Schroeder, J L AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1989 PY - 1989 DA - 1989 SP - 73 EP - 85 VL - 69 IS - 1 SN - 0009-2797, 0009-2797 KW - Phosphatidylserines KW - 0 KW - Phthalic Acids KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Diethylhexyl Phthalate KW - C42K0PH13C KW - Protein Kinase C KW - EC 2.7.11.13 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats KW - Brain -- enzymology KW - Animals KW - Phosphatidylserines -- pharmacology KW - Kinetics KW - In Vitro Techniques KW - Enzyme Activation -- drug effects KW - Calcium -- pharmacology KW - Substrate Specificity KW - Female KW - Phorbol 12,13-Dibutyrate -- pharmacology KW - Protein Kinase C -- antagonists & inhibitors KW - Phthalic Acids -- pharmacology KW - Diethylhexyl Phthalate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78847679?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=In+vitro+studies+of+the+inhibition+of+protein+kinase+C+from+rat+brain+by+di-%282-ethylhexyl%29phthalate.&rft.au=Shukla%2C+R+R%3BAlbro%2C+P+W%3BCorbett%2C+J+T%3BSchroeder%2C+J+L&rft.aulast=Shukla&rft.aufirst=R&rft.date=1989-01-01&rft.volume=69&rft.issue=1&rft.spage=73&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 - 1989-03-14 N1 - Date created - 1989-03-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparative dermal absorption of 2,3,7,8-tetrachlorodibenzo-p-dioxin and three polychlorinated dibenzofurans. AN - 78845913; 2916232 AB - Polychlorinated dibenzodioxins (PCDDs) and dibenzofurans (PCDFs) are toxic environmental contaminants which have the potential to accumulate in human tissues. In order to examine the potential for systemic exposure following dermal exposure, the absorption, distribution, and elimination of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 2,3,7,8-tetrachlorodibenzofuran (TCDF), 1,2,3,7,8-pentachlorodibenzofuran (1PeCDF), and 2,3,4,7,8-pentachlorodibenzofuran (4PeCDF) were evaluated in male F344 rats. TCDD (0.00015, 0.001, 0.01, 0.1, 0.5, and 1.0 mumol/kg) and the three PCDFs (0.1, 0.5, and 1.0 mumol/kg) were applied to a preclipped region on the back of the rat and covered with a perforated cap. The rats were held in individual metabolism cages for 3 days. In animals administered 0.1 mumol/kg, the absorption of TCDF was greater than that of 4PeCDF, 1PeCDF, and TCDD. Relative absorption (percentage of administered dose) declined with increasing dose while the absolute absorption (microgram/kg) increased nonlinearly with dose. Absorption of TCDF at 0.1 mumol/kg was 48% of the administered dose which was significantly greater than that of the other compounds. At this dose, absorption of 4PeCDF was greater than that of TCDD. Absorption at the higher doses was similar for all four compounds. Maximum relative absorption of TCDD (approximately 40% of the administered dose) was obtained at 0.001 and 0.00015 mumol/kg. Major tissue depots for these four chemicals included liver, adipose, skin, and muscle tissue; however, the liver:fat ratio for 4PeCDF was approximately fourfold higher than that for the other three compounds. When normalized to 100% of dose absorbed, the distribution of 4PeCDF-derived radioactivity in liver and adipose tissue was similar to that previously observed after oral and iv administration. In animals administered 0.1 mumol TCDF or 1PeCDF/kg, 56 and 32% of the respective absorbed dose was excreted as polar metabolites within 3 days. Very little of the absorbed dose of either TCDD (approximately 10%) or 4PeCDF (approximately 2%) was eliminated. Results indicate that the dermal absorption of these compounds is incomplete and that systemic toxicity following acute dermal exposure to levels found in the environment is unlikely. JF - Toxicology and applied pharmacology AU - Brewster, D W AU - Banks, Y B AU - Clark, A M AU - Birnbaum, L S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Triangle Park, North Carolina 27709. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 156 EP - 166 VL - 97 IS - 1 SN - 0041-008X, 0041-008X KW - Benzofurans KW - 0 KW - Dioxins KW - Environmental Pollutants KW - Industrial Waste KW - Polychlorinated Dibenzodioxins KW - Polymers KW - polychlorodibenzofuran KW - 1,2,3,7,8-pentachlorodibenzofuran KW - QNE7ZLB7SS KW - 2,3,4,7,8-pentachlorodibenzofuran KW - U4C2RV3124 KW - 2,3,7,8-tetrachlorodibenzofuran KW - XZJ41GQI5D KW - Index Medicus KW - Rats KW - Feces -- analysis KW - Animals KW - Rats, Inbred F344 KW - Administration, Cutaneous KW - Dose-Response Relationship, Drug KW - Industrial Waste -- analysis KW - Tissue Distribution KW - Male KW - Dioxins -- pharmacokinetics KW - Polychlorinated Dibenzodioxins -- analysis KW - Polychlorinated Dibenzodioxins -- pharmacokinetics KW - Skin Absorption KW - Benzofurans -- pharmacokinetics KW - Environmental Pollutants -- analysis KW - Benzofurans -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78845913?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparative+dermal+absorption+of+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin+and+three+polychlorinated+dibenzofurans.&rft.au=Brewster%2C+D+W%3BBanks%2C+Y+B%3BClark%2C+A+M%3BBirnbaum%2C+L+S&rft.aulast=Brewster&rft.aufirst=D&rft.date=1989-01-01&rft.volume=97&rft.issue=1&rft.spage=156&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 - 1989-03-23 N1 - Date created - 1989-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Attenuation of ethanol intoxication by alpha-2 adrenoceptor antagonists. AN - 78844370; 2563566 AB - The interaction of a highly potent and selective alpha-2 adrenoceptor antagonist, atipamezole with ethanol was investigated in tests assessing a number of ethanol's behavioral effects. Atipamezole antagonized ethanol's effects on directed exploration in a holeboard test, reduced observer-rated intoxication and also reduced the duration of loss of righting reflex caused by ethanol. Similar effects were produced by another alpha-2 adrenoceptor antagonist idazoxan. The magnitude of the effects was comparable to that produced in the same animal models by the imidazodiazepine Ro 15-4513, which antagonizes ethanol by an action at central benzodiazepine receptors. Whereas Ro 15-4513 possesses marked behavioral effects on its own, atipamezole is comparatively inactive in all paradigms so far tested. The data suggest that alpha-2 adrenoceptors can play an important role in modulating the intoxicating effects of ethanol. JF - Life sciences AU - Lister, R G AU - Durcan, M J AU - Nutt, D J AU - Linnoila, M AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 111 EP - 119 VL - 44 IS - 2 SN - 0024-3205, 0024-3205 KW - Adrenergic alpha-Antagonists KW - 0 KW - Azides KW - Dioxanes KW - Imidazoles KW - Receptors, GABA-A KW - atipamezole KW - 03N9U5JAF6 KW - Benzodiazepines KW - 12794-10-4 KW - Ethanol KW - 3K9958V90M KW - Ro 15-4513 KW - 91917-65-6 KW - Idazoxan KW - Y310PA316B KW - Index Medicus KW - Behavior, Animal -- drug effects KW - Animals KW - Azides -- pharmacology KW - Receptors, GABA-A -- metabolism KW - Seizures -- metabolism KW - Mice KW - Dioxanes -- pharmacology KW - Benzodiazepines -- pharmacology KW - Imidazoles -- pharmacology KW - Ethanol -- antagonists & inhibitors KW - Alcoholic Intoxication -- metabolism KW - Adrenergic alpha-Antagonists -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78844370?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Attenuation+of+ethanol+intoxication+by+alpha-2+adrenoceptor+antagonists.&rft.au=Lister%2C+R+G%3BDurcan%2C+M+J%3BNutt%2C+D+J%3BLinnoila%2C+M&rft.aulast=Lister&rft.aufirst=R&rft.date=1989-01-01&rft.volume=44&rft.issue=2&rft.spage=111&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 - 1989-03-15 N1 - Date created - 1989-03-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hematopoietic effects in mice exposed to arsine gas. AN - 78842618; 2916234 AB - Arsine gas is a potent hemolytic agent. Concern about semiconductor workers prompted an in-depth study of arsine at the National Institute of Environmental Health Sciences to determine the hematopoietic effects of prolonged exposure to this gas. Female B6C3F1 mice were exposed by inhalation to 0, 0.5, 2.5, and 5 ppm arsine, 6 hr/day for 14 days. Body weights of exposed mice were comparable to those of controls, but a marked, concentration-related splenomegaly was observed. Higher level arsine exposure produced statistically significant decreases in red blood cells, hematocrit and hemoglobin, with increases in white blood cell counts and mean corpuscular volume of red blood cells. Erythropoiesis as measured by quantitation of erythroid precursors in culture revealed a marrow reduction of colony-forming unit erythroids/femur cells for all treated groups on Day 3 postexposure and only at the 5 ppm dose group on 24 days postexposure, while splenic erythropoiesis increased at higher concentrations of arsine. There was no alteration in bone marrow cellularity and a less significant effect on granulocyte-macrophage progenitors. A 12-week study of arsine at 0, 0.025, 0.5, and 2.5 ppm (6 hr/day) by inhalation showed similar effects on hematopoiesis in mice. In conclusion, arsine exposure at low concentrations produces a stress on the hematopoietic system characterized by hemolysis, which persists for a prolonged period following exposure. JF - Toxicology and applied pharmacology AU - Hong, H L AU - Fowler, B A AU - Boorman, G A AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 173 EP - 182 VL - 97 IS - 1 SN - 0041-008X, 0041-008X KW - Arsenicals KW - 0 KW - Arsenic KW - N712M78A8G KW - arsine KW - V1I29R0RJQ KW - Index Medicus KW - Hematologic Tests KW - Animals KW - Hematopoiesis -- drug effects KW - Dose-Response Relationship, Drug KW - Body Weight -- drug effects KW - Mice KW - Colony-Forming Units Assay KW - Bone Marrow -- drug effects KW - Female KW - Organ Size -- drug effects KW - Hematopoietic Stem Cells -- pathology KW - Arsenic -- toxicity KW - Spleen -- pathology KW - Spleen -- drug effects KW - Hematopoietic Stem Cells -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78842618?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Hematopoietic+effects+in+mice+exposed+to+arsine+gas.&rft.au=Hong%2C+H+L%3BFowler%2C+B+A%3BBoorman%2C+G+A&rft.aulast=Hong&rft.aufirst=H&rft.date=1989-01-01&rft.volume=97&rft.issue=1&rft.spage=173&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 - 1989-03-23 N1 - Date created - 1989-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of serum, transforming growth factor type beta, or 12-O-tetradecanoyl-phorbol-13-acetate on ionized cytosolic calcium concentration in normal and transformed human bronchial epithelial cells. AN - 78837607; 2908852 AB - Fluctuations in ionized cytosolic calcium ([Ca2+]i) are considered important signals for induction of growth or differentiation in mammalian cells. The resting concentrations of [Ca2+]i in normal and adenovirus 12-SV40 hybrid virus-transformed (BEAS-2B) human bronchial epithelial cells were 63 +/- 15 nM (SD) and 44 +/- 15 nM, respectively. Eight % calcium-free fetal bovine serum rapidly caused a significant increase in [Ca2+]i, while causing both cell types to undergo squamous differentiation. When treated with 8% calcium-free fetal bovine serum, a serum-sensitive subclone of BEAS-2B cells exhibited a higher elevation of [Ca2+]i than a serum-resistant (i.e., not stimulated to differentiate by serum) subclone. However, a serum component involved in the induction of squamous differentiation, transforming growth factor type beta, did not increase [Ca2+]i in either normal cells or BEAS-2B cells. 12-O-Tetradecanoyl-phorbol-13-acetate, an exogenous inducer of squamous differentiation and activator of protein kinase C, did not increase [Ca2+]i, but did attenuate serum-induced elevation of [Ca2+]i. These results suggest that while an increase in [Ca2+]i is associated with serum-induced squamous differentiation, a cytosolic ionized calcium signal is not required for the initiation of the squamous differentiation pathway induced by either transforming growth factor type beta or 12-O-tetradecanoylphorbol-13-acetate. JF - Cancer research AU - Miyashita, M AU - Smith, M W AU - Willey, J C AU - Lechner, J F AU - Trump, B F AU - Harris, C C AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/01/01/ PY - 1989 DA - 1989 Jan 01 SP - 63 EP - 67 VL - 49 IS - 1 SN - 0008-5472, 0008-5472 KW - Transforming Growth Factors KW - 76057-06-2 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Epithelium -- analysis KW - Cytosol -- analysis KW - Humans KW - Protein Kinase C -- physiology KW - Cell Differentiation -- drug effects KW - Calcium -- analysis KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Transforming Growth Factors -- pharmacology KW - Bronchi -- drug effects KW - Bronchi -- analysis KW - Blood Physiological Phenomena UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78837607?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+serum%2C+transforming+growth+factor+type+beta%2C+or+12-O-tetradecanoyl-phorbol-13-acetate+on+ionized+cytosolic+calcium+concentration+in+normal+and+transformed+human+bronchial+epithelial+cells.&rft.au=Miyashita%2C+M%3BSmith%2C+M+W%3BWilley%2C+J+C%3BLechner%2C+J+F%3BTrump%2C+B+F%3BHarris%2C+C+C&rft.aulast=Miyashita&rft.aufirst=M&rft.date=1989-01-01&rft.volume=49&rft.issue=1&rft.spage=63&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 - 1989-01-25 N1 - Date created - 1989-01-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Clomipramine in obsessive-compulsive disorder. Further evidence for a serotonergic mechanism of action. AN - 78837206; 2910220 AB - Data from several previous studies link clomipramine's potent serotonergic effects to its clinical efficacy in reducing the symptoms of obsessive-compulsive disorder (OCD). To investigate this relationship further, we administered the serotonin (5-HT) receptor antagonist, metergoline, and placebo to ten patients with OCD in a crossover study carried out under double-blind, random-assignment conditions. In a previous study of untreated patients with OCD, we found no differences in the behavioral response to single-dose administration of metergoline or placebo. In the present study, patients with OCD receiving clomipramine hydrochloride on a long-term basis (with an average 40% lessening in OC symptoms) responded to a four-day period of administration of metergoline with significantly greater self- and observer-rated anxiety compared with the four-day placebo period. Obsessive-compulsive symptoms also tended to be greater during the metergoline phase, with significant drug-time interactions for both OC symptoms and anxiety peaking on day 4 of the metergoline phase. As anticipated, metergoline lowered plasma prolactin concentrations (providing evidence of physiologically significant 5-HT antagonism) but did not alter plasma clomipramine concentrations. These data further support the hypothesis that clomipramine's therapeutic behavioral effects in OCD are mediated via serotonergic mechanisms. JF - Archives of general psychiatry AU - Benkelfat, C AU - Murphy, D L AU - Zohar, J AU - Hill, J L AU - Grover, G AU - Insel, T R AD - Section on Clinical Neuropharmacology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 23 EP - 28 VL - 46 IS - 1 SN - 0003-990X, 0003-990X KW - Receptors, Serotonin KW - 0 KW - Serotonin Antagonists KW - Metergoline KW - 1501393LY5 KW - Serotonin KW - 333DO1RDJY KW - Clomipramine KW - NUV44L116D KW - Abridged Index Medicus KW - Index Medicus KW - Receptors, Serotonin -- drug effects KW - Metergoline -- pharmacology KW - Drug Interactions KW - Affect -- drug effects KW - Dose-Response Relationship, Drug KW - Humans KW - Adult KW - Middle Aged KW - Time Factors KW - Male KW - Female KW - Obsessive-Compulsive Disorder -- blood KW - Obsessive-Compulsive Disorder -- physiopathology KW - Serotonin -- physiology KW - Obsessive-Compulsive Disorder -- drug therapy KW - Clomipramine -- pharmacology KW - Clomipramine -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78837206?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Clomipramine+in+obsessive-compulsive+disorder.+Further+evidence+for+a+serotonergic+mechanism+of+action.&rft.au=Benkelfat%2C+C%3BMurphy%2C+D+L%3BZohar%2C+J%3BHill%2C+J+L%3BGrover%2C+G%3BInsel%2C+T+R&rft.aulast=Benkelfat&rft.aufirst=C&rft.date=1989-01-01&rft.volume=46&rft.issue=1&rft.spage=23&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 - 1989-01-30 N1 - Date created - 1989-01-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human anti-endoplasmic reticulum antibodies in sera of patients with halothane-induced hepatitis are directed against a trifluoroacetylated carboxylesterase. AN - 78836362; 2911577 AB - Previous studies have demonstrated that patients with halothane-induced hepatitis have serum antibodies that are directed against novel liver microsomal neoantigens and have suggested that these neoantigens may play an immunopathological role in development of the patients' liver damage. These investigations have further revealed that the antibodies are directed against distinct polypeptide fractions (100 kDa, 76 kDa, 59 kDa, 57 kDa, 54 kDa) that have been covalently modified by the reactive trifluoroacetyl halide metabolite of halothane. In this paper, the trifluoroacetylated (TFA) 59-kDa neoantigen (59-kDa-TFA) recognized by the patients' antibodies was isolated from liver microsomes of halothane-treated rats by chromatography on an immunoaffinity column of anti-TFA IgG. Antibodies were raised against the 59-kDa-TFA protein and were used to purify the native protein from liver microsomes of untreated rats. Based upon its apparent monomeric molecular mass, NH2-terminal amino acid sequence, catalytic activity, and other physical properties, the protein has been identified as a previously characterized microsomal carboxylesterase (EC 3.1.1.1). A similar strategy may be used to purify and characterized neoantigens associated with other drug toxicities that are believed to have an immunopathological basis. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Satoh, H AU - Martin, B M AU - Schulick, A H AU - Christ, D D AU - Kenna, J G AU - Pohl, L R AD - Laboratory of Chemical Pharmacology, National Heart, Lung and Blood Institute, Bethesda, MD 20892. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 322 EP - 326 VL - 86 IS - 1 SN - 0027-8424, 0027-8424 KW - Antibodies KW - 0 KW - Fluoroacetates KW - Trifluoroacetic Acid KW - E5R8Z4G708 KW - Carboxylic Ester Hydrolases KW - EC 3.1.1.- KW - Carboxylesterase KW - EC 3.1.1.1 KW - Halothane KW - UQT9G45D1P KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Humans KW - Protein Binding KW - Molecular Weight KW - Male KW - Trifluoroacetic Acid -- pharmacology KW - Carboxylic Ester Hydrolases -- metabolism KW - Antibodies -- immunology KW - Halothane -- pharmacology KW - Fluoroacetates -- metabolism KW - Microsomes, Liver -- enzymology KW - Trifluoroacetic Acid -- metabolism KW - Carboxylic Ester Hydrolases -- isolation & purification KW - Carboxylic Ester Hydrolases -- immunology KW - Endoplasmic Reticulum -- immunology KW - Chemical and Drug Induced Liver Injury -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78836362?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+anti-endoplasmic+reticulum+antibodies+in+sera+of+patients+with+halothane-induced+hepatitis+are+directed+against+a+trifluoroacetylated+carboxylesterase.&rft.au=Satoh%2C+H%3BMartin%2C+B+M%3BSchulick%2C+A+H%3BChrist%2C+D+D%3BKenna%2C+J+G%3BPohl%2C+L+R&rft.aulast=Satoh&rft.aufirst=H&rft.date=1989-01-01&rft.volume=86&rft.issue=1&rft.spage=322&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 - 1989-02-14 N1 - Date created - 1989-02-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Drug Metab Dispos. 1988 Jan-Feb;16(1):135-40 [2894942] J Biol Chem. 1987 Jul 25;262(21):10035-8 [3611052] J Biochem. 1988 Jan;103(1):149-55 [3360755] Anesthesiology. 1988 May;68(5):791-6 [3369720] Annu Rev Pharmacol Toxicol. 1988;28:367-87 [3289490] J Pharmacol Exp Ther. 1988 Jun;245(3):1103-9 [3385639] J Biol Chem. 1951 Nov;193(1):265-75 [14907713] J Pharmacol Exp Ther. 1980 Sep;214(3):716-20 [7400974] Arch Biochem Biophys. 1980 Apr 1;200(2):547-59 [6776896] Pharmacol Rev. 1982 Mar;34(1):85-104 [7041144] Biochem Pharmacol. 1983 Jun 1;32(11):1667-72 [6347200] Drug Metab Rev. 1984;15(5-6):1213-49 [6396057] J Pharmacol Exp Ther. 1985 Jun;233(3):857-62 [3891968] Mol Pharmacol. 1985 Nov;28(5):468-74 [3903473] J Pharmacol Exp Ther. 1987 Aug;242(2):733-40 [3302210] DNA. 1988 Mar;7(2):99-106 [3282855] Methods Enzymol. 1986;129:738-63 [3523163] Clin Sci (Lond). 1987 Mar;72(3):263-70 [3545644] Biochem Pharmacol. 1987 Mar 1;36(5):581-90 [2435290] Toxicol Appl Pharmacol. 1987 Jun 30;89(2):202-10 [3603557] J Biol Chem. 1988 Mar 5;263(7):3486-95 [3343253] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Toxic responses in F344 rats and B6C3F1 mice given roxarsone in their diets for up to 13 weeks. AN - 78835643; 2916249 AB - Thirteen-week toxicity studies were conducted in groups of 10 F344 rats and B6C3F1 mice of each sex fed roxarsone at 0, 50, 100, 200, 400, or 800 ppm in the diet. Arsenic levels in blood, urine, kidneys, and liver of rats were measured in additional animals of each sex dosed with 100 or 400 ppm roxarsone. Compound-related mortality occurred in both sexes of rats at 800 ppm and mice at 800 and 400 ppm. Significant body weight gain depression occurred in both sexes of rats at 200, 400, and 800 ppm and mice at 800 ppm. Clinical signs of toxicity (trembling, ataxia, and pale skin) were seen primarily in rats and mice at 800 ppm. Lesions associated with roxarsone administration were noted only in the kidney of rats and were characterized by tubular necrosis and mineralization at the corticomedullary junction. Arsenic levels in urine, blood, liver, and kidneys increased over time and were directly proportional to the level of roxarsone in feed. These levels were greater than 6 times higher in rats than in mice and were about 2 time higher in males than in females. The no-observable-effect level for roxarsone toxicity was estimated at 100 ppm for rats and 200 ppm for mice. No hematology or clinical chemistry effects were found in rats or mice of either sex. JF - Toxicology letters AU - Abdo, K M AU - Elwell, M R AU - Montgomery, C A AU - Thompson, M B AU - Thompson, R B AU - Prejean, J D AD - National Institute of Environmental Health Sciences, National Toxicology Program, Research Triangle Park, NC 27709. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 55 EP - 66 VL - 45 IS - 1 SN - 0378-4274, 0378-4274 KW - Roxarsone KW - H5GU9YQL7L KW - Arsenic KW - N712M78A8G KW - Index Medicus KW - Rats KW - Eating KW - Mice, Inbred Strains KW - Animals KW - Rats, Inbred F344 KW - Sex Factors KW - Dose-Response Relationship, Drug KW - Body Weight -- drug effects KW - Kidney Cortex -- pathology KW - Mice KW - Diet KW - Species Specificity KW - Male KW - Kidney Medulla -- pathology KW - Female KW - Kidney -- pathology KW - Arsenic Poisoning KW - Arsenic -- metabolism KW - Liver -- drug effects KW - Roxarsone -- toxicity KW - Kidney -- drug effects KW - Liver -- metabolism KW - Roxarsone -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78835643?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Toxic+responses+in+F344+rats+and+B6C3F1+mice+given+roxarsone+in+their+diets+for+up+to+13+weeks.&rft.au=Abdo%2C+K+M%3BElwell%2C+M+R%3BMontgomery%2C+C+A%3BThompson%2C+M+B%3BThompson%2C+R+B%3BPrejean%2C+J+D&rft.aulast=Abdo&rft.aufirst=K&rft.date=1989-01-01&rft.volume=45&rft.issue=1&rft.spage=55&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 - 1989-03-16 N1 - Date created - 1989-03-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immunohistochemical demonstration of Clara cell antigen in lung tumors of bronchiolar origin induced by N-nitrosodiethylamine in Syrian golden hamsters. AN - 78834521; 2464284 AB - Both alveolar type II cells and Clara cells have been suggested as cells of origin of human bronchioloalveolar lung carcinomas and other pulmonary neoplasms, based on the presence of cell specific markers identified by immunocytochemical methods. Alveolar type II cell origin of solid and papillary lung tumors of the mouse has been demonstrated, and Clara cells have been suggested as cell of origin for hamster pulmonary neoplasms. Therefore, chemically induced bronchiolar hyperplasias and pulmonary neoplasms of Syrian golden hamsters were analyzed by avidin-biotin immunohistochemistry to localize a hamster-specific Clara cell antigen (CCA) and keratin. The hamsters had been treated subcutaneously with multiple doses of N-nitrosodiethylamine (NDEA). Proliferative lesions of low cuboidal, tall columnar, or pleomorphic cells were present within bronchioles or adjacent to airways in the alveolar parenchyma. Frequently areas of squamous cell differentiation were present focally or diffusely that were immunoreactive for cytokeratin. Immunoreactivity for cytokeratin was also noted for hyperplastic bronchiolar neuroepithelial bodies. Cellular hyperplasias extending out into the alveolar parenchyma contained ciliated cells and frequently consisted of cells immunoreactive for CCA, showing them to be of bronchiolar Clara cell origin. Tumors developed from bronchiolar cell hyperplasias localized within bronchioles and from bronchiolar cells lining former alveolar walls. Neoplastic growth patterns were tubulo-papillary, forming loose networks or densely cellular areas. Immunoreactivity for cytoplasmic CCA was found in 50% of the tumors and was seen most frequently in small cuboidal cells and larger, vacuolated cells scattered throughout the neoplasms. In summary, evidence is presented that NDEA-induced pulmonary tumors of the Syrian golden hamster originated from cells lining bronchioles and from extrabronchiolar Clara cell hyperplasias of the terminal bronchioles. As the pulmonary tumors of the hamsters progressed towards a squamoid cell type, CCA was no longer detectable but cells became immunoreactive for keratin. JF - The American journal of pathology AU - Rehm, S AU - Takahashi, M AU - Ward, J M AU - Singh, G AU - Katyal, S L AU - Henneman, J R AD - Tumor Pathology and Pathogenesis Section, National Cancer Institute, Frederick, MD 21701-1013. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 79 EP - 87 VL - 134 IS - 1 SN - 0002-9440, 0002-9440 KW - Antigens KW - 0 KW - Epitopes KW - Diethylnitrosamine KW - 3IQ78TTX1A KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Hyperplasia KW - Mesocricetus KW - Lung -- pathology KW - Immunohistochemistry KW - Male KW - Female KW - Cricetinae KW - Lung Neoplasms -- chemically induced KW - Bronchi -- pathology KW - Bronchi -- immunology KW - Antigens -- analysis KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78834521?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Immunohistochemical+demonstration+of+Clara+cell+antigen+in+lung+tumors+of+bronchiolar+origin+induced+by+N-nitrosodiethylamine+in+Syrian+golden+hamsters.&rft.au=Rehm%2C+S%3BTakahashi%2C+M%3BWard%2C+J+M%3BSingh%2C+G%3BKatyal%2C+S+L%3BHenneman%2C+J+R&rft.aulast=Rehm&rft.aufirst=S&rft.date=1989-01-01&rft.volume=134&rft.issue=1&rft.spage=79&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 - 1989-03-06 N1 - Date created - 1989-03-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Exp Pathol (Jena). 1977;13(1):44-51 [849772] Am J Pathol. 1976 Dec;85(3):549-54 [999758] J Pathol. 1977 Feb;121(2):79-82 [874634] Am J Pathol. 1977 Oct;89(1):59-66 [20781] Eur J Cancer. 1977 Nov;13(11):1325-40 [590290] Lab Anim Sci. 1977 Dec;27(6):955-62 [202798] Cancer Res. 1978 Apr;38(4):1127-35 [639040] J Natl Cancer Inst. 1978 Aug;61(2):551-61 [355650] J Natl Cancer Inst. 1978 Aug;61(2):577-86 [355652] Am J Pathol. 1981 Feb;102(2):195-208 [6258440] Cancer Res. 1981 Jun;41(6):2147-50 [7237416] Proc Natl Acad Sci U S A. 1981 Aug;78(8):5170-4 [6946463] Cancer Res. 1982 Apr;42(4):1405-11 [7060014] J Immunol. 1983 Jul;131(1):132-9 [6345663] Am Rev Respir Dis. 1983 Aug;128(2 Pt 2):S37-41 [6881705] Acta Pharmacol Toxicol (Copenh). 1984 Feb;54(2):104-14 [6711317] Am J Pathol. 1985 Mar;118(3):493-9 [3883798] Exp Mol Pathol. 1985 Apr;42(2):220-33 [3920070] Cancer Res. 1985 Jun;45(6):2785-92 [3886137] Cancer Res. 1985 Jun;45(6):2807-12 [3986810] J Histochem Cytochem. 1985 Jun;33(6):564-8 [3889141] Am J Pathol. 1986 May;123(2):371-6 [3085510] J Histochem Cytochem. 1987 Jul;35(7):789-94 [2438324] Am J Clin Pathol. 1987 Nov;88(5):552-9 [2823596] Cancer Res. 1988 Jan 1;48(1):148-60 [3334989] Exp Lung Res. 1987;13(3):253-77 [3691409] Exp Lung Res. 1987;13(3):279-97 [3691410] Exp Lung Res. 1987;13(3):299-309 [3319535] Cancer. 1988 Feb 1;61(3):532-7 [3338020] Carcinogenesis. 1988 Feb;9(2):293-6 [3338113] Exp Pathol. 1987;32(3):169-77 [3436397] Cancer Res. 1968 Nov;28(11):2197-210 [5723964] Cancer Res. 1968 Jan;28(1):104-24 [5635364] Anat Embryol (Berl). 1988;178(1):29-39 [3377199] Lab Invest. 1972 Feb;26(2):210-9 [5059985] Lab Anim Sci. 1974 Dec;24(6):938-42 [4374603] Dev Biol. 1975 Oct;46(2):390-403 [1183725] Arch Pathol Lab Med. 1976 Mar;100(3):147-53 [946402] Eur J Cancer. 1975 Dec;11(12):867-72 [1240803] Lab Invest. 1976 Dec;35(6):558-68 [62893] Am J Pathol. 1977 Jun;87(3):569-80 [68683] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential oxygen radical susceptibility of adriamycin-sensitive and -resistant MCF-7 human breast tumor cells. AN - 78831646; 2535695 AB - Recent evidence supports the concept that Adriamycin cytotoxicity may be mediated by drug semiquinone free radical and oxyradical generation. We tested this hypothesis further by exposing drug-sensitive (WT) and 500-fold Adriamycin-resistant MCF-7 human breast tumor cells (ADRR) to exogenous superoxide- and hydrogen peroxide-generating systems and subsequently monitored cell proliferation as a measure of cytotoxicity. The ADRR tumor cells tolerated a 4-fold greater exposure than sensitive cells to superoxide generated by the xanthine/xanthine oxidase system. Likewise, exposure to hydrogen peroxide produced by the action of glucose oxidase on glucose revealed a 4-fold diminished susceptibility of the drug-resistant cells to this reduced form of oxygen. Similar results were obtained by the direct application of hydrogen peroxide to cells. For both cell lines, cytotoxicity was dependent upon the magnitude and the duration of reactive oxygen exposure. When WT and ADRR cells were cultured under hyperoxia (95% O2:5% CO2), in order to stimulate the intracellular production of oxyradicals, proliferation was inhibited to a greater extent in the drug-sensitive cell line. Additionally, hyperoxia potentiated the cytotoxicity of Adriamycin to both sensitive and drug-resistant cells, but the effect depended upon the concentration of the drug. Under hyperoxic conditions, Adriamycin caused oxygen radical-dependent cytotoxicity to the WT tumor cells at clinically relevant drug concentrations as low as 2 to 3 nM. With ADRR tumor cells, hyperoxia increased the cytotoxicity of Adriamycin at concentrations above 5 microM. Paradoxically, both the WT and the ADRR tumor cells were equally susceptible to the cytotoxic effects of gamma irradiation. It is known that the Adriamycin-resistant MCF-7 cells greatly overexpress glutathione peroxidase and glutathione transferase activities; however, other biochemical defenses against reactive drug intermediates and oxygen radicals have been reported to be similar in the two cell lines. We have reexamined those observations in this report. The resistance of ADRR breast tumor cells to Adriamycin appears to be associated with a developed tolerance to superoxide, most likely because of a twofold increase in superoxide dismutase activity, and a decreased susceptibility to hydrogen peroxide, most likely because of 12-fold augmented selenium-dependent glutathione peroxidase activity. Acting in concert, these two enzymes would decrease the formation of hydroxyl radical from reduced molecular oxygen intermediates.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Cancer research AU - Mimnaugh, E G AU - Dusre, L AU - Atwell, J AU - Myers, C E AD - Biochemical Pharmacology Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/01/01/ PY - 1989 DA - 1989 Jan 01 SP - 8 EP - 15 VL - 49 IS - 1 SN - 0008-5472, 0008-5472 KW - Free Radicals KW - 0 KW - Superoxides KW - 11062-77-4 KW - Doxorubicin KW - 80168379AG KW - Hydrogen Peroxide KW - BBX060AN9V KW - Glucose Oxidase KW - EC 1.1.3.4 KW - Oxygen KW - S88TT14065 KW - Index Medicus KW - Space life sciences KW - Oxygen -- toxicity KW - Cell Survival -- drug effects KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Drug Resistance KW - Glucose Oxidase -- pharmacology KW - Female KW - Superoxides -- pharmacology KW - Doxorubicin -- pharmacology KW - Breast Neoplasms -- pathology KW - Hydrogen Peroxide -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78831646?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Differential+oxygen+radical+susceptibility+of+adriamycin-sensitive+and+-resistant+MCF-7+human+breast+tumor+cells.&rft.au=Mimnaugh%2C+E+G%3BDusre%2C+L%3BAtwell%2C+J%3BMyers%2C+C+E&rft.aulast=Mimnaugh&rft.aufirst=E&rft.date=1989-01-01&rft.volume=49&rft.issue=1&rft.spage=8&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 - 1989-01-25 N1 - Date created - 1989-01-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Breast cancer after multiple chest fluoroscopies: second follow-up of Massachusetts women with tuberculosis. AN - 78831594; 2908849 AB - A second follow-up was conducted of 1742 women with tuberculosis who were treated in one of two sanatoria in Massachusetts between 1930 and 1956. One hospital treated only children under the age of 17. Patient follow-up was extended from 1975 through 1980, and an additional 18 breast cancers were identified from hospital records, death certificates, and responses to a mailed questionnaire. Vital status was established for 97% of the subjects. Among 1044 women who were examined an average of 101 times with X-ray fluoroscopies during lung collapse therapy, 55 breast cancers were observed in contrast to 35.8 expected, based on incidence rates from the general population. No excess was found for 698 women treated by other means (19 observed versus 22.8 expected). Excess breast cancer risk did not appear until 15 years after initial exposure and was present at the end of 50 years of observation. Risk appeared to decrease with increasing age at exposure. Estimates of radiation dose to the breast for individuals (mean = 96 rad) were based on the most current information for the numbers of fluoroscopies, reconstruction of exposure conditions, and absorbed dose calculations. The relation between dose and breast cancer risk was consistent with linearity up to 400 rads (4 Gy). For 10-year survivors, the absolute excess risk was 5.5/1 million woman-year-rad, the excess relative risk per rad was 0.73%, and the relative risk at 100 rad was 1.7. These data indicate that a woman's lifetime risk of breast cancer is influenced by events occurring in early reproductive life, that low-dose fractionated exposures are as effective as single exposures of the same total dose in inducing breast cancer, and that risk of radiogenic breast cancer persists for many years, and perhaps for life. JF - Cancer research AU - Hrubec, Z AU - Boice, J D AU - Monson, R R AU - Rosenstein, M AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1989/01/01/ PY - 1989 DA - 1989 Jan 01 SP - 229 EP - 234 VL - 49 IS - 1 SN - 0008-5472, 0008-5472 KW - Index Medicus KW - Age Factors KW - Massachusetts KW - Risk Factors KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Follow-Up Studies KW - Dose-Response Relationship, Radiation KW - Adolescent KW - Female KW - Neoplasms, Radiation-Induced -- etiology KW - Breast Neoplasms -- etiology KW - Tuberculosis, Pulmonary -- diagnostic imaging KW - Fluoroscopy -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78831594?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Breast+cancer+after+multiple+chest+fluoroscopies%3A+second+follow-up+of+Massachusetts+women+with+tuberculosis.&rft.au=Hrubec%2C+Z%3BBoice%2C+J+D%3BMonson%2C+R+R%3BRosenstein%2C+M&rft.aulast=Hrubec&rft.aufirst=Z&rft.date=1989-01-01&rft.volume=49&rft.issue=1&rft.spage=229&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 - 1989-01-25 N1 - Date created - 1989-01-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Autologous bone marrow transplantation. Current status and future directions. AN - 78831509; 2642282 AB - To assess the current status of high-dose chemotherapy with autologous marrow transplantation in hematologic malignancies and solid tumors. Studies reported between 1978 and May 1988 were identified through computer searches using Medline and Cancerline and through extensive manual searching of bibliographies of identified books and articles. More than 160 studies that contained adequate response, toxicity, or survival data were selected for analysis, including peer-reviewed articles, book chapters, and proceedings of meetings. The most current or complete references were used for series reported more than once. Information abstracted included regimen used, number of patients, response rates, disease-free and overall survival, and toxicities. A meta-analysis of the pooled data was done. For many tumor types, autologous marrow transplantation offers higher response rates than standard approaches. For leukemias and lymphomas, response rates of 60% to 80% may be achieved with the potential for cure. With solid tumors, response rates range from 30% in gliomas, 50% in melanomas and colon cancer, more than 60% in lung cancer, and 80% in breast cancer. Although responses tend to be short-lived, long-term survival can occasionally be seen. Results with autologous marrow transplantation can be improved through systematically developed, carefully designed clinical trials that may be facilitated by collaborative research. Studies should focus on disease-directed drug combinations, several courses of high-dose therapy, treatment at a time of lower tumor burden, and reducing toxicity with hematopoietic growth factors. JF - Annals of internal medicine AU - Cheson, B D AU - Lacerna, L AU - Leyland-Jones, B AU - Sarosy, G AU - Wittes, R E AD - National Cancer Institute, Bethesda, Maryland. Y1 - 1989/01/01/ PY - 1989 DA - 1989 Jan 01 SP - 51 EP - 65 VL - 110 IS - 1 SN - 0003-4819, 0003-4819 KW - Antineoplastic Agents KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Combined Modality Therapy KW - Humans KW - Clinical Trials as Topic KW - Transplantation, Autologous KW - Meta-Analysis as Topic KW - Remission Induction KW - Neoplasms -- drug therapy KW - Neoplasms -- radiotherapy KW - Bone Marrow Diseases -- prevention & control KW - Bone Marrow Diseases -- chemically induced KW - Antineoplastic Agents -- administration & dosage KW - Bone Marrow Transplantation KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78831509?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Autologous+bone+marrow+transplantation.+Current+status+and+future+directions.&rft.au=Cheson%2C+B+D%3BLacerna%2C+L%3BLeyland-Jones%2C+B%3BSarosy%2C+G%3BWittes%2C+R+E&rft.aulast=Cheson&rft.aufirst=B&rft.date=1989-01-01&rft.volume=110&rft.issue=1&rft.spage=51&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 - 1989-01-04 N1 - Date created - 1989-01-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Studies on phagocytosis in patients with acute bacterial infections. AN - 78830866; 2536044 AB - Polymorphonuclear leukocytes (PMN) and monocytes from 20 patients with acute bacterial infections were examined for phagocytic function. PMN of patients expressed markedly enhanced phagocytosis as measured by the ingestion of erythrocyte (E)IgG and IgG/C3b-coated E. Phagocytosis of E coated with C3b alone was not seen, while low levels of ingestion of iC3b-E by patients' PMNs was noted. Monocytes from patients and controls expressed similar phagocytic activity in a fixed endpoint assay; however, the kinetics of phagocytosis by patients' monocytes was strikingly faster. Superoxide anion (O2.) and myeloperoxidase activities were similar to controls in PMN of four patients studied on day 1 of admission. PMN from two of three patients studied longitudinally showed an initial elevation in EIgG phagocytosis, which fell to normal levels by day 4, concomitantly with increased O2. generation and clinical improvement. Phagocytosis remained elevated in the third patient who did not clear his septicemia. Surface membrane FcRII, FcRIII, CR1, and CR3 were similar on patient and control PMN. In contrast, FcRI was increased on PMN of five of seven patients by monomeric IgG binding, and on two of two patients by monoclonal anti-FcRI binding. Thus, PMN and monocytes of patients with acute bacterial infections are either upregulated with regard to phagocytic function or are less susceptible to downregulation than are normal cells. This presumably would have a beneficial effect on host defenses during infection. JF - The Journal of clinical investigation AU - Simms, H H AU - Frank, M M AU - Quinn, T C AU - Holland, S AU - Gaither, T A AD - Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 252 EP - 260 VL - 83 IS - 1 SN - 0021-9738, 0021-9738 KW - Antibodies, Monoclonal KW - 0 KW - Azides KW - Superoxides KW - 11062-77-4 KW - Sodium Azide KW - 968JJ8C9DV KW - Peroxidase KW - EC 1.11.1.7 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Peroxidase -- metabolism KW - Aged KW - Longitudinal Studies KW - Superoxides -- metabolism KW - Aged, 80 and over KW - Adult KW - Azides -- pharmacology KW - Middle Aged KW - Female KW - Male KW - Bacterial Infections -- immunology KW - Phagocytosis -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78830866?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Studies+on+phagocytosis+in+patients+with+acute+bacterial+infections.&rft.au=Simms%2C+H+H%3BFrank%2C+M+M%3BQuinn%2C+T+C%3BHolland%2C+S%3BGaither%2C+T+A&rft.aulast=Simms&rft.aufirst=H&rft.date=1989-01-01&rft.volume=83&rft.issue=1&rft.spage=252&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 - 1989-02-23 N1 - Date created - 1989-02-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Immunol. 1986 Dec 1;137(11):3378-82 [2946759] J Exp Med. 1986 Apr 1;163(4):826-36 [3005468] Inflammation. 1987 Jun;11(2):211-27 [3034783] Immunology. 1987 Nov;62(3):405-11 [3499379] Acta Paediatr Scand. 1968 Mar;57(2):110-4 [4178671] J Clin Invest. 1967 Apr;46(4):668-79 [6021213] Biochem J. 1959 Sep;73:119-26 [14434282] Scand J Clin Lab Invest Suppl. 1968;97:77-89 [4179068] Immunology. 1970 Dec;19(6):967-74 [5487543] Lancet. 1972 Oct 7;2(7780):727-30 [4116144] Inflammation. 1978 Jun;3(2):129-35 [216633] J Clin Invest. 1979 Feb;63(2):221-9 [372238] J Infect Dis. 1980 Jan;141(1):14-26 [6245144] J Infect Dis. 1980 Apr;141(4):441-9 [6768810] J Biol Chem. 1981 Apr 25;256(8):3995-4006 [6783652] Proc Natl Acad Sci U S A. 1982 May;79(10):3275-9 [6808506] Blood. 1982 Sep;60(3):618-22 [6286012] J Immunol. 1982 Sep;129(3):1041-9 [6980915] Anal Biochem. 1982 Sep 15;125(2):427-32 [6758629] Mol Immunol. 1983 Jun;20(6):623-35 [6603572] World J Surg. 1983 May;7(3):424-9 [6880231] J Clin Invest. 1984 Feb;73(2):366-73 [6321554] Arch Surg. 1985 Jan;120(1):93-8 [2981524] J Immunol. 1985 Apr;134(4):2580-7 [3156186] J Immunol. 1986 Feb 1;136(3):860-6 [3001188] J Clin Invest. 1986 Mar;77(3):925-33 [3005369] Proc Natl Acad Sci U S A. 1987 Apr;84(8):2213-7 [3031672] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Analysis of the sequence-specific interactions between Cro repressor and operator DNA by systematic base substitution experiments. AN - 78829308; 2911590 AB - We measured quantitatively the binding affinities of purified Cro repressor to the chemically synthesized wild-type and mutant OR1 operators, consisting of all three possible base-pair substitutions and of thymine to uracil substitutions at each base-pair position of the 17-base-pair operator sequence. The sequence-specific interactions between Cro repressor and the operator DNA occur at the symmetrically disposed outer 7-base-pair positions of each half operator and at the central base-pair position. The binding of Cro is almost symmetrical with respect to the pseudo-twofold symmetry of the binding site. The binding free energy changes calculated from the affinity changes are mostly additive for specific Cro binding. Also the binding affinities of Cro to the operators or any other DNA sequences can be predicted by simple addition of free energy changes of single base substitutions. We isolated cro mutants by site-directed mutagenesis and studied their DNA binding to the wild-type and base-substituted mutant operators. The sequence-specific contacts derived from such studies are significantly different from the models proposed by Ohlendorf et al. [Ohlendorf, D. H., Anderson, W. F., Takeda, Y. & Matthews, B. W. (1982) Nature (London) 298, 719-723] and by Hochschild et al. [Hochschild, A., Douhan, J., III, & Ptashne, M. (1986) Cell 47, 807-816]. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Takeda, Y AU - Sarai, A AU - Rivera, V M AD - Laboratory of Mathematical Biology, National Cancer Institute-Frederick Cancer Research Facility, MD 21701. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 439 EP - 443 VL - 86 IS - 2 SN - 0027-8424, 0027-8424 KW - Repressor Proteins KW - 0 KW - Transcription Factors KW - Uracil KW - 56HH86ZVCT KW - DNA KW - 9007-49-2 KW - Thymine KW - QR26YLT7LT KW - Index Medicus KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Mutation KW - Transcription Factors -- metabolism KW - Operator Regions, Genetic KW - DNA -- metabolism KW - Repressor Proteins -- metabolism KW - DNA -- genetics KW - Repressor Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78829308?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Analysis+of+the+sequence-specific+interactions+between+Cro+repressor+and+operator+DNA+by+systematic+base+substitution+experiments.&rft.au=Takeda%2C+Y%3BSarai%2C+A%3BRivera%2C+V+M&rft.aulast=Takeda&rft.aufirst=Y&rft.date=1989-01-01&rft.volume=86&rft.issue=2&rft.spage=439&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 - 1989-02-21 N1 - Date created - 1989-02-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1985 Feb;82(4):1084-8 [3156377] Cell. 1986 Mar 28;44(6):925-33 [3955653] J Biol Chem. 1986 Jul 5;261(19):8608-16 [3522575] Science. 1986 Oct 24;234(4775):451-7 [3532321] Cell. 1986 Dec 5;47(5):807-16 [2946418] Science. 1986 Dec 19;234(4783):1526-41 [3024321] Nature. 1987 Apr 30-May 6;326(6116):886-8 [3553960] Nature. 1987 Apr 30-May 6;326(6116):888-91 [3553961] J Mol Biol. 1987 Jul 5;196(1):149-58 [2958636] Proc Natl Acad Sci U S A. 1988 Jul;85(13):4633-7 [3387430] Genetics. 1988 Jan;118(1):21-9 [8608928] Annu Rev Biochem. 1969;38:841-80 [4896249] J Mol Biol. 1970 Feb 28;48(1):67-83 [4915295] J Mol Biol. 1970 Nov 14;53(3):401-17 [4924006] Cell. 1975 Jun;5(2):109-13 [1095210] Proc Natl Acad Sci U S A. 1976 Mar;73(3):804-8 [1062791] FEBS Lett. 1977 Feb 15;74(1):10-3 [838065] Proc Natl Acad Sci U S A. 1977 Feb;74(2):560-4 [265521] J Mol Biol. 1977 May 15;112(2):265-77 [875019] J Biol Chem. 1977 Sep 10;252(17):6177-83 [330523] Proc Natl Acad Sci U S A. 1978 Apr;75(4):1783-7 [273909] Proc Natl Acad Sci U S A. 1978 Aug;75(8):3578-82 [278973] Proc Natl Acad Sci U S A. 1979 Oct;76(10):5061-5 [159452] Nature. 1981 Apr 30;290(5809):754-8 [6452580] Nature. 1982 Aug 19;298(5876):718-23 [6213863] Science. 1983 Sep 9;221(4615):1020-6 [6308768] Annu Rev Biochem. 1984;53:293-321 [6236744] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Epididymal interstitial (Leydig) cell tumors in B6C3F1 mice. AN - 78825396; 2913705 AB - Six primary interstitial cell tumors of the epididymis were identified from 46,752 male B6C3F1 mice used in chronic toxicity and carcinogenicity studies. Five of the tumors occurred at the end of 2-year studies; none were attributed to treatment. None of the mice with epididymal tumors had a primary testicular tumor. Histologically, tumors were characterized by a nodular or diffuse proliferation of tumor cells in the epididymal interstitium. Most cells were polygonal with highly vacuolated cytoplasm (vacuolated cells) or eosinophilic cytoplasm (eosinophilic cells). Smaller hyperchromatic cells with scant basophilic cytoplasm (basophilic cells) and cells with yellow-brown pigment characteristic of lipofuscin (pigmented cells) were less common. In each tumor two or more cell types were present. Extension of these tumors through the capsule, invasion of the testis, or metastasis did not occur. By electron microscopy both eosinophilic and vacuolated cell types had a large round or oval nucleus with sparse heterochromatin, abundant mitochondria with tubulovesicular cristae, and frequent desmosome structures between cell membranes. Vacuolated cells contained numerous lipid droplets. Morphological features of the epididymal tumors are similar to those of the testicular interstitial (Leydig) cell tumor in mice and rats. JF - Veterinary pathology AU - Mitsumori, K AU - Talley, F A AU - Elwell, M R AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 65 EP - 69 VL - 26 IS - 1 SN - 0300-9858, 0300-9858 KW - Index Medicus KW - Animals KW - Microscopy, Electron KW - Mice KW - Male KW - Mice, Inbred Strains KW - Leydig Cell Tumor -- ultrastructure KW - Epididymis -- pathology KW - Testicular Neoplasms -- pathology KW - Testicular Neoplasms -- veterinary KW - Leydig Cell Tumor -- pathology KW - Leydig Cell Tumor -- veterinary KW - Testicular Neoplasms -- ultrastructure KW - Rodent Diseases -- pathology KW - Epididymis -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78825396?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Veterinary+pathology&rft.atitle=Epididymal+interstitial+%28Leydig%29+cell+tumors+in+B6C3F1+mice.&rft.au=Mitsumori%2C+K%3BTalley%2C+F+A%3BElwell%2C+M+R&rft.aulast=Mitsumori&rft.aufirst=K&rft.date=1989-01-01&rft.volume=26&rft.issue=1&rft.spage=65&rft.isbn=&rft.btitle=&rft.title=Veterinary+pathology&rft.issn=03009858&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-09 N1 - Date created - 1989-03-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Desensitization to parathyroid hormone in renal cells from aged rats is associated with alterations in G-protein activity. AN - 78823083; 2492037 AB - Parathyroid hormone (PTH)-stimulated Na+/Ca2+ exchange activity, but not forskolin-sensitive Na+-dependent Ca2+ efflux, was blunted in renal cortical cells from aged rats. PTH-sensitive adenylate cyclase activity in renal membranes from senescent rats also declined, but forskolin-stimulated activity did not change. In addition, cholera toxin- and pertussis toxin-stimulated Na+-dependent Ca2+ efflux and cAMP formation were blunted in cells from aged animals. Further, cells from aged rats had decreased Gs-alpha and Gi-alpha proteins, as detected by ADP-ribosylation. These findings would be consistent with the proposal of an age-associated heterologous desensitization that involved the G-proteins. Serum concentrations of iPTH were increased in the old rat, suggesting that the desensitization to PTH in the aging rat represented an adaptive response to prolonged stimulation by the hormone. This hypothesis was supported by the findings that the attenuated PTH-sensitive Na+/Ca2+ exchange activity, cAMP formation, and adenylate cyclase activity in cells from old rats could be reversed by parathyroidectomy. The decreased label in cholera toxin-catalyzed ADP-ribosylated Gs-alpha and pertussis toxin catalyzed ADP-ribosylated Gi-alpha found in cells from aged rats was also largely negated by the surgery. In conclusion, the results suggest that the age-related blunting in the responses of renal cells to PTH was associated with a deficit in G-protein function and that this alteration could be reversed by removal of the parathyroid gland. JF - The Journal of clinical investigation AU - Hanai, H AU - Liang, C T AU - Cheng, L AU - Sacktor, B AD - Laboratory of Biological Chemistry, National Institute on Aging, Baltimore, Maryland 21224. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 268 EP - 277 VL - 83 IS - 1 SN - 0021-9738, 0021-9738 KW - Adenylate Cyclase Toxin KW - 0 KW - Parathyroid Hormone KW - Virulence Factors, Bordetella KW - Colforsin KW - 1F7A44V6OU KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Cholera Toxin KW - 9012-63-9 KW - Sodium KW - 9NEZ333N27 KW - Pertussis Toxin KW - EC 2.4.2.31 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Calcium KW - SY7Q814VUP KW - Abridged Index Medicus KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Calcium -- metabolism KW - Virulence Factors, Bordetella -- pharmacology KW - Animals KW - Colforsin -- pharmacology KW - Cholera Toxin -- pharmacology KW - Adenosine Diphosphate Ribose -- metabolism KW - Male KW - Sodium -- metabolism KW - Parathyroid Hormone -- pharmacology KW - GTP-Binding Proteins -- metabolism KW - Aging KW - Kidney -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78823083?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Desensitization+to+parathyroid+hormone+in+renal+cells+from+aged+rats+is+associated+with+alterations+in+G-protein+activity.&rft.au=Hanai%2C+H%3BLiang%2C+C+T%3BCheng%2C+L%3BSacktor%2C+B&rft.aulast=Hanai&rft.aufirst=H&rft.date=1989-01-01&rft.volume=83&rft.issue=1&rft.spage=268&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 - 1989-02-23 N1 - Date created - 1989-02-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1951 Nov;193(1):265-75 [14907713] Endocrinology. 1986 Feb;118(2):595-602 [3002757] Nature. 1970 Aug 15;227(5259):680-5 [5432063] Ann N Y Acad Sci. 1971 Dec 30;185:386-94 [4330505] J Clin Invest. 1973 Jan;52(1):181-4 [4734167] Q J Med. 1975 Jul;44(175):505-21 [1178820] J Gerontol. 1976 Sep;31(5):523-6 [820738] Biochim Biophys Acta. 1977 May 2;466(3):474-87 [15597] Endocrinology. 1978 Jan;102(1):45-51 [217587] Am J Physiol. 1979 Apr;236(4):E401-9 [219712] N Engl J Med. 1979 Jun 21;300(25):1419-21 [440391] Biochem J. 1979 Mar 15;178(3):549-57 [454364] J Biol Chem. 1980 Feb 25;255(4):1252-8 [6766444] J Lab Clin Med. 1980 Mar;95(3):373-85 [7354241] J Biol Chem. 1981 Dec 25;256(24):12866-74 [6118367] J Biol Chem. 1982 Jan 10;257(1):20-3 [6273425] Calcif Tissue Int. 1981;33(5):477-84 [6797700] J Biol Chem. 1982 Apr 10;257(7):3739-46 [6277948] Am J Physiol. 1982 Mar;242(3):E154-63 [6278948] J Biol Chem. 1982 May 10;257(9):5312-8 [6950937] Endocrinology. 1982 Jul;111(1):252-9 [6177527] J Biol Chem. 1986 Apr 25;261(12):5419-25 [3007502] J Biol Chem. 1986 Jun 15;261(17):7906-11 [3086320] J Biol Chem. 1986 Jun 25;261(18):8182-91 [3087970] J Biol Chem. 1986 Jul 25;261(21):9587-90 [3015900] Am J Physiol. 1986 Sep;251(3 Pt 2):F399-407 [3752253] FEBS Lett. 1986 Sep 29;206(1):36-42 [3093273] Endocrinology. 1986 Dec;119(6):2864-6 [3780554] Proc Natl Acad Sci U S A. 1986 Dec;83(23):8893-7 [3024154] Exp Gerontol. 1986;21(6):515-22 [3030793] Adv Exp Med Biol. 1986;208:537-41 [3031954] Endocrinology. 1987 Aug;121(2):443-8 [3496213] Exp Gerontol. 1987;22(4):263-9 [3666071] Proc Natl Acad Sci U S A. 1987 Oct;84(20):7266-9 [2890163] J Biol Chem. 1988 Feb 5;263(4):1768-72 [3123477] J Bone Miner Res. 1987 Oct;2(5):363-6 [3455620] J Bone Miner Res. 1987 Oct;2(5):367-74 [3455621] Am J Physiol. 1982 Jul;243(1):E37-42 [6283911] Biosci Rep. 1981 Sep;1(9):709-13 [6125220] Endocrinology. 1982 Oct;111(4):1311-7 [6288355] Mech Ageing Dev. 1982 Dec;20(4):353-60 [6300573] J Biol Chem. 1983 Jul 25;258(14):8692-7 [6305997] J Clin Invest. 1983 Aug;72(2):411-21 [6308053] J Clin Invest. 1983 Aug;72(2):422-32 [6308054] Endocrinology. 1983 Nov;113(5):1638-46 [6313327] Endocrinology. 1983 Dec;113(6):1942-9 [6315338] Cell. 1984 Mar;36(3):577-9 [6321035] Am J Physiol. 1984 Mar;246(3 Pt 1):E266-70 [6608276] J Biol Chem. 1984 Sep 10;259(17):10827-33 [6469984] J Membr Biol. 1984;79(1):19-31 [6737462] J Biol Chem. 1984 Jun 25;259(12):7893-901 [6539777] Endocrinology. 1984 Oct;115(4):1239-47 [6479092] J Biol Chem. 1984 Nov 25;259(22):13806-13 [6438083] J Clin Invest. 1985 Apr;75(4):1096-105 [3988932] Proc Natl Acad Sci U S A. 1985 Jun;82(12):4270-3 [3858880] Nature. 1985 Sep 12-18;317(6033):124-9 [2993919] Recent Prog Horm Res. 1985;41:41-99 [2996090] Calcif Tissue Int. 1986 Jan;38(1):27-32 [3079648] J Clin Invest. 1969 Oct;48(10):1832-44 [4309802] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Leukemia risk following radiotherapy for breast cancer. AN - 78821955; 2909667 AB - To evaluate further the relationship between high-dose radiotherapy and leukemia incidence, a nested case-control study was conducted in a cohort of 22,753 women who were 18-month survivors of invasive breast cancer diagnosed from 1935 to 1972. Women treated for breast cancer after 1973 were excluded to minimize the possible confounding influence of treatment with chemotherapeutic agents. The cases had histologically confirmed leukemia reported to the Connecticut Tumor Registry (CTR) between 1935 and 1984. A total of 48 cases of leukemia following breast cancer were included in the study. Two controls were individually matched to each leukemia case on the basis of age, calendar year when diagnosed with breast cancer, and survival time. Leukemia diagnoses were verified by one hematologist. Radiation dose to active bone marrow was estimated by medical physicists on the basis of the original radiotherapy records of study subjects. Local radiation doses to each of the 16 bone marrow components for each patient were reconstructed; the dose averaged over the entire body was 530 rad (5.3 Gy). Based on this dosage and assuming a linear relationship between dose and affect, a relative risk (RR) in excess of 10 would have been expected. However, there was little evidence that radiotherapy increased the overall risk of leukemia (RR = 1.16; 90% confidence interval [CI], 0.6 to 2.1). The risk of chronic lymphocytic leukemia, one of the few malignancies without evidence for an association with ionizing radiation, was not significantly increased (RR = 1.8; n = 10); nor was the risk for all other forms of leukemia (RR = 1.0; n = 38). There was no indication that risk varied over categories of radiation dose. These data exclude an association between leukemia and radiotherapy for breast cancer of 2.2-fold with 90% confidence, and provide further evidence that cell death predominates over cell transformation when high radiation doses are delivered to limited volumes of tissue. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Curtis, R E AU - Boice, J D AU - Stovall, M AU - Flannery, J T AU - Moloney, W C AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 21 EP - 29 VL - 7 IS - 1 SN - 0732-183X, 0732-183X KW - Index Medicus KW - Registries KW - Epidemiologic Methods KW - Risk Factors KW - Humans KW - Aged KW - Middle Aged KW - Bone Marrow -- radiation effects KW - Female KW - Connecticut KW - Leukemia, Radiation-Induced -- epidemiology KW - Breast Neoplasms -- radiotherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78821955?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Leukemia+risk+following+radiotherapy+for+breast+cancer.&rft.au=Curtis%2C+R+E%3BBoice%2C+J+D%3BStovall%2C+M%3BFlannery%2C+J+T%3BMoloney%2C+W+C&rft.aulast=Curtis&rft.aufirst=R&rft.date=1989-01-01&rft.volume=7&rft.issue=1&rft.spage=21&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 - 1989-02-09 N1 - Date created - 1989-02-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phorbol myristate acetate and calcium ionophore A23187-stimulated human T cells do not express high-affinity IL-2 receptors. AN - 78821240; 15493263 AB - Phorbol myristate acetage (PMA) and Ca2+ ionophore A23187 mimic early signal transduction pathways and activate purified human T cells to secrete large quantities of interleukin-2 (IL-2) and to proliferate. Despite producing 50-100-fold more IL-2 than phytohaemagglutinin (PHA)-activated peripheral blood lymphocytes (PBL), PMA/A23187-stimulated human T cells proliferate less than cells activated by PHA. Washing the cells to remove PMA/A23187 was found to increase cellular proliferation two to five-fold. High-affinity IL-2R (HA-IL-2R) were found to be expressed by human T cells that had been washed 24 hr after PMA/A23187 stimulation and recultured without stimulus for an additional 48 hr, but not by T cells constantly exposed to PMA/A23187 for 72 hr. Radioligand binding studies with [125I]IL-2 demonstrated that while the alpha (p55) and beta (p70-75) subunits of HA-IL-2R were both present on the constant PMA/A23187-stimulated T cells, they did not appear to associate to form functional HA-IL-2R. This defect in the expression of bio-active HA-IL-2R on constant PMA/A23187-stimulated human T cells seems to account for their low proliferative response. JF - Immunology AU - Chopra, R K AU - Powers, D C AU - Adler, W H AU - Nagel, J E AD - Clinical Immunology Section, Gerontology Research Center, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA. Y1 - 1989/01// PY - 1989 DA - January 1989 SP - 54 EP - 60 VL - 66 IS - 1 SN - 0019-2805, 0019-2805 KW - Adjuvants, Immunologic KW - 0 KW - Ionophores KW - Receptors, Interleukin-2 KW - Calcimycin KW - 37H9VM9WZL KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Stimulation, Chemical KW - Lymphocyte Activation KW - Cells, Cultured KW - Humans KW - Biological Assay KW - T-Lymphocytes -- metabolism KW - Ionophores -- pharmacology KW - Receptors, Interleukin-2 -- analysis KW - Tetradecanoylphorbol Acetate -- pharmacology KW - T-Lymphocytes -- drug effects KW - Calcimycin -- pharmacology KW - Adjuvants, Immunologic -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78821240?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Immunology&rft.atitle=Phorbol+myristate+acetate+and+calcium+ionophore+A23187-stimulated+human+T+cells+do+not+express+high-affinity+IL-2+receptors.&rft.au=Chopra%2C+R+K%3BPowers%2C+D+C%3BAdler%2C+W+H%3BNagel%2C+J+E&rft.aulast=Chopra&rft.aufirst=R&rft.date=1989-01-01&rft.volume=66&rft.issue=1&rft.spage=54&rft.isbn=&rft.btitle=&rft.title=Immunology&rft.issn=00192805&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2004-12-17 N1 - Date created - 2004-10-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Eur J Immunol. 1973 Oct;3(10):645-9 [4587740] J Immunol. 1988 Apr 1;140(7):2249-59 [2832473] J Immunol Methods. 1982;50(1):39-49 [6979583] Proc Natl Acad Sci U S A. 1983 Jun;80(11):3444-7 [6407014] Biochem Biophys Res Commun. 1983 Jul 29;114(2):638-45 [6411090] J Exp Med. 1983 Dec 1;158(6):1895-911 [6606011] Biochem J. 1984 Jun 1;220(2):345-60 [6146314] J Exp Med. 1984 Oct 1;160(4):1126-46 [6090574] J Biol Chem. 1985 Feb 10;260(3):1366-9 [3155734] Nature. 1985 Jan 24-30;313(6000):318-20 [3918270] J Cell Physiol. 1985 Apr;123(1):46-50 [3919035] Nature. 1985 May 30-Jun 5;315(6018):419-20 [3923369] J Immunol Methods. 1985 Jul 16;81(1):15-30 [3926900] Biochem Biophys Res Commun. 1985 Jul 31;130(2):724-31 [2992482] Scand J Immunol. 1985 Nov;22(5):591-6 [3936166] Proc Natl Acad Sci U S A. 1986 Jun;83(11):3992-6 [3086875] J Biol Chem. 1986 Jun 25;261(18):8158-62 [3087969] Eur J Immunol. 1986 Oct;16(10):1217-21 [3095123] J Immunol. 1987 Apr 1;138(7):2353-8 [3104462] J Immunol. 1987 May 15;138(10):3100-7 [3106473] J Immunol. 1987 May 15;138(10):3532-8 [3033076] Nature. 1987 Jun 11-17;327(6122):518-22 [3108674] J Immunol. 1987 Sep 1;139(5):1393-9 [3114365] J Immunol. 1987 Sep 15;139(6):1918-26 [3114379] Clin Exp Immunol. 1987 Aug;69(2):433-40 [3115657] Clin Res. 1987 Sep;35(5):439-50 [2889557] J Immunol. 1988 Jan 15;140(2):361-6 [3257235] J Clin Invest. 1988 Apr;81(4):1096-102 [3127423] J Biol Chem. 1982 Jul 10;257(13):7847-51 [7085651] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Chronic Toxicity Tests of Sodium Thiocyanate With Sodium Nitrite in F344 Rats AN - 760215425; 13641448 AB - Sodium thiocyanate, a common environmental chemical, was found to increase the incidence of liver tumors in a group of rats treated with 0.08% in drinking water. To test the possibility that thiocyanate was catalyzing the formation of carcinogenic nitrosamines from amines and nitrite in the food, a group of 20 male and 20 female rats was given a higher dose of sodium thiocyanate (0.32%) together with sodium nitrite (0.2%) in drinking water. Similar groups of rats were given 0.32% sodium thiocyanate or 0.2% sodium nitrite in drinking water or were untreated. All treatments lasted most of the lifetime of the rats, at least 2 years. There was no difference between the groups, treated or untreated, in survival, or in the incidence of any tumor that could be related to the treatment. The results indicate that sodium thiocyanate is without carcinogenic activity in rats, alone or combined with sodium nitrite. JF - Toxicology and Industrial Health AU - Lijinsky, W AU - Kovatch, R M AD - NCI-Frederick Cancer Research Facility BRI-Basic Research Program Frederick, MD 21701 Y1 - 1989 PY - 1989 DA - 1989 SP - 25 EP - 29 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU UK VL - 5 IS - 1 SN - 0748-2337, 0748-2337 KW - Toxicology Abstracts; Pollution Abstracts KW - chronic toxicity KW - sodium nitrite KW - sodium thiocyanate. KW - Food KW - Survival KW - tumors KW - Sodium nitrite KW - Tumors KW - Amines KW - Rats KW - Sodium KW - Nitrosamines KW - amines KW - Nitrites KW - Carcinogenicity KW - Chronic toxicity KW - Liver KW - survival KW - Drinking water KW - Nitrite KW - P 2000:FRESHWATER POLLUTION KW - X 24350:Industrial Chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/760215425?accountid=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+Industrial+Health&rft.atitle=Chronic+Toxicity+Tests+of+Sodium+Thiocyanate+With+Sodium+Nitrite+in+F344+Rats&rft.au=Lijinsky%2C+W%3BKovatch%2C+R+M&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1989-01-01&rft.volume=5&rft.issue=1&rft.spage=25&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+Industrial+Health&rft.issn=07482337&rft_id=info:doi/10.1177%2F074823378900500102 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2010-10-01 N1 - Number of references - 10 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Sodium; Nitrosamines; amines; Chronic toxicity; Food; Liver; Survival; Tumors; Sodium nitrite; Nitrite; Drinking water; Rats; Nitrites; Carcinogenicity; tumors; Amines; survival DO - http://dx.doi.org/10.1177/074823378900500102 ER - TY - JOUR T1 - Quantification of Toxic Response and the Development of the Median Effective Dose (Ed 50)--a Historical Perspective AN - 760214376; 13641451 AB - The development of the widely-used median effective (or lethal) dose as a summary measure in quantifying toxic response to chemical stimuli is reviewed. Attention is directed at those mathematical properties noted by the originator of the median effective dose, the English physiologist John William Trevan, that make the measure a useful summary statistic for toxicological studies. Consideration is also given to the development of precursor measures to the median effective dose, such as minimal effective dose. JF - Toxicology and Industrial Health AU - Piegorsch, Walter W AD - Division of Biometry and Risk Assessment National Institute of Environmental Health Sciences Research Triangle Park, North Carolina Y1 - 1989 PY - 1989 DA - 1989 SP - 55 EP - 62 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU UK VL - 5 IS - 1 SN - 0748-2337, 0748-2337 KW - Toxicology Abstracts UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/760214376?accountid=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+Industrial+Health&rft.atitle=Quantification+of+Toxic+Response+and+the+Development+of+the+Median+Effective+Dose+%28Ed+50%29--a+Historical+Perspective&rft.au=Piegorsch%2C+Walter+W&rft.aulast=Piegorsch&rft.aufirst=Walter&rft.date=1989-01-01&rft.volume=5&rft.issue=1&rft.spage=55&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+Industrial+Health&rft.issn=07482337&rft_id=info:doi/10.1177%2F074823378900500105 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2010-10-01 N1 - Last updated - 2011-12-14 DO - http://dx.doi.org/10.1177/074823378900500105 ER - TY - JOUR T1 - The Statistical Analysis of a Carcinogen Mixture Experiment. III. Carcinogens With Different Target Systems, Aflatoxin B1, N-Butyl-N-(4-Hydroxybutyl)Nitrosamine, Lead Acetate, and Thiouracil AN - 760153000; 13641447 AB - This paper describes factorial experiments designed to determine whether two carcinogens that lead to cancers in different organ systems act synergistically to produce cancers in Fischer 344 rats. Four carcinogens, aflatoxin B sub(1) (AFLA), N-butyl-n-(4-hydroxybutyl)nitrosamine (NBBN), lead acetate (LA), and thiouracil (THIO) were studied in pairwise combinations. Each of the six possible pairs were studied by means of a 4 X 4 factorial experiment, each agent being fed at zero and at three non-zero doses. Methods of analysis designed explicitly for this study were derived to study interaction. These methods were supplemented by standard statistical methods appropriate for single agent studies. Neither synergism nor antagonism was demonstrated in these combined exposure studies. Findings for male and female animals were consistent. JF - Toxicology and Industrial Health AU - Fears, Thomas R AU - Elashoff, Robert M AU - Schneiderman, Marvin A AD - Biostatistics Branch National Cancer Institute Washington, D.C Y1 - 1989 PY - 1989 DA - 1989 SP - 1 EP - 23 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU UK VL - 5 IS - 1 SN - 0748-2337, 0748-2337 KW - Toxicology Abstracts KW - aflatoxin B1 KW - lead acetate KW - N-butyl-n-(4-hydroxybutyl)nitrosamine KW - statistical analysis KW - thiouracil. KW - Aflatoxin B1 KW - Statistics KW - N-Butyl-N-(4-hydroxybutyl)nitrosamine KW - Statistical analysis KW - Carcinogens KW - Antagonism KW - Lead KW - Cancer KW - X 24350:Industrial Chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/760153000?accountid=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+Industrial+Health&rft.atitle=The+Statistical+Analysis+of+a+Carcinogen+Mixture+Experiment.+III.+Carcinogens+With+Different+Target+Systems%2C+Aflatoxin+B1%2C+N-Butyl-N-%284-Hydroxybutyl%29Nitrosamine%2C+Lead+Acetate%2C+and+Thiouracil&rft.au=Fears%2C+Thomas+R%3BElashoff%2C+Robert+M%3BSchneiderman%2C+Marvin+A&rft.aulast=Fears&rft.aufirst=Thomas&rft.date=1989-01-01&rft.volume=5&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+Industrial+Health&rft.issn=07482337&rft_id=info:doi/10.1177%2F074823378900500101 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2010-10-01 N1 - Number of references - 14 N1 - Last updated - 2015-04-02 N1 - SubjectsTermNotLitGenreText - Aflatoxin B1; Statistics; N-Butyl-N-(4-hydroxybutyl)nitrosamine; Statistical analysis; Antagonism; Carcinogens; Cancer; Lead DO - http://dx.doi.org/10.1177/074823378900500101 ER - TY - JOUR T1 - Effects of ICRF-187 on the cardiac and renal toxicity of epirubicin in spontaneously hypertensive rats. AN - 75760463; 2495862 AB - A study was made of the protective effect of ICRF-187 against the cardiotoxicity and nephrotoxicity produced by epirubicin in spontaneously hypertensive rats (SHR). A total of 20 SHR were divided into 4 groups of 5 animals; the first group received i.v. injections of 1.5 mg/kg epirubicin; the second was treated with i.p. injections of 50 mg/kg ICRF-187 30 min before receiving 1.5 mg/kg epirubicin; the two remaining groups received ICRF-187 and saline, respectively, and served as controls. The experiment was terminated after 12 weekly injections (total cumulative dose of epirubicin, 18 mg/kg). Morphologic studies showed that severe cardiomyopathy manifested by myofibrillar loss and dilatation of the sarcoplasmic reticulum and nephropathy characterized by tubular dilatation and atrophy, protein casts in the lumina of renal tubules, and glomerular vacuolization occurred in SHR given epirubicin alone. Animals receiving the combination of ICRF-187 and epirubicin showed a marked reduction in the severity of cardiomyopathy and a moderate reduction in nephropathy. These changes, and their modification by ICRF-187, were similar to those we have previously observed in SHR treated with total cumulative doses of 12 mg/kg doxorubicin. Such pathologic changes were absent in animals receiving ICRF-187 or saline alone. The findings of this study suggest that ICRF-187 can be used clinically to prevent the cardiotoxicity of epirubicin, particularly in situations in which this drug may have to be given either in large doses or to patients at high risk of developing anthracycline cardiotoxicity. JF - Cancer chemotherapy and pharmacology AU - Dardir, M AU - Herman, E H AU - Ferrans, V J AD - Pathology Branch, National Heart, Lung and Blood Institute, Bethesda, MD 20892. Y1 - 1989 PY - 1989 DA - 1989 SP - 269 EP - 275 VL - 23 IS - 5 SN - 0344-5704, 0344-5704 KW - Piperazines KW - 0 KW - Epirubicin KW - 3Z8479ZZ5X KW - Razoxane KW - 5AR83PR647 KW - Index Medicus KW - Rats KW - Animals KW - Stereoisomerism KW - Drug Interactions KW - Rats, Inbred SHR KW - Myocardium -- pathology KW - Body Weight -- drug effects KW - Microscopy, Electron KW - Blood Pressure -- drug effects KW - Drug Evaluation, Preclinical KW - Male KW - Razoxane -- therapeutic use KW - Kidney -- pathology KW - Piperazines -- therapeutic use KW - Kidney -- drug effects KW - Heart -- drug effects KW - Epirubicin -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75760463?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effects+of+ICRF-187+on+the+cardiac+and+renal+toxicity+of+epirubicin+in+spontaneously+hypertensive+rats.&rft.au=Dardir%2C+M%3BHerman%2C+E+H%3BFerrans%2C+V+J&rft.aulast=Dardir&rft.aufirst=M&rft.date=1989-01-01&rft.volume=23&rft.issue=5&rft.spage=269&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 - 1989-06-02 N1 - Date created - 1989-06-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Correlates of Adolescents' Use of Smokeless Tobacco AN - 21158906; 11103625 AB - Data are presented on the prevalence and correlates of smokeless tobacco use among a group of 568 adolescents from five public schools located in western New York State. Two of the five schools were located in rural communities, two were located in suburbs of Buffalo, and one school was located in the city of Buffalo. Nineteen percent of males reported current use of smokeless tobacco. There was very little regular use among girls, although 18% reported having tried it. Sharp regional differ ences in the use of smokeless tobacco were observed with the highest percentage of users among students from rural communities. Experimentation with cigarette smok ing was associated with use of smokeless tobacco, however, few regular users of smoke less tobacco were current smokers. As is the case with cigarette smoking, social influ ences, especially those of peers and family members, were important factors associated with use of smokeless tobacco. Study findings suggest that programs that attempt to prepare students to cope with social pressures for using and stress the immediate negative consequences of use (i.e., stained teeth, bad breath) are more likely to be successful in discouraging adolescents from using smokeless tobacco than programs that only educate about the detrimental health effects of chewing and/or dipping tobacco. JF - Health Education & Behavior AU - Colborn, James W AU - Cummings, KMichael AU - Michalek, Arthur M AD - Health Promotions Science Branch, National Cancer Institute Y1 - 1989 PY - 1989 DA - 1989 SP - 91 EP - 100 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU UK VL - 16 IS - 1 SN - 1090-1981, 1090-1981 KW - smokeless tobacco KW - Health & Safety Science Abstracts KW - USA, New York, Buffalo KW - teeth KW - suburbs KW - Education KW - schools KW - Cigarette smoking KW - Tobacco KW - Adolescents KW - Rural areas KW - Urban areas KW - H 4000:Food and Drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/21158906?accountid=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=Health+Education+%26+Behavior&rft.atitle=Correlates+of+Adolescents%27+Use+of+Smokeless+Tobacco&rft.au=Colborn%2C+James+W%3BCummings%2C+KMichael%3BMichalek%2C+Arthur+M&rft.aulast=Colborn&rft.aufirst=James&rft.date=1989-01-01&rft.volume=16&rft.issue=1&rft.spage=91&rft.isbn=&rft.btitle=&rft.title=Health+Education+%26+Behavior&rft.issn=10901981&rft_id=info:doi/10.1177%2F109019818901600110 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2009-12-01 N1 - Last updated - 2011-12-15 N1 - SubjectsTermNotLitGenreText - suburbs; Education; schools; Cigarette smoking; Tobacco; teeth; Adolescents; Urban areas; Rural areas; USA, New York, Buffalo DO - http://dx.doi.org/10.1177/109019818901600110 ER - TY - JOUR T1 - Solution conformation of the actinomycin D related pentapeptide lactone using NMR and molecular modeling. AN - 16087754; 2647129 AB - A detailed description of the two observed solution conformations of the pentapeptide lactone fragment of actinomycin D is presented using the distance constraints obtained from two-dimensional nuclear Overhauser enhancement spectra in combination with minimum energy calculations. Low energy conformational states that are compatible with the experimental distances are found for each of the two conformers. For one conformer, an all trans peptide bond conformation is found with no intramolecular hydrogen bonds. For the other conformer, the D-Val-Pro and Pro-Sar peptide bonds were cis; this solution conformation is the same as that found in both the crystal structure of the pentapeptide lactone as well as of the native actinomycin D itself. (DBO) JF - Biopolymers AU - Mauger, AB AU - Gallagher, K S AU - Silverton, J V AU - Ferretti, JA AD - Lab. Chem., NHLBI, Natl. Inst. Health, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 1771 EP - 1780 VL - 28 IS - 10 SN - 0006-3525, 0006-3525 KW - N.M.R. KW - actinomycin D KW - conformation KW - fragments KW - lactone KW - models 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/16087754?accountid=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=unknown&rft.jtitle=Film+Index+International&rft.atitle=TERRA+INCOGNITA&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1959-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&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 - Identification and mutagenicity of the urinary metabolites of the mutagenic noncarcinogen 2,6-diaminotoluene. AN - 15832477; 2430120 AB - 2,6-Diaminotoluene (2,6-DAT) is a high production volume chemical; approximately 100 million pounds are produced annually in the synthesis of several dyes for furs and textiles and in the manufacture of 2,6-toluenediisocyanate for the manufacture of flexible polyurethane foams and elastomers. 2,6-DAT is mutagenic in the Ames/Salmonella test requiring metabolic activation, but was not carcinogenic to male or female rats or mice in 2-year bioassays. Following oral administration of super(14)C-labeled 2,6-DAT, 85% of the radioactivity was excreted in the urine within 24 hours. Resolution of the urine by reversed phase HPLC identified 4 metabolites, and no parent compound was excreted. Analysis by mass spectroscopy and nuclear magnetic resonance spectroscopy identified the metabolites as a) 3-hydroxy-2,6-DAT, b) 5-hydroxy-2-acetylamino-6-aminotoluene, c) 2-acetylamino-6-aminotoluene, and d) 2,6-di(acetylamino)-toluene. JF - Journal of Liquid Chromatography AU - Cunningham, M L AU - Burka, L T AU - Matthews, H B AD - Syst. Toxicol. Branch, NIEHS, Research Triangle Park, NC 27709, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 1407 EP - 1416 VL - 12 IS - 8 SN - 0148-3919, 0148-3919 KW - 2,6-diaminotoluene KW - identification KW - metabolites KW - mice KW - Toxicology Abstracts KW - Ames test KW - mutagenicity KW - X 24155:Biochemistry KW - X 24153:Metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15832477?accountid=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+Liquid+Chromatography&rft.atitle=Identification+and+mutagenicity+of+the+urinary+metabolites+of+the+mutagenic+noncarcinogen+2%2C6-diaminotoluene.&rft.au=Cunningham%2C+M+L%3BBurka%2C+L+T%3BMatthews%2C+H+B&rft.aulast=Cunningham&rft.aufirst=M&rft.date=1989-01-01&rft.volume=12&rft.issue=8&rft.spage=1407&rft.isbn=&rft.btitle=&rft.title=Journal+of+Liquid+Chromatography&rft.issn=01483919&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 - mutagenicity; Ames test ER - TY - JOUR T1 - Mortality associated with respiratory function and symptoms in advanced age. The Framingham Study. AN - 15829171; 2435080 AB - Pulmonary function, cigarette smoking, and respiratory symptoms were determined in 3,133 men and women at the 13th examination of the Framingham Study (1972 to 1976). Deaths in the subsequent 10-yr period were identified. Forced expiratory volume in one second and forced vital capacity were standardized for body size by dividing by the square of the height (FEV sub(1)/ht super(2), FVC/ht super(2)). As expected, mean values of these pulmonary function measures were lower in women compared to those in men, older participants compared to younger, smokers compared to non-smokers, and those with respiratory symptoms compared to those without. In men and women under 70 yr of age and women over 70 yr of age, FEV sub(1)/ht super(2) was inversely related to mortality after adjustment for age, smoking, and respiratory symptoms. In older men, FEV sub(1)/ht super(2) was not related to mortality, but symptoms of dyspnea were associated with increased risk of death. JF - American Journal of Respiratory and Critical Care Medicine AU - Sorlie, P D AU - Kannel, W B AU - O'Connor, G AD - NHLBI, NIH, Fed. Build., Rm. 3A10, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 379 EP - 384 VL - 140 IS - 2 SN - 0003-0805, 0003-0805 KW - cigarette smoking KW - function KW - Toxicology Abstracts KW - lung KW - man KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15829171?accountid=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+Respiratory+and+Critical+Care+Medicine&rft.atitle=Mortality+associated+with+respiratory+function+and+symptoms+in+advanced+age.+The+Framingham+Study.&rft.au=Sorlie%2C+P+D%3BKannel%2C+W+B%3BO%27Connor%2C+G&rft.aulast=Sorlie&rft.aufirst=P&rft.date=1989-01-01&rft.volume=140&rft.issue=2&rft.spage=379&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 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - lung; man ER - TY - JOUR T1 - The significance and scope of reproductive tract infections among Third World women. AN - 15803955; 2407513 AB - Due to biomedical, behavioral and societal factors, reproductive tract infections are widespread in the Third World. Without early diagnosis and accurate therapy, their complications severely compromise women's health, fertility and productivity; infant health and survival; and the effectiveness of family planning programs. Clinicians and public health planners can address these treatable syndromes through research and services in socially acceptable settings including family planning, prenatal and MCH clinics, Specific approaches are discussed. JF - INT. J. GYNECOL. OBSTET. AU - Wasserheit, J N AD - STD Branch, DMID-NIAID, Westwood Build., Rm. 748, NIH, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 145 EP - 168 IS - suppl. 3 KW - man KW - females KW - developing countries KW - infection KW - clinical aspects KW - Microbiology Abstracts B: Bacteriology KW - genital tract KW - sexually-transmitted diseases KW - J 02847:Genitourinary tract KW - J 02849:Sexually-transmitted diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15803955?accountid=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=INT.+J.+GYNECOL.+OBSTET.&rft.atitle=The+significance+and+scope+of+reproductive+tract+infections+among+Third+World+women.&rft.au=Wasserheit%2C+J+N&rft.aulast=Wasserheit&rft.aufirst=J&rft.date=1989-01-01&rft.volume=&rft.issue=suppl.+3&rft.spage=145&rft.isbn=&rft.btitle=&rft.title=INT.+J.+GYNECOL.+OBSTET.&rft.issn=&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 - genital tract; sexually-transmitted diseases ER - TY - JOUR T1 - Cardiorespiratory effects of immunotherapy with interleukin-2. AN - 15802253; 2413426 AB - All patients treated with recombinant IL-2 alone, with transfer of LAK cells, or with cyclophosphamide between December 1984 and September 1987 (total of 423 treatment courses in 317 total patients) were evaluated as to the development of significant cardiorespiratory toxicity. Of the 423 treatment courses, only 1.8% were associated with severe peripheral edema and only 2.8% and 3.1%, respectively, were associated with significant ascites or pleural effusions. Thirty-nine of 423 patients (9.2%) had severe respiratory distress and 27 patients required intubation (6.4%). Cardiovascular effects included tachycardia and hypotension requiring vasopressor administration in 65% and intravenous (IV) fluid administration. Weight gain greater than or equal to 10% of body weight was noted in 32% of the 423 patients. Arrhythmias were primarily supraventricular (9.7%) and responded well to conventional medical treatments. JF - Journal of Clinical Oncology AU - Lee, R E AU - Lotze, M T AU - Skibber, J M AU - Tucker, E AU - Bonow, RO AU - Ognibene, F P AU - Carrasquillo, JA AU - Shelhamer, J H AU - Parrillo, JE AU - Rosenberg, SA AD - Surg. Branch, NCI, Build. 10, Rm. 2B47, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 7 EP - 20 VL - 7 IS - 1 SN - 0732-183X, 0732-183X KW - interleukin 2 KW - Toxicology Abstracts KW - side effects KW - lung KW - heart KW - immunotherapy KW - man KW - X 24113:Side effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15802253?accountid=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+Clinical+Oncology&rft.atitle=Cardiorespiratory+effects+of+immunotherapy+with+interleukin-2.&rft.au=Lee%2C+R+E%3BLotze%2C+M+T%3BSkibber%2C+J+M%3BTucker%2C+E%3BBonow%2C+RO%3BOgnibene%2C+F+P%3BCarrasquillo%2C+JA%3BShelhamer%2C+J+H%3BParrillo%2C+JE%3BRosenberg%2C+SA&rft.aulast=Lee&rft.aufirst=R&rft.date=1989-01-01&rft.volume=7&rft.issue=1&rft.spage=7&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 - 2011-12-13 N1 - SubjectsTermNotLitGenreText - side effects; heart; lung; man; immunotherapy ER - TY - JOUR T1 - Physical activity and risk of cancer in the NHANES I population. AN - 15799077; 2411791 AB - We studied the relation between self-reported physical activity and cancer in the first National Health and Nutrition Examination Survey (NHANES I) cohort, originally examined between 1971-75, and followed prospectively through the Epidemiologic Follow-up Study (NHEFS), conducted between 1982-84. Among 5,138 men and 7,407 women 25-74 years old, for nonrecreational activity we observed increased risk of cancer among inactive individuals compared to very active persons (for men, relative risk (RR) 1.8,95% confidence interval (CI) = 1.4, 2.4; for women RR 1.3, 95% CI = 1.0, 1.8). These findings were unchanged after adjustment for cigarette smoking, body mass index (BMI), and other potential confounders. Sites which demonstrated stronger inactivity-cancer associations included colorectum and lung among men, and breast and cervix among women, although these findings for women were based on relatively few cases. JF - American Journal of Public Health AU - Albanes, D AU - Blair, A AU - Taylor, PR AD - Cancer Prev. Stud. Branch, Div. Cancer Prev. and Control, NCI, NIH, EPN 211, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 744 EP - 750 VL - 79 IS - 6 SN - 0090-0036, 0090-0036 KW - cancer KW - exercise KW - Health & Safety Science Abstracts KW - nutrition KW - surveys KW - H SM10.21:CANCER UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15799077?accountid=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+Public+Health&rft.atitle=Physical+activity+and+risk+of+cancer+in+the+NHANES+I+population.&rft.au=Albanes%2C+D%3BBlair%2C+A%3BTaylor%2C+PR&rft.aulast=Albanes&rft.aufirst=D&rft.date=1989-01-01&rft.volume=79&rft.issue=6&rft.spage=744&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 revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - nutrition; surveys ER - TY - JOUR T1 - Bioreactor operation for the production of exotoxin A by Pseudomonas aeruginosa . AN - 15798169; 2407063 AB - Discussed here are experiments aimed at developing an optimal production strategy for an exocellular protein under regulatory control, i.e. exotoxin A (ETA), which is produced by Pseudomonas aeruginosa . Using established techniques from molecular biology (i.e. Northern blots), information on ETA mRNA levels could be obtained and used to improve the production strategy for this exotoxin. The implications for other gene products under regulatory control also are presented. JF - Biotechnology and Bioengineering AU - Blumentals, I I AU - Kelly, R M AU - Shiloach, J AD - Biotechnol. Unit, Build. 6, B1-33, NIDDK, NIH, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 1214 EP - 1220 VL - 34 IS - 9 SN - 0006-3592, 0006-3592 KW - Pseudomonas aeruginosa KW - production KW - optimization KW - exotoxin A KW - bioreactors KW - Biotechnology and Bioengineering Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology KW - J 02822:Biosynthesis and physicochemical properties KW - W 30600:Fermentation and process engineering KW - A 01023:Others UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15798169?accountid=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=Biotechnology+and+Bioengineering&rft.atitle=Bioreactor+operation+for+the+production+of+exotoxin+A+by+Pseudomonas+aeruginosa+.&rft.au=Blumentals%2C+I+I%3BKelly%2C+R+M%3BShiloach%2C+J&rft.aulast=Blumentals&rft.aufirst=I&rft.date=1989-01-01&rft.volume=34&rft.issue=9&rft.spage=1214&rft.isbn=&rft.btitle=&rft.title=Biotechnology+and+Bioengineering&rft.issn=00063592&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 - bioreactors ER - TY - JOUR T1 - Nucleotide and deduced amino acid sequences for the four variable domains of the major outer membrane proteins of the 15 Chlamydia trachomatis serovars. AN - 15793048; 2398448 AB - The amino acid sequences of major outer membrane proteins (MOMPs) from Chlamydia trachomatis serovars A, B, C, L1, and L2 are predominantly conserved but have four variable domains (VDs) in which major neutralizing and serotyping antigenic determinants are located. Because these MOMP VDs are primarily responsible for antigenic differences between serovars and are associated with important immunological and biological properties, we undertook studies focused on defining these sequences within the MOMPs of all 15 C. trachomatis serovars. These findings should be useful for predicting MOMP antigenic determinants and testing the antigenic properties of these VDs by using synthetic peptides corresponding to each MOMP VD. JF - Infection and Immunity AU - Yuan, Ying AU - Zhang, Y-X AU - Watkins, NG AU - Caldwell, H D AD - Lab. Microb. Struct. and Funct., Rocky Mt. Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 1040 EP - 1049 VL - 57 IS - 4 SN - 0019-9567, 0019-9567 KW - Chlamydia trachomatis KW - amino acid sequence KW - antigenic determinants KW - genes KW - nucleotide sequence KW - outer membranes KW - predictions KW - proteins KW - serovars KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - N 14640:Structure & sequence KW - G 07320:Bacterial genetics KW - J 02727:Amino acids, peptides and proteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15793048?accountid=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=unknown&rft.jtitle=Film+Index+International&rft.atitle=JULIE+LA+ROUSSE&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1959-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&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 - outer membranes ER - TY - JOUR T1 - Preliminary study on treatment of septic shock patients with antilipopolysaccharide IgG from blood donors. AN - 15641898; 2287096 AB - A novel intravenous therapy consisting of polyvalent IgG antibodies to lipopolysaccharide (LPS, endotoxin) obtained from screening of blood donors was used for treatment of patients with profound septic endotoxin shock. Investigation of the anti-LPS IgG pharmacokinetics in the 10 patients revealed time related changes in the plasma concentrations of anti-LPS IgG, endotoxin, tumour necrosis factor (TNF) and the clinical parameters. A decrease in serum concentrations of IgG and IgM antibodies to LPS was observed prior to the immunotherapy as well as in a clinical example of lethal septicemia without anti-LPS immunotherapy. Increasing serum concentrations of anti-LPS IgG during antibody infusion was followed by a decrease in the concentration of endotoxin and TNF. JF - Scandinavian Journal of Infectious Diseases AU - Fomsgaard, A AU - Baek, L AU - Fomsgaard, J S AU - Engquist, A AD - Lab. Infect. Dis., NIAID/NIH, 12441 Parklawn Dr., Rockville, MD 20852, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 697 EP - 708 VL - 21 IS - 6 SN - 0036-5548, 0036-5548 KW - septic shock KW - treatment KW - antibodies KW - blood donors KW - lipopolysaccharides KW - Microbiology Abstracts B: Bacteriology KW - endotoxins KW - immunoglobulin G KW - J 02855:Human Bacteriology: Others UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15641898?accountid=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=unknown&rft.jtitle=Film+Index+International&rft.atitle=DR%C3%94LES+DE+PH%C3%89NOM%C3%88NES&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1959-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&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 - endotoxins; immunoglobulin G ER - TY - JOUR T1 - Heat-shock cognate protein (hsc71) and related proteins in mouse spermatogenic cells. AN - 15632032; 2279739 AB - A monoclonal antibody (13D3) has been developed that recognizes a 71 kilodalton (71 kDa) protein on two-dimensional immunoblots of proteins extracted from a mixture of mouse spermatogenic cells (mainly pachytene spermatocytes and spermatids). This protein was shown by immunoblotting and adenosine triphosphate (ATP)-binding characteristics to be identical to a 71 kDa mouse heat-shock cognate (hsc) protein, hsc71, present in 3T3 cells. Along with a 70 kDa heat-shock inducible protein (hsp70), and a 74 kDa heat-shock cognate protein (hsc74), hsc71 is a product of the mouse HSP70 multigene family. The results suggest that unique heat-shock proteins are synthesized late in spermatogenesis. JF - Biology of Reproduction AU - Maekawa, M AU - O'Brien, DA AU - Allen, R L AU - Eddy, E M AD - LRDT, C4-01, NIEHS/NIH, Research Triangle Park, NC 27709, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 843 EP - 852 VL - 40 IS - 4 SN - 0006-3363, 0006-3363 KW - heat shock KW - mice KW - protein hsc71 KW - spermatogenesis 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/15632032?accountid=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=unknown&rft.jtitle=Film+Index+International&rft.atitle=La+MAISON+DE+BERNARDA&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1959-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&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 - A shortened synthesis of 4-(3-aminopropyl) pyrazole, an affinity ligand for alcohol dehydrogenase purification. AN - 15611262; 2257166 AB - The most efficient, specific and rapid procedures for alcohol dehydrogenase (ADH) purification utilize immobilized 4-(3-aminopropyl) pyrazole to which pyrazole sensitive ADHs i.e. class I isozymes, bind. Because of the length of the reported synthesis of this affinity resin, we synthesized the 4-(3-aminopropyl) pyrazole ligand by a new method in two steps from commercially available nicotinaldehyde. The ligand synthesized by this simplified procedure was directly coupled to the chain-extended support, Activated CH-Sepharose 4B, to yield the same ligand-spacer combination. Human and hamster class I ADHs purified using this resin were homogenous by SDS-PAGE followed by silver staining. Specific activity and recovery of human class I ADH were comparable to those previously reported. JF - Preparative Biochemistry and Biotechnology AU - Miller, SPF AU - Giri, PR AU - Goldman, D AD - Lab. Clin. Stud., NIAAA, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 129 EP - 139 VL - 19 IS - 2 SN - 0032-7484, 0032-7484 KW - 4-(3-aminopropyl)pyrazole KW - affinity KW - alcohol dehydrogenase KW - ligands KW - man KW - purification KW - use 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/15611262?accountid=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=Preparative+Biochemistry+and+Biotechnology&rft.atitle=A+shortened+synthesis+of+4-%283-aminopropyl%29+pyrazole%2C+an+affinity+ligand+for+alcohol+dehydrogenase+purification.&rft.au=Miller%2C+SPF%3BGiri%2C+PR%3BGoldman%2C+D&rft.aulast=Miller&rft.aufirst=SPF&rft.date=1989-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&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 - Seasonal affective disorder and visual impairment: Two case studies. AN - 15574907; 2229001 AB - Winter depressive episodes in patients with seasonal affective disorder are induced by light deficiency and are successfully treated by enhancing environmental light. The authors investigated the role of abnormal visual information processing in the genesis of seasonal affective disorder symptoms by examining two patients with impaired vision and recurrent winter depressions. The first patient developed winter depressions after developing a traumatic cataract in one eye, and was helped by light therapy. The second patient, fully blind since she was 1 year old, nonetheless suffered as an adult from winter depressions, which responded to bright -- but not to dim -- light treatment. The authors discuss the implications of these findings. JF - Journal of Clinical Psychiatry AU - Rosenthal, N E AU - DellaBella, P AU - Hahn, L AU - Skwerer, R G AD - Unit Outpatient Stud., Clin. Psychobiol. Branch, NIMH, Build. 10/4S-239, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 469 EP - 472 VL - 50 IS - 12 SN - 0160-6689, 0160-6689 KW - seasonal affective disorder KW - vision KW - depression KW - Health & Safety Science Abstracts KW - psychology KW - H SM9.7:HUMAN FACTORS UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15574907?accountid=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=Journal+of+Clinical+Psychiatry&rft.atitle=Seasonal+affective+disorder+and+visual+impairment%3A+Two+case+studies.&rft.au=Rosenthal%2C+N+E%3BDellaBella%2C+P%3BHahn%2C+L%3BSkwerer%2C+R+G&rft.aulast=Rosenthal&rft.aufirst=N&rft.date=1989-01-01&rft.volume=50&rft.issue=12&rft.spage=469&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Psychiatry&rft.issn=01606689&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 - psychology ER - TY - JOUR T1 - Isolation and immunological properties of adenosine kinase. AN - 15562093; 2221393 AB - Bovine liver adenosine kinase is a 43 kDa protein that catalyzes the transfer of phosphate from GTP or ATP to adenosine. Its immunological properties were compared to other GTP-binding proteins of similar to 40 kDa, in particular those involved in signal transduction, such as G sub(s) and G sub(i), the stimulatory and inhibitory regulatory proteins of adenylyl cyclase, G sub(t), from the visual excitation system, and G sub(o), a similar protein of unknown function. The GTP-binding proteins do not exhibit immunological cross-reactivity. JF - Preparative Biochemistry and Biotechnology AU - Noda, M AU - Kunz, B C AU - Tsai, Su-Chen AU - Adamik, R AU - Murtagh, J J AU - Chen, Hao-Chia AU - Halpern, J L AU - Moss, J AD - Lab. Cell. Metab., NHLBI, Natl. Inst. Health, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 351 EP - 361 VL - 19 IS - 4 SN - 0032-7484, 0032-7484 KW - adenosine kinase KW - cattle KW - characterization KW - isolation KW - liver 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/15562093?accountid=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=Preparative+Biochemistry+and+Biotechnology&rft.atitle=Isolation+and+immunological+properties+of+adenosine+kinase.&rft.au=Noda%2C+M%3BKunz%2C+B+C%3BTsai%2C+Su-Chen%3BAdamik%2C+R%3BMurtagh%2C+J+J%3BChen%2C+Hao-Chia%3BHalpern%2C+J+L%3BMoss%2C+J&rft.aulast=Noda&rft.aufirst=M&rft.date=1989-01-01&rft.volume=19&rft.issue=4&rft.spage=351&rft.isbn=&rft.btitle=&rft.title=Preparative+Biochemistry+and+Biotechnology&rft.issn=00327484&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 - A rapid method for in situ hybridization for viral DNA in brain biopsies from patients with AIDS. AN - 15479759; 2214006 AB - Brain biopsy is often necessary in the diagnosis of neurological complications found in AIDS patients. We describe here a rapid method of tissue preparation and in situ DNA hybridization for detecting JC virus DNA in frozen brain biopsy sections which allows the diagnosis of progressive multifocal leukoencephalopathy to be established on the day of surgery. Once the diagnosis is established, therapeutic and management decisions can be made more easily. The commercial availability of biotinylated probes for several of the DNA viruses most frequently encountered in brain infections of AIDS patients will provide wide application of these techniques to patient management. JF - AIDS AU - Houff, SA AU - Katz, D AU - Kufta, C V AU - Major, E O AD - LVMP, NINDS, Natl. Inst. Health, Build. 36, Rm. 5D-04, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 843 EP - 845 VL - 3 IS - 12 SN - 0269-9370, 0269-9370 KW - acquired immune deficiency syndrome KW - clinical aspects KW - biopsy KW - brain KW - hybridization analysis KW - leukoencephalitis KW - tomography KW - Biotechnology and Bioengineering Abstracts; Virology & AIDS Abstracts KW - W 30507:Diagnostic KW - V 22004:AIDS: Clinical aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15479759?accountid=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&rft.atitle=A+rapid+method+for+in+situ+hybridization+for+viral+DNA+in+brain+biopsies+from+patients+with+AIDS.&rft.au=Houff%2C+SA%3BKatz%2C+D%3BKufta%2C+C+V%3BMajor%2C+E+O&rft.aulast=Houff&rft.aufirst=SA&rft.date=1989-01-01&rft.volume=3&rft.issue=12&rft.spage=843&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-12 N1 - SubjectsTermNotLitGenreText - biopsy; brain; leukoencephalitis; hybridization analysis; tomography ER - TY - JOUR T1 - Phosphorylation of myelin basic protein and peptides by ganglioside-stimulated protein kinase. AN - 15458614; 2188102 AB - Rabbit myelin basic protein (MBP) was phosphorylated by a ganglioside-stimulated protein kinase to a stoichiometry of 1.4 and 2.1 mol phosphate/mol MBP in the presence and absence of G sub(T1b), respectively. Two-dimensional peptide mapping analyses revealed that two of the sites of phosphorylation were distinct from those catalyzed by cAMP-dependent protein kinase or protein kinase C. Phosphorylation of one of these sites by ganglioside-stimulated protein kinase was inhibited by G sub(T1b), suggesting that the inhibitory effect of gangliosides on MBP phosphorylation may be substrate-directed. JF - Biochemical and Biophysical Research Communications AU - Jesse Chan, Kai-Foon AD - Lab. Exp. Neuropathol., NINDS, NIH, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 93 EP - 100 VL - 165 IS - 1 SN - 0006-291X, 0006-291X KW - gangliosides KW - myelin basic protein KW - phosphorylation KW - protein kinase KW - rabbits KW - role KW - stimulation 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/15458614?accountid=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=Phosphorylation+of+myelin+basic+protein+and+peptides+by+ganglioside-stimulated+protein+kinase.&rft.au=Jesse+Chan%2C+Kai-Foon&rft.aulast=Jesse+Chan&rft.aufirst=Kai-Foon&rft.date=1989-01-01&rft.volume=165&rft.issue=1&rft.spage=93&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 - Effect of pH on mutagenesis by thiols in Salmonella typhimurium TA102. AN - 15451773; 2180563 AB - The mutagenicity of thiol (SH)-containing compounds was tested in Salmonella typhimurium TA102 in the liquid preincubation method. Cysteinyl-glycine (CG), cysteine ethyl ester (CEE), L- and D-penicillamine (PA), cystine (Cys) and glutathione (GSH) were mutagenic to strain TA102 without metabolic activation. On a molar basis, CG was the most potent mutagen. The mutagenicity of the remaining compounds decreased in the order specified above. The mutagenic response of each thiol-containing compound was a function of the pK sub(a) of the thiol group and the pH of the preincubation mixture. This indicates that a thiolate anion, rather than a free thiol, is required for mutagenesis. JF - Mutation Research AU - Stark, A AU - Arad, A AU - Siskindovich, S AU - Pagano, DA AU - Zeiger, E AD - Cell. and Genet. Toxicol. Branch, NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 89 EP - 94 VL - 224 IS - 1 SN - 0027-5107, 0027-5107 KW - Salmonella typhimurium KW - effects on KW - cysteinyl-glycine KW - cysteine ethyl ester KW - cysteine KW - glutathione KW - L-penicillamine KW - D-penicillamine KW - thiols KW - Toxicology Abstracts; Microbiology Abstracts B: Bacteriology KW - mutagenesis KW - pH KW - X 24240:Miscellaneous KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15451773?accountid=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=Mutation+Research&rft.atitle=Effect+of+pH+on+mutagenesis+by+thiols+in+Salmonella+typhimurium+TA102.&rft.au=Stark%2C+A%3BArad%2C+A%3BSiskindovich%2C+S%3BPagano%2C+DA%3BZeiger%2C+E&rft.aulast=Stark&rft.aufirst=A&rft.date=1989-01-01&rft.volume=224&rft.issue=1&rft.spage=89&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 - 2011-12-12 N1 - SubjectsTermNotLitGenreText - mutagenesis; pH ER - TY - JOUR T1 - Partial purification and characterization of the specific protein-lysine N-methyltransferase of YL32, a yeast ribosomal protein. AN - 15447397; 2184023 AB - YL23 and YL32 are two of the three most heavily methylated ribosomal proteins of Saccharomyces cerevisiae . Using an in vitro assay, it was determined that they are methylated by two distinct enzymes. The protein-lysine N-methyltransferase that methylates YL32 was partially purified by affinity and ion-exchange chromatography. Its molecular mass was estimated to be 82 kDa, and its isoelectric point to be 4.45. Optimum activity was expressed at pH 7.5, and the enzyme was irreversibly inactivated at pH lower than 5.0. Formation of epsilon -N-dimethyllysine was observed to occur in two steps via epsilon -N-monomethyllysine. Like other protein-lysine N-methyltransferases, the methylase of YL32 exhibits a high substrate specificity. JF - Biochimica et Biophysica Acta: Protein Structure and Molecular Enzymology AU - Lobet, Y AU - Lhoest, J AU - Colson, C AD - Lab. Pathobiol., Rocky Mt. Lab., NIH/NIAID, Hamilton, MT 59840, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 224 EP - 231 VL - 997 IS - 3 SN - 0167-4838, 0167-4838 KW - Saccharomyces cerevisiae KW - activity KW - protein lysine N-methyltransferase KW - ribosomal protein YL23 KW - substrates KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - K 03020:Fungi UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15447397?accountid=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=Biochimica+et+Biophysica+Acta%3A+Protein+Structure+and+Molecular+Enzymology&rft.atitle=Partial+purification+and+characterization+of+the+specific+protein-lysine+N-methyltransferase+of+YL32%2C+a+yeast+ribosomal+protein.&rft.au=Lobet%2C+Y%3BLhoest%2C+J%3BColson%2C+C&rft.aulast=Lobet&rft.aufirst=Y&rft.date=1989-01-01&rft.volume=997&rft.issue=3&rft.spage=224&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+Biophysica+Acta%3A+Protein+Structure+and+Molecular+Enzymology&rft.issn=01674838&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 - Bradykinin and kininogens in bovine milk. AN - 15426643; 2171531 AB - Two peptides exhibiting kinin activity in an isolated rat uterus assay were purified from pasteurized skim bovine milk. The amino acid sequence of the more prominent peptide was found to be that of bradykinin. Partially purified kinin preparations were also obtained from N-tosyl-L-phenylalanyl chloromethyl ketone-treated trypsin digests of non-fat dry milk and insoluble lactalbumin. The application of fast atom bombardment/mass spectrometry permitted detection of the bradykinin protonated molecular ion in each of these samples. Fast atom bombardment/mass spectrometry analysis further confirmed the occurrence of bradykinin in a pancreatic kallikrein digest of a partially purified bovine milk kininogen preparation. In apparent contrast with bovine plasma kininogens, the forms of kininogen which occur in milk include a high M sub(r) kininogen and a low M sub(r) kininogen. Kinin formation from the high kininogen is catalyzed by porcine pancreatic kallikrein or trypsin. JF - Journal of Biological Chemistry AU - Wilson, W E AU - Lazarus, L H AU - Tomer, K B AD - P.O. Box 12233, NIEHS, Research Traingle Park, NC 27709, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 17777 EP - 17783 VL - 264 IS - 30 SN - 0021-9258, 0021-9258 KW - bradykinin KW - characterization KW - cow's milk KW - isolation KW - kininogen 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/15426643?accountid=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=Psychiatric+Quarterly&rft.atitle=The+Closing+of+a+State+Hospital%3A+What+Is+the+Quality+of+Patients%27+Lives+One+Year+Post-Release%3F&rft.au=Solomon%2C+Phyllis&rft.aulast=Solomon&rft.aufirst=Phyllis&rft.date=1992-10-01&rft.volume=63&rft.issue=3&rft.spage=279&rft.isbn=&rft.btitle=&rft.title=Psychiatric+Quarterly&rft.issn=00332720&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 - Partial unfolding of dodecameric glutamine synthetase from Escherichia coli : Temperature-induced, reversible transitions of two domains. AN - 15422056; 2154963 JF - Biochemistry (Washington) AU - Shrake, A AU - Fisher, M T AU - McFarland, P J AU - Ginsburg, A AD - NHLBI/NIH, Build. 3, Rm. 208, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 6281 EP - 6294 VL - 28 IS - 15 SN - 0006-2960, 0006-2960 KW - Escherichia coli KW - analysis KW - domains KW - glutamate-ammonia ligase KW - induction KW - temperature KW - transitions KW - unfolding 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/15422056?accountid=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=unknown&rft.jtitle=Film+Index+International&rft.atitle=La+ENCRUCIJADA&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1959-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&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 the spoT gene of Escherichia coli . AN - 15420010; 2155344 AB - The Escherichia coli spoT gene encodes a guanosine-3',5'-bispyrophosphate (ppGpp) 3'-pyrophosphohydrolase known to be responsible for cellular (ppGpp) degradation. The DNA sequence of the spoT region is presented. The spoT gene is deduced to be 702 codons long, with a probable UUG initiation codon, and a deduced mass of 79,342 daltons. JF - Journal of Biological Chemistry AU - Sarubbi, E AU - Rudd, KE AU - Xiao, Hua AU - Ikehara, K AU - Kalman, M AU - Cashel, M AD - Build. 6, Rm. 335, Lab. Mol. Genet., NICHD, NIH, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 15074 EP - 15082 VL - 264 IS - 25 SN - 0021-9258, 0021-9258 KW - Escherichia coli KW - amino acid sequence KW - genes KW - guanosine 3',5'-bis(diphosphate) 3'-pyrophosphatase KW - nucleotide sequence KW - predictions KW - spoT gene KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - N 14640:Structure & sequence KW - G 07320:Bacterial genetics KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15420010?accountid=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=unknown&rft.jtitle=Film+Index+International&rft.atitle=CINE+BALLETS+DE+PARIS&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1959-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&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 - Xenobiotic metabolism by isolated pulmonary cells. AN - 15418666; 2156243 AB - In many instances the Clara cell is a target site for chemicals requiring metabolic activation for cellular damage. Two other cell types commonly compared for their role in activation and detoxification of xenobiotics are the alveolar type II cell and the alveolar macrophage. This review compares some of the data that has been accumulated on the metabolism of xenobiotics by these three cell types. Some conclusions about the distribution of enzyme components in the cell populations of different species are reached and some suggestions are offered for future directions of research in this area. JF - Pharmacology & Therapeutics AU - Devereux, T R AU - Domin, BA AU - Philpot, R M AD - Lab. Biochem. Risk Anal., NIEHS, Research Triangle Park, NC 27709, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 243 EP - 256 VL - 41 IS - 1-2 SN - 0163-7258, 0163-7258 KW - xenobiotics KW - metabolism KW - in vitro KW - cells KW - Toxicology Abstracts KW - reviews KW - lung KW - X 24250:Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15418666?accountid=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=unknown&rft.jtitle=Film+Index+International&rft.atitle=Les+PETITS+CHATS&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1959-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-12 N1 - SubjectsTermNotLitGenreText - lung; reviews ER - TY - JOUR T1 - Crystal structure of a cAMP-independent form of catabolite gene activator protein with adenosine substituted in one of two cAMP-binding sites. AN - 15417190; 2155508 AB - Catabolite gene activator protein (CAP) in the presence of cAMP stimulates transcription from several operons in Escherichia coli . A cAMP-independent variant, in which Ala-144 is replaced by Thr (CAP91), is activated by analogues of cAMP, such as adenosine, which do not activate the wild-type CAP. In order to test the effect of adenosine on the structure, a crystal of CAP91 grown as a complex with cAMP was soaked in a solution of 10 mM adenosine, and X-ray diffraction data were measured to 3.5-angstrom resolution. JF - Biochemistry (Washington) AU - Vaney, M-C AU - Gilliland, G L AU - Harman, J G AU - Peterkofsky, A AU - Weber, I T AD - NCI-Frederick Cancer Res. Facil., BRI-Basic Res. Program, Crystallogr. Lab., Frederick, MD 21701, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 4568 EP - 4574 VL - 28 IS - 11 SN - 0006-2960, 0006-2960 KW - Escherichia coli KW - X-ray diffraction KW - binding KW - catabolite activator protein KW - cyclic AMP KW - sites KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology KW - J 02727:Amino acids, peptides and proteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15417190?accountid=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=Crystal+structure+of+a+cAMP-independent+form+of+catabolite+gene+activator+protein+with+adenosine+substituted+in+one+of+two+cAMP-binding+sites.&rft.au=Vaney%2C+M-C%3BGilliland%2C+G+L%3BHarman%2C+J+G%3BPeterkofsky%2C+A%3BWeber%2C+I+T&rft.aulast=Vaney&rft.aufirst=M-C&rft.date=1989-01-01&rft.volume=28&rft.issue=11&rft.spage=4568&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 - X-ray diffraction ER - TY - JOUR T1 - Conserved sequence elements upstream and downstream from the transcription initiation site of the Caulobacter crescentus rrnA gene cluster. AN - 15416835; 2158953 AB - The nucleotide sequence and in vivo transcription start sites for rrnA , one of the two rRNA gene clusters of the eubacterium Caulobacter crescentus , have been determined. Two transcription start sites, a major and minor, for the rRNA gene cluster are located more than 700 nucleotides upstream from the 16 S rRNA gene. Transcription was detected from only the major start site in the swarmer cells. JF - Journal of Molecular Biology AU - Amemiya, K AD - Natl. Inst. Health (NINDS), Lab. Viral and Mol. Pathog., Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 245 EP - 254 VL - 210 IS - 2 SN - 0022-2836, 0022-2836 KW - genes KW - rrnA gene KW - nucleotide sequence KW - Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts B: Bacteriology KW - promoters KW - Caulobacter crescentus KW - N 14640:Structure & sequence KW - G 07320:Bacterial genetics KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15416835?accountid=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=Conserved+sequence+elements+upstream+and+downstream+from+the+transcription+initiation+site+of+the+Caulobacter+crescentus+rrnA+gene+cluster.&rft.au=Amemiya%2C+K&rft.aulast=Amemiya&rft.aufirst=K&rft.date=1989-01-01&rft.volume=210&rft.issue=2&rft.spage=245&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 revised - 2006-11-01 N1 - Last updated - 2011-12-12 N1 - SubjectsTermNotLitGenreText - Caulobacter crescentus; promoters ER - TY - JOUR T1 - Blockade of only spinal alpha sub(1) adrenoceptors is insufficient to attenuate DDT-induced alterations in motor function. AN - 15403830; 2153070 AB - Male Fischer 344N rats were chronically implanted with an intrathecal cannula and gavaged with p,p'-DDT (1,1,1-trichloro-2,2-bis-(p-chlorophenyl)-ethane; 30 or 45 mg/kg) or corn oil. Seven hours later, subjects were intrathecally infused with vehicle, 15, 30, 60, or 120 mu g of prazosin (an alpha sub(1)-adrenergic antagonist). Spectral analysis of bodily movements was performed 7.5, 8, and 10 hr after DDT administration. The data indicate that while intrathecal prazosin will attenuate DDT induced motor dysfunction, this effect requires blockade of alpha sub(1) adrenoceptors in regions other than solely the spinal cord. JF - Toxicology and Applied Pharmacology AU - Herr, D W AU - Mailman, R B AU - Tilson, HA AD - Lab. Mol. and Integrative Neurosci. NIEHS, MD 17-01, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 11 EP - 26 VL - 101 IS - 1 SN - 0041-008X, 0041-008X KW - DDT KW - disruption KW - receptors KW - antagonists KW - injection KW - effects on KW - alpha 1-adrenergic KW - rats KW - Animal Behavior Abstracts; Toxicology Abstracts; CSA Neurosciences Abstracts KW - spinal cord KW - motor activity KW - X 24131:Acute exposure KW - Y 25667:Mammals (excluding primates) KW - N3 11139:Toxicological and psychoactive drug correlates UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15403830?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocialservices&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Administration+and+Policy+in+Mental+Health&rft.atitle=The+Future+of+CMHCs%3A+The+Role+of+the+State&rft.au=Harper%2C+Robert+J&rft.aulast=Harper&rft.aufirst=Robert&rft.date=1994-03-01&rft.volume=21&rft.issue=4&rft.spage=319&rft.isbn=&rft.btitle=&rft.title=Administration+and+Policy+in+Mental+Health&rft.issn=0894587X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-12 N1 - SubjectsTermNotLitGenreText - motor activity; spinal cord ER - TY - JOUR T1 - Crystallization and preliminary X-ray diffraction studies of bovine recombinant immune interferon. AN - 15400391; 2145797 AB - Reproducible conditions have been established for the crystallization of recombinant bovine immune interferon. Two crystalline forms of this protein were obtained. A tetragonal form, space group P422, with unit cell dimensions a = b = 59 multiplied by 0 angstrom and c = 125 multiplied by 7 angstrom and an orthorhombic form, space group P2 sub(1)2 sub(1)2 sub(1), with unit cell dimensions a = 42 multiplied by 80 angstrom, b = 79 multiplied by 90 angstrom and c = 85 multiplied by 64 angstrom were obtained under similar crystallization conditions. The orthorhombic form diffracts to 2 multiplied by 6 angstrom resolution, contains a single interferon dimer in the asymmetric unit of structure and is suitable for X-ray diffraction analysis. JF - Journal of Molecular Biology AU - Rubin, J R AU - Burton, LE AD - NCI-Frederick Cancer Res. Facil., BRI-Basic Res. Program, P.O. Box B, Frederick, MD 21701, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 829 EP - 831 VL - 209 IS - 4 SN - 0022-2836, 0022-2836 KW - 2.6 angstrom KW - X-ray crystallography KW - cattle KW - gamma -interferon KW - resolution KW - tertiary structure KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - F 06773:Interferons UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15400391?accountid=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=unknown&rft.jtitle=Film+Index+International&rft.atitle=La+VALSE+DU+GORILLE&rft.au=&rft.aulast=&rft.aufirst=Linner&rft.date=1994-10-01&rft.volume=19&rft.issue=2&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Arete&rft.issn=08859787&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 - gamma -interferon ER - TY - JOUR T1 - Structure of complex of synthetic HIV-1 protease with a substrate-based inhibitor at 2.3 angstrom resolution. AN - 15390083; 2141846 AB - The structure of a complex between a peptide inhibitor with the sequence N-acetyl-Thr-Ile-Nle- psi (CH sub(2)-NH)-Nle-Gln-Arg.amide (Nle, norleucine) with chemically synthesized HIV-1 (human immunodeficiency virus 1) protease was determined at 2.3 angstrom resolution (R factor of 0.176). Despite the symmetric nature of the unliganded enzyme, the asymmetric inhibitor lies in a single orientation and makes extensive interactions at the interface between the two subunits of the homodimeric protein. Compared with the unliganded enzyme, the protein molecule underwent substantial changes, particularly in an extended region corresponding to the "flaps" (residues 35 to 57 in each chain), where backbone movements as large as 7 angstrom are observed. JF - Science (Washington) AU - Miller, M AU - Schneider, J AU - Sathyanarayana, B K AU - Toth, M V AU - Marshall, G R AU - Clawson, L AU - Selk, L AU - Kent, SBH AU - Wlodawer, A AD - Crystallogr. Lab., NCI-Frederick Cancer Res. Facil., BRI-Basic Res. Program, P.O. Box B, Frederick, MD 21701, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 1149 EP - 1152 VL - 246 IS - 4934 SN - 0036-8075, 0036-8075 KW - E.S.R. KW - human immunodeficiency virus 1 KW - proteinase KW - subunit structure 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/15390083?accountid=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=Science+%28Washington%29&rft.atitle=Structure+of+complex+of+synthetic+HIV-1+protease+with+a+substrate-based+inhibitor+at+2.3+angstrom+resolution.&rft.au=Miller%2C+M%3BSchneider%2C+J%3BSathyanarayana%2C+B+K%3BToth%2C+M+V%3BMarshall%2C+G+R%3BClawson%2C+L%3BSelk%2C+L%3BKent%2C+SBH%3BWlodawer%2C+A&rft.aulast=Miller&rft.aufirst=M&rft.date=1989-01-01&rft.volume=246&rft.issue=4934&rft.spage=1149&rft.isbn=&rft.btitle=&rft.title=Science+%28Washington%29&rft.issn=00368075&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 - E.S.R.; subunit structure ER - TY - JOUR T1 - Attenuation of hypothermic effects of ethanol by alpha sub(2)-adrenoceptor blockers. AN - 15382541; 2135647 AB - Effects of selective alpha sub(2)-adrenoceptor antagonists, atipamezole and idazoxan, on ethanol-induced hypothermia were investigated in mice. Ethanol significantly reduced core temperature whilst both alpha d2-adrenoceptor antagonists were without effect when administered alone. However, both the 1 and 3 mg/kg doses of atipamezole significantly attenuated the ethanol-induced reduction in body temperature 20 and 40 min after administration. The 3 mg/kg dose of idazoxan (but not the 1 mg/kg dose) also significantly attenuated ethanol's hypothermic effect 20 min after administration but this effect was not statistically significant at 40 min. In a subsequent experiment using lower doses of atipamezole (0.03-1.0 mg/kg) the attenuation of ethanol-induced hypothermia caused by atipamezole was found to be dose-related. The effect of the benzodiazepine inverse agonist Ro 15-4513 on ethanol-induced hypothermia was also investigated. This compound possessed an intrinsic hypothermic action but neither attenuated nor enhanced the hypothermic effect of ethanol. JF - European Journal of Pharmacology AU - Durcan, MJ AU - Wozinak, K M AU - Lister, R G AU - Linnoila, M AD - NIAAA, Build. 10, Rm. 3C218, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 381 EP - 386 VL - 166 IS - 3 SN - 0014-2999, 0014-2999 KW - ethanol KW - atipamezole KW - idazoxan KW - mice KW - Toxicology Abstracts KW - hypothermia KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15382541?accountid=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=European+Journal+of+Pharmacology&rft.atitle=Attenuation+of+hypothermic+effects+of+ethanol+by+alpha+sub%282%29-adrenoceptor+blockers.&rft.au=Durcan%2C+MJ%3BWozinak%2C+K+M%3BLister%2C+R+G%3BLinnoila%2C+M&rft.aulast=Durcan&rft.aufirst=MJ&rft.date=1989-01-01&rft.volume=166&rft.issue=3&rft.spage=381&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 revised - 2006-11-01 N1 - Last updated - 2011-12-12 N1 - SubjectsTermNotLitGenreText - hypothermia ER - TY - JOUR T1 - Two different regions of phosphoglycoprotein are photoaffinity-labeled by azidopine. AN - 15381026; 2126100 AB - Cells that express P-glycoprotein are resistant to many unrelated anticancer drugs. All evidence suggests that P-glycoprotein is a plasma membrane protein that confers multidrug resistance by actively transporting these cytotoxic drugs out of cells. The objective of the work is to locate drug binding sites on P-glycoprotein. Azidopine is a photoaffinity drug analog that specifically labels P-glycoprotein. To determine the region of P-glycoprotein that binds azidopine, the authors labeled P-glycoprotein with azidopine and digested the labeled protein into fragments. They then identified the labeled fragments with specific antibodies. JF - Journal of Biological Chemistry AU - Bruggemann, E P AU - Germann, U A AU - Gottesman, M M AU - Pastan, I AD - Lab. Mol. Biol., NCI, NIH, Build 37, Rm. 4E16, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 15483 EP - 15488 VL - 264 IS - 26 SN - 0021-9258, 0021-9258 KW - P-glycoprotein KW - azidopine KW - binding KW - cell lines KW - man KW - photoaffinity labelling KW - sites KW - use 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/15381026?accountid=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=unknown&rft.jtitle=Film+Index+International&rft.atitle=PICKPOCKET&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1959-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Film+Index+International&rft.issn=&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 - Interaction of phencyclidine with voltage-dependent potassium channels in cultured rat hippocampal neurons: Comparison with block of the NMDA receptor-ionophore complex. AN - 15380391; 2134955 AB - Whole-cell voltage-clamp recording techniques were used to investigate the blockade of voltage-dependent K super(+) channels by phencyclidine (PCP) in cultured rat hippocampal neurons. At low doses, the behavioral effects of the drug are more likely to result from an interaction with NMDA receptor channels than voltage-dependent K super(+) channels. JF - Journal of Neuroscience AU - Ffrench-Mullen, JMH AU - Rogawski, MA AD - Med. Neurol. Branch, NINDS, NIH, Build. 10, Rm. 5N-248, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 4051 EP - 4061 VL - 9 IS - 11 SN - 0270-6474, 0270-6474 KW - phencyclidine KW - interaction KW - channels KW - potassium KW - rats KW - Toxicology Abstracts; CSA Neurosciences Abstracts KW - hippocampus KW - N3 11104:Mammals (except primates) KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15380391?accountid=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+Neuroscience&rft.atitle=Interaction+of+phencyclidine+with+voltage-dependent+potassium+channels+in+cultured+rat+hippocampal+neurons%3A+Comparison+with+block+of+the+NMDA+receptor-ionophore+complex.&rft.au=Ffrench-Mullen%2C+JMH%3BRogawski%2C+MA&rft.aulast=Ffrench-Mullen&rft.aufirst=JMH&rft.date=1989-01-01&rft.volume=13&rft.issue=17&rft.spage=2429&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-12 N1 - SubjectsTermNotLitGenreText - hippocampus ER - TY - JOUR T1 - Antagonists to metal carcinogens. AN - 15380108; 2125936 AB - Numerous studies indicate that the carcinogenic and toxic effects of certain metals such as nickel (Ni), cadmium (Cd), beryllium (Be), and lead (Pb) can be partially or totally prevented or, in some cases, enhanced by several other metals and organic compounds. These studies are important since environmental exposure to mixtures of metals is more likely to occur than is exposure to a single metal. The results may also have therapeutic implications. This review presents the most prominent antagonists of metal carcinogenesis and briefly summarizes corresponding literature data. JF - Journal of the American College of Toxicology AU - Rodriguez, R E AU - Kasprzak, K S AD - NCI-FCRF, Build. 538, Rm. 205E, Frederick, MD 21701-1013, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 1265 EP - 1269 VL - 8 IS - 7 SN - 0730-0913, 0730-0913 KW - heavy metals KW - nickel KW - cadmium KW - beryllium KW - lead KW - Toxicology Abstracts; Health & Safety Science Abstracts; Pollution Abstracts KW - carcinogenesis KW - toxicology KW - H SE4.20:POISONS AND POISONING KW - X 24162:Chronic exposure KW - P 6000:TOXICOLOGY AND HEALTH UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15380108?accountid=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+American+College+of+Toxicology&rft.atitle=Antagonists+to+metal+carcinogens.&rft.au=Rodriguez%2C+R+E%3BKasprzak%2C+K+S&rft.aulast=Rodriguez&rft.aufirst=R&rft.date=1989-01-01&rft.volume=8&rft.issue=7&rft.spage=1265&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+College+of+Toxicology&rft.issn=07300913&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - SuppNotes - Special issue: Toxicology of heavy metals. N1 - Last updated - 2011-12-12 N1 - SubjectsTermNotLitGenreText - nickel; cadmium; beryllium; lead; carcinogenesis; toxicology ER - TY - JOUR T1 - Comparative carcinogenicity of two structurally similar phenylenediamine dyes (HC Blue No. 1 and HC Blue No. 2) in F344/N rats and B6C3F sub(1) mice. AN - 15379726; 2134935 AB - Toxicology and carcinogenesis studies of 2 structurally-related p-phenylenediamines, HC Blue No. 1 and HC Blue No. 2, were conducted by administering each chemical in feed for 103 weeks to both sexes of Fischer 344/N rats and B6C3F sub(1) (C57BL/6N x C3H/HEN) mice. Diets containing 0, 1500, or 3000 ppm HC Blue 1 were fed to male and female rats and male mice; female mice received diets with 0, 3000, or 6000 ppm. Diets containing 0, 5000, or 10,000 ppm HC Blue 2 were fed to male rats and mice and the females received diets containing 0, 10,000 or 20,000 ppm. These concentrations were compatible with long-term growth and survival. The results demonstrated substantial differences in the neoplastic and non-neoplastic lesions caused by these structural analogs. HC Blue 2 caused histicytosis in lungs and hyperostosis of the skull in rats, and splenic hematopoiesis, fibrous osteodystrophy, and hyperostosis of the skull in mice. These non-neoplastic lesions were not observed in rats or mice treated with HC Blue. JF - Toxicology AU - Kari, F W AU - Mennear, J H AU - Farnell, D AU - Thompson, R B AU - Huff, JE AD - NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 155 EP - 165 VL - 56 IS - 2 SN - 0300-483X, 0300-483X KW - dyes KW - HC Blue No. 1 KW - HC Blue No. 2 KW - rats KW - mice KW - p-phenylenediamine KW - Toxicology Abstracts KW - carcinogenicity KW - X 24152:Chronic exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15379726?accountid=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=Comparative+carcinogenicity+of+two+structurally+similar+phenylenediamine+dyes+%28HC+Blue+No.+1+and+HC+Blue+No.+2%29+in+F344%2FN+rats+and+B6C3F+sub%281%29+mice.&rft.au=Kari%2C+F+W%3BMennear%2C+J+H%3BFarnell%2C+D%3BThompson%2C+R+B%3BHuff%2C+JE&rft.aulast=Kari&rft.aufirst=F&rft.date=1989-01-01&rft.volume=56&rft.issue=2&rft.spage=155&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 - 2011-12-12 N1 - SubjectsTermNotLitGenreText - carcinogenicity ER - TY - JOUR T1 - Restrained least squares refinement of native (calcium) and cadmium-substituted carp parvalbumin using X-ray crystallographic data at 1.6-(angstrom) resolution. AN - 15376250; 2131293 AB - Carp parvalbumin coordinates calcium through one carbonyl oxygen atom and the oxygen-containing side chains of 5 amino acid residues, or 4 residues and a water molecule, in a helix-loop-helix structural motif. Other calcium-binding proteins, including calmodulin and troponin C, also possess this unique calcium-binding design, which is designated EF-hand or calmodulin fold. Parvalbumin has two such sites, labeled CD and EF. Each of the calcium-binding sites of refined structures of proteins belonging to this group has a 7-oxygen coordination sphere except those of the structure of parvalbumin as it was reported in 1975. Differences between the parvalbumin structure described in 1975 and the present structure are addressed, including the discovery of 7-coordination for both the CD and EF sites. JF - Journal of Biological Chemistry AU - Swain, AL AU - Kretsinger, R H AU - Amma, EL AD - Crystallogr. Lab., NCI-Frederick Cancer Res. Facil., BRI-Basic Res. Program, P.O. Box B, Frederick, MD 21701, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 16620 EP - 16628 VL - 264 IS - 28 SN - 0021-9258, 0021-9258 KW - Cyprinus carpio KW - X-ray analysis KW - X-ray crystallography KW - biochemical analysis KW - molecular structure KW - parvalbumin KW - parvalbumin crystal structure KW - proteins KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA Aquaculture Abstracts KW - Freshwater KW - Q1 08346:Physiology, biochemistry, biophysics KW - Q3 08582:Fish culture UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15376250?accountid=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=Journal+of+Biological+Chemistry&rft.atitle=Restrained+least+squares+refinement+of+native+%28calcium%29+and+cadmium-substituted+carp+parvalbumin+using+X-ray+crystallographic+data+at+1.6-%28angstrom%29+resolution.&rft.au=Swain%2C+AL%3BKretsinger%2C+R+H%3BAmma%2C+EL&rft.aulast=Swain&rft.aufirst=AL&rft.date=1989-01-01&rft.volume=264&rft.issue=28&rft.spage=16620&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 - molecular structure; biochemical analysis; proteins; Freshwater ER - TY - JOUR T1 - Predicted structures of the cGMP binding domains of the cGMP-dependent protein kinase: A key alanine/threonine difference in evolutionary divergence of cAMP and cGMP binding sites. AN - 15371938; 2113652 AB - Mammalian cGMP- and cAMP-dependent protein kinases show considerable similarity in amino acid sequence, although they specifically bind different cyclic nucleotides. Results of cGMP analogue binding experiments, combined with modeling of the cGMP binding sites by analogy to the structure of the homologous catabolite gene activator protein, suggest that a threonine residue forms a hydrogen bond with the 2-NH sub(2) of cGMP. This threonine is invariant in all cGMP binding domains, but the corresponding residue in 23 out of 24 cAMP binding sites of protein kinases is alanine, which cannot form the same hydrogen bond. JF - Biochemistry (Washington) AU - Weber, I T AU - Shabb, J B AU - Corbin, J D AD - Crystallogr. Lab., NCI-Frederick Cancer Res. Facil., BRI-Basic Res. Program, P.O. Box B, Frederick, MD 21701, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 6122 EP - 6127 VL - 28 IS - 14 SN - 0006-2960, 0006-2960 KW - amino acid sequence KW - binding KW - cattle KW - cyclic GMP KW - dependent KW - predictions KW - protein kinase KW - sites 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/15371938?accountid=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+Offender+Therapy+and+Comparative+Criminology&rft.atitle=Music+Therapy+for+Prisoners%3A+Pilot+Randomised+Controlled+Trial+and+Implications+for+Evaluating+Psychosocial+Interventions&rft.au=Gold%2C+Christian%3BAssmus%2C+Jorg%3BHjornevik%2C+Kjetil%3BQvale%2C+Liv+Gunnhild%3BBrown%2C+Fiona+Kirkwood%3BHansen%2C+Anita+Lill%3BWaage%2C+Leif%3BStige%2C+Brynjulf&rft.aulast=Gold&rft.aufirst=Christian&rft.date=2014-12-01&rft.volume=58&rft.issue=12&rft.spage=1520&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Offender+Therapy+and+Comparative+Criminology&rft.issn=0306624X&rft_id=info:doi/10.1177%2F0306624X13498693 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Tissue inhibitor of metalloproteinase (TIMP-2). A new member of the metalloproteinase inhibitor family. AN - 15369359; 2126725 AB - Human melanoma cells secret a 21-kDa protein, termed CSC-21K, which binds with 1:1 molar stoichiometry to the matrix metalloproteinase type IV collagenase proenzyme (70-kDa gelatinase) secreted by the same cells. This binding protein has been purified and its complete primary structure determined by sequencing overlapping peptides which span the entire protein. The amino acid sequence demonstrates that this protein shares significant homology with human TIMP (tissue inhibitor of metalloproteinase), including conservation of the positions of the 12 cysteine residues and 3 of 4 tryptophan residues. The identification of CSC-21K now indicates that a family of TIMP-related proteins exists. JF - Journal of Biological Chemistry AU - Stetler-Stevenson, W G AU - Krutzsch, H C AU - Liotta, LA AD - Lab. Pathol., NCI, NIH, Build. 10, Rm. 2A33, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 17374 EP - 17378 VL - 264 IS - 19 SN - 0021-9258, 0021-9258 KW - amino acid sequence KW - cells KW - homology KW - inhibitors KW - man KW - metalloproteinase 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/15369359?accountid=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+Child+Sexual+Abuse&rft.atitle=Policy+Interventions+Designed+to+Combat+Sexual+Violence%3A+Community+Notification+and+Civil+Commitment&rft.au=Levenson%2C+Jill+S&rft.aulast=Levenson&rft.aufirst=Jill&rft.date=2003-01-01&rft.volume=12&rft.issue=3-4&rft.spage=17&rft.isbn=&rft.btitle=&rft.title=Journal+of+Child+Sexual+Abuse&rft.issn=10538712&rft_id=info:doi/10.1300%2FJ070v12n03_02 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Human immunodeficiency virus-like particles produced by a vaccinia virus expression vector. AN - 15367894; 2122198 AB - Infectious retrovirus particles consist of a core structure containing RNA and gag-pol polypeptides surrounded by a lipid membrane studded with env proteins. A recombinant vaccinia virus was designed to express the entire gag-pol precursor protein of the human immunodeficiency virus type 1. The production of noninfectious virus-like particles by expression vectors should be useful for biochemical studies and could provide a safe source of material for the development of vaccines. JF - Proceedings of the National Academy of Sciences, USA AU - Karacostas, V AU - Nagashima, K AU - Gonda, MA AU - Moss, B AD - Lab. Viral Dis., NIAID, Natl Inst. Health, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 8964 EP - 8967 VL - 86 IS - 22 SN - 0027-8424, 0027-8424 KW - human immunodeficiency virus KW - recombinants KW - cloning vectors KW - vaccinia virus KW - virus-like particles KW - Biotechnology and Bioengineering Abstracts; Virology & AIDS Abstracts KW - W 30114:Cloning vectors KW - V 22002:AIDS: Molecular and in vitro aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15367894?accountid=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=Human+immunodeficiency+virus-like+particles+produced+by+a+vaccinia+virus+expression+vector.&rft.au=Karacostas%2C+V%3BNagashima%2C+K%3BGonda%2C+MA%3BMoss%2C+B&rft.aulast=Karacostas&rft.aufirst=V&rft.date=1989-01-01&rft.volume=86&rft.issue=22&rft.spage=8964&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 - 2011-12-12 N1 - SubjectsTermNotLitGenreText - vaccinia virus; virus-like particles; cloning vectors ER - TY - JOUR T1 - Crystal structure of a retroviral protease proves relationship to aspartic protease family. AN - 15362738; 2123478 AB - Retroviral gag, pol and env gene products are translated as precursor polyproteins, which are cleaved by virus-encoded proteases to produce the mature proteins found in virions. We have now determined the crystal structure of Rous sarcoma virus (RSV) protease at 3-angstrom resolution and find it is dimeric and has a structure similar to aspartic proteases. This structure should provide a useful basis for the modelling of the structures of other retroviral proteases, such as that of HIV, and also for the rational design of protease inhibitors as potential antiviral drugs. JF - Nature AU - Miller, M AU - Jaskolski, M AU - Rao, JKM AU - Leis, J AU - Wlodawer, A AD - Crystallogr. Lab., NCI-Frederick Cancer Res. Facil., BRI-Basic Res. Program, P.O. Box B, Frederick, MD 21701, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 576 EP - 579 VL - 337 IS - 6207 SN - 0028-0836, 0028-0836 KW - Rous sarcoma virus KW - X-ray crystallography KW - proteinase 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/15362738?accountid=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=Nature&rft.atitle=Crystal+structure+of+a+retroviral+protease+proves+relationship+to+aspartic+protease+family.&rft.au=Miller%2C+M%3BJaskolski%2C+M%3BRao%2C+JKM%3BLeis%2C+J%3BWlodawer%2C+A&rft.aulast=Miller&rft.aufirst=M&rft.date=1989-01-01&rft.volume=337&rft.issue=6207&rft.spage=576&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&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 - X-ray crystallography ER - TY - JOUR T1 - Oral administration of cyclosporin does not prevent expansion of antigen-specific, gut-associated, and spleen lymphocyte populations during Chlamydia trachomatis proctitis in nonhuman primates. AN - 15358065; 2117517 AB - To study the effects of oral cyclosporin (CsA) administration on immune responses in the gastrointestinal tract, humoral and cellular immune responses were studied in CsA-treated nonhuman primates having Chlamydia trachomatis proctitis (lymphogranuloma venereum, LGV). There was no apparent effect of CsA treatment on the gross or microscopic appearance of LGV proctitis, but CsA-treated animals, with or without LGV infection, had lymphoid hyperplasia of spleen and mesenteric lymph nodes. CsA treatment inhibited the primary antibody response to LGV, inhibited peripheral blood lymphocyte mitogen-induced proliferation and IL-2 production, and inhibited LGV-specific proliferation of peripheral blood lymphocytes. In contrast, mitogen-stimulated proliferation of spleen, mesenteric lymph node, and lamina propria lymphocytes was not significantly inhibited in CsA-treated animals. JF - Digestive Diseases and Sciences AU - Zeitz, M AU - Quinn, T C AU - Graeff, A S AU - Schwarting, R AU - James, S P AD - Natl. Inst. Health, NIAID, Build. 10, Rm. 11N250, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 585 EP - 595 VL - 34 IS - 4 SN - 0163-2116, 0163-2116 KW - Primates KW - cyclosporin A KW - effects on KW - immune response KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - immunosuppression KW - lymphocytes KW - gut KW - Chlamydia trachomatis KW - proctitis KW - spleen KW - F 06801:Bacteria KW - J 02833:Immune response and immune mechanisms KW - F 06791:Experimental UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15358065?accountid=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=Digestive+Diseases+and+Sciences&rft.atitle=Oral+administration+of+cyclosporin+does+not+prevent+expansion+of+antigen-specific%2C+gut-associated%2C+and+spleen+lymphocyte+populations+during+Chlamydia+trachomatis+proctitis+in+nonhuman+primates.&rft.au=Zeitz%2C+M%3BQuinn%2C+T+C%3BGraeff%2C+A+S%3BSchwarting%2C+R%3BJames%2C+S+P&rft.aulast=Zeitz&rft.aufirst=M&rft.date=1989-01-01&rft.volume=34&rft.issue=4&rft.spage=585&rft.isbn=&rft.btitle=&rft.title=Digestive+Diseases+and+Sciences&rft.issn=01632116&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-12 N1 - SubjectsTermNotLitGenreText - Chlamydia trachomatis; immunosuppression; gut; spleen; lymphocytes; proctitis ER - TY - JOUR T1 - The sequence of a nervous system-specific, class II beta -tubulin gene from Xenopus laevis . AN - 15356835; 2114202 AB - The authors previously reported the isolation of a beta -tubulin cDNA (clone 24-10) whose RNA is expressed in the nervous system of Xenopus laevis and is accumulated early after gastrulation. The sequence of the predicted 24-10 protein shares 99% identity with the chicken beta 2-tubulin. Comparison of the C-terminal domain of the predicted 24-10 protein with other beta -tubulins indicates that the 24-10 protein is a class II isotype beta -tubulin. The 3' untranslated sequence of clone 24-10 is identical to the same region of clone D8 which was previously shown to be expressed in the nervous system of tadpoles. JF - Nucleic Acids Research AU - Good, P J AU - Richter, K AU - Dawid, IB AD - Lab. Mol. Genet., NICHD, NIH, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 8000 VL - 17 IS - 19 SN - 0305-1048, 0305-1048 KW - Xenopus laevis KW - amino acid sequence KW - beta -tubulin KW - cDNA KW - class II KW - genes KW - nervous system 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 - N 14640:Structure & sequence KW - G 07374:GENERAL UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15356835?accountid=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+sequence+of+a+nervous+system-specific%2C+class+II+beta+-tubulin+gene+from+Xenopus+laevis+.&rft.au=Good%2C+P+J%3BRichter%2C+K%3BDawid%2C+IB&rft.aulast=Good&rft.aufirst=P&rft.date=1989-01-01&rft.volume=17&rft.issue=19&rft.spage=8000&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 N1 - SubjectsTermNotLitGenreText - nervous system; genes ER - TY - JOUR T1 - A reversible unfolding reaction of swine pepsin: Implications for pepsinogen's folding mechanism. AN - 15356448; 2113910 AB - Above pH 6, swine pepsin undergoes a conformational change to a neutral form which has 80% of the secondary structure of the native protein. In contrast to native pepsin, this form of the enzyme can be reversibly unfolded by urea in a rapid, cooperative reaction. Since all of pepsin's sequence is present in its precursor pepsinogen, it is likely that this neutral structure is present in one or more of the transient intermediates previously detected in the reversible unfolding reaction of the zymogen. JF - Biochemical and Biophysical Research Communications AU - McPhie, P AD - Lab. Biochem. and Metab., NIDDK, NIH, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 115 EP - 119 VL - 158 IS - 1 SN - 0006-291X, 0006-291X KW - C.D. KW - folding KW - mechanisms KW - pepsinogen KW - secondary 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/15356448?accountid=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=A+reversible+unfolding+reaction+of+swine+pepsin%3A+Implications+for+pepsinogen%27s+folding+mechanism.&rft.au=McPhie%2C+P&rft.aulast=McPhie&rft.aufirst=P&rft.date=1989-01-01&rft.volume=158&rft.issue=1&rft.spage=115&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 - Proton detection of long-range couplings to carbon-13 using semiselective pulses. A high-resolution method for assigning amino acids in peptides. AN - 15354696; 2113259 JF - J. MAGN. RESONANCE. AU - Davis, D G AD - Lab. Mol. Biophys., NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 212 EP - 218 VL - 83 IS - 1 KW - N.M.R. KW - amino acids KW - assignment KW - detection KW - proteins KW - protons KW - semiselective pubes 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/15354696?accountid=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=J.+MAGN.+RESONANCE.&rft.atitle=Proton+detection+of+long-range+couplings+to+carbon-13+using+semiselective+pulses.+A+high-resolution+method+for+assigning+amino+acids+in+peptides.&rft.au=Davis%2C+D+G&rft.aulast=Davis&rft.aufirst=D&rft.date=1989-01-01&rft.volume=83&rft.issue=1&rft.spage=212&rft.isbn=&rft.btitle=&rft.title=J.+MAGN.+RESONANCE.&rft.issn=&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 - Single-dose ethanol administration activates the hypothalamic-pituitary-adrenal axis: Exploration of the mechanism of action. AN - 15348465; 2110381 AB - Activation of the hypothalamic-pituitary-adrenal axis (HPAA) by single-dose ethanol administration, which achieved moderately high blood ethanol levels, was explored in naive rats in order to determine the mechanism of ethanol's activation of the stress axis. The results of this study indicate that neither adrenal medulla-derived epinephrine (E) nor arginine vasopressin (AVP) are significant regulators or coregulators of corticotroph secretions following a moderately high, single-dose, intragastric administration of ethanol. JF - Neuroendocrinology AU - Thiagarajan, AB AU - Mefford, IN AU - Eskay, R L AD - Lab. Clin. Stud., NIAAA, NIH, Build. 10, Rm. 3C-216, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 427 EP - 432 VL - 5 IS - 4 SN - 0028-3835, 0028-3835 KW - ethanol KW - effects on KW - release KW - adrenocorticotropic hormone KW - rats KW - Toxicology Abstracts; CSA Neurosciences Abstracts KW - N3 11250:PROOPIOMELANOCORTICOTROPIC-DERIVED HORMONES KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15348465?accountid=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=Neuroendocrinology&rft.atitle=Single-dose+ethanol+administration+activates+the+hypothalamic-pituitary-adrenal+axis%3A+Exploration+of+the+mechanism+of+action.&rft.au=Thiagarajan%2C+AB%3BMefford%2C+IN%3BEskay%2C+R+L&rft.aulast=Thiagarajan&rft.aufirst=AB&rft.date=1989-01-01&rft.volume=5&rft.issue=4&rft.spage=427&rft.isbn=&rft.btitle=&rft.title=Neuroendocrinology&rft.issn=00283835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-12 ER - TY - JOUR T1 - Carcinogenesis in rats by nitrosodialkylureas containing methyl and ethyl groups given by gavage and in drinking water. AN - 15340384; 2098373 AB - The carcinogenic effects in male and female F344 rats of four nitrosodialkylureas containing methyl or ethyl groups have been compared by two modes of administration, gavage in oil solution or dissolved in drinking water. Weekly doses of 20 and 40 mu mol were given to each rat by either route and treatment lasted usually 30 wk, resulting in a total dose per rat of 0.6 or 1.2 mmol. Nitrosodimethylurea and nitroso-1-methyl-3-ethylurea gave rise primarily to tumors of the nervous system, whereas nitrosodiethylurea and nitroso-1-ethyl-3-methylurea gave rise to tumors of the mammary gland, lung, intestinal tract, nervous system, and testicular mesotheliomas. The effect of nitrosodimethylurea was weaker than that of the other three compounds, as measured by rate of mortality with tumors. Drinking water treatment was less effective than treatment by gavage, by the same criterion. JF - Journal of Toxicology and Environmental Health AU - Lijinsky, W AU - Saavedra, JE AU - Kovatch, R M AD - BRI-Basic Res. Program, NCI-Frederick Cancer Res. Fac., Frederick, MD 21701, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 27 EP - 38 VL - 28 IS - 1 SN - 0093-4108, 0093-4108 KW - nitrosodialkylureas KW - structure-activity relationships KW - potable water KW - rats KW - Health & Safety Science Abstracts; Pollution Abstracts; Toxicology Abstracts KW - carcinogenesis KW - P 3000:SEWAGE & WASTEWATER TREATMENT KW - X 24200:Nitrosamines & related compounds KW - H SE3.21:WATER POLLUTION/WATER QUALITY UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15340384?accountid=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+Toxicology+and+Environmental+Health&rft.atitle=Carcinogenesis+in+rats+by+nitrosodialkylureas+containing+methyl+and+ethyl+groups+given+by+gavage+and+in+drinking+water.&rft.au=Lijinsky%2C+W%3BSaavedra%2C+JE%3BKovatch%2C+R+M&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1989-01-01&rft.volume=28&rft.issue=1&rft.spage=27&rft.isbn=&rft.btitle=&rft.title=Journal+of+Toxicology+and+Environmental+Health&rft.issn=00934108&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-12 N1 - SubjectsTermNotLitGenreText - carcinogenesis; rats ER - TY - JOUR T1 - Deaths from all causes in non-smokers who lived with smokers. AN - 15327566; 2083349 AB - Mortality associated with passive smoking was evaluated in a 12-year study of 27,891 White adult smokers and 19,035 never smokers identified in 1963. Death rates were calculated using an estimate of the person-years at risk. Adjusted for age, marital status, education, and quality of housing, the estimated relative risks of death from all causes were 1.17 for men and 1.15 for women with passive exposure. These relative risks were similar to those for ex-smokers and for pipe or cigar smokers. Risks increased slightly with level of exposure. The relative risk from passive smoking was greatest for men under age 50. Risks from passive smoking were slightly elevated for several causes among men and women, and may be broader than those previously reported. On the other hand, these small nonspecific increases in death rates may reflect other characteristics of passive smokers that increase mortality. JF - American Journal of Public Health AU - Sandler, D P AU - Comstock, G W AU - Helsing, K J AU - Shore, D L AD - Epidemiol. Branch, MD A3-05, NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 163 EP - 167 VL - 79 IS - 2 SN - 0090-0036, 0090-0036 KW - smoking KW - man KW - Health & Safety Science Abstracts; Toxicology Abstracts KW - cigarettes KW - passive smoking KW - mortality KW - public health KW - H SE4.26:DRUGS AND ALCOHOL KW - H SM3.8.4:DRUGS AND ALCOHOL KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15327566?accountid=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+Public+Health&rft.atitle=Deaths+from+all+causes+in+non-smokers+who+lived+with+smokers.&rft.au=Sandler%2C+D+P%3BComstock%2C+G+W%3BHelsing%2C+K+J%3BShore%2C+D+L&rft.aulast=Sandler&rft.aufirst=D&rft.date=1989-01-01&rft.volume=79&rft.issue=2&rft.spage=163&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 revised - 2006-11-01 N1 - SuppNotes - Special issue: Tobacco and health. N1 - Last updated - 2011-12-12 N1 - SubjectsTermNotLitGenreText - public health; passive smoking; cigarettes; mortality; man ER - TY - JOUR T1 - The oxidation of methylglyoxal by mammalian pyruvate dehydrogenase. AN - 15323024; 2081052 AB - Mammalian pyruvate dehydrogenase actively catalyzed the oxidation of methylglyoxal to acetyl-CoA. The reaction was fully enzymatic with an estimated K sub(m) of 1.89 mM. On the other hand, methylglyoxal was a competitive inhibitor of the enzyme for pyruvate, the K sub(i) being in the 1 mM range. The reaction was inhibited in the presence of HgCl sub(2). The reaction products were quantitatively identified as acetyl-CoA and formic acid. A mechanism for the reaction is proposed. JF - Archives of Biochemistry and Biophysics AU - Argiles, J M AD - Lab. Metab., NIAAA, 12501 Washington Ave., Rockville, MD 20852, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 238 EP - 244 VL - 273 IS - 1 SN - 0003-9861, 0003-9861 KW - activity KW - mammalian cells KW - methylglyoxal KW - oxidation KW - pyruvate dehydrogenase 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/15323024?accountid=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=The+oxidation+of+methylglyoxal+by+mammalian+pyruvate+dehydrogenase.&rft.au=Argiles%2C+J+M&rft.aulast=Argiles&rft.aufirst=J&rft.date=1989-01-01&rft.volume=273&rft.issue=1&rft.spage=238&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 - 2015-03-24 ER - TY - JOUR T1 - Practical aspects of 3D heteronuclear NMR of proteins. AN - 15322857; 2080330 AB - Practical aspects regarding the acquisition and processing of 3D heteronuclear data sets are discussed, with particular emphasis on the 3D NOESY-HMQC experiment which combines the 2D NOE and the heteronuclear multiple-quantum coherence (HMQC) experiments. Slices through the 3D spectrum are equivalent to super(15)N-filtered 2D NOESY spectra and exhibit sensitivity similar to that obtained in regular 2D NOE experiments. The authors discuss experimental procedures for obtaining maximum resolution with a relatively small number of t sub(1) and t sub(2) increments. JF - J. MAGN. RESONANCE. AU - Kay, LE AU - Marion, D AU - Bax, A AD - Lab. Chem. Phys., NIDDK, Natl. Inst. Health, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 72 EP - 84 VL - 84 IS - 1 KW - 3D heteronuclear KW - N.M.R. 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/15322857?accountid=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=J.+MAGN.+RESONANCE.&rft.atitle=Practical+aspects+of+3D+heteronuclear+NMR+of+proteins.&rft.au=Kay%2C+LE%3BMarion%2C+D%3BBax%2C+A&rft.aulast=Kay&rft.aufirst=LE&rft.date=1989-01-01&rft.volume=84&rft.issue=1&rft.spage=72&rft.isbn=&rft.btitle=&rft.title=J.+MAGN.+RESONANCE.&rft.issn=&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 - Detection of glutathione thiyl free radical catalyzed by prostaglandin H synthase present in keratinocytes. Study of cooxidation in a cellular system. AN - 15320567; 2080875 AB - The authors report here the application of the electron spin resonance technique to detect free radicals formed by the hydroperoxidase activity of prostaglandin H synthase in cells. Studies were done using keratinocytes obtained from hairless mice. These cells can be prepared in large number and possess significant prostaglandin H synthase activity. Initial attempts to directly detect free radical metabolites of several amines in cells were unsuccessful. A technique was developed based on the ability of some free radicals formed by prostaglandin hydroperoxidase to oxidize reduced glutathione (GSH) to a thiyl radical, which was trapped by 5,5-dimethyl-1-pyrroline N-oxide (DMPO). The results suggest that prostaglandin hydroperoxidase-dependent co-oxidation of chemicals can result in the intracellular formation of free radical metabolites. JF - Journal of Biological Chemistry AU - Schreiber, J AU - Foureman, G L AU - Hughes, M F AU - Mason, R P AU - Eling, TE AD - NIEHS, Lab. Mol. Biophys., P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 7936 EP - 7943 VL - 264 IS - 14 SN - 0021-9258, 0021-9258 KW - activity KW - detection KW - free radicals KW - keratinocytes KW - mice KW - prostaglandin H synthase 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/15320567?accountid=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=Detection+of+glutathione+thiyl+free+radical+catalyzed+by+prostaglandin+H+synthase+present+in+keratinocytes.+Study+of+cooxidation+in+a+cellular+system.&rft.au=Schreiber%2C+J%3BFoureman%2C+G+L%3BHughes%2C+M+F%3BMason%2C+R+P%3BEling%2C+TE&rft.aulast=Schreiber&rft.aufirst=J&rft.date=1989-01-01&rft.volume=264&rft.issue=14&rft.spage=7936&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 - Hybrid DNA artifact from PCR of closely related target sequences. AN - 15318142; 2081755 AB - The authors have recently determined through standard molecular cloning methods that Xenopus laevis contains two different nonallelic preproinsulin genes which are very similar to each other (i.e. 94% identity in the coding region). In order to obtain the remaining sequence of the 5'-untranslated regions they used the anchored polymerase chain reaction and reverse-transcribed Xenopus pancreatic RNA using an antisense oligonucleotide common to both preproinsulin I and II mRNAs. The resulting single-stranded DNA was tailed using terminal 3'-deoxyribonucleotide transferase (TdT) and dATP. Amplification was accomplished by PCR using two antisense oligonucleotides, one common to both preproinsulin I and II mRNAs, and the second oligonucleotide, oligo-dT sub(20). The resulting amplified DNA fragment, approximately 350 base-pairs in length, hybridized strongly to a radiolabeled preproinsulin cDNA probe. JF - Nucleic Acids Research AU - Shuldiner, A R AU - Nirula, A AU - Roth, J AD - Diabetes Branch, NIDDK, NIH, Build. 10, Rm. 8-S-243, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 4409 VL - 17 IS - 11 SN - 0305-1048, 0305-1048 KW - polymerase chain reaction KW - methodology KW - artifacts KW - hybrids KW - generation KW - DNA KW - Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - N 14610:Occurrence, isolation & assay KW - W 30119:Others UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15318142?accountid=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=Hybrid+DNA+artifact+from+PCR+of+closely+related+target+sequences.&rft.au=Shuldiner%2C+A+R%3BNirula%2C+A%3BRoth%2C+J&rft.aulast=Shuldiner&rft.aufirst=A&rft.date=1989-01-01&rft.volume=17&rft.issue=11&rft.spage=4409&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 - 2011-12-12 N1 - SubjectsTermNotLitGenreText - DNA ER - TY - JOUR T1 - Sulfur-containing 1,3-dialkylxanthine derivatives as selective antagonists at A sub(1)-adenosine receptors. AN - 15305826; 2063734 AB - Sulfur-containing analogues of 8-substituted xanthines were prepared in an effort to increase selectivity or potency as antagonists at adenosine receptors. Either cyclopentyl or various aryl substituents were utilized at the 8-position, because of the association of these group with high potency at A sub(1)-adenosine receptors. JF - Journal of Medicinal Chemistry AU - Jacobson, KA AU - Kiriasis, L AU - Barone, S AU - Bradbury, B J AU - Kammula, U AU - Campagne, J M AU - Secunda, S AU - Daly, J W AU - Neumeyer, J L AD - Lab. Chem., NIDDK, NIH, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 1873 EP - 1879 VL - 32 IS - 8 SN - 0022-2623, 0022-2623 KW - 1,3-dialkylxanthine KW - A1 KW - adenosine KW - analysis KW - containing KW - derivatives KW - interaction KW - receptors KW - sulphur 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/15305826?accountid=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=Dyslexia+%28Chichester%2C+England%29&rft.atitle=Early+home-based+intervention+in+the+Netherlands+for+children+at+familial+risk+of+dyslexia.&rft.au=van+Otterloo%2C+Sandra+G%3Bvan+der+Leij%2C+Aryan%3BHenrichs%2C+Lotte+F&rft.aulast=van+Otterloo&rft.aufirst=Sandra&rft.date=2009-08-01&rft.volume=15&rft.issue=3&rft.spage=187&rft.isbn=&rft.btitle=&rft.title=Dyslexia+%28Chichester%2C+England%29&rft.issn=10769242&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 - Conserved folding in retroviral proteases: Crystal structure of a synthetic HIV-1 protease. AN - 15276955; 2036739 AB - The rational design of drugs that can inhibit the action of viral proteases depends on obtaining accurate structures of these enzymes. The crystal structure of chemically synthesized HIV-1 protease has been determined at 2.8 angstrom resolution (R factor of 0.184) with the use of a model based on the Rous sarcoma virus protease structure. In this enzymatically active protein, the cysteines were replaced by alpha -amino-n-butyric acid, a nongenetically coded amino acid. This structure, in which all 99 amino acids were located, differs in several important details from that reported previously by other. JF - Science (Washington) AU - Wlodawer, A AU - Miller, M AU - Jaskolski, M AU - Sathyanarayana, B K AU - Baldwin, E AU - Weber, I T AU - Selk, L M AU - Clawson, L AU - Schneider, J AD - Crystallogr. Lab., NCI-Frederick Cancer Res. Facil., BRI Basic Res. Program, P.O. Box B, Frederick, MD 21701, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 616 EP - 621 VL - 245 IS - 4918 SN - 0036-8075, 0036-8075 KW - crystal structure KW - folding KW - human immunodeficiency virus 1 KW - proteinase KW - synthetic 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 KW - V 22032:Viral proteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15276955?accountid=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=Science+%28Washington%29&rft.atitle=Conserved+folding+in+retroviral+proteases%3A+Crystal+structure+of+a+synthetic+HIV-1+protease.&rft.au=Wlodawer%2C+A%3BMiller%2C+M%3BJaskolski%2C+M%3BSathyanarayana%2C+B+K%3BBaldwin%2C+E%3BWeber%2C+I+T%3BSelk%2C+L+M%3BClawson%2C+L%3BSchneider%2C+J&rft.aulast=Wlodawer&rft.aufirst=A&rft.date=1989-01-01&rft.volume=245&rft.issue=4918&rft.spage=616&rft.isbn=&rft.btitle=&rft.title=Science+%28Washington%29&rft.issn=00368075&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 - Database and search techniques for two dimensional gel protein data: A comparison of paradigms for exploratory data analysis and prospects for biological modeling. AN - 15276215; 2032220 AB - In this paper, the GELLAB-II system is discussed with respect to how data reduction and exploratory data analysis can be aided by computer data management and statistical search techniques. By encoding the gel patterns in a "Three-dimensional" (3-D) database, an exploratory data analysis can be carried out in an environment that might be called a "spread sheet for 2-D gel protein data". From such databases, complex parametric network models of protein expression during events such as differentiation might be constructed. For this, 2-D gel databases must be able to include data from other domains external to the gel itself. Because of the increasing complexity of such databases, new tools are required to help manage this complexity. Two such tools, object-oriented databases and expert-system rule-based analysis, are discussed in this context. JF - Electrophoresis AU - Lemkin, P F AU - Lester, E P AD - IPS, LTB, NCI/FCRF, Build. 469 Rm. 150B, Frederick, MD 21701, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 122 EP - 140 VL - 10 IS - 2 SN - 0170-0835, 0170-0835 KW - computer applications KW - data banks KW - gel electrophoresis KW - two-dimensional 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/15276215?accountid=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=Database+and+search+techniques+for+two+dimensional+gel+protein+data%3A+A+comparison+of+paradigms+for+exploratory+data+analysis+and+prospects+for+biological+modeling.&rft.au=Lemkin%2C+P+F%3BLester%2C+E+P&rft.aulast=Lemkin&rft.aufirst=P&rft.date=1989-01-01&rft.volume=10&rft.issue=2&rft.spage=122&rft.isbn=&rft.btitle=&rft.title=Electrophoresis&rft.issn=01700835&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 - Affinity generation of single-stranded DNA for dideoxy sequencing following the polymerase chain reaction. AN - 15270194; 2028927 AB - A method to rapidly generate single stranded DNA for dideoxy sequencing following the polymerase chain reaction is described. By incorporating biotin in one of the amplification primers, the authors are able to physically separate the two DNA strands produced in the polymerase chain reaction. After amplification, the mixture is passed through a column containing streptavidin agarose. This method was utilized to sequence mitochondrial DNA from crude genomic DNA and to determine the sequences of four clones containing human mitochondrial DNA as a test of its accuracy. The use of biotin-facilitated separation permitted us to amplify and sequence DNA samples in a single day. JF - Analytical Biochemistry AU - Mitchell, L G AU - Merril, C R AD - NIMH, Lab. Biochem. Genet., NIH, Build. 10, Rm. 3N218, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 239 EP - 242 VL - 178 IS - 2 SN - 0003-2697, 0003-2697 KW - DNA KW - synthesis KW - use KW - polymerase chain reaction KW - biotin KW - streptavidin KW - Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - W 30111:Oligonucleotide synthesis KW - N 14220:Chemical synthesis & properties UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15270194?accountid=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=Analytical+Biochemistry&rft.atitle=Affinity+generation+of+single-stranded+DNA+for+dideoxy+sequencing+following+the+polymerase+chain+reaction.&rft.au=Mitchell%2C+L+G%3BMerril%2C+C+R&rft.aulast=Mitchell&rft.aufirst=L&rft.date=1989-01-01&rft.volume=178&rft.issue=2&rft.spage=239&rft.isbn=&rft.btitle=&rft.title=Analytical+Biochemistry&rft.issn=00032697&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-12 ER - TY - JOUR T1 - Human non-transformed monocyte-derived macrophage cell lines. AN - 15270119; 2027443 AB - The authors have demonstrated that human blood monocyte-derived macrophages can be passaged from primary cultures and replicate. Randomly selected lines were examined to look for cell proliferation by looking at numbers of cells over time and by labelling cells with tritiated thymidine to determine the number of cells synthesizing DNA. In addition, the cells can be frozen at the time of isolation and stored for at least 1 year, and then thawed and shown to retain functional activity. Human monocyte-derived macrophages can be cultured as finite cell lines. JF - Journal of Immunological Methods AU - Sechler, JMG AU - Warren, M K AU - Gallin, JI AD - Build. 10, Rm. 11C103, NIAID, NIH, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 277 EP - 285 VL - 119 IS - 2 SN - 0022-1759, 0022-1759 KW - macrophages KW - cell lines KW - passage KW - man KW - Biotechnology and Bioengineering Abstracts; Immunology Abstracts KW - W 30330:Animals KW - F 06764:Function UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15270119?accountid=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+Immunological+Methods&rft.atitle=Human+non-transformed+monocyte-derived+macrophage+cell+lines.&rft.au=Sechler%2C+JMG%3BWarren%2C+M+K%3BGallin%2C+JI&rft.aulast=Sechler&rft.aufirst=JMG&rft.date=1989-01-01&rft.volume=119&rft.issue=2&rft.spage=277&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 revised - 2006-11-01 N1 - Last updated - 2011-12-12 ER - TY - JOUR T1 - Effect of subchronic arsine inhalation on immune function and host resistance. AN - 15265955; 2020102 AB - Arsine is a toxic gas known for its hemolytic effects. Immunological parameters were examined in female B6C3F sub(1) mice after a 14-day (6 h/day) exposure to air or to 0.5, 2.5 or 5.0 ppm arsine. Arsine induced marked changes in splenic cellular populations. Although there was no effect on the total number of splenic lymphocytes, the percentage of lymphocytes fell in all arsine-exposed groups, from 83.4% in air controls to 45.6% in 5.0 ppm arsine, while there was a concomitant increase in rubricyte percentages. Splenic T-cell percentages were depressed at all arsine concentrations, while the percentages of B-cells were depressed only at 5.0 ppm arisen. Neither the numbers of peritoneal exudate macrophages nor their function was affected by arsine exposure. In vitro analysis showed an arsine concentration-dependent decrease in natural killer cell and cytotoxic T-lymphocyte function. JF - Inhalation Toxicology AU - Rosenthal, G J AU - Fort, M M AU - Germolec AU - Ackermann, M F AU - Lamm, K R AU - Blair, P C AU - Fowler, BA AU - Luster, MI AU - Thomas, P T AD - NIEHS/NTP, P.O. Box 12233 MD C1-04, Research Triangle Park, NC 27709, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 113 EP - 127 VL - 1 IS - 2 SN - 0895-8378, 0895-8378 KW - arsine KW - effects on KW - immune response KW - spleen KW - mice KW - Health & Safety Science Abstracts; Immunology Abstracts; Toxicology Abstracts KW - inhalation KW - lymphocytes KW - immunology KW - H SM8.8.2:CHEMICALS (CORROSION) KW - F 06791:Experimental KW - X 24152:Chronic exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15265955?accountid=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=Effect+of+subchronic+arsine+inhalation+on+immune+function+and+host+resistance.&rft.au=Rosenthal%2C+G+J%3BFort%2C+M+M%3BGermolec%3BAckermann%2C+M+F%3BLamm%2C+K+R%3BBlair%2C+P+C%3BFowler%2C+BA%3BLuster%2C+MI%3BThomas%2C+P+T&rft.aulast=Rosenthal&rft.aufirst=G&rft.date=1989-01-01&rft.volume=1&rft.issue=2&rft.spage=113&rft.isbn=&rft.btitle=&rft.title=Inhalation+Toxicology&rft.issn=08958378&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-12 N1 - SubjectsTermNotLitGenreText - inhalation; mice; lymphocytes; immunology; immune response; spleen ER - TY - JOUR T1 - Binding of thyroxine to human plasma low density lipoprotein through specific interaction with apolipoprotein B (apoB-100). AN - 15252563; 2015828 AB - Human plasma low density lipoprotein (LDL), which binds 0.2% of plasma T sub(4), was shown to interact with the hormone through its protein moiety, apolipoprotein B-100. LDL and LDL sub(2), the major subfraction of LDL, were found to have 3 equivalent binding sites for T sub(4) with K sub(a) = 2.5 x 10 super(6) M super(-1). Photoaffinity labeling of LDL with inner ring-labeled ( super(125)I)T sub(4), followed by SDS-PAGE or agarose-SDS-PAGE of the labeled products, revealed that apoB-100 and its proteolytic cleavage products, apoB-74 and apoB-26, bound ( super(125)I)T sub(4). In the presence of 1 or 10 mu M T sub(4), labeling was decreased in 7 separate experiments by 40-53% or 65-86%, respectively, consistent with a K sub(a) of approximately equals 10 super(6) M super(-1). Binding of T sub(4) to apoB-100 associated with VLDL was also demonstrated by photoaffinity labeling. JF - Biochimie. Paris AU - Benvenga, S AU - Cahnmann, H AU - Gregg, R AU - Robbins, J AD - Clin. Endocrinol. Branch, NIDDK, Build. 10, Rm. 8N 311, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 263 EP - 268 VL - 71 IS - 2 SN - 0300-9084, 0300-9084 KW - apolipoprotein B KW - binding KW - interaction KW - lipoprotein (low density) KW - man KW - plasma KW - thyroxine 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/15252563?accountid=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+pediatric+otorhinolaryngology&rft.atitle=The+development+of+snoring+and+sleep+related+breathing+distress+from+4+to+6+years+in+a+cohort+of+Swedish+children.&rft.au=L%C3%B6fstrand-Tidestr%C3%B6m%2C+Britta%3BHultcrantz%2C+Elisabeth&rft.aulast=L%C3%B6fstrand-Tidestr%C3%B6m&rft.aufirst=Britta&rft.date=2007-07-01&rft.volume=71&rft.issue=7&rft.spage=1025&rft.isbn=&rft.btitle=&rft.title=International+journal+of+pediatric+otorhinolaryngology&rft.issn=01655876&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 - Gene conversion in Escherichia coli : The recF pathway for resolution of heteroduplex DNA. AN - 15249607; 2009357 AB - The independent repair of mismatched nucleotides present in heteroduplex DNA, has been used to explain gene conversion and map expansion after general genetic recombination. The authors have constructed and purified heteroduplex plasmid DNAs that contain heteroallelic 10-base-pair insertion-deletion mismatches. These DNA substrates are similar in structure to the heteroduplex DNA intermediates that have been proposed to be produced during the genetic recombination of plasmids. These DNA substrates were transformed into wild-type and mutant Escherichia coli strains, and the fate of the heteroduplex DNA was determined by both restriction mapping and genetic tests. Independent repair events that yielded a wild-type Tet super(r) gene were observed at a frequency of approximately 1% in both wild-type and recB recC sbcB) mutant E. coli strains. JF - Journal of Bacteriology AU - Fishel, R AU - Kolodner, R AD - Lab. Chromosome Biol., BRI-Basic Res. Program, NCI-Frederick Cancer Res. Facil., Frederick, MD 21701, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 3046 EP - 3052 VL - 171 IS - 6 SN - 0021-9193, 0021-9193 KW - gene conversion KW - recF gene KW - Biochemistry Abstracts 2: Nucleic Acids; Genetics Abstracts; Microbiology Abstracts B: Bacteriology KW - genes KW - Escherichia coli KW - DNA repair KW - G 07320:Bacterial genetics KW - N 14652:DNA repair KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15249607?accountid=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=Gene+conversion+in+Escherichia+coli+%3A+The+recF+pathway+for+resolution+of+heteroduplex+DNA.&rft.au=Fishel%2C+R%3BKolodner%2C+R&rft.aulast=Fishel&rft.aufirst=R&rft.date=1989-01-01&rft.volume=171&rft.issue=6&rft.spage=3046&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 - 2011-12-12 N1 - SubjectsTermNotLitGenreText - Escherichia coli; genes; DNA repair ER - TY - JOUR T1 - Water: Africa's most precious resource. AN - 15241031; 2001364 AB - Water is arguably Africa's most precious resource. And while pumping and maintaining a pure water supply is the number one priority, water storage is a vital area of activity. The author reports on the important role for the specialist tank manufacturer in helping to meet the World Health Organization's aim of clean water for all. JF - Water and Waste Treatment AU - Hayes, P AD - NEI Thompson Horsley Bridge, UK Y1 - 1989 PY - 1989 DA - 1989 SP - 31 EP - 32 VL - 32 IS - 3 SN - 0043-1133, 0043-1133 KW - Africa KW - Pollution Abstracts KW - water supplies KW - resource management KW - pollution control KW - P 3000:SEWAGE & WASTEWATER TREATMENT UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15241031?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Apollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+language+%26+communication+disorders+%2F+Royal+College+of+Speech+%26+Language+Therapists&rft.atitle=Modal+verbs+with+and+without+tense%3A+a+study+of+English-+and+Cantonese-speaking+children+with+specific+language+impairment.&rft.au=Leonard%2C+Laurence+B%3BDeevy%2C+Patricia%3BWong%2C+Anita+M-Y%3BStokes%2C+Stephanie+F%3BFletcher%2C+Paul&rft.aulast=Leonard&rft.aufirst=Laurence&rft.date=2007-03-01&rft.volume=42&rft.issue=2&rft.spage=209&rft.isbn=&rft.btitle=&rft.title=International+journal+of+language+%26+communication+disorders+%2F+Royal+College+of+Speech+%26+Language+Therapists&rft.issn=13682822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-12 N1 - SubjectsTermNotLitGenreText - water supplies; pollution control; resource management ER - TY - JOUR T1 - Purified human erythrocyte pyrroline-5-carboxylate reductase. Preferential oxidation of NADPH. AN - 15227793; 1989836 AB - Pyrroline-5-carboxylate reductase catalyzes the final step in proline synthesis by NAD(P)H-dependent reduction of pyrroline-5-carboxylate. The authors have purified and characterized this enzyme from human erythrocytes. Purification to homogeneity ( similar to 600,000-fold) was accomplished by sonication, ultracentrifugation, 2',5'-ADP-Sepharose affinity chromatography, and DEAE-Sephacel ion exchange chromatography. The enzyme runs as a single band of 30,000 M sub(r) on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The authors suggest that, in some cell types including human erythrocytes, a physiologic function of pyrroline-5-carboxylate reductase is the generation of NADP super(+). JF - Journal of Biological Chemistry AU - Merrill, MJ AU - Yeh, G C AU - Phang, J M AD - Endocrinol. Sect., Metab. Branch, NCI, Build. 10, Rm. 4N115, NIH, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 9352 EP - 9358 VL - 264 IS - 16 SN - 0021-9258, 0021-9258 KW - NADPH KW - activity KW - erythrocytes KW - man KW - oxidation KW - pyrroline-5-carboxylate reductase 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/15227793?accountid=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=Purified+human+erythrocyte+pyrroline-5-carboxylate+reductase.+Preferential+oxidation+of+NADPH.&rft.au=Merrill%2C+MJ%3BYeh%2C+G+C%3BPhang%2C+J+M&rft.aulast=Merrill&rft.aufirst=MJ&rft.date=1989-01-01&rft.volume=264&rft.issue=16&rft.spage=9352&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 - Spontaneous polymerization of the antibiotic peptide magainin 2. AN - 15225465; 1990843 AB - The authors describe here the ability of the magainin 2 peptide to assemble spontaneously into characteristic 13-nm diameter filaments having a 30 nm periodic helical substructure. Optimal conditions for extensive polymerization into filaments of several hundred microns required low pH and high ionic strength. Polymerization of the magainin 2 peptide may be involved in its recently described in vitro membrane-disrupting and antibiotic activities. JF - FEBS Letters AU - Urrutia, R AU - Cruciani, R A AU - Barker, J L AU - Kachar, B AD - NIDCD, Natl. Inst. Health, Build. 36, Rm. 5D 08, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 17 EP - 21 VL - 247 IS - 1 SN - 0014-5793, 0014-5793 KW - antibiotics KW - characterization KW - magainin 2 KW - polymerization 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/15225465?accountid=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=Spontaneous+polymerization+of+the+antibiotic+peptide+magainin+2.&rft.au=Urrutia%2C+R%3BCruciani%2C+R+A%3BBarker%2C+J+L%3BKachar%2C+B&rft.aulast=Urrutia&rft.aufirst=R&rft.date=1989-01-01&rft.volume=247&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 revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - In vitro binding characteristics of ( super(3)H)spiperone to the pituitary of the goldfish (Carassius auratus)). AN - 15224246; 1990927 AB - Homogenates of the pituitary of the goldfish (Carassius auratus ) were incubated with ( super(3)H)spiperone under various experimental paradigms to evaluate the binding characteristics of the goldfish pituitary dopamine receptor. The data agree with previous in vivo and in vitro findings of the biological actions of dopamine agonists and antagonists in modifying gonadotropic hormone release in the goldfish and represent the first demonstration of the existence and binding characteristics of a dopamine/neuroleptic receptor in the pituitary of a nonmammalian vertebrate. JF - General and Comparative Endocrinology AU - Omeljaniuk, R J AU - Peter, R E AD - ERRB NICHD, Build. 10, Room 8C-407, Natl. Inst. Health, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 57 EP - 67 VL - 74 IS - 1 SN - 0016-6480, 0016-6480 KW - binding KW - pituitary KW - pituitary gland KW - spiperone KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA Aquaculture Abstracts; CSA Neurosciences Abstracts KW - neurotransmitters KW - inhibitors KW - receptors KW - Freshwater KW - Carassius auratus KW - hormones KW - Q1 08346:Physiology, biochemistry, biophysics KW - Q3 08582:Fish culture KW - N3 11080:Neuroendocrinology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15224246?accountid=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=General+and+Comparative+Endocrinology&rft.atitle=In+vitro+binding+characteristics+of+%28+super%283%29H%29spiperone+to+the+pituitary+of+the+goldfish+%28Carassius+auratus%29%29.&rft.au=Omeljaniuk%2C+R+J%3BPeter%2C+R+E&rft.aulast=Omeljaniuk&rft.aufirst=R&rft.date=1989-01-01&rft.volume=74&rft.issue=1&rft.spage=57&rft.isbn=&rft.btitle=&rft.title=General+and+Comparative+Endocrinology&rft.issn=00166480&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 - neurotransmitters; inhibitors; pituitary gland; receptors; hormones; pituitary; Carassius auratus; Freshwater ER - TY - JOUR T1 - Experimental evidence of an alpha helix in Desulfovibrio desulfuricans Norway ferredoxin I: A two-dimensional NMR study. AN - 15224242; 1989748 AB - Desulfovibrio ferredoxins are small proteins involved in biological oxido-reduction reactions and contain either one or two (4Fe-4S) clusters. The conformation of D. desulfuricans Norway ferredoxin I in solution was studied by two-dimensional NMR and various conformational parameters indicate the presence of an alpha -helix involving residues 41 to 50. JF - Biochemical and Biophysical Research Communications AU - Marion, D AU - Guerlesquin, F AD - Lab. Chem. Phys., NIDDK, Natl. Inst. Health, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 592 EP - 598 VL - 159 IS - 2 SN - 0006-291X, 0006-291X KW - Desulfovibrio desulfuricans KW - N.M.R. KW - alpha KW - ferredoxin I KW - helix KW - identification KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology KW - J 02723:Photosynthesis, electron transport and related phenomena UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15224242?accountid=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=Experimental+evidence+of+an+alpha+helix+in+Desulfovibrio+desulfuricans+Norway+ferredoxin+I%3A+A+two-dimensional+NMR+study.&rft.au=Marion%2C+D%3BGuerlesquin%2C+F&rft.aulast=Marion&rft.aufirst=D&rft.date=1989-01-01&rft.volume=159&rft.issue=2&rft.spage=592&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 - Dopamine inhibition of gonadotropin and alpha -melanocyte-stimulating hormone release in vitro from the pituitary of the goldfish (Carassius auratus ). AN - 15219665; 1987797 AB - The purpose of the present investigation was to examine the receptor specificity of dopamine inhibition of gonadotropin (GtH) and alpha -melanocyte-stimulating hormone ( alpha -MSH) release from the goldfish (Carassius auratus ) pituitary in vitro. The results suggest the involvement of a low-affinity dopamine/neuroleptic receptor in dopamine inhibition of GtH and alpha -MSH release from the pituitary of the goldfish. JF - General and Comparative Endocrinology AU - Omeljaniuk, R J AU - Tonon, M C AU - Peter, R E AD - ERRB NICHD, Build., 10, Room 8C-407, Natl. Inst. Health, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 451 EP - 467 VL - 74 IS - 3 SN - 0016-6480, 0016-6480 KW - dopamine KW - gonadotropins KW - inhibition KW - pituitary gland KW - release KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA Aquaculture Abstracts; CSA Neurosciences Abstracts KW - Freshwater KW - Carassius auratus KW - endocrinology KW - hormones KW - chemoreceptors KW - Q1 08346:Physiology, biochemistry, biophysics KW - Q3 08582:Fish culture KW - N3 11260:GONADOTROPINS AND PREGNANCY-RELATED HORMONES UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15219665?accountid=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=General+and+Comparative+Endocrinology&rft.atitle=Dopamine+inhibition+of+gonadotropin+and+alpha+-melanocyte-stimulating+hormone+release+in+vitro+from+the+pituitary+of+the+goldfish+%28Carassius+auratus+%29.&rft.au=Omeljaniuk%2C+R+J%3BTonon%2C+M+C%3BPeter%2C+R+E&rft.aulast=Omeljaniuk&rft.aufirst=R&rft.date=1989-01-01&rft.volume=74&rft.issue=3&rft.spage=451&rft.isbn=&rft.btitle=&rft.title=General+and+Comparative+Endocrinology&rft.issn=00166480&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 - pituitary gland; endocrinology; chemoreceptors; hormones; Carassius auratus; Freshwater ER - TY - JOUR T1 - Cloning of the rat adrenal medullary phenylethanolamine-N-methyltransferase. AN - 15219244; 1985879 AB - The authors have cloned phenylethanolamine-N-methyltransferase (PNMT - the enzyme that converts noradrenaline to adrenaline) using a rat adrenal library. Compared to the bovine cDNA the clone sequenced is missing 72 nucleotides of the coding region at the 5' end of the sequence and shows an 83% and 84% homology in the coding region to the bovine and human sequences, respectively. The protein sequence shows a 83% similarity to the bovine and a 92% similarity to the human enzyme (excluding conservative substitutions these percentages are 79% and 87%, respectively). JF - Nucleic Acids Research AU - Mezey, E AD - Lab. Cell Biol., NIMH, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 2125 VL - 17 IS - 5 SN - 0305-1048, 0305-1048 KW - adrenal medulla KW - amino acid sequence KW - genes KW - nucleotide sequence KW - phenylethanolamine-N-methyltransferase 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/15219244?accountid=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=Cloning+of+the+rat+adrenal+medullary+phenylethanolamine-N-methyltransferase.&rft.au=Mezey%2C+E&rft.aulast=Mezey&rft.aufirst=E&rft.date=1989-01-01&rft.volume=17&rft.issue=5&rft.spage=2125&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 N1 - SubjectsTermNotLitGenreText - genes; adrenal medulla ER - TY - JOUR T1 - Alterations in pituitary GnRH and dopamine receptors associated with the seasonal variation and regulation of gonadotropin release in the goldfish (Carassius auratus ). AN - 15217070; 1987673 AB - Seasonal variations in the serum concentrations of gonadotropin (GtH) and the serum GtH response to intraperitoneal injection of domperidone, a specific dopamine receptor antagonist, were examined in goldfish. In addition, the effects of in vivo treatment of goldfish with a superactive analog of salmon gonadotropin-releasing hormone (sGnRH-A) and domperidone on the binding parameters of pituitary GnRH and dopamine receptors were investigated in goldfish. The results provide information on the interaction of GnRH and dopamine on regulation of serum concentrations of GtH in goldfish, and suggest that this interaction partly involves changes in the number of pituitary receptors for GnRH and dopamine. JF - General and Comparative Endocrinology AU - Omeljaniuk, R J AU - Habibi, H R AU - Peter, R E AD - ERRB NICHD, Build. 10, Rm. 8C-407, Natl. Inst. Health, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 392 EP - 399 VL - 74 IS - 3 SN - 0016-6480, 0016-6480 KW - dopamine KW - gonadotropins KW - pituitary gland KW - regulation KW - release KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA Aquaculture Abstracts; CSA Neurosciences Abstracts KW - secretion KW - Freshwater KW - Carassius auratus KW - hormones KW - Q3 08582:Fish culture KW - Q1 08344:Reproduction and development KW - N3 11080:Neuroendocrinology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15217070?accountid=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=General+and+Comparative+Endocrinology&rft.atitle=Alterations+in+pituitary+GnRH+and+dopamine+receptors+associated+with+the+seasonal+variation+and+regulation+of+gonadotropin+release+in+the+goldfish+%28Carassius+auratus+%29.&rft.au=Omeljaniuk%2C+R+J%3BHabibi%2C+H+R%3BPeter%2C+R+E&rft.aulast=Omeljaniuk&rft.aufirst=R&rft.date=1989-01-01&rft.volume=74&rft.issue=3&rft.spage=392&rft.isbn=&rft.btitle=&rft.title=General+and+Comparative+Endocrinology&rft.issn=00166480&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 - secretion; pituitary gland; hormones; Carassius auratus; Freshwater ER - TY - JOUR T1 - Hepatotoxicity of agents that enhance formation of focal hepatocellular proliferative lesions (putative preneoplastic foci) in a rapid rat liver bioassay. AN - 15197006; 1968669 AB - The histopathology of hepatic toxicity for 58 chemicals previously tested in a rapid rat liver bioassay for demonstrating potential hepatocellular carcinogens and/or tumor promoters was reviewed. Rats received the test diet for 1 week prior to partial hepatectomy and for an additional 5 weeks thereafter at doses near the estimated maximally tolerated dose. These rats served as controls for others receiving initiation by N-nitrosodiethylamine (DEN) and the test diets. Twenty-two of these chemicals were previously found to enhance the formation of glutathione S-transferase, placental form (GST-P)-positive putative preneoplastic hepatocellular foci (promoters) following DEN initiation in this rapid bioassay, whereas 36 chemicals did not. Of the agents that promoted GST-P-positive foci, 14/22 (63.6%) produced toxic hepatocyte lesions while only 4/36 (11.1%) of the nonpromoters did so at the doses used. Biliary toxicity was found for 7/22 (31.8%) of the promoters and 6/36 (16.7%) of the nonpromoters. JF - Fundamental and Applied Toxicology AU - Ward, J M AU - Tsuda, H AU - Tatematsu, M AU - Hagiwara, A AU - Ito, N AD - NCI-FCRF, Build. 538, Frederick, MD 21701-1013, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 163 EP - 171 VL - 12 IS - 1 SN - 0272-0590, 0272-0590 KW - xenobiotics KW - histopathology KW - rapid KW - rats KW - Toxicology Abstracts KW - bioassays KW - liver KW - X 24221:Toxicity testing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15197006?accountid=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=Hepatotoxicity+of+agents+that+enhance+formation+of+focal+hepatocellular+proliferative+lesions+%28putative+preneoplastic+foci%29+in+a+rapid+rat+liver+bioassay.&rft.au=Ward%2C+J+M%3BTsuda%2C+H%3BTatematsu%2C+M%3BHagiwara%2C+A%3BIto%2C+N&rft.aulast=Ward&rft.aufirst=J&rft.date=1989-01-01&rft.volume=12&rft.issue=1&rft.spage=163&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 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-12 N1 - SubjectsTermNotLitGenreText - liver; bioassays ER - TY - JOUR T1 - A method for the rapid screening of human blood samples for the presence of HIV-1 sequences: The probe-shift assay. AN - 15193458; 1972164 AB - In theory, screening directly for the human immunodeficiency virus (HIV) DNA has advantages over screening for HIV-related antibodies; however, the HIV genome appears to be present only in a small fraction of peripheral blood cells from infected individuals. The polymerase chain reaction (PCR) specifically amplifies defined DNA segments, permitting the identification of specific DNA segments even if they are present in a fraction of cells. The authors describe here an alternative approach to specific detection of PCR-amplified DNA segments, the probe-shift assay, that is simpler, faster, and less subject to erroneous identification than the previously described techniques. JF - AIDS Research and Human Retroviruses AU - Kumar, R AU - Goedert, J J AU - Hughes, SH AD - NCI-Frederick Cancer Res. Facil., BRI-Basic Res. Program, P.O. Box B, Frederick, MD 21701, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 345 EP - 354 VL - 5 IS - 3 SN - 0889-2229, 0889-2229 KW - man KW - blood KW - detection KW - probes KW - probe-shift assay KW - polymerase chain reaction KW - oligonucleotides KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts KW - human immunodeficiency virus 1 KW - DNA KW - hybridization KW - A 01114:Viruses KW - V 22121:Diagnosis KW - V 22004:AIDS: Clinical aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15193458?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+Research+and+Human+Retroviruses&rft.atitle=A+method+for+the+rapid+screening+of+human+blood+samples+for+the+presence+of+HIV-1+sequences%3A+The+probe-shift+assay.&rft.au=Kumar%2C+R%3BGoedert%2C+J+J%3BHughes%2C+SH&rft.aulast=Kumar&rft.aufirst=R&rft.date=1989-01-01&rft.volume=5&rft.issue=3&rft.spage=345&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 revised - 2006-11-01 N1 - Last updated - 2011-12-12 N1 - SubjectsTermNotLitGenreText - human immunodeficiency virus 1; DNA; hybridization ER - TY - JOUR T1 - Human monocyte chemoattractant protein-1 (MCP-1). Full-length cDNA cloning, expression in mitogen-stimulated blood mononuclear leukocytes, and sequence similarity to mouse competence gene JE. AN - 15175381; 1952768 AB - The purpose of this work was to analyze cDNA encoding human monocyte chemoattractant protein-1 (MCP-1), previously isolated from glioma cell line culture fluid. Screening of a cDNA library from total poly(A) RNA of glioma cell line U-105MG yielded a clone that coded for the entire MCP-1. Nucleotide sequence analysis and comparison with the amino acid sequence of purified MCP-1 showed that the cDNA clone comprises a 53-nucleotide 5'-non-coding region, an open reading frame coding for a 99-residue protein of which the last 76 residues correspond exactly to pure MCP-1, and a 389-nucleotide 3'-untranslated region. The hydrophobicity of the first 23 residues is typical of a signal peptide. Southern blot analysis of human and animal genomic DNA showed that there is a single MCP-1 gene, which is conserved in several primates. JF - FEBS Letters AU - Yoshimura, T AU - Yuhki, N AU - Moore, S K AU - Appella, E AU - Lerman, MI AU - Leonard, E J AD - Lab. Immunobiol., Build. 560, Rm. 12-71, NCI-FCRF, Frederick, MD 21701, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 487 EP - 493 VL - 244 IS - 2 SN - 0014-5793, 0014-5793 KW - amino acid sequence KW - cDNA KW - chemoattractant protein 1 KW - comparison KW - genes KW - homology KW - leukocytes (mononuclear) KW - man 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 - N 14640:Structure & sequence KW - G 07430:Chromosome studies/nucleotide sequence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15175381?accountid=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=Human+monocyte+chemoattractant+protein-1+%28MCP-1%29.+Full-length+cDNA+cloning%2C+expression+in+mitogen-stimulated+blood+mononuclear+leukocytes%2C+and+sequence+similarity+to+mouse+competence+gene+JE.&rft.au=Yoshimura%2C+T%3BYuhki%2C+N%3BMoore%2C+S+K%3BAppella%2C+E%3BLerman%2C+MI%3BLeonard%2C+E+J&rft.aulast=Yoshimura&rft.aufirst=T&rft.date=1989-01-01&rft.volume=244&rft.issue=2&rft.spage=487&rft.isbn=&rft.btitle=&rft.title=FEBS+Letters&rft.issn=00145793&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 - leukocytes (mononuclear); genes; man ER - TY - JOUR T1 - Cytoskeletal effects of acrylamide and 2,5-hexanedione: Selective aggregation of vimentin filaments. AN - 15169830; 1943645 AB - Several neurotoxic compounds cause aggregation of neurofilaments in peripheral axons. This may represent a primary action of these chemicals or a secondary response to other cellular damage. To distinguish between these possibilities, the effects of acrylamide and 2,5-hexanedione (2,5-HD) on vimentin were examined in PtK sub(2) cultured cells. Both acrylamide and 2,5-HD caused aggregation of vimentin filaments in a concentration-dependent fashion; these effects occurred at a lower concentration than alterations in other cytoskeletal filaments. The effects of both acrylamide and 2,5-HD were reversible, except at high concentrations of 2,5-HD. Crosslinking of cytoskeletal proteins was also examined. High-molecular-weight proteins with vimentin-like immunoreactivity were detected on blots from cells exposed to high concentrations of 2,5-HD. No crosslinked protein was detected after acrylamide treatment. These results suggest that both acrylamide and 2,5-HD cause a primary collapse of vimentin intermediate filaments in cultured cells. JF - Toxicology and Applied Pharmacology AU - Sager, PR AD - AIDS Program, NIAID, NIH, 6003 Executive Blvd., Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 141 EP - 155 VL - 97 IS - 1 SN - 0041-008X, 0041-008X KW - effects on KW - cell lines KW - acrylamide KW - acetonylacetone KW - CSA Neurosciences Abstracts; Toxicology Abstracts KW - neurofilaments KW - cytoskeleton KW - X 24151:Acute exposure KW - N3 11104:Mammals (except primates) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15169830?accountid=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=Cytoskeletal+effects+of+acrylamide+and+2%2C5-hexanedione%3A+Selective+aggregation+of+vimentin+filaments.&rft.au=Sager%2C+PR&rft.aulast=Sager&rft.aufirst=PR&rft.date=1989-01-01&rft.volume=97&rft.issue=1&rft.spage=141&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 revised - 2006-11-01 N1 - Last updated - 2011-12-12 N1 - SubjectsTermNotLitGenreText - cytoskeleton; neurofilaments ER - TY - JOUR T1 - Hippocampal and cerebellar beta -adrenergic receptors and adenylate cyclase are differentially altered by chronic ethanol ingestion. AN - 15168717; 1943579 AB - Chronic ethanol ingestion by mice resulted in the loss of high-affinity beta -adrenergic agonist binding sites and a significant decrease in activation of adenylate cyclase by guanine nucleotides and beta -adrenergic agonists in the hippocampus. Different responses to ethanol in hippocampus and cerebellum may result from quantitative differences in distribution of beta sub(1)- and beta sub(2)-adrenergic receptors in the tested brain areas and/or differential effects of ethanol on stimulatory guanine nucleotide binding protein in these brain areas. JF - Journal of Neurochemistry AU - Valverius, P AU - Hoffman, P L AU - Tabakoff, B AD - NIAAA/DICBR, Build. 10, Rm. 3C103, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 492 EP - 497 VL - 52 IS - 2 SN - 0022-3042, 0022-3042 KW - chronic effects KW - receptors KW - density KW - ethanol KW - beta -adrenergic KW - mice KW - Toxicology Abstracts; CSA Neurosciences Abstracts KW - brain KW - N3 11104:Mammals (except primates) KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15168717?accountid=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+Neurochemistry&rft.atitle=Hippocampal+and+cerebellar+beta+-adrenergic+receptors+and+adenylate+cyclase+are+differentially+altered+by+chronic+ethanol+ingestion.&rft.au=Valverius%2C+P%3BHoffman%2C+P+L%3BTabakoff%2C+B&rft.aulast=Valverius&rft.aufirst=P&rft.date=1989-01-01&rft.volume=52&rft.issue=2&rft.spage=492&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 revised - 2006-11-01 N1 - Last updated - 2011-12-12 N1 - SubjectsTermNotLitGenreText - brain ER - TY - JOUR T1 - Molecular modeling of the HIV-1 protease and its substrate binding site. AN - 15145742; 1924458 AB - The human immunodeficiency virus (HIV-1) encodes a protease that is essential for viral replication and is a member of the aspartic protease family. The recently determined three-dimensional structure of the related protease from Rous sarcoma virus has been used to model the smaller HIV-1 dimer. The active site has been analyzed by comparison to the structure of the aspartic protease, rhizopuspepsin, complexed with a peptide inhibitor. The HIV-1 protease is predicted to interact with seven residues of the protein substrate. This information can be used to design protease inhibitors and possible antiviral drugs. JF - Science (Washington) AU - Weber, I T AU - Miller, M AU - Jaskolski, M AU - Leis, J AU - Skalka, A M AU - Wlodawer, A AD - Crystallogr. Lab., NCI-Frederick Cancer Res. Facil., BRI-Basic Res. Program, Frederick, MD 21701, USA Y1 - 1989 PY - 1989 DA - 1989 SP - 928 EP - 931 VL - 243 IS - 4893 SN - 0036-8075, 0036-8075 KW - binding KW - human immunodeficiency virus 1 KW - models KW - proteinase KW - sites KW - substrates KW - tertiary structure 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 KW - V 22032:Viral proteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15145742?accountid=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=Science+%28Washington%29&rft.atitle=Molecular+modeling+of+the+HIV-1+protease+and+its+substrate+binding+site.&rft.au=Weber%2C+I+T%3BMiller%2C+M%3BJaskolski%2C+M%3BLeis%2C+J%3BSkalka%2C+A+M%3BWlodawer%2C+A&rft.aulast=Weber&rft.aufirst=I&rft.date=1989-01-01&rft.volume=243&rft.issue=4893&rft.spage=928&rft.isbn=&rft.btitle=&rft.title=Science+%28Washington%29&rft.issn=00368075&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 - tertiary structure ER - TY - JOUR T1 - Africa's most precious resource AN - 13749236; 199001033 AB - The role of sectional steel water storage tanks in ensuring water supplies in Africa, particularly in Nigeria, is discussed. Multi-state water supply projects, water rehabilitation schemes, and agricultural development projects throughout Nigeria would generally require water storage tanks. NEI Thompson, Horseley Bridge, of the U.K. and their Nigerian associate, CFAO Structor, were participating in these developments. JF - Water Services AU - Hayes, PR AD - NEI Thompson, Horseley Bridge Y1 - 1989 PY - 1989 DA - 1989 SP - 387 EP - 387,389 VL - 93 IS - 1123 SN - 0301-7028, 0301-7028 KW - Aqualine Abstracts KW - AQ 00005:Underground Services and Water Use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/13749236?accountid=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=Water+Services&rft.atitle=Africa%27s+most+precious+resource&rft.au=Hayes%2C+PR&rft.aulast=Hayes&rft.aufirst=PR&rft.date=1989-01-01&rft.volume=93&rft.issue=1123&rft.spage=387&rft.isbn=&rft.btitle=&rft.title=Water+Services&rft.issn=03017028&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2000-09-01 N1 - SuppNotes - Publication focus: General. N1 - Last updated - 2011-12-12 ER - TY - JOUR T1 - New yeast-Escherichia coli shuttle vectors constructed with in vitro mutagenized yeast genes lacking six-base pair restriction sites. AN - 78747021; 3073106 AB - We describe the production of new alleles of the LEU2, URA3 and TRP1 genes of Saccharomyces cerevisiae by in vitro mutagenesis. Each new allele, which lacks restriction enzyme recognition sequences found in the pUC19 multicloning site, was used to construct a unique series of yeast-Escherichia coli shuttle vectors derived from the plasmid pUC19. For each gene a 2 mu vector (YEplac), an ARS1 CEN4 vector (YCplac) and an integrative vector (YIplac) was constructed. The features of these vectors include (i) small size; (ii) unique recognition site for each restriction enzyme found in the pUC19 multicloning site; (iii) screening for plasmids containing inserts by color assay; (iv) high plasmid yield; (v) efficient transformation of S. cerevisiae. These vectors should allow greater flexibility with regard to DNA restriction fragment manipulation and subcloning. JF - Gene AU - Gietz, R D AU - Sugino, A AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/12/30/ PY - 1988 DA - 1988 Dec 30 SP - 527 EP - 534 VL - 74 IS - 2 SN - 0378-1119, 0378-1119 KW - DNA, Recombinant KW - 0 KW - Oligodeoxyribonucleotides KW - Index Medicus KW - Genotype KW - Alleles KW - Transformation, Genetic KW - Oligodeoxyribonucleotides -- chemical synthesis KW - Plasmids KW - Saccharomyces cerevisiae -- genetics KW - Genes, Fungal KW - Genetic Vectors KW - Restriction Mapping KW - Escherichia coli -- genetics KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78747021?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=New+yeast-Escherichia+coli+shuttle+vectors+constructed+with+in+vitro+mutagenized+yeast+genes+lacking+six-base+pair+restriction+sites.&rft.au=Gietz%2C+R+D%3BSugino%2C+A&rft.aulast=Gietz&rft.aufirst=R&rft.date=1988-12-30&rft.volume=74&rft.issue=2&rft.spage=527&rft.isbn=&rft.btitle=&rft.title=Gene&rft.issn=03781119&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-06-19 N1 - Date created - 1989-06-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Acyclovir treatment of the chronic fatigue syndrome. Lack of efficacy in a placebo-controlled trial. AN - 78594167; 2849717 AB - Twenty-seven adults with a diagnosis of the chronic fatigue syndrome were enrolled in a double-blind, placebo-controlled study of acyclovir therapy. The patients had had debilitating fatigue for an average of 6.8 years, accompanied by persisting antibodies to Epstein-Barr virus early antigens (titers greater than or equal to 1:40) or undetectable levels of antibodies to Epstein-Barr virus nuclear antigens (titers less than 1:2) or both. Each course of treatment consisted of intravenous placebo or acyclovir (500 mg per square meter of body-surface area) administered every eight hours for seven days. The same drug was then given orally for 30 days (acyclovir, 800 mg four times daily). There were six-week observation periods before, between, and after the treatments. Three patients had acyclovir-induced nephrotoxicity and were withdrawn from the study. Of the 24 patients who completed the trial, similar numbers improved with acyclovir therapy and with placebo (11 and 10, respectively). Neither acyclovir treatment nor clinical improvement correlated with alterations in laboratory findings, including titers of antibody to Epstein-Barr virus or levels of circulating immune complexes or of leukocyte 2',5'-oligoadenylate synthetase. Subjective improvement correlated with various measures of mood. We conclude that acyclovir, as used in this study, does not ameliorate the chronic fatigue syndrome. We believe that the clinical improvement observed in most patients reflected either spontaneous remission of the syndrome or a placebo effect. JF - The New England journal of medicine AU - Straus, S E AU - Dale, J K AU - Tobi, M AU - Lawley, T AU - Preble, O AU - Blaese, R M AU - Hallahan, C AU - Henle, W AD - Medical Virology Section, National Institute of Allergy and Infectious Diseases, Bethesda, Md 20892. Y1 - 1988/12/29/ PY - 1988 DA - 1988 Dec 29 SP - 1692 EP - 1698 VL - 319 IS - 26 SN - 0028-4793, 0028-4793 KW - Antibodies, Viral KW - 0 KW - Antigens, Viral KW - Acyclovir KW - X4HES1O11F KW - Abridged Index Medicus KW - Index Medicus KW - Affect -- drug effects KW - Body Temperature -- drug effects KW - Humans KW - Clinical Trials as Topic KW - Antigens, Viral -- analysis KW - Antibodies, Viral -- analysis KW - Syndrome KW - Adult KW - Rest KW - Chronic Disease KW - Herpesviridae Infections -- drug therapy KW - Herpesvirus 4, Human -- immunology KW - Female KW - Male KW - Fatigue -- immunology KW - Acyclovir -- therapeutic use KW - Acyclovir -- administration & dosage KW - Acyclovir -- adverse effects KW - Fatigue -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78594167?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Acyclovir+treatment+of+the+chronic+fatigue+syndrome.+Lack+of+efficacy+in+a+placebo-controlled+trial.&rft.au=Straus%2C+S+E%3BDale%2C+J+K%3BTobi%2C+M%3BLawley%2C+T%3BPreble%2C+O%3BBlaese%2C+R+M%3BHallahan%2C+C%3BHenle%2C+W&rft.aulast=Straus&rft.aufirst=S&rft.date=1988-12-29&rft.volume=319&rft.issue=26&rft.spage=1692&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 - 1989-01-30 N1 - Date created - 1989-01-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of tumor-infiltrating lymphocytes and interleukin-2 in the immunotherapy of patients with metastatic melanoma. A preliminary report. AN - 78576305; 3264384 AB - Lymphocytes extracted from freshly resected melanomas can be expanded in vitro and can often mediate specific lysis of autologous tumor cells but not allogeneic tumor or autologous normal cells. We treated 20 patients with metastatic melanoma by means of adoptive transfer of these tumor-infiltrating lymphocytes and interleukin-2, after the patients had received a single intravenous dose of cyclophosphamide. Objective regression of the cancer was observed in 9 of 15 patients (60 percent) who had not previously been treated with interleukin-2 and in 2 of 5 patients (40 percent) in whom previous therapy with interleukin-2 had failed. Regression of cancer occurred in the lungs, liver, bone, skin, and subcutaneous sites and lasted from 2 to more than 13 months. Toxic effects of interleukin-2 occurred, although the treatment course was short (five days); these side effects were reversible. It appears that in patients with metastatic melanoma, this experimental treatment regimen can produce higher response rates than those achieved with interleukin-2 administered alone or with lymphokine-activated killer cells. It is too early to determine whether this new form of immunotherapy can improve survival, but further trials seem warranted. JF - The New England journal of medicine AU - Rosenberg, S A AU - Packard, B S AU - Aebersold, P M AU - Solomon, D AU - Topalian, S L AU - Toy, S T AU - Simon, P AU - Lotze, M T AU - Yang, J C AU - Seipp, C A AD - Surgery Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/12/22/ PY - 1988 DA - 1988 Dec 22 SP - 1676 EP - 1680 VL - 319 IS - 25 SN - 0028-4793, 0028-4793 KW - Interleukin-2 KW - 0 KW - Cyclophosphamide KW - 8N3DW7272P KW - Abridged Index Medicus KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Combined Modality Therapy KW - Cells, Cultured KW - Humans KW - Adult KW - Neoplasm Metastasis KW - Middle Aged KW - Male KW - Female KW - Lymphocytes -- immunology KW - Interleukin-2 -- adverse effects KW - Interleukin-2 -- administration & dosage KW - Melanoma -- therapy KW - Immunotherapy -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78576305?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Use+of+tumor-infiltrating+lymphocytes+and+interleukin-2+in+the+immunotherapy+of+patients+with+metastatic+melanoma.+A+preliminary+report.&rft.au=Rosenberg%2C+S+A%3BPackard%2C+B+S%3BAebersold%2C+P+M%3BSolomon%2C+D%3BTopalian%2C+S+L%3BToy%2C+S+T%3BSimon%2C+P%3BLotze%2C+M+T%3BYang%2C+J+C%3BSeipp%2C+C+A&rft.aulast=Rosenberg&rft.aufirst=S&rft.date=1988-12-22&rft.volume=319&rft.issue=25&rft.spage=1676&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 - 1989-01-23 N1 - Date created - 1989-01-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: N Engl J Med. 1989 May 25;320(21):1418-9 [2785641] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Studies of the mechanism of spontaneous germline ecotropic provirus acquisition in mice. AN - 78738394; 2854055 AB - SWR/J--RF/J hybrid mice spontaneously acquire new germline ecotropic proviruses at high frequency. We have performed ovarian transplantation and in situ hybridization studies to delineate the mechanism and developmental stage of germline provirus acquisition. In addition, we have developed a novel, efficient and simple method to introduce single copy proviruses into the mouse germline. The results reported here have direct implications for understanding how proviruses are acquired in the germline, for using murine leukemia viruses as insertional mutagens, and for using retroviral vectors to introduce foreign genes into the mouse germline. JF - The EMBO journal AU - Lock, L F AU - Keshet, E AU - Gilbert, D J AU - Jenkins, N A AU - Copeland, N G AD - Mammalian Genetics Laboratory, NCI--Frederick Cancer Research Facility, MD 21701. Y1 - 1988/12/20/ PY - 1988 DA - 1988 Dec 20 SP - 4169 EP - 4177 VL - 7 IS - 13 SN - 0261-4189, 0261-4189 KW - DNA, Viral KW - 0 KW - Index Medicus KW - Animals KW - Ovary -- microbiology KW - Crosses, Genetic KW - Mice KW - DNA, Viral -- isolation & purification KW - Nucleic Acid Hybridization KW - Ovary -- transplantation KW - Oocytes -- microbiology KW - DNA, Viral -- genetics KW - Ovary -- anatomy & histology KW - Male KW - Female KW - Pregnancy KW - Leukemia Virus, Murine -- genetics KW - Proviruses -- isolation & purification KW - Proviruses -- genetics KW - Leukemia Virus, Murine -- isolation & purification KW - Mice, Inbred Strains -- microbiology KW - Mice, Inbred Strains -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78738394?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Studies+of+the+mechanism+of+spontaneous+germline+ecotropic+provirus+acquisition+in+mice.&rft.au=Lock%2C+L+F%3BKeshet%2C+E%3BGilbert%2C+D+J%3BJenkins%2C+N+A%3BCopeland%2C+N+G&rft.aulast=Lock&rft.aufirst=L&rft.date=1988-12-20&rft.volume=7&rft.issue=13&rft.spage=4169&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 - 1989-06-02 N1 - Date created - 1989-06-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Virol. 1986 Nov;60(2):693-701 [3773055] Nature. 1987 Mar 19-25;326(6110):292-5 [3821905] Nature. 1987 Mar 19-25;326(6110):295-8 [3029599] Genetics. 1987 Sep;117(1):85-92 [2822532] Genetics. 1987 Sep;117(1):93-100 [3666442] Genes Dev. 1987 Jun;1(4):366-75 [2824282] Virology. 1984 Feb;133(1):183-90 [6322428] Cell. 1985 Dec;43(3 Pt 2):811-9 [3000616] Virology. 1988 Jan;162(1):1-11 [2447699] Proc Natl Acad Sci U S A. 1988 Feb;85(4):1156-60 [2829217] J Endocrinol. 1960 Apr;20:135-46 [14407693] Virology. 1970 Dec;42(4):1136-9 [4099080] Nature. 1971 Apr 30;230(5296):591-2 [4324231] J Exp Med. 1971 Jun 1;133(6):1219-33 [4325132] J Exp Med. 1972 Nov 1;136(5):1272-85 [4343244] J Exp Med. 1972 Nov 1;136(5):1286-301 [4343245] Proc Natl Acad Sci U S A. 1973 Nov;70(11):3067-71 [4361674] Proc Natl Acad Sci U S A. 1974 Sep;71(9):3555-9 [4372624] Exp Cell Res. 1975 May;92(2):361-71 [1132434] Virology. 1975 Oct;67(2):404-14 [52941] Proc Natl Acad Sci U S A. 1976 Apr;73(4):1260-4 [1063407] J Virol. 1976 May;18(2):383-400 [178885] Exp Cell Res. 1978 Mar 1;112(1):199-205 [631211] Cell. 1978 Oct;15(2):429-35 [214239] Cell. 1979 Feb;16(2):347-56 [222457] Cell. 1980 Jan;19(1):181-8 [7357600] Cell. 1980 Feb;19(2):431-6 [6244110] Proc Natl Acad Sci U S A. 1980 Jan;77(1):614-8 [6244569] Proc Natl Acad Sci U S A. 1980 Aug;77(8):4871-4 [6254044] Proc Natl Acad Sci U S A. 1980 Oct;77(10):5774-8 [6255464] Nature. 1981 Oct 1;293(5831):370-4 [6268990] Nature. 1982 Apr 29;296(5860):865-8 [7070527] J Virol. 1982 Feb;41(2):542-56 [6281466] J Virol. 1982 Apr;42(1):165-75 [6283136] J Virol. 1982 Jul;43(1):26-36 [6287001] J Virol. 1982 Aug;43(2):629-40 [6287036] J Exp Med. 1982 Nov 1;156(5):1461-74 [6290589] Cell. 1983 Jan;32(1):209-16 [6825169] J Exp Med. 1983 Aug 1;158(2):506-14 [6310018] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sequencing and synthesis of pardaxin, a polypeptide from the Red Sea Moses sole with ionophore activity. AN - 78586956; 2462511 AB - Pardaxin, an amphipathic polypeptide secreted by the Red Sea flatfish Pardachirus marmoratus whose sequence is NH2-G-F-F-A-L-I-P-K-I-I-S-S-P-L-F-K-T-L-L-S-A-V-G-S-A-L-S-S-S-G-G-Q-E, was synthesized by the solid-phase method. The structure was verified by sequencing. The synthetic polypeptide changed the resistance of lipid bilayers by forming pores. At 10(-7)-10(-8) M, the synthetic pardaxin increased the frequency of the spontaneous release of quanta of acetylcholine at the neuromuscular junction by up to 100-fold, resembling the native product. Synthetic pardaxin seems to be a suitable tool for investigating the molecular structures underlying channel selectivity. JF - FEBS letters AU - Shai, Y AU - Fox, J AU - Caratsch, C AU - Shih, Y L AU - Edwards, C AU - Lazarovici, P AD - Molecular, Cellular and Nutritional Endocrinology Branch, NIDDK, Bethesda, MD 20892. Y1 - 1988/12/19/ PY - 1988 DA - 1988 Dec 19 SP - 161 EP - 166 VL - 242 IS - 1 SN - 0014-5793, 0014-5793 KW - Fish Venoms KW - 0 KW - Ion Channels KW - Ionophores KW - Lipid Bilayers KW - pardaxin KW - 67995-63-5 KW - Acetylcholine KW - N9YNS0M02X KW - Index Medicus KW - Neuromuscular Junction -- drug effects KW - Animals KW - Electric Conductivity KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Acetylcholine -- secretion KW - Neuromuscular Junction -- secretion KW - Lipid Bilayers -- metabolism KW - Chromatography, High Pressure Liquid KW - Protein Conformation KW - Ion Channels -- metabolism KW - Ionophores -- pharmacology KW - Flatfishes -- metabolism KW - Fish Venoms -- pharmacology KW - Fish Venoms -- chemical synthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78586956?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Sequencing+and+synthesis+of+pardaxin%2C+a+polypeptide+from+the+Red+Sea+Moses+sole+with+ionophore+activity.&rft.au=Shai%2C+Y%3BFox%2C+J%3BCaratsch%2C+C%3BShih%2C+Y+L%3BEdwards%2C+C%3BLazarovici%2C+P&rft.aulast=Shai&rft.aufirst=Y&rft.date=1988-12-19&rft.volume=242&rft.issue=1&rft.spage=161&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 - 1989-02-06 N1 - Date created - 1989-02-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Residual hematopoietic effect in mice exposed to ochratoxin A prior to irradiation. AN - 78580018; 3059580 AB - Ochratoxin A (OCT A) has the potential to cause myelotoxicity in addition to the well-known toxic effects on the liver and kidney. Whereas in previous studies the bone marrow parameters were examined shortly after injection, experiments reported here were designed to determine whether mice would recover from the myelotoxic effects induced to OCT A injection and secondly whether mice previously injected to OCT A would be more sensitive to radiation-induced myelotoxicity than vehicle controls. Six-week old female B6C3F1 mice were injected intraperitoneally on alternate days over a week with a total dose of 20 or 40 mg/kg of OCT A and bone marrow parameters monitored for up to 16 weeks. Controls received vehicle alone. There was a suppression of marrow granulocyte macrophage progenitors (CFU-C) in OCT A-treated animals which returned to normal values by 2 weeks (20 mg/kg group) or by 5 weeks (40 mg/kg group) following the last treatment. Some of the OCT A-treated mice were additionally irradiated with 200 rads of whole body irradiation (WBI) at 10 and 52 days following OCT A injections. Irradiation caused a significant reduction in CFU-Cs in all mice but the effects were more pronounced in the mice that had received OCT A previously. The bone marrow parameters of 40 mg/kg OCT A-treated mice returned to normal by 6 weeks after first WBI. A second WBI produced similar depression in CFU-Cs with again a delayed 8 weeks recovery as compared to controls in both dose groups of OCT A-treated mice. The delayed recovery in bone marrow progenitors was also reflected in lower peripheral white blood counts after the second irradiation in 40 mg/kg OCT A-treated mice as compared to the untreated irradiated controls. This indicated that residual bone marrow effect of OCT A makes the mice more sensitive to subsequent irradiation induced injury. JF - Toxicology AU - Hong, H H AU - Jameson, C W AU - Boorman, G A AD - Chemical Pathology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/12/16/ PY - 1988 DA - 1988 Dec 16 SP - 57 EP - 67 VL - 53 IS - 1 SN - 0300-483X, 0300-483X KW - Ochratoxins KW - 0 KW - ochratoxin A KW - 1779SX6LUY KW - Index Medicus KW - Leukocyte Count -- drug effects KW - Animals KW - Whole-Body Irradiation KW - Leukocyte Count -- radiation effects KW - Hematopoiesis -- radiation effects KW - Hematopoiesis -- drug effects KW - Mice KW - Colony-Forming Units Assay KW - Time Factors KW - Ochratoxins -- toxicity KW - Ochratoxins -- administration & dosage KW - Bone Marrow -- radiation effects KW - Bone Marrow -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78580018?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Residual+hematopoietic+effect+in+mice+exposed+to+ochratoxin+A+prior+to+irradiation.&rft.au=Hong%2C+H+H%3BJameson%2C+C+W%3BBoorman%2C+G+A&rft.aulast=Hong&rft.aufirst=H&rft.date=1988-12-16&rft.volume=53&rft.issue=1&rft.spage=57&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-24 N1 - Date created - 1989-01-24 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Toxicology 1989 Feb;54(2):227 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Enhanced DNA repair and resistance to cisplatin in human ovarian cancer. AN - 78584626; 3144285 JF - Biochemical pharmacology AU - Lai, G M AU - Ozols, R F AU - Smyth, J F AU - Young, R C AU - Hamilton, T C AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/12/15/ PY - 1988 DA - 1988 Dec 15 SP - 4597 EP - 4600 VL - 37 IS - 24 SN - 0006-2952, 0006-2952 KW - Diterpenes KW - 0 KW - Aphidicolin KW - 38966-21-1 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Diterpenes -- pharmacology KW - Tumor Cells, Cultured KW - Dose-Response Relationship, Drug KW - Humans KW - Female KW - Ovarian Neoplasms -- genetics KW - Cisplatin -- toxicity KW - Drug Resistance KW - DNA Repair -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78584626?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Enhanced+DNA+repair+and+resistance+to+cisplatin+in+human+ovarian+cancer.&rft.au=Lai%2C+G+M%3BOzols%2C+R+F%3BSmyth%2C+J+F%3BYoung%2C+R+C%3BHamilton%2C+T+C&rft.aulast=Lai&rft.aufirst=G&rft.date=1988-12-15&rft.volume=37&rft.issue=24&rft.spage=4597&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 - 1989-01-26 N1 - Date created - 1989-01-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Altered regulation of P-450IA1 expression in a multidrug-resistant MCF-7 human breast cancer cell line. AN - 78571033; 3143724 AB - MCF-7 human breast cancer cells, selected for resistance to adriamycin (AdrR), exhibit the phenotype of multidrug resistance (MDR). Previous studies have shown that resistance in AdrR MCF-7 cells is associated with several biochemical changes that are similar to those induced in rat hyperplastic nodules, preneoplastic liver lesions which display broad spectrum resistance to carcinogens and hepatotoxins. In this report, we show that these changes in the AdrR MCF-7 cells are also associated with the development of cross-resistance to the procarcinogen benzo(a)pyrene (BP) and are associated with a marked defect in the conversion of BP to its cytotoxic, carcinogenic metabolites by AdrR cells. Since aryl hydrocarbon hydroxylase is the principle enzyme activity which converts benzo(a)pyrene to toxic hydroxylated forms, the regulation of cytochrome P-450IA1 expression, the gene encoding this enzyme activity in MCF-7 cells, was examined. Incubation with 100 nM 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for 24 h results in a marked increase in aryl hydrocarbon hydroxylase activity in wild type (WT) but not AdrR MCF-7 cells. The alteration in aryl hydrocarbon hydroxylase expression in the AdrR cells is not overcome by incubation either with higher concentrations of TCDD (1 microM) or for longer periods of time (4 days). Northern blot analysis indicates that this defect in AdrR MCF-7 cells involves a regulatory defect at the level of P-450IA1 RNA. Following transfection of a construct containing the normal mouse P-450IA1 promoter fused to a reporter gene (bacterial chloramphenicol acetyltransferase) into WT and AdrR MCF-7 cells, TCDD induced chloramphenicol acetyltransferase activity in WT MCF-7 cells only. Furthermore, TCDD also induces both DT-diaphorase and UDP-glucuronyltransferase activities in WT, but not AdrR cells. These data suggest that the defect in the AdrR MCF-7 cells is not due to a structural P-450IA1 gene mutation, but rather involves a product regulating the polycyclic hydrocarbon-inducible expression of several drug-metabolizing enzyme activities. This defect in the AdrR MCF-7 cells is also associated with the development of resistance to ellipticine, an anticancer agent which is converted to more toxic hydroxylated species by aryl hydrocarbon hydroxylase or a similar mixed function oxidase. The WT and AdrR MCF-7 cells represent a useful model to study the regulation of the P-450IA1 gene in human cells. JF - The Journal of biological chemistry AU - Ivy, S P AU - Tulpule, A AU - Fairchild, C R AU - Averbuch, S D AU - Myers, C E AU - Nebert, D W AU - Baird, W M AU - Cowan, K H AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/12/15/ PY - 1988 DA - 1988 Dec 15 SP - 19119 EP - 19125 VL - 263 IS - 35 SN - 0021-9258, 0021-9258 KW - Ellipticines KW - 0 KW - Polychlorinated Dibenzodioxins KW - ellipticine KW - 117VLW7484 KW - Benzo(a)pyrene KW - 3417WMA06D KW - Doxorubicin KW - 80168379AG KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - NAD(P)H Dehydrogenase (Quinone) KW - EC 1.6.5.2 KW - Quinone Reductases KW - EC 1.6.99.- KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Glucuronosyltransferase KW - EC 2.4.1.17 KW - Index Medicus KW - Blotting, Northern KW - Chloramphenicol O-Acetyltransferase -- biosynthesis KW - Humans KW - Polychlorinated Dibenzodioxins -- pharmacology KW - Quinone Reductases -- biosynthesis KW - Drug Resistance KW - Glucuronosyltransferase -- metabolism KW - Phenotype KW - Aryl Hydrocarbon Hydroxylases -- metabolism KW - Cell Line KW - Ellipticines -- pharmacology KW - Benzo(a)pyrene -- metabolism KW - Breast Neoplasms -- genetics KW - Doxorubicin -- pharmacology KW - Breast Neoplasms -- metabolism KW - Gene Expression Regulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78571033?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Altered+regulation+of+P-450IA1+expression+in+a+multidrug-resistant+MCF-7+human+breast+cancer+cell+line.&rft.au=Ivy%2C+S+P%3BTulpule%2C+A%3BFairchild%2C+C+R%3BAverbuch%2C+S+D%3BMyers%2C+C+E%3BNebert%2C+D+W%3BBaird%2C+W+M%3BCowan%2C+K+H&rft.aulast=Ivy&rft.aufirst=S&rft.date=1988-12-15&rft.volume=263&rft.issue=35&rft.spage=19119&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 - 1989-01-20 N1 - Date created - 1989-01-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - IL-2-PE40 is cytotoxic for activated T lymphocytes expressing IL-2 receptors. AN - 78569311; 3264309 AB - IL-2-PE40 is a chimeric molecule in which IL-2 is attached to the amino end of modified Pseudomonas exotoxin molecule lacking cell recognition domain. This molecule was extremely toxic for Con A-stimulated spleen cells from mice. Moreover, IL-2-PE40 has suppressive effect against Ag-activated cells; it inhibits the generation of cytotoxic T lymphocyte activity in a MLC. IL-2-PE40 could be a useful agent in IL-2R targeting therapy including immunosuppressive therapy for allograft rejection or some autoimmune diseases. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Ogata, M AU - Lorberboum-Galski, H AU - FitzGerald, D AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/12/15/ PY - 1988 DA - 1988 Dec 15 SP - 4224 EP - 4228 VL - 141 IS - 12 SN - 0022-1767, 0022-1767 KW - Bacterial Proteins KW - 0 KW - Exotoxins KW - IL-2-PE40 chimeric protein, recombinant KW - Immunosuppressive Agents KW - Immunotoxins KW - Interleukin-2 KW - Protein Synthesis Inhibitors KW - Receptors, Interleukin-2 KW - Recombinant Proteins KW - Concanavalin A KW - 11028-71-0 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Spleen KW - Mice KW - Mice, Inbred BALB C KW - Bacterial Proteins -- toxicity KW - Lymphocyte Activation -- drug effects KW - T-Lymphocytes -- metabolism KW - Protein Synthesis Inhibitors -- toxicity KW - Immunosuppressive Agents -- toxicity KW - Mice, Inbred C57BL KW - T-Lymphocytes -- drug effects KW - T-Lymphocytes -- immunology KW - Recombinant Proteins -- toxicity KW - Immunotoxins -- toxicity KW - Exotoxins -- toxicity KW - Pseudomonas -- immunology KW - Interleukin-2 -- toxicity KW - Receptors, Interleukin-2 -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78569311?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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-2-PE40+is+cytotoxic+for+activated+T+lymphocytes+expressing+IL-2+receptors.&rft.au=Ogata%2C+M%3BLorberboum-Galski%2C+H%3BFitzGerald%2C+D%3BPastan%2C+I&rft.aulast=Ogata&rft.aufirst=M&rft.date=1988-12-15&rft.volume=141&rft.issue=12&rft.spage=4224&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 - 1989-01-18 N1 - Date created - 1989-01-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dependence of secretory responses to gonadotropin-releasing hormone on diacylglycerol metabolism. Studies with a diacylglycerol lipase inhibitor, RHC 80267. AN - 78567122; 3143714 AB - The role of diacylglycerol (DG) as a source of arachidonic acid during gonadotropin-releasing hormone (GnRH) stimulation of gonadotropin secretion was analyzed in primary cultures of rat anterior pituitary cells. An inhibitor of DG lipase (RHC 80267, RHC) caused dose-dependent blockade of GnRH-stimulated luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion. The DG lipase inhibitor did not alter gonadotropin responses to arachidonic acid, and addition of arachidonic acid reversed its inhibition of GnRH-stimulated LH and FSH release. In [3H]arachidonic acid-prelabeled cells, incubation with RHC increased the accumulation of [3H]DG. These results suggest that DG lipase participates in GnRH action and that arachidonic acid mobilization from DG is involved in the mechanism of gonadotropin release. Gonadotropin responses to tetradecanoyl phorbol acetate and dioctanoyl glycerol were not altered by RHC, and the addition of these activators of protein kinase C (Ca2+- and phospholipid-dependent enzyme) did not prevent the inhibition of GnRH-induced gonadotropin release by RHC. Activation of phospholipase A2 by melittin increased LH and FSH secretion, whereas blockade of this enzyme by quinacrine reduced GnRH-stimulated hormone release. However, RHC did not diminish the gonadotropin response to melittin. The inhibitory actions of RHC and quinacrine were additive and were reversed by concomitant treatment with arachidonic acid. Ionomycin also increased LH and FSH release, and the gonadotropin responses to the ionophore were unaltered by RHC but were reduced by quinacrine. Incubation of cells in Ca2+-depleted (+/- [ethylenebis(oxyethylenenitrilo)]tetraacetic acid) medium reduced but did not abolish the LH and FSH releasing activity of GnRH. Treatment with RHC also reduced the gonadotropin responses to GnRH under Ca2+-depleted conditions. These observations indicate that RHC inhibition of GnRH action is not due to nonspecific actions on Ca2+ entry, protein kinase C activation and actions, nor phospholipase A2 enzyme activity. The results of this study provide further evidence for an extracellular Ca2+-independent mechanism of GnRH action, and suggest that GnRH causes mobilization of arachidonic acid by two distinct lipases, namely, phospholipase A2 and DG lipase, during stimulation of gonadotropin secretion. JF - The Journal of biological chemistry AU - Chang, J P AU - Morgan, R O AU - Catt, K J AD - Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1988/12/15/ PY - 1988 DA - 1988 Dec 15 SP - 18614 EP - 18620 VL - 263 IS - 35 SN - 0021-9258, 0021-9258 KW - Arachidonic Acids KW - 0 KW - Cyclohexanes KW - Cyclohexanones KW - Diglycerides KW - Ethers KW - Glycerides KW - 1,2-dioctanoylglycerol KW - 1069-87-0 KW - Arachidonic Acid KW - 27YG812J1I KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 KW - Ionomycin KW - 56092-81-0 KW - 1,6-bis(cyclohexyloximinocarbonyl)hexane KW - 83654-05-1 KW - Luteinizing Hormone KW - 9002-67-9 KW - Follicle Stimulating Hormone KW - 9002-68-0 KW - Lipoprotein Lipase KW - EC 3.1.1.34 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Rats KW - Luteinizing Hormone -- secretion KW - Animals KW - Ethers -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Follicle Stimulating Hormone -- secretion KW - Female KW - Arachidonic Acids -- pharmacology KW - Glycerides -- metabolism KW - Pituitary Gland, Anterior -- drug effects KW - Diglycerides -- pharmacology KW - Cyclohexanes -- pharmacology KW - Pituitary Gland, Anterior -- metabolism KW - Cyclohexanones -- pharmacology KW - Lipoprotein Lipase -- antagonists & inhibitors KW - Gonadotropin-Releasing Hormone -- pharmacology KW - Diglycerides -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78567122?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dependence+of+secretory+responses+to+gonadotropin-releasing+hormone+on+diacylglycerol+metabolism.+Studies+with+a+diacylglycerol+lipase+inhibitor%2C+RHC+80267.&rft.au=Chang%2C+J+P%3BMorgan%2C+R+O%3BCatt%2C+K+J&rft.aulast=Chang&rft.aufirst=J&rft.date=1988-12-15&rft.volume=263&rft.issue=35&rft.spage=18614&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 - 1989-01-20 N1 - Date created - 1989-01-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Restricted expression of mitogen-induced high affinity IL-2 receptors in aging mice. AN - 78566911; 3264308 AB - Several lines of indirect evidence suggest that the number and/or affinity of IL-2R expressed by activated T lymphocytes declines with age and that this decline is implicated in the age-related proliferative impairment of Ag or mitogen-stimulated T cells. In an attempt to provide a direct demonstration of such a defect, various experimental approaches were used to analyze the expression of high and low affinity IL-2R as well as their functional properties in relation to age in purified populations of murine T lymphocytes. IL-2R were induced by Con A-activation which involves a transmembrane signaling mechanism or by exposure to phorbol dibutyrate (PDBu) which bypasses such a pathway. Consistent with the previously reported age-related defect in signal transduction, a major deficiency in the expression of high affinity IL-2R was observed in mitogen-activated cells derived from aged animals. As expected, PDBu-induction circumvented the transmembrane signaling defect and resulted in the restoration of a measurable amount of high affinity IL-2R expressed by cells from aged mice early after activation. The functional properties of the IL-2R expressed as a consequence of Con A or PDBu induction were investigated by assessing the proliferative response induced through the high affinity IL-2R as compared to that mediated by the beta-chain alone. Although Con A-induction resulted in a decreased expression of high affinity IL-2R by T lymphocytes derived from aged mice, the ability of these receptors as well as that of their beta-chain component to transmit a proliferative signal was identical in both age groups. In contrast, PDBu induced in both cell populations the expression of functionally aberrant IL-2R, unable to signal for proliferation unless excessively high concentrations of rIL-2 were available. The quantitative minimal estimate of the frequency of Con A-activated, IL-2-responsive cells showed a fourfold age-associated decrease, confirming the inability of a subpopulation of T lymphocytes from aged mice to express a sufficient density of high affinity IL-2R as a consequence of mitogenic activation. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Proust, J J AU - Kittur, D S AU - Buchholz, M A AU - Nordin, A A AD - Clinical Immunology Section, National Institute on Aging, Baltimore, MD 21224. Y1 - 1988/12/15/ PY - 1988 DA - 1988 Dec 15 SP - 4209 EP - 4216 VL - 141 IS - 12 SN - 0022-1767, 0022-1767 KW - Interleukin-2 KW - 0 KW - Mitogens KW - Receptors, Interleukin-2 KW - Recombinant Proteins KW - Concanavalin A KW - 11028-71-0 KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Interleukin-2 -- metabolism KW - T-Lymphocytes -- physiology KW - Mice KW - Leukocyte Count KW - Interleukin-2 -- physiology KW - T-Lymphocytes -- metabolism KW - Cell Survival -- drug effects KW - Recombinant Proteins -- metabolism KW - Mice, Inbred C57BL KW - Male KW - T-Lymphocytes -- immunology KW - Lymphocyte Activation -- drug effects KW - Receptors, Interleukin-2 -- biosynthesis KW - Aging KW - Receptors, Interleukin-2 -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78566911?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Restricted+expression+of+mitogen-induced+high+affinity+IL-2+receptors+in+aging+mice.&rft.au=Proust%2C+J+J%3BKittur%2C+D+S%3BBuchholz%2C+M+A%3BNordin%2C+A+A&rft.aulast=Proust&rft.aufirst=J&rft.date=1988-12-15&rft.volume=141&rft.issue=12&rft.spage=4209&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 - 1989-01-18 N1 - Date created - 1989-01-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chromosome alterations in Syrian hamster cells transformed in vitro by sodium bisulfite, a nonclastogenic carcinogen. AN - 78535123; 3191496 AB - Sodium bisulfite, a nonmutagen at neutral pH, induces neoplastic transformation of cultured Syrian hamster fetal cells. Morphologically transformed fibroblast colonies were isolated, and derived cell lines formed anchorage-independent colonies in agarose and progressively growing s.c. fibrosarcomas in nu/nu mice. Five tumorigenic cell lines analyzed by G- and C-banding were chromosomally abnormal with numerical deviations and structural alterations. Three tumors that developed in nude mice had the chromosome constitution of the inoculated transformed cell as well as secondary changes associated with tumor progression. Transformed cell lines had either a predominantly near-diploid or a near-tetraploid population with consistent chromosome gain and loss. Monosomy of the chromosome 13 observed in three cell lines was a nonrandom numerical alteration. Four lines had abnormal chromosomes resulting from deletions, unbalanced translocations, or centric fusions, and one cell line had a chromosome with a homogeneously staining region. Changes of chromosomes 1 and X were observed in three lines. The breakpoints on X chromosome nonrandomly involved the region qa5 which is frequently affected in hamster cells transformed by other carcinogens and may result in loss of genes essential for the maintenance of a normal phenotype. The formation of abnormal chromosomes cannot be directly attributed to the initial DNA damage as bisulfite concentrations effective in causing neoplastic transformation induced a significant but minimal increase in sister chromatid exchanges and failed to cause chromosome aberrations. Bisulfite inhibition of DNA replication might be a contributing factor in the occurrence of abnormal chromosomes. This cytogenetic analysis provides the first evidence that neoplastically transformed cells by a nonclastogenic carcinogen exhibit persistent chromosome rearrangements, a genetic alteration essential to the process of malignant transformation. JF - Cancer research AU - Popescu, N C AU - DiPaolo, J A AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/12/15/ PY - 1988 DA - 1988 Dec 15 SP - 7246 EP - 7251 VL - 48 IS - 24 Pt 1 SN - 0008-5472, 0008-5472 KW - Sulfites KW - 0 KW - sodium bisulfite KW - TZX5469Z6I KW - Index Medicus KW - Karyotyping KW - Animals KW - X Chromosome KW - Sister Chromatid Exchange KW - Chromosome Banding KW - Cells, Cultured KW - Mesocricetus KW - Mice, Nude KW - Mice KW - Cricetinae KW - Chromosome Aberrations KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78535123?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Chromosome+alterations+in+Syrian+hamster+cells+transformed+in+vitro+by+sodium+bisulfite%2C+a+nonclastogenic+carcinogen.&rft.au=Popescu%2C+N+C%3BDiPaolo%2C+J+A&rft.aulast=Popescu&rft.aufirst=N&rft.date=1988-12-15&rft.volume=48&rft.issue=24+Pt+1&rft.spage=7246&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 - 1989-01-09 N1 - Date created - 1989-01-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Four-day duration of tumor promoter exposure required to transform JB6 promotion-sensitive cells to anchorage independence. AN - 78534990; 3191489 AB - The JB6 mouse epidermal cell lines have been developed to study promotion of neoplastic transformation in vitro. Treatment of JB6 cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) at 1 to 100 ng/ml results in the irreversible acquisition of tumorigenicity in nude mice and anchorage-independent growth. Among the biochemical responses which occur during TPA treatment is a decrease in procollagen synthesis. During a study of the possible role of H2O2 in the process of promotion, it was observed that catalase purchased commercially would inhibit TPA promotion as well as the reduction of collagen synthesis in a dose-dependent manner. A highly purified catalase preparation failed to demonstrate the TPA blocking activity, suggesting that this activity was due to a contaminating factor. We have separated the TPA blocking factor from the catalase itself using concanavalin A affinity chromatography. The factor is a Mr 60,000 glycoprotein showing TPA hydrolase activity. The enzyme, which is similar to a murine liver-derived TPA hydrolase, produces a single phorbol product from TPA that has been identified as phorbol-13-acetate. TPA hydrolase was used to terminate TPA action in soft agar. This made it possible to establish that approximately 4 days of exposure to phorbol esters are required for promotion of transformation in the JB6 model system. JF - Cancer research AU - Dion, L D AU - Gindhart, T D AU - Colburn, N H AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, Maryland 21701. Y1 - 1988/12/15/ PY - 1988 DA - 1988 Dec 15 SP - 7126 EP - 7131 VL - 48 IS - 24 Pt 1 SN - 0008-5472, 0008-5472 KW - Collagen KW - 9007-34-5 KW - Catalase KW - EC 1.11.1.6 KW - Hydrolases KW - EC 3.- KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Chromatography, Affinity KW - Catalase -- metabolism KW - Animals KW - Epidermis -- drug effects KW - Hydrolases -- metabolism KW - Mice KW - Cell Adhesion -- drug effects KW - Collagen -- biosynthesis KW - Time Factors KW - Molecular Weight KW - Cell Line KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Skin -- cytology KW - Cell Transformation, Neoplastic -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78534990?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Four-day+duration+of+tumor+promoter+exposure+required+to+transform+JB6+promotion-sensitive+cells+to+anchorage+independence.&rft.au=Dion%2C+L+D%3BGindhart%2C+T+D%3BColburn%2C+N+H&rft.aulast=Dion&rft.aufirst=L&rft.date=1988-12-15&rft.volume=48&rft.issue=24+Pt+1&rft.spage=7126&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 - 1989-01-09 N1 - Date created - 1989-01-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human ethanol-inducible P450IIE1: complete gene sequence, promoter characterization, chromosome mapping, and cDNA-directed expression. AN - 78709506; 3233219 AB - The human P450IIE1 gene, coding for an ethanol-inducible nitrosamine-metabolizing P-450, was isolated from a lambda EMBL3 genomic library and completely sequenced. The human gene spanned 11,413 base pairs and contained nine exons and a typical TATA box. Upstream and downstream DNAs of 2788 and 559 base pairs were also sequenced and compared to the rat gene. Significant areas of sequence similarity were observed within 140 base pairs upstream of the transcription start site in the rat and human genes. Human DNA 539 base pairs upstream of the transcription start site was inserted into the expression vector pSVOAL delta 5', and luciferase activity was detected when the constructs were introduced into a rat hepatoma cell line. The activity was over 100-fold lower than that of pRSVL, a Rous sarcoma virus LTR-driven luciferase gene. By use of panels of rodent-human cell hybrids, the gene was mapped to chromosome 10 (CYP2E locus). A full-length cDNA, constructed with the first exon of the genomic clone and a partial cDNA clone, was expressed in COS cells and found to code for N-nitrosodimethylamine demethylase activity. JF - Biochemistry AU - Umeno, M AU - McBride, O W AU - Yang, C S AU - Gelboin, H V AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/12/13/ PY - 1988 DA - 1988 Dec 13 SP - 9006 EP - 9013 VL - 27 IS - 25 SN - 0006-2960, 0006-2960 KW - Nitrosamines KW - 0 KW - Ethanol KW - 3K9958V90M KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Luciferases KW - EC 1.13.12.- KW - Index Medicus KW - Animals KW - Exons KW - Sequence Homology, Nucleic Acid KW - Humans KW - Nitrosamines -- metabolism KW - Transcription, Genetic KW - Cloning, Molecular KW - Rats KW - Base Sequence KW - Enzyme Induction -- drug effects KW - Transfection KW - Molecular Sequence Data KW - Luciferases -- genetics KW - Promoter Regions, Genetic KW - Ethanol -- pharmacology KW - Cytochrome P-450 Enzyme System -- genetics KW - DNA -- genetics KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Gene Expression Regulation KW - Chromosome Mapping UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78709506?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+ethanol-inducible+P450IIE1%3A+complete+gene+sequence%2C+promoter+characterization%2C+chromosome+mapping%2C+and+cDNA-directed+expression.&rft.au=Umeno%2C+M%3BMcBride%2C+O+W%3BYang%2C+C+S%3BGelboin%2C+H+V%3BGonzalez%2C+F+J&rft.aulast=Umeno&rft.aufirst=M&rft.date=1988-12-13&rft.volume=27&rft.issue=25&rft.spage=9006&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-01 N1 - Date created - 1989-05-01 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - J02843; GENBANK N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Enhancement of fluorinated pyrimidine-induced cytotoxicity by leucovorin in human colorectal carcinoma cell lines. AN - 78540062; 2973527 AB - Reduced folates have been shown to increase the cytotoxicity of 5-fluorouracil (5-FU) by stabilizing the 5-fluoro-2'-deoxyuridine-5'-monophosphate-thymidylate synthase complex, thus increasing the block in the DNA synthetic pathway. Using an in vitro colorimetric [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] cytotoxicity assay, we tested the effects of 5-FU and 5-fluoro-2'-deoxyuridine (FdUrd) with and without leucovorin (LV) on a panel of 11 human colorectal carcinoma cell lines. The effect of LV on 5-FU and FdUrd was quantitatively similar. A clinically achievable level of LV (20 microM) increased the cytotoxicity in all three replicate experiments in 10 of the 11 cell lines (P less than .05, binomial test). LV alone at a concentration of 20 microM had no effect on cell survival. In three cell lines, 50% inhibition of growth occurred at a clinically achievable area under the curve of 5-FU alone. With the addition of LV, one additional cell line showed 50% growth inhibition at a clinically achievable level of 5-FU. Hence large clinical trials may be necessary to detect a significant improvement in survival as a result of adding LV to the fluorinated pyrimidines. JF - Journal of the National Cancer Institute AU - Park, J G AU - Collins, J M AU - Gazdar, A F AU - Allegra, C J AU - Steinberg, S M AU - Greene, R F AU - Kramer, B S AD - NCI-Navy Medical Oncology Branch, Bethesda, MD. Y1 - 1988/12/07/ PY - 1988 DA - 1988 Dec 07 SP - 1560 EP - 1564 VL - 80 IS - 19 SN - 0027-8874, 0027-8874 KW - Floxuridine KW - 039LU44I5M KW - Leucovorin KW - Q573I9DVLP KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - Cell Survival -- drug effects KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Drug Synergism KW - Fluorouracil -- administration & dosage KW - Floxuridine -- administration & dosage KW - Floxuridine -- pharmacology KW - Carcinoma -- pathology KW - Colorectal Neoplasms -- pathology KW - Leucovorin -- administration & dosage KW - Floxuridine -- pharmacokinetics KW - Fluorouracil -- pharmacology KW - Leucovorin -- pharmacology KW - Fluorouracil -- pharmacokinetics KW - Colorectal Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78540062?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Enhancement+of+fluorinated+pyrimidine-induced+cytotoxicity+by+leucovorin+in+human+colorectal+carcinoma+cell+lines.&rft.au=Park%2C+J+G%3BCollins%2C+J+M%3BGazdar%2C+A+F%3BAllegra%2C+C+J%3BSteinberg%2C+S+M%3BGreene%2C+R+F%3BKramer%2C+B+S&rft.aulast=Park&rft.aufirst=J&rft.date=1988-12-07&rft.volume=80&rft.issue=19&rft.spage=1560&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 - 1988-12-28 N1 - Date created - 1988-12-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Gene conversion and differential regulation in the rat P-450 IIA gene subfamily. Purification, catalytic activity, cDNA and deduced amino acid sequence, and regulation of an adult male-specific hepatic testosterone 15 alpha-hydroxylase. AN - 78536636; 3192524 AB - Previous studies on regulation of the rat hepatic P-450 IIA1 cDNA have provided evidence for a second gene closely related to but regulated in a manner quite distinct from P-450 IIA1. Experiments were carried out to isolate the cDNA for this second P-450 gene, designated IIA2, in order to study more directly its regulation and relationship to IIA1. A full length cDNA to IIA2 was isolated from an adult male rat liver lambda gt11 library and sequenced completely. The IIA2 cDNA shared 93% nucleotide and 88% deduced amino acid similarities with the previously characterized IIA1 cDNA (Nagata, K., Matsunaga, T., Gillette, J., Gelboin, H. V., and Gonzalez, F. J. (1987) J. Biol. Chem. 262, 2787-2793). The protein, deduced from the cDNA, contained 492 amino acids and a calculated Mr of 56,352. Comparison of the IIA1 and IIA2 cDNAs revealed areas of low nucleotide similarity interspersed with areas of absolute identity, suggesting that gene conversions have played a role in the evolution of the IIA subfamily. Expression of IIA1 and IIA2 mRNAs in rat liver during development was studied with use of specific oligonucleotide probes. IIA1 mRNA was increased within 1 week after birth in both male and female rats; however, its postpubertal expression was decreased in males yet remained elevated in females. In contrast, IIA2 mRNA was markedly induced in male rat liver at puberty but was not detectable in females at any age examined. Furthermore, only IIA1 mRNA was induced by treatment of rats with 3-methylcholanthrene. Although IIA1 and IIA2 mRNAs were actively expressed in hepatic tissue, no evidence for their expression was found in lung, kidney, or intestine, suggesting that the IIA genes have tissue-specific promoters. Reconstituted enzyme assays on the purified protein products P-450 IIA1 and P-450 IIA2 showed that, although both enzymes share considerable sequence similarity, their positional specificities toward the prototype substrate testosterone are strikingly different. JF - The Journal of biological chemistry AU - Matsunaga, T AU - Nagata, K AU - Holsztynska, E J AU - Lapenson, D P AU - Smith, A AU - Kato, R AU - Gelboin, H V AU - Waxman, D J AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/12/05/ PY - 1988 DA - 1988 Dec 05 SP - 17995 EP - 18002 VL - 263 IS - 34 SN - 0021-9258, 0021-9258 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 15-alpha-hydroxylase KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Base Sequence KW - Sex Factors KW - Sequence Homology, Nucleic Acid KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Species Specificity KW - Male KW - Gene Conversion KW - Genes KW - Cytochrome P-450 Enzyme System -- genetics KW - Microsomes, Liver -- enzymology KW - Cytochrome P-450 Enzyme System -- isolation & purification KW - Steroid Hydroxylases -- metabolism KW - Steroid Hydroxylases -- isolation & purification KW - Cytochrome P-450 Enzyme System -- metabolism KW - Steroid Hydroxylases -- genetics KW - Gene Expression Regulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78536636?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Gene+conversion+and+differential+regulation+in+the+rat+P-450+IIA+gene+subfamily.+Purification%2C+catalytic+activity%2C+cDNA+and+deduced+amino+acid+sequence%2C+and+regulation+of+an+adult+male-specific+hepatic+testosterone+15+alpha-hydroxylase.&rft.au=Matsunaga%2C+T%3BNagata%2C+K%3BHolsztynska%2C+E+J%3BLapenson%2C+D+P%3BSmith%2C+A%3BKato%2C+R%3BGelboin%2C+H+V%3BWaxman%2C+D+J%3BGonzalez%2C+F+J&rft.aulast=Matsunaga&rft.aufirst=T&rft.date=1988-12-05&rft.volume=263&rft.issue=34&rft.spage=17995&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 - 1989-01-03 N1 - Date created - 1989-01-03 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - J04187; GENBANK N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The molecular biology of cytochrome P450s. AN - 78747186; 3072575 JF - Pharmacological reviews AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 243 EP - 288 VL - 40 IS - 4 SN - 0031-6997, 0031-6997 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Animals KW - Multigene Family KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Chromosome Mapping KW - Cytochrome P-450 Enzyme System -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78747186?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacological+reviews&rft.atitle=The+molecular+biology+of+cytochrome+P450s.&rft.au=Gonzalez%2C+F+J&rft.aulast=Gonzalez&rft.aufirst=F&rft.date=1988-12-01&rft.volume=40&rft.issue=4&rft.spage=243&rft.isbn=&rft.btitle=&rft.title=Pharmacological+reviews&rft.issn=00316997&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-26 N1 - Date created - 1989-05-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Pharmacol Rev 1989 Mar;41(1):91-2 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Species correlation of chemical carcinogens. AN - 78742640; 3244862 JF - Risk analysis : an official publication of the Society for Risk Analysis AU - Portier, C J AD - Statistics and Biomathematics Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 551 EP - 553 VL - 8 IS - 4 SN - 0272-4332, 0272-4332 KW - Carcinogens KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Carcinogenicity Tests KW - Data Interpretation, Statistical KW - Predictive Value of Tests KW - Species Specificity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78742640?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Species+correlation+of+chemical+carcinogens.&rft.au=Portier%2C+C+J&rft.aulast=Portier&rft.aufirst=C&rft.date=1988-12-01&rft.volume=8&rft.issue=4&rft.spage=551&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 - 1989-06-01 N1 - Date created - 1989-06-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intravenous cocaine: psychiatric effects, biological mechanisms. AN - 78707704; 3233231 AB - Volunteer addicts were administered iv loading doses of cocaine, followed by 4-hr cocaine infusions that maintained steady-state conditions. The loading doses were followed by the "rush" and "high" subjective effects that users typically experience; cocaine infusions maintained the experience of drug "high", but not "rush". In a subsequent experiment, haloperidol pretreatment did not alter cocaine "rush" but partially attenuated cocaine "high." During cocaine infusions, we also noted suspicious and paranoid behavior, which were blindly rated by nurses. During one of the infusion conditions, the degree of suspiciousness observed was related to the amount of cocaine previously administered. Although cardiovascular responses to cocaine were marked, we found no alterations in plasma catecholamines following cocaine administrations. Baseline homovanillic acid (HVA) levels, however, were related to the degree of suspiciousness observed following cocaine dosing. The potential contributions of dopaminergic systems and physiological sensitization to the development of the psychiatric toxicity of cocaine are discussed. JF - Biological psychiatry AU - Sherer, M A AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 865 EP - 885 VL - 24 IS - 8 SN - 0006-3223, 0006-3223 KW - Methoxyhydroxyphenylglycol KW - 534-82-7 KW - Cocaine KW - I5Y540LHVR KW - Haloperidol KW - J6292F8L3D KW - Norepinephrine KW - X4W3ENH1CV KW - Homovanillic Acid KW - X77S6GMS36 KW - Index Medicus KW - Euphoria -- drug effects KW - Haloperidol -- adverse effects KW - Infusions, Intravenous KW - Dose-Response Relationship, Drug KW - Humans KW - Methoxyhydroxyphenylglycol -- blood KW - Norepinephrine -- blood KW - Chromatography, High Pressure Liquid KW - Homovanillic Acid -- blood KW - Arousal -- drug effects KW - Premedication KW - Adult KW - Male KW - Brain -- drug effects KW - Substance-Related Disorders -- complications KW - Psychoses, Substance-Induced -- blood KW - Cocaine -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78707704?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Intravenous+cocaine%3A+psychiatric+effects%2C+biological+mechanisms.&rft.au=Sherer%2C+M+A&rft.aulast=Sherer&rft.aufirst=M&rft.date=1988-12-01&rft.volume=24&rft.issue=8&rft.spage=865&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 - 1989-04-28 N1 - Date created - 1989-04-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: NIH Guide Grants Contracts. 1993 Jun 25;22(23):1-4 [8390275] Biol Psychiatry. 1989 Dec;26(8):847-8 [2590695] Erratum In: Biol Psychiatry 1992 Aug 15;32(4):381 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human hepatocyte and kidney cell metabolism of 2-acetylaminofluorene and comparison to the respective rat cells. AN - 78677623; 3228713 AB - The metabolism and mutagenic activation of 2-acetylaminofluorene by human and rat hepatocytes and kidney cells were measured. High performance liquid chromatography was used to separate the 2-acetylaminofluorene metabolites, and a cell-mediated Salmonella typhimurium mutagenesis assay was used to detect mutagenic intermediates. Rat and human differences were observed with cells from both organs and levels of metabolism and mutagenesis were higher in human cells. Within a species, liver and kidney cell differences were also evident, with levels of hepatocyte-mediated metabolism and mutagenesis being greater than kidney cells. Human inter-individual variation was apparent with cells from both organs, but the variation observed was significantly greater in hepatocytes than kidney cells. A knowledge of such differences, including an understanding that they may vary with the chemical being studied, should be useful in the extrapolation of rodent carcinogenesis data to humans. JF - Cell biology and toxicology AU - Langenbach, R AU - Rudo, K AD - Cellular and Genetic Toxicology Branch, National Institute of Environmental Health Sciences Research Triangle Park, North Carolina 27709. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 453 EP - 465 VL - 4 IS - 4 SN - 0742-2091, 0742-2091 KW - 2-Acetylaminofluorene KW - 9M98QLJ2DL KW - Index Medicus KW - Rats KW - Animals KW - Mutagenicity Tests KW - Biotransformation KW - Humans KW - Carcinogenicity Tests KW - Species Specificity KW - Male KW - Female KW - Kidney -- metabolism KW - 2-Acetylaminofluorene -- toxicity KW - Liver -- drug effects KW - Kidney -- drug effects KW - Liver -- metabolism KW - 2-Acetylaminofluorene -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78677623?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biology+and+toxicology&rft.atitle=Human+hepatocyte+and+kidney+cell+metabolism+of+2-acetylaminofluorene+and+comparison+to+the+respective+rat+cells.&rft.au=Langenbach%2C+R%3BRudo%2C+K&rft.aulast=Langenbach&rft.aufirst=R&rft.date=1988-12-01&rft.volume=4&rft.issue=4&rft.spage=453&rft.isbn=&rft.btitle=&rft.title=Cell+biology+and+toxicology&rft.issn=07422091&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-17 N1 - Date created - 1989-04-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Protein kinase C-dependent and -independent mechanisms regulating the parotid substance P receptor as revealed by differential effects of protein kinase C inhibitors. AN - 78668707; 2464997 AB - Substance P-induced inositol trisphosphate (InsP3) formation was inhibited by 1 microM-4 beta-phorbol 12,13-dibutyrate (PDBu) in rat parotid acinar cells. The inhibitory effect of PDBu was reversed by the protein kinase C inhibitors H-7 or K252a. Substance P also elicits a persistent desensitization of subsequent substance P-stimulated InsP3 formation. However, this desensitization was not inhibited by H-7. In addition, H-7 had no effect on the time course of substance P-induced InsP3 formation. These results suggest that, although activation of protein kinase C by phorbol esters can inhibit the substance P receptor-linked phospholipase C pathway, this mechanism apparently plays little, if any, role in regulating this system after activation by substance P. JF - The Biochemical journal AU - Sugiya, H AU - Putney, J W AD - Calcium Regulation Section, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/12/01/ PY - 1988 DA - 1988 Dec 01 SP - 677 EP - 680 VL - 256 IS - 2 SN - 0264-6021, 0264-6021 KW - Carbazoles KW - 0 KW - Indole Alkaloids KW - Inositol Phosphates KW - Isoquinolines KW - Piperazines KW - Receptors, Neurokinin-1 KW - Receptors, Neurotransmitter KW - Sugar Phosphates KW - Substance P KW - 33507-63-0 KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine KW - 84477-87-2 KW - Inositol 1,4,5-Trisphosphate KW - 85166-31-0 KW - staurosporine aglycone KW - 97161-97-2 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Isoquinolines -- pharmacology KW - Animals KW - Carbazoles -- pharmacology KW - Receptors, Neurotransmitter -- drug effects KW - Piperazines -- pharmacology KW - Male KW - Sugar Phosphates -- metabolism KW - Protein Kinase C -- antagonists & inhibitors KW - Substance P -- pharmacology KW - Inositol Phosphates -- metabolism KW - Parotid Gland -- metabolism KW - Phorbol 12,13-Dibutyrate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78668707?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Protein+kinase+C-dependent+and+-independent+mechanisms+regulating+the+parotid+substance+P+receptor+as+revealed+by+differential+effects+of+protein+kinase+C+inhibitors.&rft.au=Sugiya%2C+H%3BPutney%2C+J+W&rft.aulast=Sugiya&rft.aufirst=H&rft.date=1988-12-01&rft.volume=256&rft.issue=2&rft.spage=677&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 - 1989-03-16 N1 - Date created - 1989-03-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1985 Sep 12-18;317(6033):124-9 [2993919] J Biol Chem. 1985 Mar 25;260(6):3281-8 [3919020] J Biol Chem. 1986 Apr 25;261(12):5307-13 [3082882] Proc Natl Acad Sci U S A. 1986 Apr;83(7):2032-6 [3083411] Biochem Biophys Res Commun. 1986 May 29;137(1):50-60 [3013192] J Biol Chem. 1987 Feb 5;262(4):1638-43 [3543007] J Cell Physiol. 1987 Jan;130(1):29-36 [3492499] J Pharmacol Exp Ther. 1987 Feb;240(2):617-22 [2879910] Eur J Biochem. 1987 Mar 2;163(2):417-21 [3028803] J Biol Chem. 1987 May 5;262(13):6121-7 [3032956] J Biol Chem. 1987 May 15;262(14):6766-70 [3471761] Biochem Biophys Res Commun. 1987 Apr 14;144(1):35-40 [3579911] J Biol Chem. 1987 Nov 5;262(31):14912-6 [2444592] Mol Pharmacol. 1987 Dec;32(6):737-42 [2892124] Biochem J. 1987 Jun 15;244(3):647-53 [2451500] Biochem J. 1988 Jul 15;253(2):459-66 [2460079] J Physiol. 1977 Jun;268(1):139-49 [195043] Mol Pharmacol. 1980 Jul;18(1):78-83 [6157980] Biochem J. 1982 Sep 15;206(3):555-60 [6184051] Biochem J. 1983 May 15;212(2):473-82 [6309146] Life Sci. 1984 Apr 2;34(14):1347-55 [6323902] Biochem J. 1984 Jun 1;220(2):345-60 [6146314] Mol Pharmacol. 1984 Sep;26(2):261-6 [6237255] Biochem Biophys Res Commun. 1984 Sep 17;123(2):703-9 [6593069] Biochemistry. 1984 Oct 9;23(21):5036-41 [6238627] Biochem Biophys Res Commun. 1984 Nov 30;125(1):258-64 [6239622] Biochem Biophys Res Commun. 1986 Jan 29;134(2):868-75 [3004469] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chemotherapy/radiation therapy plus/minus lonidamine in the treatment of non-small cell lung cancer (limited disease): preliminary results. AN - 78641031; 2851173 AB - One hundred sixteen patients with unresectable locally advanced non-small cell lung cancer (NSCLC) were accrued in a prospective randomized trial comparing (A), chemotherapy (cisplatin and etoposide [VP-16]) for two courses plus radiation therapy (30 + 20 Gy split course), followed by an additional two courses to (B), the same regimen plus the addition of lonidamine (LND). There were 93 patients evaluable for response (46 in the chemotherapy/radiation arm and 47 in the chemotherapy/radiation/LND arm). One hundred fifteen patients were evaluable for toxicity. The overall response rates, median time to progression, and median survival time were similar in both arms. For the group of patients with squamous cell histology, time to progression was 27 weeks on arm A and 38 weeks on arm B (P = 0.01). Two-year survival in the squamous cell group in arm A was 9%, in arm B, 39%. LND does not give rise to additional toxicity, although myalgia and testicular pain are characteristic side effects. JF - Seminars in oncology AU - Gallo-Curcio, C AU - Verturo, I AU - Rinaldi, M AU - Ambesi Impiombato, F AU - Del Vecchio, M R AU - Tonachella, R AU - Tropea, F AU - Antilli, A AU - Ciottoli, G B AU - De Gregorio, M AD - National Cancer Institute, Regina Elena, C. Forlanini Hospital, Rome, Italy. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 26 EP - 31 VL - 15 IS - 6 Suppl 7 SN - 0093-7754, 0093-7754 KW - Indazoles KW - 0 KW - Pyrazoles KW - lonidamine KW - U78804BIDR KW - Index Medicus KW - Prospective Studies KW - Random Allocation KW - Combined Modality Therapy KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Time Factors KW - Male KW - Female KW - Pyrazoles -- administration & dosage KW - Indazoles -- administration & dosage KW - Lung Neoplasms -- therapy KW - Carcinoma, Non-Small-Cell Lung -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78641031?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Chemotherapy%2Fradiation+therapy+plus%2Fminus+lonidamine+in+the+treatment+of+non-small+cell+lung+cancer+%28limited+disease%29%3A+preliminary+results.&rft.au=Gallo-Curcio%2C+C%3BVerturo%2C+I%3BRinaldi%2C+M%3BAmbesi+Impiombato%2C+F%3BDel+Vecchio%2C+M+R%3BTonachella%2C+R%3BTropea%2C+F%3BAntilli%2C+A%3BCiottoli%2C+G+B%3BDe+Gregorio%2C+M&rft.aulast=Gallo-Curcio&rft.aufirst=C&rft.date=1988-12-01&rft.volume=15&rft.issue=6+Suppl+7&rft.spage=26&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 - 1989-02-28 N1 - Date created - 1989-02-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prenatal exposure of male mice to diethylstilbestrol alter the expression of the lactotransferrin gene in seminal vesicles. AN - 78638766; 3216864 AB - We have previously isolated an estrogen-inducible secretory protein, lactotransferrin (LTF), and a cDNA to its messenger RNA from the uterus of mice. In this report we determined that the level of LTF mRNA is minimal in the seminal vesicles of normal mice. In contrast, expression of LTF mRNA in the seminal vesicles of developmentally estrogenized males was both constitutive and estrogen inducible. The results suggested that this alteration may be an example of atypical gene expression after hormonal manipulation early in development. JF - Molecular endocrinology (Baltimore, Md.) AU - Pentecost, B T AU - Newbold, R R AU - Teng, C T AU - McLachlan, J A AD - Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences Research Triangle Park, North Carolina 27709. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 1243 EP - 1248 VL - 2 IS - 12 SN - 0888-8809, 0888-8809 KW - Androgens KW - 0 KW - Estrogens KW - Genetic Markers KW - Lactoglobulins KW - Prostatic Secretory Proteins KW - Proteins KW - Seminal Plasma Proteins KW - beta-microseminoprotein KW - Diethylstilbestrol KW - 731DCA35BT KW - Lactoferrin KW - EC 3.4.21.- KW - Index Medicus KW - Animals KW - Genetic Markers -- genetics KW - Estrogens -- pharmacology KW - Estrogens -- metabolism KW - Mice KW - Androgens -- pharmacology KW - Proteins -- genetics KW - Male KW - Female KW - Androgens -- metabolism KW - Pregnancy KW - Seminal Vesicles -- metabolism KW - Lactoferrin -- genetics KW - Diethylstilbestrol -- pharmacology KW - Lactoglobulins -- genetics KW - Gene Expression Regulation -- drug effects KW - Seminal Vesicles -- drug effects KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78638766?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prenatal+exposure+of+male+mice+to+diethylstilbestrol+alter+the+expression+of+the+lactotransferrin+gene+in+seminal+vesicles.&rft.au=Pentecost%2C+B+T%3BNewbold%2C+R+R%3BTeng%2C+C+T%3BMcLachlan%2C+J+A&rft.aulast=Pentecost&rft.aufirst=B&rft.date=1988-12-01&rft.volume=2&rft.issue=12&rft.spage=1243&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 - 1989-03-03 N1 - Date created - 1989-03-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Proteolytic degradation of protein kinase C in the phorbol ester-induced interleukin-2 secreting thymoma cells. AN - 78628299; 3265048 AB - Effects of phorbol 12-myristate 13-acetate (PMA) on the fate of protein kinase C in two mouse thymoma cell lines, which are either responsive (EL4) or unresponsive (IEL4) to PMA-induced interleukin-2 (IL-2) production, were investigated with polyclonal antibodies raised against rat brain enzyme. These antibodies immunoprecipitated completely the protein kinase C from both cell lines and detected mainly an 82-kDa protein by immunoblot analysis of the crude homogenates as well as the partially purified kinase preparations. PMA elicited a time- and dose-dependent redistribution of protein kinase C from cytosol to the particulate fraction and proteolytic degradation of the kinase from both cell lines. The dose of PMA required for half-maximum protein kinase C translocation and degradation was at least five times lower for EL4 than for IEL4. In the presence of 16 nM PMA the rates of protein kinase C translocation and degradation were faster in EL4 than in IEL4, and the half-lives of protein kinase C in EL4 and IEL4 were less than 5 min and greater than 2 h, respectively. Analysis of the tryptic fragments of the immunoprecipitated enzyme, previously phosphorylated in the presence of [gamma-32P]ATP, revealed minor structural differences between the protein kinase C from these two cell lines. In neither cell line did the PMA-induced degradation of protein kinase C result in an accumulation of the Ca2+/phospholipid-independent kinase (catalytic unit) as analyzed by immunoblotting and gel filtration chromatography. Thus, activation of protein kinase C through the proteolytic conversion to the effector-independent catalytic unit plays little role in IL-2 production. The role of protein kinase C translocation and degradation in the PMA-induced responses in EL4 cells is unknown. However, IL-2 production in EL4 cells was reduced when PMA-induced degradation of protein kinase C was retarded by exogenously added protease inhibitors. JF - Archives of biochemistry and biophysics AU - Huang, F L AU - Arora, P K AU - Hanna, E E AU - Huang, K P AD - Section on Metabolic Regulation, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 503 EP - 514 VL - 267 IS - 2 SN - 0003-9861, 0003-9861 KW - Interleukin-2 KW - 0 KW - Peptide Fragments KW - Protease Inhibitors KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Protease Inhibitors -- pharmacology KW - Immunoblotting KW - Animals KW - Phosphorylation KW - Peptide Mapping KW - Cytosol -- enzymology KW - Cell Line -- drug effects KW - Peptide Fragments -- analysis KW - Mice KW - Precipitin Tests KW - Hydrolysis KW - Protein Kinase C -- metabolism KW - Thymoma -- secretion KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Protein Kinase C -- isolation & purification KW - Interleukin-2 -- secretion KW - Thymoma -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78628299?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Proteolytic+degradation+of+protein+kinase+C+in+the+phorbol+ester-induced+interleukin-2+secreting+thymoma+cells.&rft.au=Huang%2C+F+L%3BArora%2C+P+K%3BHanna%2C+E+E%3BHuang%2C+K+P&rft.aulast=Huang&rft.aufirst=F&rft.date=1988-12-01&rft.volume=267&rft.issue=2&rft.spage=503&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 - 1989-02-16 N1 - Date created - 1989-02-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The chronic hepatic or renal toxicity of di(2-ethylhexyl) phthalate, acetaminophen, sodium barbital, and phenobarbital in male B6C3F1 mice: autoradiographic, immunohistochemical, and biochemical evidence for levels of DNA synthesis not associated with carcinogenesis or tumor promotion. AN - 78599205; 3206528 AB - Male B6C3F1 mice, 6 weeks of age, were fed diets or water containing di(2-ethylhexyl) phthalate (DEHP) at 12,000 or 6000 ppm, acetaminophen (ACT) at 10,000 or 5000 ppm, sodium barbital (BBS) at 1000 ppm, or phenobarbital (PB) at 500 ppm for 40 weeks. Groups of six mice were terminated at 2, 8, 24, and 40 weeks for evaluation of liver and kidney weights, histopathology, and thymidine kinase (TK) activity in liver and kidney and levels of DNA synthesis, measured by tritiated thymidine [( 3H]T) autoradiography or bromodeoxyuridine (BrdU) immunohistochemistry. Liver weights, as percentage of body weight, were significantly elevated at most time intervals for mice exposed to all chemicals at each dose. The hepatocyte labeling indices (LI) with [3H]T autoradiography or BrdU immunocytochemistry were significantly elevated in mice fed DEHP at 12,000 ppm at 24 and 40 weeks or BBS and ACT at 2 weeks. LI were not elevated in mice fed PB. Hepatic TK activity was significantly elevated in mice fed DEHP, BBS, or ACT at Weeks 2 and 8. Histopathologic hepatic lesions were associated with these elevations, while hepatic lesions were not associated with changes in TK activity in PB-treated mice. In contrast, only DEHP and BBS induced toxic renal lesions. Persistent or transient elevation of the renal LI and TK activity accompanied renal toxicity. Thus, the hepatic toxin DEHP induced chronic renal hyperplasia without evidence of renal carcinogenicity or tumor promotion in previous studies at the doses used. ACT, a hepatotoxin, produced transient chronic hepatic hyperplasia without evidence of carcinogenicity in B6C3F1 mice in earlier studies at the same doses used. Thus, persistent or transient hepatic or renal hyperplasia was associated with carcinogenic or tumor promoting activity of these chemicals in some cases but not in others. JF - Toxicology and applied pharmacology AU - Ward, J M AU - Hagiwara, A AU - Anderson, L M AU - Lindsey, K AU - Diwan, B A AD - Division of Cancer Etiology, National Cancer Institute, Frederick, Maryland 21701-1013. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 494 EP - 506 VL - 96 IS - 3 SN - 0041-008X, 0041-008X KW - Barbiturates KW - 0 KW - Phthalic Acids KW - Acetaminophen KW - 362O9ITL9D KW - Barbital KW - 5WZ53ENE2P KW - DNA KW - 9007-49-2 KW - Diethylhexyl Phthalate KW - C42K0PH13C KW - Thymidine Kinase KW - EC 2.7.1.21 KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Animals KW - Thymidine Kinase -- analysis KW - Mice, Inbred C3H KW - Mice KW - Autoradiography KW - Immunohistochemistry KW - Male KW - Liver -- pathology KW - Kidney -- pathology KW - Kidney Neoplasms -- chemically induced KW - Diethylhexyl Phthalate -- toxicity KW - Kidney -- drug effects KW - Liver Neoplasms, Experimental -- chemically induced KW - Barbiturates -- toxicity KW - Barbital -- toxicity KW - DNA -- biosynthesis KW - Phthalic Acids -- toxicity KW - Liver -- drug effects KW - Phenobarbital -- toxicity KW - Acetaminophen -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78599205?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+chronic+hepatic+or+renal+toxicity+of+di%282-ethylhexyl%29+phthalate%2C+acetaminophen%2C+sodium+barbital%2C+and+phenobarbital+in+male+B6C3F1+mice%3A+autoradiographic%2C+immunohistochemical%2C+and+biochemical+evidence+for+levels+of+DNA+synthesis+not+associated+with+carcinogenesis+or+tumor+promotion.&rft.au=Ward%2C+J+M%3BHagiwara%2C+A%3BAnderson%2C+L+M%3BLindsey%2C+K%3BDiwan%2C+B+A&rft.aulast=Ward&rft.aufirst=J&rft.date=1988-12-01&rft.volume=96&rft.issue=3&rft.spage=494&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 - 1989-02-03 N1 - Date created - 1989-02-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Concomitant infection of HTLV-I and HIV-1: prevalence of IgG and IgM antibodies in Washington, D.C. area. AN - 78582697; 2904886 AB - Serum samples collected from four groups of individuals in the Washington, D.C. area were examined for the presence of IgG and IgM classes of antibody reacting against HTLV-I and HIV-1. These four groups were: (1) healthy adults with negative premarital VDRL test for syphilis (n = 113), (2) miscellaneous common disease patients (n = 155), (3) drug abusers (n = 130), and (4) homosexual men (n = 187). The former two groups are considered to be low-risk groups, and the latter two, high-risk groups. The prevalence of IgG antibody on ELISA/Western blot tests for these groups were respectively: (1) 5.3%/1.8%, (2) 5.2%/1.9%, (3) 13.9%/4.6%, and (4) 4.3%/1.6% for HTLV-I, and (1) 2.7%/0.9%, (2) 4.5%/0%, (3) 12.3%/5.4%, and (4) 8.0%/5.9% for HIV-1. Instances of possible concomitant infection as shown by the presence of antibodies against both HTLV-I and HIV-1 were found only in the latter two high-risk groups, i.e. two (1.5%) in group (3), and three (1.6%) in group (4) as confirmed by both Western blot and immunofluorescence tests. Out of 97 sera collected from drug abusers in 1985-86 which had IgG antibody by Western blot test against HIV-1, 23 (23.7%) were HTLV-I antibody positive by ELISA test (Group 5), and 8 of these were confirmed by Western blot test. Among these 8 persons, IgM antibody against HTLV-I was found in 2, while that against HIV-1 was positive in 7 persons.(ABSTRACT TRUNCATED AT 250 WORDS) JF - European journal of epidemiology AU - Chang, K S AU - Wang, L C AU - Gao, C L AU - Alexander, S AU - Ting, R C AU - Bodner, A AU - Log, T AU - Kuo, A F AU - Strickland, P AD - Laboratory of Cellular Oncology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 426 EP - 434 VL - 4 IS - 4 SN - 0393-2990, 0393-2990 KW - HIV Antibodies KW - 0 KW - HTLV-I Antibodies KW - Immunoglobulin G KW - Immunoglobulin M KW - Index Medicus KW - AIDS/HIV KW - Deltaretrovirus Infections -- immunology KW - Acquired Immunodeficiency Syndrome -- complications KW - Deltaretrovirus Infections -- epidemiology KW - Injections, Intravenous KW - Random Allocation KW - Humans KW - Retrospective Studies KW - Aged KW - Blotting, Western -- methods KW - Homosexuality KW - Deltaretrovirus Infections -- complications KW - District of Columbia KW - Acquired Immunodeficiency Syndrome -- epidemiology KW - Acquired Immunodeficiency Syndrome -- immunology KW - Adult KW - Enzyme-Linked Immunosorbent Assay KW - Middle Aged KW - Substance-Related Disorders -- immunology KW - Fluorescent Antibody Technique KW - Male KW - Female KW - HTLV-I Antibodies -- analysis KW - Immunoglobulin G -- analysis KW - HIV -- immunology KW - Immunoglobulin M -- analysis KW - HIV Antibodies -- analysis KW - Human T-lymphotropic virus 1 -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78582697?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+epidemiology&rft.atitle=Concomitant+infection+of+HTLV-I+and+HIV-1%3A+prevalence+of+IgG+and+IgM+antibodies+in+Washington%2C+D.C.+area.&rft.au=Chang%2C+K+S%3BWang%2C+L+C%3BGao%2C+C+L%3BAlexander%2C+S%3BTing%2C+R+C%3BBodner%2C+A%3BLog%2C+T%3BKuo%2C+A+F%3BStrickland%2C+P&rft.aulast=Chang&rft.aufirst=K&rft.date=1988-12-01&rft.volume=4&rft.issue=4&rft.spage=426&rft.isbn=&rft.btitle=&rft.title=European+journal+of+epidemiology&rft.issn=03932990&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-07 N1 - Date created - 1989-02-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Eur J Epidemiol 1989 Mar;5(1):128-9 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Caffeinated beverages and decreased fertility. AN - 78576350; 2904572 AB - 104 healthy women who had been attempting to become pregnant for three months were interviewed about their use of caffeinated beverages, alcohol, and cigarettes. In their subsequent cycles, women who consumed more than the equivalent of one cup of coffee per day were half as likely to become pregnant, per cycle, as women who drank less. A dose-response effect was present. JF - Lancet (London, England) AU - Wilcox, A AU - Weinberg, C AU - Baird, D AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1988 SP - 1453 EP - 1456 VL - 2 IS - 8626-8627 SN - 0140-6736, 0140-6736 KW - Coffee KW - 0 KW - Caffeine KW - 3G6A5W338E KW - Abridged Index Medicus KW - Index Medicus KW - Population KW - United States KW - Infertility KW - Fertility KW - Organic Chemicals KW - Population Dynamics KW - Health KW - Treatment KW - Nutrition KW - Developed Countries KW - Ingredients And Chemicals KW - Alkaloids KW - Demographic Factors KW - Drugs KW - North America KW - Americas KW - Maternal Nutrition KW - Fecundability KW - Differential Fertility KW - Northern America KW - Fecundity KW - North Carolina KW - Reproduction KW - Developing Countries KW - Smoking KW - Risk Factors KW - Humans KW - Adult KW - Alcohol Drinking KW - Female KW - Pregnancy KW - Beverages KW - Caffeine -- adverse effects KW - Coffee -- adverse effects KW - Infertility, Female -- chemically induced KW - Fertility -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78576350?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Caffeinated+beverages+and+decreased+fertility.&rft.au=Wilcox%2C+A%3BWeinberg%2C+C%3BBaird%2C+D&rft.aulast=Wilcox&rft.aufirst=A&rft.date=1988-12-01&rft.volume=2&rft.issue=8626-8627&rft.spage=1453&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 - 1989-01-26 N1 - Date created - 1989-01-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Lancet. 1989 Feb 18;1(8634):378 [2563522] Lancet. 1990 Mar 31;335(8692):792-3 [1969535] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lineage-specific regulation of the vasoactive intestinal peptide gene in neuroblastoma cells is conferred by 5.2 kilobases of 5'-flanking sequence. AN - 78575001; 3200839 AB - The expression of a transfected plasmid containing 5.2 kilobases (kb) of 5' regulatory DNA sequence of the human vasoactive intestinal peptide (VIP) gene attached to coding sequences of the reporter gene chloramphenicol acetyltransferase (CAT) was compared with endogenous VIP expression in subclones of the human neuroblastoma cell line SK-N-SH. These subclones vary widely in basal and inducible quantities of VIP and its precursor mRNA and can be interconverted under specified culture conditions. Endogenous VIP immunoreactivity, detectable in all subclones, was lowest in the neuronal subclone SH-SY-5Y, whereas 15- to 25-fold higher levels were observed in the epithelial-appearing SH-EP and intermediate SH-IN subclones. Treatment with 10 nM phorbol 12-myristate 13-acetate (PMA) stimulated VIP peptide levels approximately 5-fold in SH-SY-5Y cells but did not increase appreciably VIP levels in the other subclones. Treatment with 2.5 microM forskolin resulted in less than 50% stimulation of VIP expression in all subclones. Levels of mRNA encoding the VIP precursor generally paralleled these differences in VIP immunoreactivity. In cells transfected with the VIP/CAT fusion gene, CAT activity reflected closely these differences in basal VIP expression and the changes in response to PMA and forskolin. Deletion of 2.7 kb of the most upstream sequences resulted in an 80-90% reduction in basal CAT activity in SH-IN, but not SH-SY-5Y cells, and resulted in an 80% reduction in PMA stimulation in SH-SY-5Y cells. Deletion to within 74 nucleotides of the transcription start site resulted in CAT expression in SH-IN cells that was only 3% of that seen with the full 5.2-kb flanking sequences and further diminished the remaining PMA responsiveness in SH-SY-5Y cells. The data indicate that important cell-type-specific transcription regulatory sequences reside greater than 2.5 kb upstream from the VIP transcription start site. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Waschek, J A AU - Hsu, C M AU - Eiden, L E AD - Unit on Molecular and Cellular Neurobiology, National Institutes of Health, Bethesda, MD 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 9547 EP - 9551 VL - 85 IS - 24 SN - 0027-8424, 0027-8424 KW - Colforsin KW - 1F7A44V6OU KW - Vasoactive Intestinal Peptide KW - 37221-79-7 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Colforsin -- pharmacology KW - Chromosome Deletion KW - Base Sequence KW - Transfection KW - Humans KW - Enhancer Elements, Genetic KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Plasmids KW - Molecular Weight KW - Cell Line KW - Neuroblastoma -- genetics KW - Vasoactive Intestinal Peptide -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78575001?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Lineage-specific+regulation+of+the+vasoactive+intestinal+peptide+gene+in+neuroblastoma+cells+is+conferred+by+5.2+kilobases+of+5%27-flanking+sequence.&rft.au=Waschek%2C+J+A%3BHsu%2C+C+M%3BEiden%2C+L+E&rft.aulast=Waschek&rft.aufirst=J&rft.date=1988-12-01&rft.volume=85&rft.issue=24&rft.spage=9547&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 - 1989-01-26 N1 - Date created - 1989-01-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell. 1978 Dec;15(4):1157-74 [728996] Mol Cell Biol. 1988 Feb;8(2):605-14 [2895420] Brain Res. 1982 Jan 14;231(2):472-7 [7055688] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Nature. 1983 Aug 11-17;304(5926):547-9 [6571696] Life Sci. 1983 Aug 22;33(8):687-93 [6888186] J Natl Cancer Inst. 1983 Oct;71(4):741-7 [6137586] Lancet. 1983 Nov 19;2(8360):1163-5 [6139527] Proc Natl Acad Sci U S A. 1984 Jul;81(13):3949-53 [6330725] Endocrinology. 1985 Sep;117(3):1020-6 [3839453] DNA. 1985 Aug;4(4):293-300 [3899557] Biochem Biophys Res Commun. 1985 Nov 15;132(3):885-91 [2416313] Cell. 1986 Aug 29;46(5):705-16 [3091258] Proc Natl Acad Sci U S A. 1986 Oct;83(20):7653-7 [2429314] J Biol Chem. 1986 Nov 5;261(31):14373-6 [3464596] Nature. 1986 Oct 23-29;323(6090):731-4 [3022151] Mol Cell Biol. 1986 Dec;6(12):4305-16 [3025651] Proc Natl Acad Sci U S A. 1987 Jan;84(2):605-9 [3025882] Cell. 1987 Jan 30;48(2):331-42 [3643061] Nature. 1987 Jan 22-28;325(6102):368-72 [3027570] Cancer Res. 1987 Mar 1;47(5):1383-9 [3028608] Mol Cell Biol. 1987 Feb;7(2):725-37 [3821727] Cell. 1987 Jun 19;49(6):729-39 [3034432] Cell. 1987 Jun 19;49(6):741-52 [3034433] Science. 1987 Jun 5;236(4806):1237-45 [3296191] J Biol Chem. 1987 Jun 25;262(18):8743-7 [3036825] Nature. 1987 Jul 9-15;328(6126):175-8 [2885756] Cell. 1987 Oct 23;51(2):251-60 [2822255] Mol Cell Biol. 1987 Aug;7(8):2745-52 [3670292] Mol Cell Biol. 1987 Nov;7(11):3994-4002 [2828923] Mol Cell Biol. 1987 Nov;7(11):4058-64 [3431549] Science. 1988 Mar 18;239(4846):1400-5 [2831625] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pharmacokinetics of subcutaneous methotrexate. AN - 78570070; 3199171 AB - The pharmacokinetics of subcutaneously administered methotrexate was studied as a parenteral alternative to oral administration. An initial feasibility study was performed in Rhesus monkeys comparing the subcutaneous route to intravenous (IV) injection and oral administration. The subcutaneous dose was completely absorbed and a sustained-release effect was observed when compared with the IV dose. No local or systemic toxicities resulted from subcutaneous methotrexate in the animals. Twelve children with acute lymphoblastic leukemia on maintenance therapy protocols prescribing either 7.5 mg/m2 biweekly or 40 mg/m2 weekly were also monitored after both a subcutaneous and an oral dose of methotrexate. Four children at the higher dosage level were also studied after an equal IV dose. The subcutaneous dose was again completely absorbed in these children at both dose levels, whereas the oral dose, which produced comparable plasma drug concentrations at the lower dosage level, resulted in a total drug exposure (area under the plasma concentration-time curve) that was one third that of the equal subcutaneous dose at the higher dosage level. No local or systemic toxicity was attributed to the subcutaneous methotrexate. Subcutaneous administration of methotrexate is well tolerated and well absorbed and appears to overcome the problems associated with oral administration, including variable absorption and saturation of the absorption mechanism with increasing doses. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Balis, F M AU - Mirro, J AU - Reaman, G H AU - Evans, W E AU - McCully, C AU - Doherty, K M AU - Murphy, R F AU - Jeffries, S AU - Poplack, D G AD - Pediatric Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 1882 EP - 1886 VL - 6 IS - 12 SN - 0732-183X, 0732-183X KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Administration, Oral KW - Animals KW - Humans KW - Child KW - Child, Preschool KW - Adult KW - Absorption KW - Injections, Subcutaneous KW - Macaca mulatta KW - Adolescent KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- drug therapy KW - Female KW - Male KW - Methotrexate -- pharmacokinetics KW - Methotrexate -- blood KW - Methotrexate -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78570070?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pharmacokinetics+of+subcutaneous+methotrexate.&rft.au=Balis%2C+F+M%3BMirro%2C+J%3BReaman%2C+G+H%3BEvans%2C+W+E%3BMcCully%2C+C%3BDoherty%2C+K+M%3BMurphy%2C+R+F%3BJeffries%2C+S%3BPoplack%2C+D+G&rft.aulast=Balis&rft.aufirst=F&rft.date=1988-12-01&rft.volume=6&rft.issue=12&rft.spage=1882&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 - 1989-01-18 N1 - Date created - 1989-01-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Binding region for human immunodeficiency virus (HIV) and epitopes for HIV-blocking monoclonal antibodies of the CD4 molecule defined by site-directed mutagenesis. AN - 78560726; 2461565 AB - The binding region for human immunodeficiency virus (HIV) and epitopes for a panel of HIV-blocking anti-CD4 monoclonal antibodies of the CD4 molecule were defined by using in vitro site-directed mutagenesis. Codons for two amino acid residues (Ser-Arg) were inserted at selected positions within the region encoding the first and second immunoglobulin-like domains of CD4. A vaccinia virus-based expression system was used to produce soluble full-length extracellular CD4 fragments containing the insertions. The mutant proteins were tested for direct binding to soluble gp120 (the CD4-binding subunit of the viral envelope glycoprotein) and to a series of HIV-blocking anti-CD4 monoclonal antibodies. Impaired gp120 binding activity resulted from insertions after amino acid residues 31, 44, 48, 52, 55, and 57 in the first immunoglobulin-like domain. The epitopes for two HIV-blocking monoclonal antibodies, OKT4A and OKT4D, were also mapped in the gp120-binding region in the first domain. Insertions after amino acid residues 21 and 91 in the first domain had no effect on gp120 binding but impaired the binding of OKT4E, suggesting that this antibody recognizes a discontinuous epitope not directly involved in gp120 binding. Moderate impairment of gp120 binding resulted from the insertion after amino acid residues 164 in the second immunoglobulin-like domain, where the epitopes for monoclonal antibodies MT151 and OKT4B were also mapped. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Mizukami, T AU - Fuerst, T R AU - Berger, E A AU - Moss, B AD - Laboratory of Viral Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 9273 EP - 9277 VL - 85 IS - 23 SN - 0027-8424, 0027-8424 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Differentiation, T-Lymphocyte KW - Epitopes KW - HIV Antibodies KW - Immunoglobulins KW - Receptors, HIV KW - Receptors, Virus KW - Index Medicus KW - AIDS/HIV KW - Vaccinia virus -- genetics KW - Animals KW - Base Sequence KW - Molecular Sequence Data KW - Immunoglobulins -- immunology KW - Mice KW - Amino Acid Sequence KW - Antigens, Differentiation, T-Lymphocyte -- genetics KW - HIV Antibodies -- immunology KW - Receptors, Virus -- immunology KW - Receptors, Virus -- genetics KW - Antigens, Differentiation, T-Lymphocyte -- immunology KW - Epitopes -- immunology KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78560726?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Binding+region+for+human+immunodeficiency+virus+%28HIV%29+and+epitopes+for+HIV-blocking+monoclonal+antibodies+of+the+CD4+molecule+defined+by+site-directed+mutagenesis.&rft.au=Mizukami%2C+T%3BFuerst%2C+T+R%3BBerger%2C+E+A%3BMoss%2C+B&rft.aulast=Mizukami&rft.aufirst=T&rft.date=1988-12-01&rft.volume=85&rft.issue=23&rft.spage=9273&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 - 1988-12-30 N1 - Date created - 1988-12-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1970 Aug 15;227(5259):680-5 [5432063] Nature. 1988 Sep 22;335(6188):363-6 [2843773] Proc Natl Acad Sci U S A. 1981 Jun;78(6):3824-8 [6167991] Cell Immunol. 1983 Sep;80(2):310-9 [6192938] Hum Immunol. 1984 Feb;9(2):89-102 [6199335] Science. 1984 Jul 6;225(4657):59-63 [6328660] Nature. 1984 Dec 20-1985 Jan 2;312(5996):763-7 [6096719] Nature. 1984 Dec 20-1985 Jan 2;312(5996):767-8 [6083454] Proc Natl Acad Sci U S A. 1985 Jan;82(2):488-92 [3881765] Cell. 1985 Aug;42(1):93-104 [2990730] J Immunol. 1985 Nov;135(5):3151-62 [2995487] J Immunol. 1986 Jan;136(2):361-3 [2416802] Science. 1986 Jan 24;231(4736):382-5 [3001934] Nature. 1986 Jul 31-Aug 6;322(6078):470-4 [3016552] J Immunol. 1986 Nov 1;137(9):2937-44 [2428879] Cell. 1986 Nov 7;47(3):333-48 [3094962] Nature. 1986 Oct 23-29;323(6090):725-8 [3095663] Proc Natl Acad Sci U S A. 1986 Nov;83(21):8122-6 [3095828] Science. 1986 Nov 28;234(4780):1120-3 [2430333] J Immunol Methods. 1987 Feb 26;97(1):93-100 [3029227] Proc Natl Acad Sci U S A. 1987 Mar;84(6):1649-53 [3104900] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3891-5 [3495801] Mol Cell Biol. 1987 Jul;7(7):2538-44 [3112559] Cell. 1987 Sep 11;50(6):975-85 [2441877] Nature. 1987 Dec 3-9;330(6147):487-9 [2446142] Science. 1987 Dec 18;238(4834):1704-7 [3500514] Proc Natl Acad Sci U S A. 1987 Dec;84(24):9155-9 [3501122] Nature. 1988 Jan 7;331(6151):76-8 [2829022] Nature. 1988 Jan 7;331(6151):78-81 [2829023] Nature. 1988 Jan 7;331(6151):82-4 [3257544] Nature. 1988 Jan 7;331(6151):84-6 [2829024] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2357-61 [2451247] Science. 1988 Jun 3;240(4857):1335-9 [2453925] AIDS. 1988 Apr;2(2):101-5 [2454642] Annu Rev Immunol. 1988;6:381-405 [3289571] Annu Rev Immunol. 1988;6:555-80 [2454644] Cell. 1988 Jul 1;54(1):65-72 [2454749] Nature. 1988 Jul 14;334(6178):159-62 [3260352] J Mol Biol. 1978 Mar 25;120(1):97-120 [642007] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mood changes associated with reproductive life events: an overview of research and treatment strategies. AN - 78559651; 3198579 JF - The Journal of clinical psychiatry AU - Blumenthal, S J AU - Nadelson, C C AD - Health and Behavior Research Branch, National Institute of Mental Health, Rockville, MD 20857. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 466 EP - 468 VL - 49 IS - 12 SN - 0160-6689, 0160-6689 KW - Contraceptives, Oral KW - 0 KW - Index Medicus KW - Contraceptives, Oral -- adverse effects KW - Humans KW - Menstrual Cycle KW - Aging KW - Male KW - Female KW - Pregnancy KW - Premenstrual Syndrome -- psychology KW - Reproduction KW - Affect UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78559651?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+psychiatry&rft.atitle=Mood+changes+associated+with+reproductive+life+events%3A+an+overview+of+research+and+treatment+strategies.&rft.au=Blumenthal%2C+S+J%3BNadelson%2C+C+C&rft.aulast=Blumenthal&rft.aufirst=S&rft.date=1988-12-01&rft.volume=49&rft.issue=12&rft.spage=466&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+clinical+psychiatry&rft.issn=01606689&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-17 N1 - Date created - 1989-01-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA damage-inducible transcripts in mammalian cells. AN - 78557692; 3194391 AB - Hybridization subtraction at low ratios of RNA to cDNA was used to enrich for the cDNA of transcripts increased in Chinese hamster cells after UV irradiation. Forty-nine different cDNA clones were isolated. Most coded for nonabundant transcripts rapidly induced 2- to 10-fold after UV irradiation. Only 2 of the 20 cDNA clones sequenced matched known sequences (metallothionein I and II). The predicted amino acid sequence of one cDNA had two localized areas of homology with the rat helix-destabilizing protein. These areas of homology were at the two DNA-binding sites of this nucleic acid single-strand-binding protein. The induced transcripts were separated into two general classes. Class I transcripts were induced by UV radiation and not by the alkylating agent methyl methanesulfonate. Class II transcripts were induced by UV radiation and by methyl methanesulfonate. Many class II transcripts were induced also by H2O2 and various alkylating agents but not by heat shock, phorbol 12-tetradecanoate 13-acetate, or DNA-damaging agents which do not produce high levels of base damage. Since many of the cDNA clones coded for transcripts which were induced rapidly and only by certain types of DNA-damaging agents, their induction is likely a specific response to such damage rather than a general response to cell injury. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Fornace, A J AU - Alamo, I AU - Hollander, M C AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 8800 EP - 8804 VL - 85 IS - 23 SN - 0027-8424, 0027-8424 KW - DNA, Single-Stranded KW - 0 KW - Acetoxyacetylaminofluorene KW - 6098-44-8 KW - Index Medicus KW - Xeroderma Pigmentosum KW - Ultraviolet Rays KW - DNA, Single-Stranded -- genetics KW - Humans KW - Acetoxyacetylaminofluorene -- pharmacology KW - Dose-Response Relationship, Radiation KW - Cell Line KW - Cloning, Molecular KW - Transcription, Genetic -- drug effects KW - Transcription, Genetic -- radiation effects KW - DNA Damage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78557692?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=DNA+damage-inducible+transcripts+in+mammalian+cells.&rft.au=Fornace%2C+A+J%3BAlamo%2C+I%3BHollander%2C+M+C&rft.aulast=Fornace&rft.aufirst=A&rft.date=1988-12-01&rft.volume=85&rft.issue=23&rft.spage=8800&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 - 1988-12-30 N1 - Date created - 1988-12-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 1974 Dec;34(12):3318-25 [4371955] Mol Cell Biol. 1988 Nov;8(11):4716-20 [2463464] Proc Natl Acad Sci U S A. 1977 Apr;74(4):1553-7 [266196] Mutat Res. 1982 Jun;94(2):263-76 [7110177] J Mol Biol. 1983 Jun 5;166(4):557-80 [6345791] Anal Biochem. 1983 Jul 1;132(1):6-13 [6312838] Nucleic Acids Res. 1984 Jan 11;12(1 Pt 1):417-28 [6546426] Microbiol Rev. 1984 Mar;48(1):60-93 [6371470] Cell. 1985 Feb;40(2):359-69 [3838150] Mol Cell Biol. 1985 Feb;5(2):320-9 [2983189] Mol Cell Biol. 1985 Jan;5(1):75-84 [3920512] J Biol Chem. 1986 Mar 15;261(8):3536-43 [3005291] Proc Natl Acad Sci U S A. 1986 Mar;83(6):1842-6 [3081903] Anal Biochem. 1986 Feb 1;152(2):232-8 [3516005] Nucleic Acids Res. 1986 Jul 25;14(14):5793-811 [2426659] Mol Cell Biol. 1986 May;6(5):1760-6 [3785178] Mol Cell Biol. 1987 Feb;7(2):622-31 [3102944] Int J Radiat Biol Relat Stud Phys Chem Med. 1987 Mar;51(3):493-503 [3553051] Nucleic Acids Res. 1987 Aug 11;15(15):5945-62 [2442723] J Biol Chem. 1988 Mar 5;263(7):3307-13 [2830282] J Biol Chem. 1976 Apr 10;251(7):2133-41 [1270426] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Localization of alpha-casein gene transcription in sections of epoxy resin-embedded mouse mammary tissues by in situ hybridization. AN - 78556720; 3057071 AB - The objective of our study was to evaluate the suitability of aldehyde-fixed, epoxy resin-embedded tissue for efficient and reproducible detection of casein mRNA in mouse mammary tissue by in situ hybridization. We used mouse alpha-casein-specific, 35S-labeled riboprobes generated from a Gemini-3 vector. Both complementary (anti-sense) and homologous (sense) RNA probes were utilized in our study (specific activity ranged from 5-7 x 10(8) cpm/micrograms). We tested the stability of newly synthesized [3H]-uridine-labeled RNA in tissue sections subjected to epoxy plastic solvents and found that no detectable loss of label occurred during preparation of semi-thin (1-2 micron) plastic sections for situ hybridization. In addition, it was possible to detect alpha-casein mRNA in deplasticized sections of mammary gland tissue taken from normal, pregnant, or lactating mice, pre-neoplastic mammary alveolar hyperplasias, explant cultures, and mammary tumors. A positive hybridization signal was consistently obtained in sections of mammary tissues where the estimated average copy number for total casein mRNA was greater than or equal to 250/cell. In mammary tumors, where the estimated casein mRNA content was much lower (less than 5/cell), our positive hybridization signal occurred in regions of the tumor that, in consecutive sections, stained positive for casein by immunoperoxidase. After formaldehyde-glutaraldehyde fixation, loss of hybridizable RNA from epoxy-embedded tissues and sections appears to be minimal. Image resolution was greatly enhanced over frozen or paraffin sections of mammary tissue. Non-specific binding of the radioactive probes was very low. Protease treatment of the sections was not necessary for detection of hybridizable signal. JF - The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society AU - Liscia, D S AU - Doherty, P J AU - Smith, G H AD - Oncogenetics Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 1503 EP - 1510 VL - 36 IS - 12 SN - 0022-1554, 0022-1554 KW - Caseins KW - 0 KW - Epoxy Resins KW - RNA Probes KW - RNA, Messenger KW - Diethylstilbestrol KW - 731DCA35BT KW - Index Medicus KW - Mammary Neoplasms, Experimental -- analysis KW - Histological Techniques KW - Animals KW - Lactation -- metabolism KW - Mice, Inbred C3H KW - Diethylstilbestrol -- pharmacology KW - Transcription, Genetic KW - Mice KW - Male KW - Female KW - Pregnancy KW - Mammary Glands, Animal -- analysis KW - Mammary Glands, Animal -- drug effects KW - Caseins -- genetics KW - RNA, Messenger -- analysis KW - Nucleic Acid Hybridization UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78556720?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+histochemistry+and+cytochemistry+%3A+official+journal+of+the+Histochemistry+Society&rft.atitle=Localization+of+alpha-casein+gene+transcription+in+sections+of+epoxy+resin-embedded+mouse+mammary+tissues+by+in+situ+hybridization.&rft.au=Liscia%2C+D+S%3BDoherty%2C+P+J%3BSmith%2C+G+H&rft.aulast=Liscia&rft.aufirst=D&rft.date=1988-12-01&rft.volume=36&rft.issue=12&rft.spage=1503&rft.isbn=&rft.btitle=&rft.title=The+journal+of+histochemistry+and+cytochemistry+%3A+official+journal+of+the+Histochemistry+Society&rft.issn=00221554&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-03 N1 - Date created - 1989-01-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Development after exposure to polychlorinated biphenyls and dichlorodiphenyl dichloroethene transplacentally and through human milk. AN - 78548636; 3142988 AB - To determine whether exposure to polychlorinated biphenyls (PCBs) or dichlorodiphenyl dichloroethene (DDE), either transplacentally or through breast feeding, affected scores on the Bayley Scales of Infant Development at 6 or 12 months of age. Cohort followed from birth to 1 year of age. General community. Volunteer sample of 858 infants, of whom 802 had Bayley scores available at either 6 months or 12 months or both. None. Bayley scales and chemical measurements were done independently. Higher transplacental exposure to PCBs was associated with lower psychomotor scores at both 6 and 12 months of age; the difference between the mean scores in the lowest and highest PCB groups was 7 points at 6 months and 8 points at 12 months. Higher transplacental exposure to DDE was associated with higher mental scores at 6 months of age (the difference between the mean scores in the lowest and highest DDE groups was 6 points), but no relationship was seen at 12 months. Exposure to either chemical through breast feeding was apparently unrelated to Bayley scores. Transplacental exposure to PCBs was associated with lower psychomotor scores. No deleterious effects were associated with breast feeding. JF - The Journal of pediatrics AU - Gladen, B C AU - Rogan, W J AU - Hardy, P AU - Thullen, J AU - Tingelstad, J AU - Tully, M AD - Statistics and Biomathematics Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 991 EP - 995 VL - 113 IS - 6 SN - 0022-3476, 0022-3476 KW - Dichlorodiphenyl Dichloroethylene KW - 4M7FS82U08 KW - Polychlorinated Biphenyls KW - DFC2HB4I0K KW - Abridged Index Medicus KW - Index Medicus KW - Infant KW - Intelligence -- drug effects KW - Psychomotor Performance -- drug effects KW - Humans KW - Brain -- drug effects KW - Infant, Newborn KW - Follow-Up Studies KW - Neuropsychological Tests KW - Female KW - Pregnancy KW - Child, Preschool KW - Milk, Human -- analysis KW - Dichlorodiphenyl Dichloroethylene -- analysis KW - Breast Feeding KW - Child Development -- drug effects KW - Polychlorinated Biphenyls -- analysis KW - Dichlorodiphenyl Dichloroethylene -- adverse effects KW - Prenatal Exposure Delayed Effects KW - Polychlorinated Biphenyls -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78548636?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Development+after+exposure+to+polychlorinated+biphenyls+and+dichlorodiphenyl+dichloroethene+transplacentally+and+through+human+milk.&rft.au=Gladen%2C+B+C%3BRogan%2C+W+J%3BHardy%2C+P%3BThullen%2C+J%3BTingelstad%2C+J%3BTully%2C+M&rft.aulast=Gladen&rft.aufirst=B&rft.date=1988-12-01&rft.volume=113&rft.issue=6&rft.spage=991&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 - 1989-01-10 N1 - Date created - 1989-01-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Return of symptoms after discontinuation of clomipramine in patients with obsessive-compulsive disorder. AN - 78546968; 3057923 AB - To evaluate the need for maintenance drug therapy in patients with obsessive-compulsive disorder, the authors assessed 21 patients with obsessive-compulsive disorder who manifested sustained improvement during 5 to 27 months of clomipramine treatment and who agreed to participate in a double-blind discontinuation study. Of 18 patients who completed the study, 16 had substantial recurrence of obsessive-compulsive symptoms by the end of the 7-week placebo period. In addition, 11 had a significant increase in depressive symptoms. Treatment duration before discontinuation of clomipramine was not related to the frequency or severity of obsessive-compulsive or depressive symptom appearance. These findings suggest that prolonged drug treatment may be warranted for obsessive-compulsive disorder. JF - The American journal of psychiatry AU - Pato, M T AU - Zohar-Kadouch, R AU - Zohar, J AU - Murphy, D L AD - Laboratory of Clinical Science, NIMH, Bethesda, MD 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 1521 EP - 1525 VL - 145 IS - 12 SN - 0002-953X, 0002-953X KW - Clomipramine KW - NUV44L116D KW - Abridged Index Medicus KW - Index Medicus KW - Psychiatric Status Rating Scales KW - Double-Blind Method KW - Psychotherapy KW - Combined Modality Therapy KW - Humans KW - Adult KW - Clinical Trials as Topic KW - Substance Withdrawal Syndrome -- psychology KW - Middle Aged KW - Recurrence KW - Male KW - Female KW - Obsessive-Compulsive Disorder -- psychology KW - Obsessive-Compulsive Disorder -- drug therapy KW - Clomipramine -- adverse effects KW - Clomipramine -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78546968?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Return+of+symptoms+after+discontinuation+of+clomipramine+in+patients+with+obsessive-compulsive+disorder.&rft.au=Pato%2C+M+T%3BZohar-Kadouch%2C+R%3BZohar%2C+J%3BMurphy%2C+D+L&rft.aulast=Pato&rft.aufirst=M&rft.date=1988-12-01&rft.volume=145&rft.issue=12&rft.spage=1521&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 - 1989-01-10 N1 - Date created - 1989-01-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Enflurane metabolism produces covalently bound liver adducts recognized by antibodies from patients with halothane hepatitis. AN - 78546813; 3195754 AB - The existence of a rare syndrome of "enflurane hepatitis" similar to that described for halothane and of a cross-sensitization between halothane and enflurane has been controversial, largely due to equivocal clinical case reports and a lack of a plausible molecular mechanism for the hepatotoxicity. The present study suggests a possible hypersensitivity basis for enflurane hepatitis and the apparent cross-sensitization between halothane and enflurane involving covalently bound liver microsomal adducts. Immunoblotting studies have revealed that antibodies in the sera of six patients with halothane hepatitis recognize liver microsomal antigens of Mr = 100,000, or both 100,000 and 76,000, formed in rats treated with enflurane or halothane. These antigens were not detected in microsomes from isoflurane- or sesame oil-treated rats. The recognition of these antigens could be abolished by preincubation of the sera with microsomes from halothane-treated rats. These data suggest that the difluoromethoxydifluoroacetyl halide metabolite of enflurane, as well as the trifluoroacetyl halide metabolite of halothane, covalently bind to similar hepatic proteins, and may become immunogens in susceptible patients. This mechanism may also account for the apparent cross-sensitization between halothane and enflurane anesthesia, and the development of hepatic necrosis. JF - Anesthesiology AU - Christ, D D AU - Kenna, J G AU - Kammerer, W AU - Satoh, H AU - Pohl, L R AD - Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 833 EP - 838 VL - 69 IS - 6 SN - 0003-3022, 0003-3022 KW - Isoantigens KW - 0 KW - liver specific F antigen KW - Enflurane KW - 91I69L5AY5 KW - Halothane KW - UQT9G45D1P KW - Abridged Index Medicus KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Halothane -- adverse effects KW - Male KW - Enflurane -- metabolism KW - Chemical and Drug Induced Liver Injury -- etiology KW - Enflurane -- adverse effects KW - Isoantigens -- immunology KW - Enflurane -- immunology KW - Chemical and Drug Induced Liver Injury -- metabolism KW - Chemical and Drug Induced Liver Injury -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78546813?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Anesthesiology&rft.atitle=Enflurane+metabolism+produces+covalently+bound+liver+adducts+recognized+by+antibodies+from+patients+with+halothane+hepatitis.&rft.au=Christ%2C+D+D%3BKenna%2C+J+G%3BKammerer%2C+W%3BSatoh%2C+H%3BPohl%2C+L+R&rft.aulast=Christ&rft.aufirst=D&rft.date=1988-12-01&rft.volume=69&rft.issue=6&rft.spage=833&rft.isbn=&rft.btitle=&rft.title=Anesthesiology&rft.issn=00033022&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-05 N1 - Date created - 1989-01-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activated neutrophils induce prolonged DNA damage in neighboring cells. AN - 78534852; 2847879 AB - We have measured the capacity of highly-purified, paraffin oil-elicited neutrophils to induce DNA single-strand breaks in a newly established plasmacytoma cell line, RIMPC 2304, which was induced by a retrovirus containing the c-myc and V-Ha-ras oncogenes. This cell line effectively repairs DNA damage induced by gamma-irradiation. DNA damage induced by neutrophils was correlated with the oxidative burst of the neutrophils. The levels of superoxide anion, H2O2, and HOCl produced after stimulation of the neutrophils (6 X 10(5)/cm3) with the tumor promoter phorbol myristate acetate (100 nM) were 33.8 microM, 12.8 microM and 1.7 microM respectively in 15 min, and 98 microM, 20 microM and 8.7 microM respectively in 90 min. The results of alkaline elution experiments revealed that when the same concentration of neutrophils was co-incubated for 15 min in serum-free medium with an equal number of radioactively labeled RIMPC 2304 cells, the latter incurred a level of damage that approximated that caused by 300 rad equivalents of gamma-irradiation or by a 1-min treatment with 20 microM H2O2 at 37 degrees C. Damage from neutrophils was coincident with the oxidative burst; it was induced rapidly (within 5 min) but remained high for more than 90 min. The level of damage achieved was dependent upon the ratio of neutrophils: target cells and was clearly detectable at ratios as low as 0.25:1. Induction of single-strand breaks was completely inhibited by catalase and partially inhibited by superoxide dismutase, mannitol, and reduced glutathione but not by Na azide. Addition of the non-steroidal anti-inflammatory drug indomethacin either enhanced (at 50 microM) or had no effect (at 2 microM) on the damage detected. Finally, repair of strand breaks induced by neutrophils was significantly slower (half-time approximately 10 min) than that observed for repair of similar levels of damage induced by H2O2 or gamma-irradiation (half-times approximately 3 min, each). The results indicate that neutrophils cause prolonged DNA damage in neighboring cells. Moreover, they indicate that although H2O2 produced in the oxidative burst is an essential mediator of the damage observed, additional reactive oxygen intermediates including the superoxide anion are also implicated. The data are discussed in relation to the possible role of neutrophils in chronic inflammation and in pristane-induced plasmacytoma formation in mice. JF - Carcinogenesis AU - Shacter, E AU - Beecham, E J AU - Covey, J M AU - Kohn, K W AU - Potter, M AD - Laboratory of Genetics, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 2297 EP - 2304 VL - 9 IS - 12 SN - 0143-3334, 0143-3334 KW - Terpenes KW - 0 KW - Superoxides KW - 11062-77-4 KW - pristane KW - 26HZV48DT1 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Oxygen KW - S88TT14065 KW - Indomethacin KW - XXE1CET956 KW - Index Medicus KW - Animals KW - Superoxides -- metabolism KW - DNA Repair KW - Tumor Cells, Cultured KW - Oxygen -- metabolism KW - Hydrogen Peroxide -- metabolism KW - Mice KW - Terpenes -- pharmacology KW - Mice, Inbred BALB C KW - Time Factors KW - Indomethacin -- pharmacology KW - Neutrophils -- metabolism KW - DNA Damage KW - Neutrophils -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78534852?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Activated+neutrophils+induce+prolonged+DNA+damage+in+neighboring+cells.&rft.au=Shacter%2C+E%3BBeecham%2C+E+J%3BCovey%2C+J+M%3BKohn%2C+K+W%3BPotter%2C+M&rft.aulast=Shacter&rft.aufirst=E&rft.date=1988-12-01&rft.volume=9&rft.issue=12&rft.spage=2297&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-12 N1 - Date created - 1989-01-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Carcinogenesis 1989 Mar;10(3):628 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genomic 5-methyldeoxycytidine decreases associated with the induction of squamous differentiation in cultured normal human bronchial epithelial cells. AN - 78532040; 2461263 AB - The terminal squamous differentiation of epithelial cells involves a number of cellular changes. However, the mechanisms underlying this differentiation process are unknown. The present study demonstrates that 5-azacytidine, 12-O-tetradecanoylphorbol-13-acetate (TPA) and type beta-transforming growth factor (TGF-beta) significantly diminish the genomic 5-methyldeoxycytidine (5mdC) content of normal human bronchial epithelial cells concomitantly with the induction of squamous differentiation. 5-Azacytidine or TPA, but not type beta-transforming growth factor, also initiated decreases in the genomic 5mdC content of differentiation nonresponsive human tumor A549 cells. These effects of TPA or type beta-transforming growth factor occurred at concentrations of 1 nM and 1.2 pM, respectively, which were approximately one tenth of kd values of their specific receptors. Therefore, the decreases in genomic 5mdC induced by these agents were probably mediated, directly or indirectly, by receptor--ligand interactions. JF - Carcinogenesis AU - Wilson, V L AU - Masui, T AU - Smith, R A AU - Harris, C C AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 2155 EP - 2159 VL - 9 IS - 12 SN - 0143-3334, 0143-3334 KW - Deoxycytidine KW - 0W860991D6 KW - Transforming Growth Factors KW - 76057-06-2 KW - DNA KW - 9007-49-2 KW - 5-methyldeoxycytidine KW - B200GV71QM KW - Azacitidine KW - M801H13NRU KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Azacitidine -- pharmacology KW - Cells, Cultured KW - Humans KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Epithelium -- metabolism KW - Transforming Growth Factors -- pharmacology KW - Cell Differentiation -- drug effects KW - Epithelium -- drug effects KW - Deoxycytidine -- metabolism KW - Deoxycytidine -- analogs & derivatives KW - DNA -- metabolism KW - Bronchi -- metabolism KW - Bronchi -- drug effects KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78532040?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Genomic+5-methyldeoxycytidine+decreases+associated+with+the+induction+of+squamous+differentiation+in+cultured+normal+human+bronchial+epithelial+cells.&rft.au=Wilson%2C+V+L%3BMasui%2C+T%3BSmith%2C+R+A%3BHarris%2C+C+C&rft.aulast=Wilson&rft.aufirst=V&rft.date=1988-12-01&rft.volume=9&rft.issue=12&rft.spage=2155&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-12 N1 - Date created - 1989-01-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transformation of rat liver epithelial cells with v-H-ras or v-raf causes expression of MDR-1, glutathione-S-transferase-P and increased resistance to cytotoxic chemicals. AN - 78530743; 2903802 AB - We have examined the relationship between transformation and multidrug resistance by employing the v-H-ras or v-raf oncogenes to transform rat liver epithelial (RLE) cells in vitro. The data indicate that transformation of RLE cells with v-H-ras or v-raf results in increased resistance to the cytotoxins adriamycin, vinblastine and 2-acetylaminofluorene. This multidrug resistance is accompanied by increasing expression of P-glycoprotein (MDR-1) and glutathione-S-transferase P (GST-P). Thus, neoplastic transformation of RLE cells with v-raf or v-H-ras, independently of chemical exposure, results in multidrug resistance. JF - Carcinogenesis AU - Burt, R K AU - Garfield, S AU - Johnson, K AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 2329 EP - 2332 VL - 9 IS - 12 SN - 0143-3334, 0143-3334 KW - Antineoplastic Agents KW - 0 KW - Membrane Glycoproteins KW - P-Glycoprotein KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Index Medicus KW - Rats KW - Animals KW - Drug Resistance -- genetics KW - Placenta -- enzymology KW - Cell Survival -- drug effects KW - Oncogenes KW - Membrane Glycoproteins -- biosynthesis KW - Liver -- drug effects KW - Cell Transformation, Neoplastic -- metabolism KW - Glutathione Transferase -- biosynthesis KW - Glutathione Transferase -- genetics KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78530743?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Transformation+of+rat+liver+epithelial+cells+with+v-H-ras+or+v-raf+causes+expression+of+MDR-1%2C+glutathione-S-transferase-P+and+increased+resistance+to+cytotoxic+chemicals.&rft.au=Burt%2C+R+K%3BGarfield%2C+S%3BJohnson%2C+K%3BThorgeirsson%2C+S+S&rft.aulast=Burt&rft.aufirst=R&rft.date=1988-12-01&rft.volume=9&rft.issue=12&rft.spage=2329&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-12 N1 - Date created - 1989-01-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Drug abuse discharges from non-federal short-stay hospitals. AN - 78525391; 3189633 AB - An analysis of inpatient drug abuse cases was done using the National Hospital Discharge Survey (NHDS). An estimated two million discharges with a drug abuse diagnosis occurred in non-federal short-stay hospitals during 1979-85, a figure which is believed to be an underestimate. Compared to other hospital inpatients, drug abuse inpatients are more likely to be male, ages 15-44, and other than White race. Increases in hospital use for drug abuse treatment were found to have occurred between 1979 and 1985, with discharge rates per 10,000 population increasing from 3.1 to 6.0 for drug dependence and from 3.8 to 7.7 for nondependent drug abuse. Concurrent increases in availability of hospital-based inpatient drug and alcohol treatment programs and insurance coverage for drug abuse treatment were found to have occurred during the same period. JF - American journal of public health AU - Gfroerer, J C AU - Adams, E H AU - Moien, M AD - Statistical and Epidemiologic Analysis Branch, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 1559 EP - 1562 VL - 78 IS - 12 SN - 0090-0036, 0090-0036 KW - Abridged Index Medicus KW - Index Medicus KW - United States KW - Patient Admission KW - Humans KW - Adult KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Substance-Related Disorders -- therapy KW - Length of Stay KW - Patient Discharge KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78525391?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Drug+abuse+discharges+from+non-federal+short-stay+hospitals.&rft.au=Gfroerer%2C+J+C%3BAdams%2C+E+H%3BMoien%2C+M&rft.aulast=Gfroerer&rft.aufirst=J&rft.date=1988-12-01&rft.volume=78&rft.issue=12&rft.spage=1559&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 - 1988-12-19 N1 - Date created - 1988-12-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Arch Intern Med. 1987 Feb;147(2):349-52 [3813755] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cyclosporin A in severe, treatment-refractory rheumatoid arthritis. A randomized study. AN - 78521017; 3190040 AB - To assess the efficacy and toxicity of cyclosporin A in patients with severe, treatment-refractory rheumatoid arthritis. Prospective randomized, double-blind 6-month trial. Thirty-one patients who had classic seropositive rheumatoid arthritis with active synovitis unresponsive to conventional therapy. Patients were randomly assigned to high-dose (10 mg/kg body weight.d) or low-dose (1 mg/kg.d) cyclosporin A therapy. A reduction in the dose was permitted for adverse side effects. After 6 months of therapy, patients who showed clinically relevant improvement, defined as a 40% or greater reduction in their total joint activity score, were given the option to continue receiving the therapy for an additional 6 months. At 6 months, clinically relevant improvement occurred in 10 of 15 patients (95% CI, 38 to 88) receiving high-dose therapy and in 4 of 16 patients (CI, 7 to 52) receiving low-dose therapy (P = 0.02). Statistically significant improvements in individual measures were shown only in the high-dose group. Improvements were noted in the number of tender joints (-18.8; CI, -24.5 to -13.1) and swollen joints (-12.1; CI, -15.4 to -8.6), as well as in physician's global scores (-1.5; CI, -2.1 to -0.9) and patient's global scores (-1.1; CI, -1.9 to -0.5). Improvement in disease activity was maintained through 12 months in the high-dose group. The clinical responses to cyclosporin A were most evident in patients with depressed in-vitro proliferative responses of peripheral blood mononuclear lymphocytes to soluble recall antigens. Toxicities, such as fatigue, gastrointestinal and neurologic complaints, and hypertrichosis were frequent but often reversible with a reduction in the dose. Nephrotoxicity, with a 20% increase in the serum creatinine level, was seen in 27 of 31 patients (CI, 71 to 97). Cyclosporin A is an effective therapy for severe, treatment-refractory rheumatoid arthritis. Side effects, particularly nephrotoxicity, are common. JF - Annals of internal medicine AU - Yocum, D E AU - Klippel, J H AU - Wilder, R L AU - Gerber, N L AU - Austin, H A AU - Wahl, S M AU - Lesko, L AU - Minor, J R AU - Preuss, H G AU - Yarboro, C AD - National Institutes of Health, Bethesda, Maryland. Y1 - 1988/12/01/ PY - 1988 DA - 1988 Dec 01 SP - 863 EP - 869 VL - 109 IS - 11 SN - 0003-4819, 0003-4819 KW - Cyclosporins KW - 0 KW - C-Reactive Protein KW - 9007-41-4 KW - Creatinine KW - AYI8EX34EU KW - Abridged Index Medicus KW - Index Medicus KW - C-Reactive Protein -- drug effects KW - Double-Blind Method KW - Random Allocation KW - Dose-Response Relationship, Drug KW - Humans KW - Nervous System Diseases -- chemically induced KW - Creatinine -- blood KW - Drug Evaluation KW - Prospective Studies KW - Adult KW - Middle Aged KW - Leukocytes, Mononuclear -- drug effects KW - Female KW - Male KW - Kidney Diseases -- chemically induced KW - Cyclosporins -- adverse effects KW - Arthritis, Rheumatoid -- drug therapy KW - Arthritis, Rheumatoid -- blood KW - Cyclosporins -- therapeutic use KW - Cyclosporins -- administration & dosage KW - Arthritis, Rheumatoid -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78521017?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cyclosporin+A+in+severe%2C+treatment-refractory+rheumatoid+arthritis.+A+randomized+study.&rft.au=Yocum%2C+D+E%3BKlippel%2C+J+H%3BWilder%2C+R+L%3BGerber%2C+N+L%3BAustin%2C+H+A%3BWahl%2C+S+M%3BLesko%2C+L%3BMinor%2C+J+R%3BPreuss%2C+H+G%3BYarboro%2C+C&rft.aulast=Yocum&rft.aufirst=D&rft.date=1988-12-01&rft.volume=109&rft.issue=11&rft.spage=863&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 - 1988-12-16 N1 - Date created - 1988-12-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Colonic perforation. An unusual complication of therapy with high-dose interleukin-2. AN - 78500988; 3263182 AB - The majority (85%) of patients receiving high dose Interleukin-2 (IL-2) experience gastrointestinal side effects, namely nausea, vomiting and diarrhea. In this article we describe four cancer patients that developed localized necrosis or perforation of the colon during IL-2 treatment. They represent 1.3% of patients (n = 315) or 0.9% of treatment courses (n = 452). All underwent surgical intervention and survived to leave the hospital. No common etiologic factor was apparent. Two patients were subsequently retreated with IL-2 without complication. Localized colonic necrosis or perforation is a rare complication associated with high dose IL-2 treatments. Aggressive surgical intervention is advocated and retreatment following recovery is safe. JF - Cancer AU - Schwartzentruber, D AU - Lotze, M T AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/12/01/ PY - 1988 DA - 1988 Dec 01 SP - 2350 EP - 2353 VL - 62 IS - 11 SN - 0008-543X, 0008-543X KW - Interleukin-2 KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Interleukin-2 -- adverse effects KW - Interleukin-2 -- administration & dosage KW - Colonic Diseases -- surgery KW - Intestinal Perforation -- chemically induced KW - Colonic Diseases -- chemically induced KW - Intestinal Perforation -- surgery UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78500988?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Colonic+perforation.+An+unusual+complication+of+therapy+with+high-dose+interleukin-2.&rft.au=Schwartzentruber%2C+D%3BLotze%2C+M+T%3BRosenberg%2C+S+A&rft.aulast=Schwartzentruber&rft.aufirst=D&rft.date=1988-12-01&rft.volume=62&rft.issue=11&rft.spage=2350&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-12 N1 - Date created - 1988-12-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of CD2 in activation and cytotoxic function of CD8/Leu-7-positive T cells. AN - 78499693; 2903195 AB - CD3/CD8-positive, Leu-7-positive cells comprise about 3 to 5% of PBL in normal individuals, but the proportion of these cells is increased in patients with a variety of diseases including chronic viral infection, Crohn's disease, and AIDS. To study further the function of these cells, the proliferative and cytotoxic responses of highly purified CD8/Leu-7-positive cells were studied in vitro. These cells had low proliferative responses when exposed to PHA or mitogenic anti-CD3 mAb compared to CD8/Leu-7-negative cells, and their proliferative responses were significantly lower after addition of IL-2 or autologous adherent cells. However, the proliferative responses of both Leu-7-positive and Leu-7-negative CD8 cells were similar when stimulated with PHA, Ionomycin, or anti-CD3 in combination with phorbol ester. In addition, CD8/Leu-7-positive cells demonstrated high proliferative responses when exposed to a combination of both PHA and SRBC, and these responses could be inhibited by prior addition of non-stimulating anti-CD2.1 mAb. CD8/Leu-7-positive cells, but not CD8/Leu-7-negative cells, mediated lectin- and anti-CD3-induced cytotoxicity against K562 target cells. Cytotoxicity was in part dependent on the CD2 Ag because it was inhibited by anti-CD2.1 mAb. Finally, when small CD8-positive T cells having low cytotoxic potential were activated with PHA plus SRBC, but not PHA alone, there was significant enhancement of their cytotoxic function. Thus, the CD2 receptor may be an important activation pathway for cytotoxic cells. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Rüthlein, J AU - James, S P AU - Strober, W AD - Mucosal Immunity Section, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1988/12/01/ PY - 1988 DA - 1988 Dec 01 SP - 3791 EP - 3797 VL - 141 IS - 11 SN - 0022-1767, 0022-1767 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, CD2 KW - Antigens, CD8 KW - Antigens, Differentiation, T-Lymphocyte KW - Ethers KW - Immunosuppressive Agents KW - Lymphokines KW - Phytohemagglutinins KW - Receptors, Immunologic KW - Ionomycin KW - 56092-81-0 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Sheep KW - Humans KW - Cell Separation KW - Phenotype KW - Immunosuppressive Agents -- physiology KW - Antigen-Presenting Cells -- immunology KW - Antibodies, Monoclonal -- physiology KW - Erythrocytes -- immunology KW - Lymphocyte Activation KW - Cytotoxicity, Immunologic KW - Receptors, Immunologic -- immunology KW - T-Lymphocytes, Cytotoxic -- classification KW - T-Lymphocytes, Cytotoxic -- immunology KW - Antigens, Differentiation, T-Lymphocyte -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78499693?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Role+of+CD2+in+activation+and+cytotoxic+function+of+CD8%2FLeu-7-positive+T+cells.&rft.au=R%C3%BCthlein%2C+J%3BJames%2C+S+P%3BStrober%2C+W&rft.aulast=R%C3%BCthlein&rft.aufirst=J&rft.date=1988-12-01&rft.volume=141&rft.issue=11&rft.spage=3791&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 - 1988-12-20 N1 - Date created - 1988-12-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects and mechanism of action of lithium chloride on gastric acid secretion in rats. AN - 78493266; 2846401 AB - Lithium chloride reduce the measured parameters of gastric secretion (gastric volume, hydrogen ion concentration, and gastric acid output) 2 h after intracerebroventricular, intravenous, or subcutaneous administration in pylorus-ligated rats, in a dose-dependent manner. Intracerebroventricular administration of lithium was approximately five times and 10 times more potent than intravenous and subcutaneous injection, respectively. Time-course study demonstrated that the action of lithium (400 micrograms) on gastric secretion reached a peak at 1 h after intracerebroventricular administration; however, the effects on volume and output were still significant after 8 h. Prior intracerebroventricular injection of indomethacin (400 micrograms) reversed the action of centrally administered lithium on gastric secretion. However, central administration of the opiate receptor blocker naltrexone (100 micrograms), as well as subcutaneous administration of indomethacin (5 mg/kg), failed to modify the effect of lithium on gastric acid secretion. Our data suggest that lithium appears to act centrally to modulate gastric acid secretion in rats through a mechanism involving the synthesis of prostaglandinlike material(s) in the brain. Furthermore, the effect of centrally administered lithium is independent of stimulation of opiate receptor(s) in the brain. JF - Gastroenterology AU - Guglietta, A AU - Irons, B J AU - Lazarus, L H AU - Sivam, S P AD - Laboratory of Molecular and Integrative Neuroscience, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 1454 EP - 1459 VL - 95 IS - 6 SN - 0016-5085, 0016-5085 KW - Chlorides KW - 0 KW - Naltrexone KW - 5S6W795CQM KW - Lithium KW - 9FN79X2M3F KW - Lithium Chloride KW - G4962QA067 KW - Indomethacin KW - XXE1CET956 KW - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Animals KW - Drug Interactions KW - Injections, Intravenous KW - Dose-Response Relationship, Drug KW - Brain -- drug effects KW - Naltrexone -- pharmacology KW - Injections, Subcutaneous KW - Time Factors KW - Male KW - Injections, Intraventricular KW - Indomethacin -- pharmacology KW - Depression, Chemical KW - Chlorides -- administration & dosage KW - Lithium -- administration & dosage KW - Lithium -- pharmacology KW - Gastric Acid -- secretion KW - Chlorides -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78493266?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gastroenterology&rft.atitle=Effects+and+mechanism+of+action+of+lithium+chloride+on+gastric+acid+secretion+in+rats.&rft.au=Guglietta%2C+A%3BIrons%2C+B+J%3BLazarus%2C+L+H%3BSivam%2C+S+P&rft.aulast=Guglietta&rft.aufirst=A&rft.date=1988-12-01&rft.volume=95&rft.issue=6&rft.spage=1454&rft.isbn=&rft.btitle=&rft.title=Gastroenterology&rft.issn=00165085&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-20 N1 - Date created - 1988-12-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparative carcinogenesis by nitrosomethylalkylamines in Syrian hamsters. AN - 78487706; 3180074 AB - Six homologous nitrosomethyl-n-alkylamines, from n-propyl (C-3) to n-octyl (C-8), were administered by gavage to groups of 12 male and 12 female Syrian golden hamsters as solutions in corn oil:ethyl acetate (2:1). The solutions of C-8 to C-4 were equimolar; nitrosomethyl-n-butylamine (C-4) and nitrosomethyl-n-propylamine (C-3) were given at a lower concentration. Treatment with 0.2 ml of solution lasted 23 to 50 wk, being stopped when several hamsters had died. Additional groups of hamsters were treated similarly with nitrosomethylaniline and nitrosomethylcyclohexylamine. Excepting hamsters given the latter, treated animals had reduced survival compared with controls. The incidence of tumors in hamsters given nitrosomethylaniline and nitrosomethylcyclohexylamine was low and occurred in the liver, lungs, and spleen. Hamsters treated with nitrosomethyl-n-propylamine and nitrosomethyl-n-butylamine suffered the greatest decrease in survival. Potency judged by this criterion decreased as the size of the molecule increased in the homologous series. Virtually all of these treated hamsters died with tumors not seen in controls. These tumors, which were common in hamsters given all of the nitrosomethyl-n-alkylamines, were in the liver, lung, forestomach, and nasal mucosa, but the incidences varied somewhat between the compounds and between sexes. Bladder tumors were seen only in hamsters given nitrosamines containing even numbers of carbon atoms in the chain, namely, nitrosomethyl-n-hexylamine and nitrosomethyl-n-octylamine. JF - Cancer research AU - Lijinsky, W AU - Kovatch, R M AD - National Cancer Institute-Frederick Cancer Research Facility, Bionetics Research, Inc., Maryland 21701. Y1 - 1988/12/01/ PY - 1988 DA - 1988 Dec 01 SP - 6648 EP - 6652 VL - 48 IS - 23 SN - 0008-5472, 0008-5472 KW - Nitrosamines KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - DNA -- metabolism KW - Mesocricetus KW - Methylation KW - Male KW - Female KW - Structure-Activity Relationship KW - Cricetinae KW - Nitrosamines -- toxicity KW - Neoplasms, Experimental -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78487706?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparative+carcinogenesis+by+nitrosomethylalkylamines+in+Syrian+hamsters.&rft.au=Lijinsky%2C+W%3BKovatch%2C+R+M&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1988-12-01&rft.volume=48&rft.issue=23&rft.spage=6648&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 - 1988-12-20 N1 - Date created - 1988-12-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Two-year inhalation carcinogenesis studies of methyl methacrylate in rats and mice: inflammation and degeneration of nasal epithelium. AN - 78530642; 3188037 AB - Methyl methacrylate (MMA), a liquid monomer, is used as a chemical intermediate in the manufacture of plexiglass and other acrylic products and as "bone cement" in orthopedic and dental surgery. Toxicology and carcinogenesis inhalation studies of MMA were conducted because of: (1) widespread human exposure; (2) evidence of mutagenicity; and (3) inadequacy of previously conducted long-term oral, dermal, and inhalation studies. Groups of 50 male F344/N rats were exposed to MMA by inhalation at 0, 500, or 1000 ppm, female F344/N rats at 0, 250, or 500 ppm, and male and female B6C3F1 mice at 0, 500, or 1000 ppm, 6 h a day, 5 days a week for 102 weeks. Survival rates of male and female rats and mice exposed to MMA were similar to those of their respective controls. Body weights were reduced in the low and high dose male (3-6% and 5-10%, respectively) and female (5-7% and 8-10%) rats exposed to MMA for more than 80 weeks and in male (7-19% and 6-17%) and female (0-13% and 0-17%) mice for more than 20 weeks. Inhalation exposure of MMA for 102 weeks did not induce any increased incidences of neoplasms in male or female rats or mice. Non-neoplastic lesions in the nasal cavity of MMA-exposed rats and mice were significantly increased and these included inflammation and degeneration of the olfactory epithelium of MMA-exposed male and female rats and inflammation, hyperplasia, cytoplasmic inclusions in the respiratory epithelium, and degeneration of the olfactory epithelium in male and female mice. JF - Toxicology AU - Chan, P C AU - Eustis, S L AU - Huff, J E AU - Haseman, J K AU - Ragan, H AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/11/30/ PY - 1988 DA - 1988 Nov 30 SP - 237 EP - 252 VL - 52 IS - 3 SN - 0300-483X, 0300-483X KW - Carcinogens KW - 0 KW - Methylmethacrylates KW - Methylmethacrylate KW - 196OC77688 KW - Index Medicus KW - Animals KW - Nasal Septum -- drug effects KW - Sex Factors KW - Mice KW - Rats KW - Rats, Inbred F344 KW - Nasal Septum -- pathology KW - Body Weight -- drug effects KW - Lung -- drug effects KW - Administration, Inhalation KW - Species Specificity KW - Female KW - Male KW - Rhinitis -- chemically induced KW - Nasal Mucosa -- pathology KW - Methylmethacrylates -- administration & dosage KW - Nasal Mucosa -- drug effects KW - Methylmethacrylates -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78530642?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Two-year+inhalation+carcinogenesis+studies+of+methyl+methacrylate+in+rats+and+mice%3A+inflammation+and+degeneration+of+nasal+epithelium.&rft.au=Chan%2C+P+C%3BEustis%2C+S+L%3BHuff%2C+J+E%3BHaseman%2C+J+K%3BRagan%2C+H&rft.aulast=Chan&rft.aufirst=P&rft.date=1988-11-30&rft.volume=52&rft.issue=3&rft.spage=237&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-22 N1 - Date created - 1988-12-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibitory effect of zinc on nickel subsulfide carcinogenesis in Fischer rats. AN - 78518029; 3188038 AB - The effects of zinc oxide (ZnO) and zinc acetate (ZnAcet) administered i.m. together with nickel subsulfide (Ni3S2), a potent muscle carcinogen, were observed over 66 weeks in male F344/NCr rats. The rats (20/group) received a single injection of 2.5 mg Ni3S2 (equal to 31 mumol Ni) alone or combined with different molar proportions of ZnO or ZnAcet (8-60 mumol Zn) into both thighs. One more group of rats given i.m. Ni3S2 received s.c. ZnO (60 mumol Zn) at the nape of the neck. Control rats were treated with i.m. ZnO (60 mumol Zn) or the injection vehicle, water. In rats given Ni3S2 alone the incidence of local tumors reached 100% in 40 weeks. In rats treated locally with Ni3S2 + ZnO or ZnAcet, the tumor incidence at week 40 was only 40-60%; it reached 85-100% in 66 weeks, with no significant differences among the treatments. Treatment with i.m. Ni3S2 + s.c. ZnO resulted in 100% muscle tumors at week 58. One local tumor was found in rats given ZnO alone and none in the water injected animals. Statistical analysis revealed highly significant differences in the tumor occurrence rates between rats treated with Ni3S2 alone and rats treated with Ni3S2 combined with ZnO or ZnAcet, whereas the final tumor incidences at week 66 were not different. The first tumors were found at weeks 24-31 regardless of the treatment. Hence, administration of zinc slows the carcinogenic process induced by nickel. This effect has a systemic character and is produced by both water-soluble and insoluble zinc compounds despite their different retention times in the muscle. The half-lives of ZnO and ZnAcet in the muscle were approx. 24 days and 2.5 days, respectively; that of Ni3S2 was 21 days. Zinc in either form exerted no apparent influence upon the retention of nickel at the injection site and did not significantly affect the early local cellular reactions to nickel. JF - Toxicology AU - Kasprzak, K S AU - Kovatch, R M AU - Poirier, L A AD - Division of Cancer Etiology, National Cancer Institute, FCRF, Frederick, MD 21701. Y1 - 1988/11/30/ PY - 1988 DA - 1988 Nov 30 SP - 253 EP - 262 VL - 52 IS - 3 SN - 0300-483X, 0300-483X KW - Acetates KW - 0 KW - Carcinogens KW - nickel subsulfide KW - 12035-72-2 KW - Nickel KW - 7OV03QG267 KW - Zinc KW - J41CSQ7QDS KW - Acetic Acid KW - Q40Q9N063P KW - Zinc Oxide KW - SOI2LOH54Z KW - Index Medicus KW - Rats KW - Animals KW - Sarcoma, Experimental -- prevention & control KW - Rats, Inbred F344 KW - Male KW - Zinc Oxide -- pharmacology KW - Zinc -- pharmacology KW - Nickel -- antagonists & inhibitors KW - Muscular Diseases -- chemically induced KW - Nickel -- toxicity KW - Muscular Diseases -- prevention & control KW - Carcinogens -- antagonists & inhibitors KW - Acetates -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78518029?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inhibitory+effect+of+zinc+on+nickel+subsulfide+carcinogenesis+in+Fischer+rats.&rft.au=Kasprzak%2C+K+S%3BKovatch%2C+R+M%3BPoirier%2C+L+A&rft.aulast=Kasprzak&rft.aufirst=K&rft.date=1988-11-30&rft.volume=52&rft.issue=3&rft.spage=253&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-22 N1 - Date created - 1988-12-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanisms of secretory responses to gonadotropin-releasing hormone and phorbol esters in cultured pituitary cells. Participation of protein kinase C and extracellular calcium mobilization. AN - 78494552; 2460461 AB - The role of protein kinase C in luteinizing hormone (LH) release was analyzed in studies on the actions of gonadotropin releasing hormone (GnRH) and phorbol esters in cultured pituitary cells. During incubation in normal medium, GnRH stimulated LH release with an ED50 of 0.35 nM. Incubation in Ca2+-deficient medium (Ca2+-free, 10 microM) substantially decreased but did not abolish the LH responses to GnRH. The extracellular Ca2+-dependent component of GnRH action could be mimicked by high K+ concentrations, consistent with the presence of voltage-sensitive calcium channels (VSCC) in pituitary gonadotrophs. Ca2+ channel agonist (Bay K 8644) and antagonist (nifedipine) analogs, respectively, enhanced or partially inhibited LH responses to GnRH and also to K+, the latter confirming the participation of two types of VSCC (dihydropyridine-sensitive and -insensitive) in K+-induced secretion. Phorbol esters, including 12-O-tetradecanoylphorbol-13-acetate (TPA), 4 beta-phorbol-12,13-dibenzoate, and 4 beta-phorbol-12,13-diacetate, stimulated LH release with ED50s of 5, 10, and 1000 nM, respectively, and with about 70% of the efficacy of GnRH. Phorbol ester-stimulated LH secretion was decreased but not abolished by progressive reduction of [Ca2+]e in the incubation medium, and the residual LH response was identical with that elicited by GnRH in Ca2+-deficient medium. TPA increased [Ca2+]i to a peak after 20 s in normal medium but not in the absence of extracellular Ca2+, indicating that protein kinase C (Ca2+/phospholipid-dependent enzyme) promotes calcium entry but can also mediate secretory responses without changes in calcium influx and [Ca2+]i. The extracellular Ca2+-dependent action of TPA on LH release was blocked by Co2+. However, nifedipine did not alter TPA action on [Ca2+]i and LH release. These observations indicate that protein kinase C can participate in GnRH-induced LH release that is independent of Ca2+ entry, but also promotes the influx of extracellular Ca2+ through dihydropyridine-insensitive Ca2+-channels. JF - The Journal of biological chemistry AU - Stojilković, S S AU - Chang, J P AU - Izumi, S AU - Tasaka, K AU - Catt, K J AD - Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20982. Y1 - 1988/11/25/ PY - 1988 DA - 1988 Nov 25 SP - 17301 EP - 17306 VL - 263 IS - 33 SN - 0021-9258, 0021-9258 KW - Phorbol Esters KW - 0 KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 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 - Rats, Inbred Strains KW - Rats KW - Animals KW - Reference Values KW - Cells, Cultured KW - Kinetics 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 - Ovariectomy KW - Female KW - Luteinizing Hormone -- secretion KW - Calcium -- metabolism KW - Pituitary Gland, Anterior -- drug effects KW - Phorbol Esters -- pharmacology KW - Pituitary Gland, Anterior -- secretion KW - Pituitary Gland, Anterior -- physiology KW - Calcium -- pharmacology KW - Protein Kinase C -- physiology KW - Gonadotropin-Releasing Hormone -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78494552?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mechanisms+of+secretory+responses+to+gonadotropin-releasing+hormone+and+phorbol+esters+in+cultured+pituitary+cells.+Participation+of+protein+kinase+C+and+extracellular+calcium+mobilization.&rft.au=Stojilkovi%C4%87%2C+S+S%3BChang%2C+J+P%3BIzumi%2C+S%3BTasaka%2C+K%3BCatt%2C+K+J&rft.aulast=Stojilkovi%C4%87&rft.aufirst=S&rft.date=1988-11-25&rft.volume=263&rft.issue=33&rft.spage=17301&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 - 1988-12-20 N1 - Date created - 1988-12-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evidence for a role of protein kinase C in luteinizing hormone synthesis and secretion. Impaired responses to gonadotropin-releasing hormone in protein kinase C-depleted pituitary cells. AN - 78494227; 3053708 AB - The role of protein kinase C in luteinizing hormone (LH) release was analyzed in studies on the actions of phorbol esters and gonadotropin-releasing hormone (GnRH) in normal and protein kinase C (Ca2+/phospholipid-dependent enzyme)-depleted pituitary cell cultures. LH secretory responses of normal pituitary cells to GnRH were reduced but not abolished in Ca2+-deficient medium, consistent with the existence of extracellular Ca2+-dependent and -independent components of GnRH action. Both of these components could be elicited by treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA). The LH secretory responses to TPA and GnRH were additive only at low doses and converged to a common maximum at high concentrations of the agonists in the presence or absence of extracellular Ca2+. The release of stored LH by GnRH and TPA was accompanied by secretion of newly synthesized LH from 2 to 5 h during stimulation by either of the agonists. LH synthesis was increased in a progressive and dose-dependent manner by GnRH and TPA, and the ratio between newly synthesized and released hormone was near 1:2. TPA caused rapid and complete translocation of cytosolic protein kinase C to the particulate fraction of pituitary cells, followed by a progressive decrease in total enzyme content to approximately 10% after 6 h. Partial recovery of the cytosolic enzyme (to 20%) occurred after washing and reincubation for 15 h. Such kinase C-depleted cells showed prominent, dose-dependent reductions in the actions of GnRH and TPA on LH release and synthesis in both normal and Ca2+-deficient media. These observations support the hypothesis that protein kinase C participates in LH biosynthesis and secretion in pituitary gonadotrophs and is involved in the actions of GnRH upon these processes. JF - The Journal of biological chemistry AU - Stojilković, S S AU - Chang, J P AU - Ngo, D AU - Catt, K J AD - Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20982. Y1 - 1988/11/25/ PY - 1988 DA - 1988 Nov 25 SP - 17307 EP - 17311 VL - 263 IS - 33 SN - 0021-9258, 0021-9258 KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 KW - Luteinizing Hormone KW - 9002-67-9 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Reference Values KW - Cells, Cultured KW - Kinetics KW - Ovariectomy KW - Female KW - Luteinizing Hormone -- secretion KW - Pituitary Gland, Anterior -- drug effects KW - Pituitary Gland, Anterior -- metabolism KW - Pituitary Gland, Anterior -- secretion KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Luteinizing Hormone -- biosynthesis KW - Protein Kinase C -- physiology KW - Gonadotropin-Releasing Hormone -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78494227?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+a+role+of+protein+kinase+C+in+luteinizing+hormone+synthesis+and+secretion.+Impaired+responses+to+gonadotropin-releasing+hormone+in+protein+kinase+C-depleted+pituitary+cells.&rft.au=Stojilkovi%C4%87%2C+S+S%3BChang%2C+J+P%3BNgo%2C+D%3BCatt%2C+K+J&rft.aulast=Stojilkovi%C4%87&rft.aufirst=S&rft.date=1988-11-25&rft.volume=263&rft.issue=33&rft.spage=17307&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 - 1988-12-20 N1 - Date created - 1988-12-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phorbol ester stimulates the synthesis of sphingomyelin in NIH 3T3 cells. A diminished response in cells transformed with human A-raf carrying retrovirus. AN - 78534606; 3191996 AB - The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) stimulated the synthesis of sphingomyelin (CerPCho) from a [14C]choline-labelled phosphatidylcholine (PtdCho) pool in NIH 3T3 cells. Maximal stimulation (68%) of CerPCho synthesis, accompanied by an increase (38%) in its cellular content, required only 2 nM TPA. Higher concentrations of TPA (2-100 nM) had progressively less effect on CerPCho synthesis which correlated with increased hydrolysis of precursor PtdCho. In cells transformed with human or mouse A-raf carrying retroviruses TPA-stimulated PtdCho hydrolysis, but not CerPCho synthesis, suggesting independent regulation of these processes by the TPA-stimulated signal transduction system. JF - FEBS letters AU - Kiss, Z AU - Rapp, U R AU - Anderson, W B AD - Division of Cancer Biology and Diagnosis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/11/21/ PY - 1988 DA - 1988 Nov 21 SP - 221 EP - 226 VL - 240 IS - 1-2 SN - 0014-5793, 0014-5793 KW - Sphingomyelins KW - 0 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Oncogenes KW - Enzyme Activation -- drug effects KW - Mice KW - Protein Kinase C -- physiology KW - Cell Line KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Transformation, Viral KW - Sphingomyelins -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78534606?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phorbol+ester+stimulates+the+synthesis+of+sphingomyelin+in+NIH+3T3+cells.+A+diminished+response+in+cells+transformed+with+human+A-raf+carrying+retrovirus.&rft.au=Kiss%2C+Z%3BRapp%2C+U+R%3BAnderson%2C+W+B&rft.aulast=Kiss&rft.aufirst=Z&rft.date=1988-11-21&rft.volume=240&rft.issue=1-2&rft.spage=221&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 - 1988-12-30 N1 - Date created - 1988-12-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - High-dose carboplatin with diethyldithiocarbamate chemoprotection in treatment of women with relapsed ovarian cancer. AN - 78506061; 2846858 AB - Diethyldithiocarbamate (DDTC) has been found to protect the bone marrow, kidneys, and gastrointestinal tract from the toxic effects of cisplatin and carboplatin (CBDCA) in animal models. In an attempt to minimize the toxic effects of high-dose CBDCA (800 mg/m2), a pilot study was undertaken in which women with relapsed or refractory epithelial ovarian cancer were treated with high-dose CBDCA, which was followed 3 hours later with DDTC (4 g/m2). There were four partial responses and no complete response in 21 patients who could be evaluated (overall response rate, 19%). Significant toxic effects, including three treatment-related deaths, were associated with the regimen. This study suggests that while high-dose CBDCA plus DDTC may be active in relapsed or refractory ovarian cancer, it is associated with clinically significant hematologic and autonomic toxic effects. JF - Journal of the National Cancer Institute AU - Rothenberg, M L AU - Ostchega, Y AU - Steinberg, S M AU - Young, R C AU - Hummel, S AU - Ozols, R F AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/11/16/ PY - 1988 DA - 1988 Nov 16 SP - 1488 EP - 1492 VL - 80 IS - 18 SN - 0027-8874, 0027-8874 KW - Organoplatinum Compounds KW - 0 KW - Ditiocarb KW - 99Z2744345 KW - Carboplatin KW - BG3F62OND5 KW - Index Medicus KW - Drug Evaluation KW - Organoplatinum Compounds -- administration & dosage KW - Neoplasm Recurrence, Local -- drug therapy KW - Humans KW - Autonomic Nervous System -- drug effects KW - Adult KW - Aged KW - Middle Aged KW - Bone Marrow -- drug effects KW - Female KW - Ditiocarb -- administration & dosage 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/78506061?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=High-dose+carboplatin+with+diethyldithiocarbamate+chemoprotection+in+treatment+of+women+with+relapsed+ovarian+cancer.&rft.au=Rothenberg%2C+M+L%3BOstchega%2C+Y%3BSteinberg%2C+S+M%3BYoung%2C+R+C%3BHummel%2C+S%3BOzols%2C+R+F&rft.aulast=Rothenberg&rft.aufirst=M&rft.date=1988-11-16&rft.volume=80&rft.issue=18&rft.spage=1488&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 - 1988-11-25 N1 - Date created - 1988-11-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Whither the modulation of platinum? AN - 78505314; 2846854 JF - Journal of the National Cancer Institute AU - Leyland-Jones, B AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/11/16/ PY - 1988 DA - 1988 Nov 16 SP - 1432 EP - 1433 VL - 80 IS - 18 SN - 0027-8874, 0027-8874 KW - Antimetabolites KW - 0 KW - Methionine Sulfoximine KW - 1982-67-8 KW - Buthionine Sulfoximine KW - 5072-26-4 KW - Ditiocarb KW - 99Z2744345 KW - Amifostine KW - M487QF2F4V KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Antimetabolites -- pharmacology KW - Amifostine -- pharmacology KW - Ditiocarb -- pharmacology KW - Humans KW - Methionine Sulfoximine -- pharmacology KW - Methionine Sulfoximine -- analogs & derivatives KW - Cisplatin -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78505314?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Whither+the+modulation+of+platinum%3F&rft.au=Leyland-Jones%2C+B&rft.aulast=Leyland-Jones&rft.aufirst=B&rft.date=1988-11-16&rft.volume=80&rft.issue=18&rft.spage=1432&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 - 1988-11-25 N1 - Date created - 1988-11-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fetal hippocampal cell suspensions ameliorate behavioral effects of intradentate colchicine in the rat. AN - 78704737; 3233493 AB - Colchicine, a neurotoxin that preferentially destroys dentate gyrus granule cells and mossy fibers, was injected into the hippocampus of adult rats. Three weeks later, the rats were tested for colchicine-induced hypermotility after which they received fetal hippocampal explants. Locomotor activity was retested three weeks later, after which the rats were trained over a period of four weeks on a food-reinforced, spatial, working memory task in an 8-arm radial maze. Fetal hippocampal explants were found to attenuate significantly the colchicine-induced hypermotility and spatial learning deficits. Histological observations showed the presence of surviving hippocampal explants in both the lesioned and the control rat brains, suggesting that the presence of viable implants facilitates the recovery of behavioral function in rats with spatial memory deficits. JF - Brain research AU - Tandon, P AU - McLamb, R L AU - Novicki, D AU - Shuey, D L AU - Tilson, H A AD - Laboratory of Molecular and Integrative Neuroscience, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/11/15/ PY - 1988 DA - 1988 Nov 15 SP - 241 EP - 248 VL - 473 IS - 2 SN - 0006-8993, 0006-8993 KW - Neurotoxins KW - 0 KW - Colchicine KW - SML2Y3J35T KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Fetus KW - Animals KW - Reference Values KW - Cells, Cultured KW - Motor Activity KW - Male KW - Colchicine -- toxicity KW - Hippocampus -- transplantation KW - Hippocampus -- physiology KW - Hippocampus -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78704737?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Fetal+hippocampal+cell+suspensions+ameliorate+behavioral+effects+of+intradentate+colchicine+in+the+rat.&rft.au=Tandon%2C+P%3BMcLamb%2C+R+L%3BNovicki%2C+D%3BShuey%2C+D+L%3BTilson%2C+H+A&rft.aulast=Tandon&rft.aufirst=P&rft.date=1988-11-15&rft.volume=473&rft.issue=2&rft.spage=241&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 - 1989-05-10 N1 - Date created - 1989-05-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Isolation and partial characterization of the low-molecular-mass zinc/cadmium-binding protein from the testes of the patas monkey (Erythrocebus patas). Distinction from metallothionein. AN - 78663660; 3223896 AB - The mammalian testes are generally quite susceptible to cadmium. A deficiency of metallothionein (MT), a metal-binding protein linked to Cd tolerance, has been observed in rat testes and may explain the sensitivity in rats. Little is known about the metal-binding proteins in primate testes. Thus this study examined the nature of these proteins in a non-human primate species, the patas monkey (Erythrocebus patas). In all cases proteins isolated from testes were compared with authentic MT isolated from the liver of a zinc-treated monkey. A low-molecular-mass Zn/Cd-binding protein was seen in testicular and hepatic cytosol after gel filtration. Neither protein had substantial amounts of associated copper. These proteins could be partially purified from both sources by heat treatment and acetone precipitation. When such extracts were further separated by reverse-phase h.p.l.c., four hepatic forms were isolated, all of which proved to be authentic MT by amino acid analysis. However, only two testicular forms were separated by h.p.l.c., both of which had amino acid compositions quite unlike that of MT, having a much lower cysteine content and amino acids which are absent from MT (leucine and phenylalanine). The testicular protein appeared to be uninducible by Zn treatment. These results suggest that the low-molecular-mass Cd/Zn-binding proteins in the patas testes are not MTs and further support the hypothesis that a MT deficiency may be an important determinate of the marked testicular sensitivity to Cd toxicity. JF - The Biochemical journal AU - Waalkes, M P AU - Perantoni, A AU - Palmer, A E AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, MD 21701. Y1 - 1988/11/15/ PY - 1988 DA - 1988 Nov 15 SP - 131 EP - 137 VL - 256 IS - 1 SN - 0264-6021, 0264-6021 KW - Amino Acids KW - 0 KW - Carrier Proteins KW - cadmium-binding protein KW - zinc-binding protein KW - Cadmium KW - 00BH33GNGH KW - Metallothionein KW - 9038-94-2 KW - Iron KW - E1UOL152H7 KW - Zinc KW - J41CSQ7QDS KW - Index Medicus KW - Animals KW - Cytosol -- analysis KW - Iron -- analysis KW - Chromatography, Gel KW - Amino Acids -- analysis KW - Erythrocebus patas KW - Molecular Weight KW - Male KW - Liver -- analysis KW - Chromatography, High Pressure Liquid KW - Zinc -- analysis KW - Cadmium -- analysis KW - Testis -- analysis KW - Metallothionein -- isolation & purification KW - Carrier Proteins -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78663660?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Isolation+and+partial+characterization+of+the+low-molecular-mass+zinc%2Fcadmium-binding+protein+from+the+testes+of+the+patas+monkey+%28Erythrocebus+patas%29.+Distinction+from+metallothionein.&rft.au=Waalkes%2C+M+P%3BPerantoni%2C+A%3BPalmer%2C+A+E&rft.aulast=Waalkes&rft.aufirst=M&rft.date=1988-11-15&rft.volume=256&rft.issue=1&rft.spage=131&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 - 1989-03-17 N1 - Date created - 1989-03-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Reprod Fertil. 1965 Oct;10(2):273-5 [5836275] Biochem J. 1984 Jun 15;220(3):811-8 [6466305] J Nutr. 1974 Mar;104(3):345-78 [4590708] Biochem Soc Trans. 1975;3(5):632-4 [1193255] Environ Physiol Biochem. 1975;5(6):378-88 [1213026] Anal Biochem. 1976 May 7;72:248-54 [942051] Toxicol Appl Pharmacol. 1977 Jan;39(1):51-60 [841573] Acta Eur Fertil. 1976 Dec;7(4):339-48 [829013] Am J Physiol. 1978 Apr;234(4):E399-406 [645856] J Biol Chem. 1979 Dec 25;254(24):12399-403 [500722] Anal Biochem. 1980 Feb;102(1):31-4 [7356160] Toxicology. 1980;16(1):1-37 [6250252] J Biol Chem. 1981 Apr 25;256(8):3931-5 [7217064] J Biol Chem. 1981 Jun 10;256(11):5712-6 [7240167] Toxicology. 1981;22(2):91-101 [7324075] J Chromatogr. 1982 Mar 12;228:285-91 [7076751] Biochem J. 1984 Jun 15;220(3):819-24 [6466306] J Toxicol Environ Health. 1984;14(5-6):803-12 [6520888] Toxicol Appl Pharmacol. 1985 Jul;79(3):511-23 [4035692] Biochem J. 1985 Oct 15;231(2):279-83 [4062897] J Biol Chem. 1986 Oct 5;261(28):13097-103 [3759948] J Biol Chem. 1961 Sep;236:2435-42 [13750714] J Natl Cancer Inst. 1963 Oct;31:745-59 [14069825] C R Seances Soc Biol Fil. 1964;158:297-9 [14188425] C R Seances Soc Biol Fil. 1964;158:2113-5 [14282126] Toxicology. 1982;23(1):11-20 [7089981] Toxicol Appl Pharmacol. 1982 Oct;66(1):134-42 [7157381] Biochem J. 1983 Jan 1;209(1):71-80 [6847618] Toxicol Lett. 1984 Jan;20(1):33-9 [6695394] Toxicology. 1984 Mar;30(2):157-69 [6710540] Arch Toxikol. 1971;28(1):46-55 [5569102] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Preliminary applications of cross-axis synchronous flow-through coil planet centrifuge for large-scale preparative counter-current chromatography. AN - 78700866; 3069856 AB - The cross-axis synchronous flow-through coil planet centrifuge with a 20-cm revolutional radius and a total capacity of 1600 ml was successfully applied to preparative counter-current chromatography of various biological samples, which include sea buckthorn extract, steroid reaction mixture, indole plant hormones, and dinitrophenylamino acids. The present system offers advantages of stable balance of the centrifuge, a large column capacity, and high resolution. JF - Journal of chromatography AU - Zhang, T Y AU - Lee, Y W AU - Fang, Q C AU - Xiao, R AU - Ito, Y AD - Laboratory of Technical Development, National Heart, Lung, and Blood Institute, Bethesda, MD 20892. Y1 - 1988/11/11/ PY - 1988 DA - 1988 Nov 11 SP - 185 EP - 193 VL - 454 KW - Amino Acids KW - 0 KW - Indoleacetic Acids KW - Steroids KW - Index Medicus KW - Space life sciences KW - Plants, Toxic KW - Centrifugation -- methods KW - Plants, Medicinal KW - Steroids -- analysis KW - Rhamnus -- analysis KW - Amino Acids -- analysis KW - Indoleacetic Acids -- analysis KW - Chromatography -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78700866?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Preliminary+applications+of+cross-axis+synchronous+flow-through+coil+planet+centrifuge+for+large-scale+preparative+counter-current+chromatography.&rft.au=Zhang%2C+T+Y%3BLee%2C+Y+W%3BFang%2C+Q+C%3BXiao%2C+R%3BIto%2C+Y&rft.aulast=Zhang&rft.aufirst=T&rft.date=1988-11-11&rft.volume=454&rft.issue=&rft.spage=185&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 - 1989-04-26 N1 - Date created - 1989-04-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mouse non-histone chromosomal protein HMG-17 cDNA sequence. AN - 78560034; 3194220 JF - Nucleic acids research AU - Landsman, D AU - Zavou, S AU - Soares, N AU - Goodwin, G H AU - Bustin, M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/11/11/ PY - 1988 DA - 1988 Nov 11 SP - 10386 VL - 16 IS - 21 SN - 0305-1048, 0305-1048 KW - High Mobility Group Proteins KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Base Sequence KW - Genes KW - L Cells (Cell Line) -- metabolism KW - Molecular Sequence Data KW - Mice KW - Amino Acid Sequence KW - High Mobility Group Proteins -- genetics KW - DNA -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78560034?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mouse+non-histone+chromosomal+protein+HMG-17+cDNA+sequence.&rft.au=Landsman%2C+D%3BZavou%2C+S%3BSoares%2C+N%3BGoodwin%2C+G+H%3BBustin%2C+M&rft.aulast=Landsman&rft.aufirst=D&rft.date=1988-11-11&rft.volume=16&rft.issue=21&rft.spage=10386&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 - 1989-01-05 N1 - Date created - 1989-01-05 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - X12944; GENBANK N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] J Biol Chem. 1986 Jun 5;261(16):7479-84 [3754870] Mol Cell Biol. 1983 Feb;3(2):280-9 [6300662] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antibody-mediated routing of diphtheria toxin in murine cells results in a highly efficacious immunotoxin. AN - 78500506; 3263366 AB - The chemical coupling of diphtheria toxin to an antimurine Thy1 antibody resulted in the most efficacious immunotoxin to date. At 1 micrograms/ml the immunotoxin inhibited protein synthesis of a Thy+ AKR murine cell at a rate of 1.4 logs/h, within the order of magnitude of the efficacy of native toxins. This is unusual since murine cells are highly resistant to diphtheria toxin. The conjugate is highly specific; Thy- AKR cells display no intoxication at 1 microgram/ml even after 18 h. The effects of ammonia, acid pulsing of external media, and low temperature reveal some similarities and some differences between intoxication of sensitive cells by toxin and of murine cells by the antibody-toxin conjugate. The differences that result in the high efficacy of the antibody-toxin conjugate appear to result from the antibody-mediated routing. These results imply that murine cells possess an acidic compartment which can mediate toxin cytosolic entry. Unlike the Thy antigen, the toxin receptor on murine cells is unable to route the toxin to this cellular site. JF - The Journal of biological chemistry AU - Marsh, J W AD - Laboratory of Molecular Biology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1988/11/05/ PY - 1988 DA - 1988 Nov 05 SP - 15993 EP - 15999 VL - 263 IS - 31 SN - 0021-9258, 0021-9258 KW - Diphtheria Toxin KW - 0 KW - Immunotoxins KW - Isoantibodies KW - Proteins KW - anti-Thy antibody KW - Ammonia KW - 7664-41-7 KW - Index Medicus KW - Proteins -- pharmacology KW - Ammonia -- pharmacology KW - Animals KW - Thermodynamics KW - Kinetics KW - Cell Line KW - Diphtheria Toxin -- immunology KW - Diphtheria Toxin -- pharmacology KW - Immunotoxins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78500506?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Antibody-mediated+routing+of+diphtheria+toxin+in+murine+cells+results+in+a+highly+efficacious+immunotoxin.&rft.au=Marsh%2C+J+W&rft.aulast=Marsh&rft.aufirst=J&rft.date=1988-11-05&rft.volume=263&rft.issue=31&rft.spage=15993&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 - 1988-12-02 N1 - Date created - 1988-12-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Coinduction of MDR-1 multidrug-resistance and cytochrome P-450 genes in rat liver by xenobiotics. AN - 78466446; 2845109 AB - The levels of mRNA for multidrug-resistance (MDR-1) and selective cytochrome P-450 genes were determined in adult rat liver following administration of various natural and synthetic xenobiotics. MDR-1 (also known as PGY1) was induced following administration of aflatoxin B1, 2-(acetylamino)fluorene (AAF), N-hydroxy-2-(acetylamino)fluorene, isosafrole, phenothiazine, and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), but not after phenobarbital or 7-hydroxy-2-(acetylamino)fluorene treatment. Cytochrome P-450 isoform d was induced by TCDD, isosafrole, phenothiazine, and AAF, while cytochrome P-450 isoform b was induced by phenobarbital, and to a lesser extent by isosafrole. These observations suggest that both MDR and cytochrome P-450 gene families are evolutionarily selected by the capacity of various xenobiotics to induce their own detoxification either through metabolism to hydrophilic derivatives by the cytochrome P-450 system or direct excretion from the cell by the MDR gene family. Furthermore, the data indicate that induction of selective members of the MDR and the cytochrome P-450 gene families may depend on overlapping regulatory elements. JF - Journal of the National Cancer Institute AU - Burt, R K AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/11/02/ PY - 1988 DA - 1988 Nov 02 SP - 1383 EP - 1386 VL - 80 IS - 17 SN - 0027-8874, 0027-8874 KW - Polychlorinated Dibenzodioxins KW - 0 KW - Receptors, Aryl Hydrocarbon KW - Receptors, Drug KW - Xenobiotics KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - 2-Acetylaminofluorene KW - 9M98QLJ2DL KW - Index Medicus KW - Rats KW - Animals KW - 2-Acetylaminofluorene -- pharmacology KW - Multigene Family KW - Polychlorinated Dibenzodioxins -- pharmacology KW - Liver -- metabolism KW - Mice KW - Receptors, Drug -- physiology KW - Drug Resistance -- genetics KW - Cytochrome P-450 Enzyme System -- genetics KW - Xenobiotics -- pharmacology KW - Gene Expression Regulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78466446?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Coinduction+of+MDR-1+multidrug-resistance+and+cytochrome+P-450+genes+in+rat+liver+by+xenobiotics.&rft.au=Burt%2C+R+K%3BThorgeirsson%2C+S+S&rft.aulast=Burt&rft.aufirst=R&rft.date=1988-11-02&rft.volume=80&rft.issue=17&rft.spage=1383&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 - 1988-11-18 N1 - Date created - 1988-11-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cunninghamella bertholletiae infection associated with deferoxamine therapy. AN - 78596245; 3060947 AB - Cunninghamella bertholletiae, an uncommon cause of human infection, has been reported with increasing frequency in recent years. C. bertholletiae belongs to the order Mucorales and produces infections similar to those produced by the other agents of mucormycosis. Infections with this group of organisms have typically been seen either in patients with diabetes mellitus or in those receiving chemotherapy. Recent reports of mucormycosis in dialysis patients receiving deferoxamine for iron or aluminum overload have raised the possibility that deferoxamine therapy is a risk factor for mucormycosis. A case of C. bertholletiae infection in a patient receiving deferoxamine for iron overload unrelated to hemodialysis was investigated in detail, and possible explanations for this patient's infection were assessed. JF - Reviews of infectious diseases AU - Rex, J H AU - Ginsberg, A M AU - Fries, L F AU - Pass, H I AU - Kwon-Chung, K J AD - Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. PY - 1988 SP - 1187 EP - 1194 VL - 10 IS - 6 SN - 0162-0886, 0162-0886 KW - Iron KW - E1UOL152H7 KW - Deferoxamine KW - J06Y7MXW4D KW - Index Medicus KW - Mucorales KW - Risk Factors KW - Humans KW - Middle Aged KW - Iron -- metabolism KW - Female KW - Deferoxamine -- adverse effects KW - Lung Diseases, Fungal -- etiology KW - Mucormycosis -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78596245?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+infectious+diseases&rft.atitle=Cunninghamella+bertholletiae+infection+associated+with+deferoxamine+therapy.&rft.au=Rex%2C+J+H%3BGinsberg%2C+A+M%3BFries%2C+L+F%3BPass%2C+H+I%3BKwon-Chung%2C+K+J&rft.aulast=Rex&rft.aufirst=J&rft.date=1988-11-01&rft.volume=10&rft.issue=6&rft.spage=1187&rft.isbn=&rft.btitle=&rft.title=Reviews+of+infectious+diseases&rft.issn=01620886&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-02 N1 - Date created - 1989-02-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - MPTP and MPTP analogs induced cell death in cultured rat hepatocytes involving the formation of pyridinium metabolites. AN - 78551743; 3143167 AB - MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) which has been shown to produce a Parkinson-like syndrome in humans and monkeys also causes cell death in cultures of rat hepatocytes. Treatment of cells with MPTP or its metabolite MPP+ (1-methyl-4-phenyl pyridinium ion), resulted in leakage of lactic acid dehydrogenase and 14C-labeled adenine nucleotides, as well as marked depletion of ATP and glutathione. Deprenyl, a specific inhibitor of monoamine oxidase-B, the enzyme catalyzing the oxidation of MPTP into MPP+, blocked the lethal effect of MPTP, but gave no protection from MPP+-induced cell death. The 4'-fluoro and 4'-chloro analogs of MPTP evoked toxicities similar to that of the parent compound, while N-butyl-PTP, 4'-amino-MPTP, and 2'-methyl-MPTP were relatively less toxic. N-Acetylamino-MPTP was found virtually nontoxic. The cell death produced by these analogs was also associated with leakage of [14C]adenine nucleotides, which is an indicator of loss of ATP from cells. All these compounds except the N-acetylamino analog were converted to corresponding pyridinium metabolites by liver cells when analyzed by high-pressure liquid chromatography and plasma desorption mass spectrometry. MPTP and its analogs also served as substrates for rat liver mitochondrial monoamine oxidase to varying degrees. Toxicity of various analogs, with the noticeable exception of 2'-methyl-MPTP, was inhibited by deprenyl. These findings indicate that the conversion of MPTP and its analogs to corresponding pyridinium metabolites is essential for the expression of toxicity. JF - Toxicology and applied pharmacology AU - Singh, Y AU - Swanson, E AU - Sokoloski, E AU - Kutty, R K AU - Krishna, G AD - Section on Drug Tissue Interaction, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 347 EP - 359 VL - 96 IS - 2 SN - 0041-008X, 0041-008X KW - Pyridines KW - 0 KW - Pyridinium Compounds KW - Selegiline KW - 2K1V7GP655 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Glutathione KW - GAN16C9B8O KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Selegiline -- pharmacology KW - Cell Survival -- drug effects KW - Glutathione -- metabolism KW - Adenosine Triphosphate -- metabolism KW - Male KW - Pyridinium Compounds -- metabolism KW - Liver -- drug effects KW - Pyridines -- toxicity KW - Liver -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78551743?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=MPTP+and+MPTP+analogs+induced+cell+death+in+cultured+rat+hepatocytes+involving+the+formation+of+pyridinium+metabolites.&rft.au=Singh%2C+Y%3BSwanson%2C+E%3BSokoloski%2C+E%3BKutty%2C+R+K%3BKrishna%2C+G&rft.aulast=Singh&rft.aufirst=Y&rft.date=1988-11-01&rft.volume=96&rft.issue=2&rft.spage=347&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 - 1989-01-09 N1 - Date created - 1989-01-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dexamethasone accelerates differentiation of A6 epithelia and increases response to vasopressin. AN - 78534709; 3189533 AB - When seeded heavily on a porous tissue culture dish, A6 cells, derived from the kidney of Xenopus laevis, form a highly differentiated epithelium within 4-6 days. When dexamethasone is added to the culture medium, morphological differentiation is completed by day 2, a time at which the control (untreated) is still a disorganized multilayer of cells. In addition to the morphologically evident monolayer of cuboidal cells, the accelerated differentiation is expressed as high transepithelial electrical resistance, short-circuit current, and adenylate cyclase response to vasopressin. When grown on impermeable plastic tissue culture dishes, A6 epithelia are less differentiated and do not respond to vasopressin. With the addition of dexamethasone at the time of seeding on a plastic tissue culture dish, vasopressin responsive adenylate cyclase activity is expressed, albeit at a slower rate than when grown on a porous surface. In addition, dexamethasone treatment of mature epithelia grown on a porous surface results, in hours, in an increase in the adenylate cyclase response to vasopressin. These results reveal two previously unrecognized interactions between adrenal steroid hormones and vasopressin, namely, accelerated differentiation and increased responsiveness of adenylate cyclase. JF - The American journal of physiology AU - Preston, A S AU - Muller, J AU - Handler, J S AD - Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - C661 EP - C666 VL - 255 IS - 5 Pt 1 SN - 0002-9513, 0002-9513 KW - Vasopressins KW - 11000-17-2 KW - Dexamethasone KW - 7S5I7G3JQL KW - Index Medicus KW - Stimulation, Chemical KW - Xenopus laevis KW - Animals KW - Epithelial Cells KW - In Vitro Techniques KW - Drug Synergism KW - Epithelium -- drug effects KW - Cell Line KW - Dexamethasone -- pharmacology KW - Kidney -- drug effects KW - Kidney -- cytology KW - Vasopressins -- pharmacology KW - Cell Differentiation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78534709?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dexamethasone+accelerates+differentiation+of+A6+epithelia+and+increases+response+to+vasopressin.&rft.au=Preston%2C+A+S%3BMuller%2C+J%3BHandler%2C+J+S&rft.aulast=Preston&rft.aufirst=A&rft.date=1988-11-01&rft.volume=255&rft.issue=5+Pt+1&rft.spage=C661&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 - 1988-12-09 N1 - Date created - 1988-12-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Applications of fast atom bombardment and tandem mass spectrometry. AN - 78724896; 3242706 AB - The application of fast atom bombardment combined with tandem mass spectrometry to the structure elucidation of carcinogen-modified oligonucleotides, glutathione, cysteine and N-acetyl cysteine conjugates of exogenous toxins and chemically modified peptides is described. JF - Biomedical & environmental mass spectrometry AU - Tomer, K B AU - Guenat, C AU - Dino, J J AU - Deterding, L J AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 473 EP - 476 VL - 16 IS - 1-12 SN - 0887-6134, 0887-6134 KW - Carcinogens KW - 0 KW - Oligonucleotides KW - Peptides KW - Toxins, Biological KW - Glutathione KW - GAN16C9B8O KW - Cysteine KW - K848JZ4886 KW - Acetylcysteine KW - WYQ7N0BPYC KW - Index Medicus KW - Oligonucleotides -- analysis KW - Glutathione -- analysis KW - Cysteine -- analysis KW - Acetylcysteine -- analysis KW - Peptides -- analysis KW - Carcinogens -- analysis KW - Toxins, Biological -- analysis KW - Mass Spectrometry -- instrumentation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78724896?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biomedical+%26+environmental+mass+spectrometry&rft.atitle=Applications+of+fast+atom+bombardment+and+tandem+mass+spectrometry.&rft.au=Tomer%2C+K+B%3BGuenat%2C+C%3BDino%2C+J+J%3BDeterding%2C+L+J&rft.aulast=Tomer&rft.aufirst=K&rft.date=1988-10-01&rft.volume=16&rft.issue=1-12&rft.spage=473&rft.isbn=&rft.btitle=&rft.title=Biomedical+%26+environmental+mass+spectrometry&rft.issn=08876134&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-26 N1 - Date created - 1989-05-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genetic tools in the study of drug self-administration. AN - 78671578; 3067599 AB - Recent studies have shown that large genetic differences exist in the extent to which orally delivered ethanol will come to serve as a positive reinforcer under operantly defined conditions. In addition, these studies suggest that a significant correlation exists between results from two-bottle choice studies of ethanol drinking and operant self-administration studies of ethanol functioning as a reinforcer. The present paper reports further genetic influences on ethanol self-administration which were found using Long Sleep and Short Sleep mice, bred selectively for high and low duration of loss of the righting reflex in responses to ethanol, respectively. It was possible to establish ethanol as a reinforcer in Long Sleep mice but not in Short Sleep mice. These results indicate that neurosensitivity to ethanol may determine the absolute amount of ethanol consumption but is not highly related to the ability of ethanol to serve as a positive reinforcer. In addition, this paper presents genetic correlations which indicate that (a) ethanol preference and self-administration are highly correlated across genotype; (b) sensitivity to ethanol and self-administration of this drug are not highly genetically correlated; (c) ethanol is not self-administered in operant studies solely for its caloric value; and (d) there exist important genetic determinants of drug reinforced behavior. JF - Alcoholism, clinical and experimental research AU - George, F R AD - Behavior Genetics Laboratory, National Institute on Drug Abuse, Addiction Research Center, Baltimore, Maryland 21224. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 586 EP - 590 VL - 12 IS - 5 SN - 0145-6008, 0145-6008 KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Reinforcement Schedule KW - Reflex -- drug effects KW - Motor Skills -- drug effects KW - Ethanol -- administration & dosage KW - Conditioning, Operant KW - Mice KW - Sleep Stages -- drug effects KW - Postural Balance -- drug effects KW - Alcohol Drinking -- psychology KW - Alcoholism -- genetics KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78671578?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Genetic+tools+in+the+study+of+drug+self-administration.&rft.au=George%2C+F+R&rft.aulast=George&rft.aufirst=F&rft.date=1988-10-01&rft.volume=12&rft.issue=5&rft.spage=586&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 - 1989-03-31 N1 - Date created - 1989-03-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antihypertensive therapy with ketanserin: metabolic and hemodynamic effects. AN - 78667362; 2465437 AB - Ketanserin, a serotonin-2-receptor antagonist, was administered to 12 subjects with mild to moderate hypertension in a randomized, double-blind, placebo-controlled crossover trial. After 6 weeks of ketanserin (40 mg every 12 h), blood pressures measured 12 h after dosing were not significantly different from those obtained during the placebo period. However, 2 h after ketanserin administration, supine systolic and diastolic blood pressures declined 11 +/- 10 mm Hg (p less than 0.01) and 6 +/- 5 mm Hg (p less than 0.005) from predose values, whereas placebo caused no change in either systolic or diastolic blood pressure. At the time of peak antihypertensive activity, plasma renin activity, aldosterone, growth hormone, and prolactin levels were unchanged. Prolactin levels decreased slightly (4.1 +/- 3.0 vs. 3.7 +/- 2.9 ng/ml, p less than 0.05) during ketanserin therapy when measured 12 h after dosing. Other pituitary hormones, serum testosterone, plasma catecholamines, and plasma lipids showed no changes. Heart rate was also unchanged. Stroke volume, measured 2 h after dosing, increased (70 +/- 22 vs. 85 +/- 31 ml, p less than 0.05) with ketanserin therapy, but cardiac output did not change significantly. Ketanserin has a moderate antihypertensive effect and neutral metabolic-hormonal profile when used as monotherapy for the treatment of hypertension. However, further studies are needed to define the frequency of dosing that will provide 24-h antihypertensive activity. JF - Journal of cardiovascular pharmacology AU - Levinson, P D AU - Zimlichman, R AU - Goldstein, D S AU - Keiser, H R AD - Hypertension-Endocrine Branch, National Heart, Lung, and Blood Institute, Bethesda, Maryland. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 384 EP - 389 VL - 12 IS - 4 SN - 0160-2446, 0160-2446 KW - Hormones KW - 0 KW - Ketanserin KW - 97F9DE4CT4 KW - Index Medicus KW - Heart Rate -- drug effects KW - Double-Blind Method KW - Random Allocation KW - Humans KW - Adult KW - Hormones -- blood KW - Clinical Trials as Topic KW - Middle Aged KW - Blood Pressure -- drug effects KW - Hemodynamics -- drug effects KW - Ketanserin -- therapeutic use KW - Hypertension -- physiopathology KW - Ketanserin -- adverse effects KW - Hypertension -- metabolism KW - Hypertension -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78667362?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+cardiovascular+pharmacology&rft.atitle=Antihypertensive+therapy+with+ketanserin%3A+metabolic+and+hemodynamic+effects.&rft.au=Levinson%2C+P+D%3BZimlichman%2C+R%3BGoldstein%2C+D+S%3BKeiser%2C+H+R&rft.aulast=Levinson&rft.aufirst=P&rft.date=1988-10-01&rft.volume=12&rft.issue=4&rft.spage=384&rft.isbn=&rft.btitle=&rft.title=Journal+of+cardiovascular+pharmacology&rft.issn=01602446&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-05 N1 - Date created - 1989-04-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of changes in serum androgen binding protein with germinal epithelial damage and infertility induced by di-n-pentyl phthalate. AN - 78650693; 3220221 AB - Androgen binding protein (ABP), produced by Sertoli cells and released into seminiferous tubules and blood, was measured in the serum of di-n-pentyl phthalate (DPP)-treated rats as a potential index of germinal epithelial damage. A single oral dose of DPP (0, 0.25, 1.0, or 2.0 g/kg body wt in corn oil) was given to four groups of 110 Fischer 344 rats; 10 rats per group were killed weekly for 10 weeks. Effects of treatment on serum ABP were then compared with effects on other reproductive endpoints. Treatment did not produce any significant effect on body weight or weights of liver, kidney, prostate, and seminal vesicles. In high-dose rats, serum ABP values more than doubled 2 days after injection, remained significantly elevated for 3 weeks, then fell and remained significantly below control values from Week 4 through Week 10. Accordingly, 95% of the rats in this group showed greater than 50% of the seminiferous tubules degenerated, decreased epididymal sperm density, reduced testicular and epididymal weights, and up to 97% morphologically abnormal sperm. In medium-dose rats, serum ABP increased up to 48% during the first week, returned to control values by Week 2, and remained at control levels thereafter. Of these rats, 20% showed 20-50% degenerated tubules, decreased sperm density, reduced testicular and epididymal weights (which were not always statistically significant), and up to 23% abnormal sperm morphology. In low-dose rats, serum ABP levels were similar to those of controls, and the other parameters, except sperm density, also remained unchanged. To examine the effects of DPP on fertility, a second group of rats was exposed in an identical manner [gavaged once with DPP in corn oil (0, 0.25, 1.0, and 2.0 g/kg body wt)], then mated to untreated females at 3, 6, and 10 weeks postexposure. DPP at 2 (but not 1.0 or 0.25) g/kg caused a significant reduction in pregnancies and live pups and a significant increase in preimplantation loss. Histopathology of the testis in the first experiment suggested a very slow recovery. Therefore, controls and high-dose rats in the mating trial were killed 14, 18, and 30 weeks after dosing and the germinal epithelium was evaluated histologically. All high-dose animals showed testicular lesions typical of phthalate ester exposure and the epithelium did not recover within 30 weeks.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Lindström, P AU - Harris, M AU - Ross, M AU - Lamb, J C AU - Chapin, R E AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 528 EP - 539 VL - 11 IS - 3 SN - 0272-0590, 0272-0590 KW - Androgen-Binding Protein KW - 0 KW - Phthalic Acids KW - di-n-pentyl phthalate KW - 131-18-0 KW - Index Medicus KW - Sexual Behavior, Animal -- drug effects KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Testis -- drug effects KW - Epithelial Cells KW - Spermatozoa -- drug effects KW - Body Weight -- drug effects KW - Time Factors KW - Male KW - Female KW - Organ Size -- drug effects KW - Androgen-Binding Protein -- blood KW - Phthalic Acids -- toxicity KW - Infertility, Female -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78650693?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparison+of+changes+in+serum+androgen+binding+protein+with+germinal+epithelial+damage+and+infertility+induced+by+di-n-pentyl+phthalate.&rft.au=Lindstr%C3%B6m%2C+P%3BHarris%2C+M%3BRoss%2C+M%3BLamb%2C+J+C%3BChapin%2C+R+E&rft.aulast=Lindstr%C3%B6m&rft.aufirst=P&rft.date=1988-10-01&rft.volume=11&rft.issue=3&rft.spage=528&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 - 1989-03-22 N1 - Date created - 1989-03-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Subchronic toxicity of orally administered (gavage and dosed-feed) theophylline in Fischer 344 rats and B6C3F1 mice. AN - 78643732; 3220218 AB - Theophylline, a methylated xanthine closely resembling caffeine and theobromine, is a widely used pharmaceutical agent for the treatment of respiratory disorders and certain acute cardiovascular conditions. The National Toxicology Program has conducted 13-week subchronic toxicity studies in F344 rats and B6C3F1 mice (10 animals/group) following administration of theophylline via the diet or by gavage. Administration of theophylline in the feed (0, 1000, 2000, and 4000 ppm) resulted in no mortality or body weight effects in F344 rats, but did induce periarteritis of the arteries adjacent to mesenteric lymph nodes and the pancreas, particularly arterioles in the latter. Also observed in rats dosed with theophylline via the diet was an increased severity of chronic nephropathy in males, especially at the high dose. Administration of theophylline at the same concentrations in the feed to B6C3F1 mice resulted in no mortality, but terminal body weights were significantly decreased in all dosed groups. An increased incidence of hepatocellular glycogen depletion was observed in male and female mice, and this change is believed to represent a physiological alteration exacerbated by the administration of theophylline. Administration of theophylline by gavage to F344 rats (0, 37.5, 75, and 150 mg/kg) resulted in the early death of one high-dose male and female and significantly decreased or increased terminal body weights of high-dose males and females, respectively. Similar to the results of the dosed-feed study, male and female rats receiving theophylline by gavage demonstrated a dose-related increase in the incidence and severity of perivascular inflammation of mesenteric arteries. Gavage administration of theophylline to B6C3F1 mice (0, 75, 150, and 300 mg/kg) resulted in the early death of all high-dose females and 3/10 high-dose males and significant depression of terminal body weights in high- and mid-dose males and low-dose females. As in the dosed-feed study, the primary histopathologic change in the mouse subchronic gavage study was hepatocellular glycogen depletion, although in this case it was seen only in females. In summary, the major target organs for orally administered theophylline in 13-week subchronic toxicity studies appear to be the mesenteric arteries in F344 rats and the liver in B6C3F1 mice. On the basis of organ weight changes and/or minor histopathologic effects, many other tissues were also affected, particularly the kidneys in dosed-feed male rats and the uterus in gavage-dosed female rats. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Collins, J J AU - Elwell, M R AU - Lamb, J C AU - Manus, A G AU - Heath, J E AU - Makovec, G T AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 472 EP - 484 VL - 11 IS - 3 SN - 0272-0590, 0272-0590 KW - Theophylline KW - C137DTR5RG KW - Index Medicus KW - Rats KW - Pancreas -- pathology KW - Eating -- drug effects KW - Administration, Oral KW - Mice, Inbred Strains KW - Animals KW - Rats, Inbred F344 KW - Kidney -- pathology KW - Body Weight -- drug effects KW - Mice KW - Mesenteric Arteries -- pathology KW - Species Specificity KW - Male KW - Female KW - Theophylline -- toxicity KW - Theophylline -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78643732?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+toxicity+of+orally+administered+%28gavage+and+dosed-feed%29+theophylline+in+Fischer+344+rats+and+B6C3F1+mice.&rft.au=Collins%2C+J+J%3BElwell%2C+M+R%3BLamb%2C+J+C%3BManus%2C+A+G%3BHeath%2C+J+E%3BMakovec%2C+G+T&rft.aulast=Collins&rft.aufirst=J&rft.date=1988-10-01&rft.volume=11&rft.issue=3&rft.spage=472&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 - 1989-03-22 N1 - Date created - 1989-03-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Quantification of quinolinic acid in rat brain, whole blood, and plasma by gas chromatography and negative chemical ionization mass spectrometry: effects of systemic L-tryptophan administration on brain and blood quinolinic acid concentrations. AN - 78639644; 2975477 AB - A gas chromatography/mass spectrometry assay is described to quantify the endogenous neurotoxin quinolinic acid (QUIN) in brain, whole blood, and plasma. High specificity and high sensitivity were obtained by using negative chemical ionization and accuracy was achieved by using [18O]QUIN as internal standard. Neutralized perchloric acid extracts were washed with chloroform, applied to Dowex 1 x 8 (formate form), and eluted with 6 M formic acid. After lyophilization, QUIN and [18O]QUIN were esterified with hexafluoroisopropanol (to mass 467 and 471, respectively) using trifluoroacetylimidazole as catalyst. The esters were extracted into heptane and injected onto a gas chromatograph, DB-5 capillary column. QUIN and [18O]QUIN were quantified by selected ion monitoring of QUIN-specific anion currents from the molecular anions (m/z 467 and 471, respectively) and a specific anion fragment (m/z 316 from QUIN and m/z 320 from [18O]QUIN). Minimum sensitivity was 3 fmol, intraassay variability was 3.2%, and interassay variability was 8.1% QUIN concentrations in frontal cortex from over 200 rats ranged from 20 to 180 fmol/mg wet wt. Two hours after systemic L-tryptophan (L-Trp; 0.370 mmol/kg) administration, QUIN increased in whole blood 134.8-fold and in plasma, 74.3-fold. In frontal cortex, increases in QUIN (22.6-fold, corrected for QUIN in blood) exceeded increases in cortical L-Trp (2.54-fold), 5-HT (1.35-fold), and 5-HIAA (1.74-fold). These studies demonstrate that QUIN is present in brain and is sensitive to the availability of systemic L-Trp. JF - Analytical biochemistry AU - Heyes, M P AU - Markey, S P AD - Laboratory of Neurophysiology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 349 EP - 359 VL - 174 IS - 1 SN - 0003-2697, 0003-2697 KW - Pyridines KW - 0 KW - Quinolinic Acids KW - Tryptophan KW - 8DUH1N11BX KW - Quinolinic Acid KW - F6F0HK1URN KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Tryptophan -- pharmacology KW - Reference Values KW - Brain -- drug effects KW - Reference Standards KW - Brain -- metabolism KW - Male KW - Quinolinic Acids -- blood KW - Pyridines -- analysis KW - Gas Chromatography-Mass Spectrometry -- methods KW - Brain Chemistry KW - Quinolinic Acids -- analysis KW - Quinolinic Acids -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78639644?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Quantification+of+quinolinic+acid+in+rat+brain%2C+whole+blood%2C+and+plasma+by+gas+chromatography+and+negative+chemical+ionization+mass+spectrometry%3A+effects+of+systemic+L-tryptophan+administration+on+brain+and+blood+quinolinic+acid+concentrations.&rft.au=Heyes%2C+M+P%3BMarkey%2C+S+P&rft.aulast=Heyes&rft.aufirst=M&rft.date=1988-10-01&rft.volume=174&rft.issue=1&rft.spage=349&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 - 1989-03-08 N1 - Date created - 1989-03-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of T-cell associated antigens by porcine natural killer cells. AN - 78538508; 3263943 AB - We have examined the cell surface phenotype of porcine natural killer (NK) cells and compared them with classic porcine cytotoxic T lymphocytes (CTL). NK cells were susceptible to treatment with monoclonal antibodies to CD2 (PT11), CD8 (PT8) and Ia plus complement (C), as well as with antiserum to asialo-GM1 (ASGM1) plus C. In addition, monoclonal antibodies to leucocyte function antigen 1 (LFA-1) but not to CD8 blocked NK-mediated lysis in the absence of C. This is in contrast to porcine CTL, which were eliminated by antibodies to CD2, CD8 and Ia plus C, but not by anti-ASGMI plus C, and which were blocked by anti-CD8 in the absence of C. Therefore, although porcine NK cells are similar to porcine CTL, they are distinguished by several important differences. JF - Immunology AU - Pescovitz, M D AU - Lowman, M A AU - Sachs, D H AD - Transplantation Biology Section, National Cancer Institute, Bethesda, Maryland. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 267 EP - 271 VL - 65 IS - 2 SN - 0019-2805, 0019-2805 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Differentiation, T-Lymphocyte KW - Complement System Proteins KW - 9007-36-7 KW - Index Medicus KW - Swine KW - Animals KW - Cytotoxicity Tests, Immunologic KW - T-Lymphocytes, Cytotoxic -- immunology KW - Complement System Proteins -- immunology KW - Antibodies, Monoclonal -- immunology KW - Antigens, Differentiation, T-Lymphocyte -- analysis KW - Killer Cells, Natural -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78538508?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Immunology&rft.atitle=Expression+of+T-cell+associated+antigens+by+porcine+natural+killer+cells.&rft.au=Pescovitz%2C+M+D%3BLowman%2C+M+A%3BSachs%2C+D+H&rft.aulast=Pescovitz&rft.aufirst=M&rft.date=1988-10-01&rft.volume=65&rft.issue=2&rft.spage=267&rft.isbn=&rft.btitle=&rft.title=Immunology&rft.issn=00192805&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-06 N1 - Date created - 1989-01-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Exp Med. 1974 Dec 1;140(6):1534-46 [4139231] Vet Immunol Immunopathol. 1986 Feb;11(2):107-21 [3962168] Proc Natl Acad Sci U S A. 1978 Oct;75(10):5127-31 [154104] J Exp Med. 1979 Sep 19;150(3):471-81 [479761] J Immunol. 1980 Jan;124(1):199-201 [6985637] J Immunol. 1980 Feb;124(2):533-40 [7188699] J Immunol. 1980 Aug;125(2):755-62 [6446578] J Immunol. 1981 Jan;126(1):359-64 [7451976] J Immunol. 1981 Dec;127(6):2401-9 [6975321] J Immunol. 1981 Dec;127(6):2575-80 [7299137] J Exp Med. 1982 May 1;155(5):1579-84 [6978378] Transplantation. 1983 Apr;35(4):394-400 [6404028] J Immunol. 1983 Jun;130(6):2786-93 [6406596] J Immunol. 1983 Jul;131(1):223-31 [6408172] J Immunol. 1983 Aug;131(2):1024-7 [6863925] J Immunol. 1984 May;132(5):2183-4 [6609190] J Immunol. 1984 Jul;133(1):368-75 [6609988] J Immunol. 1985 Jan;134(1):37-44 [3871107] Res Vet Sci. 1984 Sep;37(2):211-8 [6095387] J Exp Med. 1985 Mar 1;161(3):563-76 [2579185] J Immunol. 1985 May;134(5):3272-80 [2580022] J Immunol. 1986 Mar 1;136(5):1586-91 [2936802] Transplantation. 1976 Dec;22(6):559-67 [137560] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of CD 4-, CD 8- thymocytes with IL 4 vs IL 1 + IL 2. AN - 78464775; 3262653 AB - Thymocytes from C57BL/6 mice were highly purified to obtain the CD 4-, CD 8- subpopulation which constitutes only 5% of all thymocytes. Substantial proliferation was induced in vitro with either IL-1 + IL-2 or with IL-4 in the presence of PMA. IL-1 and IL-2 synergized in inducing proliferation of these purified CD 4-, CD 8- thymocytes whereas neither synergized with IL-4. In order to determine whether stimulation with IL-1 + IL-2 acted via IL-4 or vice versa, cultures were treated reciprocally with affinity-purified anti-IL-2 or anti-IL-4 antibodies. Cultures with IL-4 were inhibited by anti-IL-4 but were unaffected by anti-IL-2. The CD 4-, CD 8- thymocytes cultured with IL-1 + IL-2 + anti-IL-2 were inhibited to baseline IL-1 stimulation. At low concentrations of IL-1 (1 U/ml) and IL-2 (100 U/ml), anti-IL-4 had no effect, whereas at higher levels of IL-1 (2 U/ml IL-1), and 100 or 200 U/ml IL-2, anti-IL-4 significantly reduced DNA synthesis. This result suggests that at higher concentrations the combination of IL-1 + IL-2 can induce cells to produce IL-4 which then contributes to overall proliferation. When CD 4-, CD 8- thymocytes were cultured with the low doses of IL-1 + IL-2 for 72 h, 62% expressed cell surface T3 complex (vs 11% at initiation) and 27% were F23.1+ (vs 5% at initiation). In contrast, culture with IL-4 led to no increase in numbers of T3+ cells and none were F23.1+; however, there was coexpression of Thy1 and 6B2 on 20% of cells at the end of culture (vs 4% at initiation). Thus, IL-1 + IL-2 causes expansion of a CD 4-, CD 8- thymocyte population expressing the alpha, beta-T cell receptor, whereas IL-4 induces cells to express a phenotype present in small numbers in the periphery of normal mice and in larger numbers in mice bearing the lpr gene. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Gause, W C AU - Takashi, T AU - Mountz, J D AU - Finkelman, F D AU - Steinberg, A D AD - Cellular Immunology Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, MD 20892. Y1 - 1988/10/01/ PY - 1988 DA - 1988 Oct 01 SP - 2240 EP - 2245 VL - 141 IS - 7 SN - 0022-1767, 0022-1767 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Differentiation, T-Lymphocyte KW - Drug Combinations KW - Interleukin-1 KW - Interleukin-2 KW - Interleukins KW - Interleukin-4 KW - 207137-56-2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Interleukin-2 -- pharmacology KW - Interleukin-1 -- pharmacology KW - Mice KW - Phenotype KW - Mice, Inbred C57BL KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Interleukin-2 -- immunology KW - Drug Synergism KW - Female KW - T-Lymphocytes -- classification KW - Lymphocyte Activation -- drug effects KW - Interleukins -- pharmacology KW - Interleukins -- immunology KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78464775?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Activation+of+CD+4-%2C+CD+8-+thymocytes+with+IL+4+vs+IL+1+%2B+IL+2.&rft.au=Gause%2C+W+C%3BTakashi%2C+T%3BMountz%2C+J+D%3BFinkelman%2C+F+D%3BSteinberg%2C+A+D&rft.aulast=Gause&rft.aufirst=W&rft.date=1988-10-01&rft.volume=141&rft.issue=7&rft.spage=2240&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 - 1988-11-03 N1 - Date created - 1988-11-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cell-mediated immune response toward viral envelope and core antigens in gibbon apes (Hylobates lar) chronically infected with human immunodeficiency virus-1. AN - 78458673; 3262661 AB - The specific cellular immune response toward envelope and core proteins of human immunodeficiency virus-1 (HIV-1) was investigated in gibbon apes chronically infected with the HTLV-IIIB isolate. After in vitro stimulation of PBMC from infected and control animals with HIV-1 Ag, DNA synthesis, IL-2R expression and IL-2 release were assayed. Cells from infected gibbon apes demonstrated a group-specific response toward whole virus preparations from three divergent HIV-1 isolates (HTLV-IIIB, HTLV-IIIRF, HTLV-IIIMN). Consistent responses were also detected against purified HIV-1 Ag, i.e., native gp120 envelope glycoprotein, recombinant gp160 glycoprotein, a synthetic peptide (peptide 7) representing a highly conserved region of gp120, and purified native core protein p24. In addition, lymphocytes from infected gibbon apes displayed a specific, MHC-restricted, cytotoxic activity against autologous cells expressing HIV-1 envelope or gag proteins. The specific T cell reactivity toward HIV-1 proteins observed in infected gibbons contrasts with findings in HIV-1 infected humans, and may help to explain the apparent discrepancy in the natural history of the infection between the two species. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Lusso, P AU - Markham, P D AU - Ranki, A AU - Earl, P AU - Moss, B AU - Dorner, F AU - Gallo, R C AU - Krohn, K J AD - Laboratory of Tumor Cell Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/10/01/ PY - 1988 DA - 1988 Oct 01 SP - 2467 EP - 2473 VL - 141 IS - 7 SN - 0022-1767, 0022-1767 KW - HIV Antigens KW - 0 KW - Interleukin-2 KW - Receptors, Interleukin-2 KW - Viral Core Proteins KW - Viral Envelope Proteins KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Animals KW - T-Lymphocytes -- metabolism KW - Interleukin-2 -- metabolism KW - Receptors, Interleukin-2 -- analysis KW - Hylobates KW - Humans KW - Cytotoxicity Tests, Immunologic KW - T-Lymphocytes, Cytotoxic -- immunology KW - Chronic Disease KW - T-Lymphocytes -- immunology KW - Lymphocyte Activation KW - Viral Envelope Proteins -- immunology KW - HIV Antigens -- isolation & purification KW - Viral Core Proteins -- immunology KW - Acquired Immunodeficiency Syndrome -- immunology KW - Viral Envelope Proteins -- isolation & purification KW - Viral Core Proteins -- isolation & purification KW - HIV Antigens -- immunology KW - Acquired Immunodeficiency Syndrome -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78458673?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cell-mediated+immune+response+toward+viral+envelope+and+core+antigens+in+gibbon+apes+%28Hylobates+lar%29+chronically+infected+with+human+immunodeficiency+virus-1.&rft.au=Lusso%2C+P%3BMarkham%2C+P+D%3BRanki%2C+A%3BEarl%2C+P%3BMoss%2C+B%3BDorner%2C+F%3BGallo%2C+R+C%3BKrohn%2C+K+J&rft.aulast=Lusso&rft.aufirst=P&rft.date=1988-10-01&rft.volume=141&rft.issue=7&rft.spage=2467&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 - 1988-11-03 N1 - Date created - 1988-11-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The measurement of cisplatin-DNA adduct levels in testicular cancer patients. AN - 78453567; 2458857 AB - Seventeen patients with 'poor prognosis' non-seminomatous testicular cancer were monitored for formation of intrastrand bidentate N7-d(ApG)- and N7-d(GpG)-diammineplatinum adducts in peripheral blood cell DNA during the course of cisplatin-based chemotherapy. Adduct values from blood cell DNA samples were compared with disease response data from the same individuals. Patients who received a dose of 40 mg/m2 cisplatin for 5 days generally formed more adducts than patients receiving 20 mg/m2 for 5 days, and adduct levels ranged from 0 to approximately 300 amol/micrograms DNA. Among the individuals who achieved a complete response, the median adduct level was 170 amol/micrograms DNA and the mean was 162. Among the individuals who achieved a partial response, the median adduct level was 78 amol/micrograms DNA and the mean was 83. Comparison of adduct levels between response groups using the Mann-Whitney test gave a two-sided P value of 0.072 (one-sided P value 0.036). Of 11 patients forming high levels of adduct (greater than 140 amol/micrograms DNA), 10 achieved a complete response; this compares with two complete responders in the group of six patients forming low levels (less than 100 amol/micrograms DNA) of adduct (P = 0.055, two-sided Fisher exact test). We conclude that cisplatin-DNA adduct formation in peripheral blood cell DNA correlates with the occurrence of complete response in patients with poor prognosis testicular cancer. JF - Carcinogenesis AU - Reed, E AU - Ozols, R F AU - Tarone, R AU - Yuspa, S H AU - Poirier, M C AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 1909 EP - 1911 VL - 9 IS - 10 SN - 0143-3334, 0143-3334 KW - Biomarkers, Tumor KW - 0 KW - DNA Adducts KW - DNA, Neoplasm KW - cisplatin-DNA adduct KW - Bleomycin KW - 11056-06-7 KW - Vinblastine KW - 5V9KLZ54CY KW - Etoposide KW - 6PLQ3CP4P3 KW - DNA KW - 9007-49-2 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Etoposide -- administration & dosage KW - Bleomycin -- administration & dosage KW - Humans KW - Vinblastine -- administration & dosage KW - Prognosis KW - Male KW - Testicular Neoplasms -- drug therapy KW - Testicular Neoplasms -- blood KW - DNA, Neoplasm -- blood KW - DNA -- blood KW - Cisplatin -- blood KW - Biomarkers, Tumor -- blood KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Cisplatin -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78453567?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+measurement+of+cisplatin-DNA+adduct+levels+in+testicular+cancer+patients.&rft.au=Reed%2C+E%3BOzols%2C+R+F%3BTarone%2C+R%3BYuspa%2C+S+H%3BPoirier%2C+M+C&rft.aulast=Reed&rft.aufirst=E&rft.date=1988-10-01&rft.volume=9&rft.issue=10&rft.spage=1909&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-11-08 N1 - Date created - 1988-11-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenesis--a synopsis of human experience with external exposure in medicine. AN - 78447707; 3049457 AB - Studies in the 1980s of medically irradiated populations have increased our knowledge of radiation carcinogenesis. (1) Investigations of prenatal x-ray exposures, especially in twins, provide evidence that very low doses of ionizing radiation may cause cancer in humans. (2) Fractionated doses appear as effective as single exposures of the same total dose in causing breast cancer, but seem less effective for lung cancer. (3) Excess breast cancers can occur among women exposed under age 10, indicating that the immature breast is susceptible to the carcinogenic action of radiation. (4) Moderate doses on the order of 1 Gy to the brains of children can cause tumors later in life; moderately high doses to the skin can cause cancer when followed by frequent exposure to ultraviolet light. (5) Radiotherapy for cervical cancer can increase the rate of subsequent leukemia with the best fitting dose-response functions including a negative exponential term to account for cell-killing. (6) Low-dose exposures of about 10 cGy may increase the risk of thyroid cancer. (7) Second cancers following radiotherapy for a variety of cancers occur primarily among long-term survivors. (8) Radiotherapy may not significantly increase the risk of leukemia following childhood cancer, whereas chemotherapy with alkylating agents is a major risk factor. (9) Bone cancer occurs after high-dose radiotherapy for childhood cancer, but children with retinoblastoma are not more susceptible to radiation-induced disease than children with other malignancies. (10) High-dose external beam therapy can cause thyroid cancer, whereas high-dose radioactive 131I may not. (11) Studies of cervical cancer patients indicate that the risk of radiation-induced second malignancies follows a time-response model consistent with a constant multiplication of the underlying background incidence, i.e. a relative risk model seems to hold for projecting risks forward in time. JF - Health physics AU - Boice, J D AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 621 EP - 630 VL - 55 IS - 4 SN - 0017-9078, 0017-9078 KW - Index Medicus KW - Humans KW - Adult KW - Clinical Trials as Topic KW - Child KW - Male KW - Female KW - Neoplasms, Radiation-Induced -- etiology KW - Radiography -- adverse effects KW - Radiotherapy -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78447707?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Carcinogenesis--a+synopsis+of+human+experience+with+external+exposure+in+medicine.&rft.au=Boice%2C+J+D&rft.aulast=Boice&rft.aufirst=J&rft.date=1988-10-01&rft.volume=55&rft.issue=4&rft.spage=621&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 - 1988-11-18 N1 - Date created - 1988-11-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of the 32P-postlabeling method to detect DNA adducts of 2-amino-3-methylimidazolo[4,5-f]quinoline (IQ) in monkeys fed IQ: identification of the N-(deoxyguanosin-8-yl)-IQ adduct. AN - 78432965; 3168152 AB - Eight DNA adducts of 2-amino-3-methylimidazolo[4,5-f]-quinoline (IQ) were found by the standard 32P-postlabeling method in livers from male Cynomolgus monkeys fed IQ (5 days/week, 3 weeks, 20 mg/kg, nasal-gastric intubation). The IQ-DNA adduct fingerprints observed in monkeys were identical to those observed in rats that received IQ (0.03%) in the diet for 2 weeks. The C8-guanine-IQ adduct was identified by comigration with the synthetic 3',5'-bisphosphate derivative of N(-deoxyguanosin-8-yl)-IQ. DNA modified in vitro with N-hydroxy-IQ showed seven adducts, including the C8-guanine-IQ adduct, that were identical to those found in monkeys and rats. Thus it appears that N-hydroxy-IQ, the reactive metabolite of IQ, was responsible for all adducts found in vivo, except one. In order to detect adducts in other organs that were present at lower levels, the intensification (ATP-deficient) method for 32P-postlabeling was used. Five of the adducts detected under standard conditions, including the C8-guanine-IQ adduct, were also detected under intensification conditions. The total level of DNA-IQ adducts was highest in the liver, followed by the kidney, colon and stomach, and bladder. The adduct patterns were identical in all organs examined. The results indicate that IQ is potentially genotoxic in primates and therefore a likely human carcinogen. JF - Carcinogenesis AU - Snyderwine, E G AU - Yamashita, K AU - Adamson, R H AU - Sato, S AU - Nagao, M AU - Sugimura, T AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 1739 EP - 1743 VL - 9 IS - 10 SN - 0143-3334, 0143-3334 KW - Mutagens KW - 0 KW - Phosphorus Radioisotopes KW - Quinolines KW - N-(deoxyguanosin-8-yl)-2-amino-3-methylimidazolo(4,5-f)quinoline KW - 115747-35-8 KW - 2-amino-3-methylimidazo(4,5-f)quinoline KW - 30GL3D3T0G KW - DNA KW - 9007-49-2 KW - Deoxyguanosine KW - G9481N71RO KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Macaca fascicularis KW - Tissue Distribution KW - Autoradiography -- methods KW - Male KW - Quinolines -- metabolism KW - Mutagens -- metabolism KW - DNA -- metabolism KW - Deoxyguanosine -- isolation & purification KW - Quinolines -- isolation & purification KW - Quinolines -- pharmacokinetics KW - Deoxyguanosine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78432965?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Use+of+the+32P-postlabeling+method+to+detect+DNA+adducts+of+2-amino-3-methylimidazolo%5B4%2C5-f%5Dquinoline+%28IQ%29+in+monkeys+fed+IQ%3A+identification+of+the+N-%28deoxyguanosin-8-yl%29-IQ+adduct.&rft.au=Snyderwine%2C+E+G%3BYamashita%2C+K%3BAdamson%2C+R+H%3BSato%2C+S%3BNagao%2C+M%3BSugimura%2C+T%3BThorgeirsson%2C+S+S&rft.aulast=Snyderwine&rft.aufirst=E&rft.date=1988-10-01&rft.volume=9&rft.issue=10&rft.spage=1739&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-11-08 N1 - Date created - 1988-11-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cellular distribution of c-myc transcripts during chemical hepatocarcinogenesis in rats. AN - 78414332; 3416306 AB - The expression of cellular myc (c-myc) was studied during early and late stages of chemical hepatocarcinogenesis in the rat using Northern blot analysis and in situ hybridization. Hepatocarcinogenesis was induced according to the resistant hepatocyte model of Solt and Farber. An uninitiated version of this model was also used to examine the expression of c-myc during proliferation and differentiation of oval cells. The expression of c-myc was increased throughout hepatocarcinogenesis starting with early preneoplastic foci and oval cells. Similar levels of c-myc transcripts were detected in oval cells and basophilic hepatocytes generated by the uninitiated version of the protocol as were found in preneoplastic foci and oval cells during hepatocarcinogenesis. Whereas c-myc expression remained elevated in late neoplastic nodules and carcinomas, it gradually declined in both "remodelling" nodules and uninitiated livers. Our data indicate that c-myc expression is elevated during the undifferentiated stages of hepatocyte development. Furthermore, the data support the hypothesis that a critical early step in chemical hepatocarcinogenesis involves a block in the normal differentiation program of the hepatocytes. JF - Cancer research AU - Nagy, P AU - Evarts, R P AU - Marsden, E AU - Roach, J AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/10/01/ PY - 1988 DA - 1988 Oct 01 SP - 5522 EP - 5527 VL - 48 IS - 19 SN - 0008-5472, 0008-5472 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Nucleic Acid Hybridization KW - Liver Neoplasms, Experimental -- genetics KW - Oncogenes KW - Liver Neoplasms, Experimental -- chemically induced KW - Transcription, Genetic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78414332?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cellular+distribution+of+c-myc+transcripts+during+chemical+hepatocarcinogenesis+in+rats.&rft.au=Nagy%2C+P%3BEvarts%2C+R+P%3BMarsden%2C+E%3BRoach%2C+J%3BThorgeirsson%2C+S+S&rft.aulast=Nagy&rft.aufirst=P&rft.date=1988-10-01&rft.volume=48&rft.issue=19&rft.spage=5522&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 - 1988-10-25 N1 - Date created - 1988-10-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Acetylcholine and coronary artery spasm: important insight or squeeze play? AN - 78412865; 3262132 JF - Journal of the American College of Cardiology AU - Cannon, R O AD - Cardiology Branch, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 889 EP - 891 VL - 12 IS - 4 SN - 0735-1097, 0735-1097 KW - Biological Products KW - 0 KW - Nitric Oxide KW - 31C4KY9ESH KW - Acetylcholine KW - N9YNS0M02X KW - Ergonovine KW - WH41D8433D KW - Abridged Index Medicus KW - Index Medicus KW - Coronary Vessels KW - Humans KW - Biological Products -- physiology KW - Injections KW - Acetylcholine -- administration & dosage KW - Coronary Vasospasm -- chemically induced KW - Angina Pectoris, Variant -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78412865?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+American+College+of+Cardiology&rft.atitle=Acetylcholine+and+coronary+artery+spasm%3A+important+insight+or+squeeze+play%3F&rft.au=Cannon%2C+R+O&rft.aulast=Cannon&rft.aufirst=R&rft.date=1988-10-01&rft.volume=12&rft.issue=4&rft.spage=889&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+College+of+Cardiology&rft.issn=07351097&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-27 N1 - Date created - 1988-10-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cancer families: human models of susceptibility to neoplasia--the Richard and Hinda Rosenthal Foundation Award lecture. AN - 78401259; 2843281 AB - Members of cancer families are at exceptionally high risk and can be studied as human models of cancer susceptibility. These patients represent rare "experiments of nature" that can reveal new insights into carcinogenic processes. We use clinical observations to identify the high risk patient, epidemiological studies to quantitate the excess risk, and laboratory investigations to examine the biological basis of susceptibility. We have uncovered a series of new family cancer syndromes that are under study for molecular mechanisms involved in the pathogenesis of cancers in general. This presentation describes our investigations of four disorders: the syndrome of sarcomas, breast cancer, and other neoplasms; inheritance of both renal cell carcinoma and a constitutional chromosome translocation in a kindred; familial Wilms' tumor; and the hepatoblastoma-adenomatous polyposis association. JF - Cancer research AU - Li, F P AD - Clinical Studies Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/10/01/ PY - 1988 DA - 1988 Oct 01 SP - 5381 EP - 5386 VL - 48 IS - 19 SN - 0008-5472, 0008-5472 KW - Index Medicus KW - Breast Neoplasms -- genetics KW - Kidney Neoplasms -- genetics KW - Pedigree KW - Adenomatous Polyposis Coli -- genetics KW - Chromosome Banding KW - Humans KW - Wilms Tumor -- genetics KW - Carcinoma, Hepatocellular -- genetics KW - Sarcoma -- genetics KW - Adenoma -- genetics KW - Carcinoma, Renal Cell -- genetics KW - Female KW - Male KW - Liver Neoplasms -- genetics KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78401259?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cancer+families%3A+human+models+of+susceptibility+to+neoplasia--the+Richard+and+Hinda+Rosenthal+Foundation+Award+lecture.&rft.au=Li%2C+F+P&rft.aulast=Li&rft.aufirst=F&rft.date=1988-10-01&rft.volume=48&rft.issue=19&rft.spage=5381&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 - 1988-10-25 N1 - Date created - 1988-10-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Disposition of 1,2,3,7,8-pentachlorodibenzofuran in the rat. AN - 78514411; 3188012 AB - 1,2,3,7,8-Pentachlorodibenzofuran (1PeCDF) is one of several toxic polychlorinated dibenzofurans (PCDFs) which are ubiquitous environmental contaminants. Related in structure and toxicity to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), PCDFs have been detected in municipal and industrial effluents, PCB mixtures, and in a variety of antiseptics and preservative solutions. The objective of this study was to evaluate the distribution and elimination of 1PeCDF in the rat and to compare these parameters with that of 2,3,4,7,8-pentachlorodibenzofuran (4PeCDF) and 2,3,7,8-tetrachlorodibenzofuran (TCDF). After iv administration of 0.1 mumol [3H]1PeCDF/kg, 1PeCDF was rapidly cleared from the blood and distributed to the liver, muscle, skin, and adipose tissue in a manner similar to that for other dibenzofurans. The initial pool sizes of 1PeCDF-derived radioactivity in the liver, muscle, skin, and adipose tissue were 43,35,10, and 7% of the administered dose, respectively. In all cases, loss of radioactivity from these tissues could be described by exponential decay and the initial half-lives for these tissues were 1.36, 0.03, 13, and 1 day, respectively. After redistribution from the muscle, skin, and adipose tissues to the liver, 1PeCDF was metabolized to a polar metabolite(s) and excreted from the body via the bile into the feces. No parent compound was detected in the bile and fecal excretion was the major route of elimination. Most of the radioactivity in the urine was excreted within the first day, after which less than 0.5% of the dose/day was detected. More than half of the administered dose was excreted in the urine and feces within 2 days. The whole-body half-life of related compounds is 4PeCDF much greater than 1PeCDF greater than or equal to TCDF. Therefore, persistence appears to be inversely related to the metabolism of these compounds and metabolism is inhibited by chlorine-substituted carbon atoms adjacent to the oxygen atom in the dibenzofuran ring. JF - Toxicology and applied pharmacology AU - Brewster, D W AU - Birnbaum, L S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/09/30/ PY - 1988 DA - 1988 Sep 30 SP - 490 EP - 498 VL - 95 IS - 3 SN - 0041-008X, 0041-008X KW - Benzofurans KW - 0 KW - Environmental Pollutants KW - 1,2,3,7,8-pentachlorodibenzofuran KW - QNE7ZLB7SS KW - 2,3,4,7,8-pentachlorodibenzofuran KW - U4C2RV3124 KW - 2,3,7,8-tetrachlorodibenzofuran KW - XZJ41GQI5D KW - Index Medicus KW - Rats KW - Feces -- analysis KW - Animals KW - Rats, Inbred F344 KW - Lethal Dose 50 KW - Bile -- metabolism KW - Tissue Distribution KW - Male KW - Structure-Activity Relationship KW - Benzofurans -- pharmacokinetics KW - Environmental Pollutants -- pharmacokinetics KW - Benzofurans -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78514411?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Disposition+of+1%2C2%2C3%2C7%2C8-pentachlorodibenzofuran+in+the+rat.&rft.au=Brewster%2C+D+W%3BBirnbaum%2C+L+S&rft.aulast=Brewster&rft.aufirst=D&rft.date=1988-09-30&rft.volume=95&rft.issue=3&rft.spage=490&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 - 1988-12-05 N1 - Date created - 1988-12-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression and amplification in transgenic mice of a polyoma virus mutant regulatory region. AN - 19624922; 8728494 AB - Two hybrid gene constructs consisting of wild-type and mutant polyoma regulatory regions fused to a bacterial reporter gene were inserted in the mouse germline. Both transgenes were expressed in a large number of different organs. However, marker gene expression controlled by the polyoma wild-type regulatory region was not detectable in the early embryo and remained low throughout the life of the animal while expression controlled by the polyoma F9-1 mutation was detectable in blastocysts and was significantly higher at later stages of development. The F9-1 hybrid gene was also amplifiable when large T-antigen was supplied in trans to mice or to kidney cells derived from these transgenic mice. Amplification resulted in the appearance of several hundred copies of episomal transgenes and a marked increase of marker gene RNA and protein. Our results suggest that the F9-1 mutation does not alter the target spectrum of gene expression in vivo but does create a more efficient enhancer element in the polyoma early control region. Transgene amplification based upon use of the polyoma regulatory elements may be a means of increasing expression of genes in transgenic mice. Images JF - Nucleic Acids Research AU - Krippl, B AU - Griep, A E AU - Mahon, K A AU - Boehnlein, E AU - Gruss, P AU - Westphal, H AD - Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1988/09/26/ PY - 1988 DA - 1988 Sep 26 SP - 8963 EP - 8976 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 16 IS - 18 SN - 0305-1048, 0305-1048 KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - Regulatory sequences KW - Transgenes KW - Developmental stages KW - Polyomavirus KW - Transgenic mice KW - Gene expression KW - Enhancers KW - blastocysts KW - RNA KW - Reporter gene KW - Hybrids KW - Kidney KW - Embryos KW - Mutation KW - J 02310:Genetics & Taxonomy KW - W 30925:Genetic Engineering KW - V 22410:Animal Diseases KW - N 14830:RNA KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19624922?accountid=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=Expression+and+amplification+in+transgenic+mice+of+a+polyoma+virus+mutant+regulatory+region.&rft.au=Krippl%2C+B%3BGriep%2C+A+E%3BMahon%2C+K+A%3BBoehnlein%2C+E%3BGruss%2C+P%3BWestphal%2C+H&rft.aulast=Krippl&rft.aufirst=B&rft.date=1988-09-26&rft.volume=16&rft.issue=18&rft.spage=8963&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 - Regulatory sequences; Transgenes; Developmental stages; Transgenic mice; Gene expression; Enhancers; blastocysts; RNA; Reporter gene; Hybrids; Kidney; Embryos; Mutation; Polyomavirus ER - TY - JOUR T1 - Cloning of the chicken chromosomal protein HMG-14 cDNA reveals a unique protein with a conserved DNA binding domain. AN - 78427530; 3417670 AB - The isolation and sequencing of a cDNA clone coding for the entire sequence of chicken chromosomal protein HMG-14 is described. The open reading frame constitutes only 25% of the transcript; the 5'-untranslated region is extremely rich in GC residues; and the 3'-untranslated region is highly enriched in AT residues. Comparison with other cDNAs coding for HMG-14 and HMG-17 reveals that the transcripts of genes coding for this family of chromosomal proteins have a characteristic structure. The deduced amino acid sequence is unique and different from all other known HMG-14 and -17 sequences. Analysis of amino acid position identity between the chicken HMG-14 and other HMG-14/-17 proteins revealed that the protein has 37% similarity to the HMG-17 group and 69% similarity to the HMG-14 group; therefore, the protein is classified as belonging to the HMG-14 group. Additional analysis leads to the conclusion that the chicken cDNA described here codes for the true homolog of calf and human HMG-14 protein. Comparison of all the known HMG-14 sequences reveals the DNA binding domain is conserved and contains the invariant dodecapeptide PKRRSARLSAKP. The HMG-14 proteins have a distinct charge distribution along the polypeptide chain: while the central region is positively charged the C-terminal domain is negatively charged. JF - The Journal of biological chemistry AU - Srikantha, T AU - Landsman, D AU - Bustin, M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/09/25/ PY - 1988 DA - 1988 Sep 25 SP - 13500 EP - 13503 VL - 263 IS - 27 SN - 0021-9258, 0021-9258 KW - High Mobility Group Proteins KW - 0 KW - Nucleosomes KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Protein Biosynthesis KW - Oviducts -- analysis KW - Animals KW - Chickens KW - Base Sequence KW - Sequence Homology, Nucleic Acid KW - Biological Evolution KW - Humans KW - Nucleosomes -- metabolism KW - Molecular Sequence Data KW - Binding Sites KW - DNA -- isolation & purification KW - High Mobility Group Proteins -- genetics KW - DNA -- metabolism KW - DNA -- genetics KW - High Mobility Group Proteins -- metabolism KW - Cloning, Molecular UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78427530?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cloning+of+the+chicken+chromosomal+protein+HMG-14+cDNA+reveals+a+unique+protein+with+a+conserved+DNA+binding+domain.&rft.au=Srikantha%2C+T%3BLandsman%2C+D%3BBustin%2C+M&rft.aulast=Srikantha&rft.aufirst=T&rft.date=1988-09-25&rft.volume=263&rft.issue=27&rft.spage=13500&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 - 1988-10-19 N1 - Date created - 1988-10-19 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M20817; GENBANK N1 - SuppNotes - Erratum In: J Biol Chem 1989 Jul 25;264(21):12744 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hydroxyl radical production by stimulated neutrophils reappraised. AN - 78414055; 2843536 AB - Release of active oxygen species during the human neutrophil respiratory burst is thought to be mandatory for effective defense against bacterial infections and may play an important role in damage to host tissues. Part of the critical bacterial and host tissue damage has been attributed to hydroxyl radicals produced from superoxide and hydrogen peroxide. Because of the short life time of the very reactive hydroxyl radical, direct study of hydroxyl radical production is not possible; therefore, indirect detection methods such as electron spin resonance (ESR) coupled with appropriate spin-trapping agents such as 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) have been used. Superoxide production during the oxidative burst has been unambiguously demonstrated. Recent reports claim that hydroxyl radicals are not made during neutrophil stimulation and offer as an explanation the presence of granular components that interfere with hydroxyl radical production. When using the spin-trap agent DMPO, absence of the relatively long-lived adducts DMPO-OH and DMPO-CH3 has been assumed to be prima facie evidence for lack of hydroxyl radical participation. We show that high superoxide flux produced during stimulation of human neutrophils rapidly destroys both DMPO-OH and DMPO-CH3. In accord with previous implications, our results provide an alternative explanation for the absence of .OH adduct in spin-trapping studies and corroborate results obtained using other methods that implicate hydroxyl radical production during neutrophil stimulation. JF - The Journal of biological chemistry AU - Samuni, A AU - Black, C D AU - Krishna, C M AU - Malech, H L AU - Bernstein, E F AU - Russo, A AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, Maryland. Y1 - 1988/09/25/ PY - 1988 DA - 1988 Sep 25 SP - 13797 EP - 13801 VL - 263 IS - 27 SN - 0021-9258, 0021-9258 KW - Cyclic N-Oxides KW - 0 KW - Free Radicals KW - Hydroxides KW - Spin Labels KW - Superoxides KW - 11062-77-4 KW - Hydroxyl Radical KW - 3352-57-6 KW - 5,5-dimethyl-1-pyrroline-1-oxide KW - 7170JZ1QF3 KW - Zymosan KW - 9010-72-4 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Zymosan -- pharmacology KW - Humans KW - Electron Spin Resonance Spectroscopy KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Superoxides -- blood KW - Neutrophils -- metabolism KW - Neutrophils -- drug effects KW - Hydroxides -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78414055?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Hydroxyl+radical+production+by+stimulated+neutrophils+reappraised.&rft.au=Samuni%2C+A%3BBlack%2C+C+D%3BKrishna%2C+C+M%3BMalech%2C+H+L%3BBernstein%2C+E+F%3BRusso%2C+A&rft.aulast=Samuni&rft.aufirst=A&rft.date=1988-09-25&rft.volume=263&rft.issue=27&rft.spage=13797&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 - 1988-10-19 N1 - Date created - 1988-10-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of cyclosporine A on T cell development and clonal deletion. AN - 78431014; 3262237 AB - Cyclosporine A (CsA) is an important immunosuppressive drug that is widely used in transplantation medicine. Many of its suppressive effects on T cells appear to be related to the inhibition of T cell receptor (TCR)-mediated activation events. Paradoxically, in certain situations CsA is responsible for the induction of a T cell-mediated autoimmunity. The effects of CsA on T cell development in the thymus were investigated to elucidate the physiologic events underlying this phenomenon. Two major effects were revealed: (i) CsA inhibits the development of mature single positive (CD4+8- or CD4-8+) TCR-alpha beta+ thymocytes without discernibly affecting CD4-8- TCR-gamma delta+ thymocytes and (ii) CsA interferes with the deletion of cells bearing self-reactive TCRs in the population of single positive thymocytes that do develop. This suggests a direct mechanism for CsA-induced autoimmunity and may have implications for the relative contribution of TCR-mediated signaling events in the development of the various T cell lineages. JF - Science (New York, N.Y.) AU - Jenkins, M K AU - Schwartz, R H AU - Pardoll, D M AD - Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1988/09/23/ PY - 1988 DA - 1988 Sep 23 SP - 1655 EP - 1658 VL - 241 IS - 4873 SN - 0036-8075, 0036-8075 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Differentiation, T-Lymphocyte KW - Cyclosporins KW - Receptors, Antigen, T-Cell KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Antigens, Differentiation, T-Lymphocyte -- genetics KW - Autoimmune Diseases -- chemically induced KW - Mice KW - Receptors, Antigen, T-Cell -- drug effects KW - Cell Differentiation -- drug effects KW - Receptors, Antigen, T-Cell -- genetics KW - T-Lymphocytes -- drug effects KW - Cyclosporins -- pharmacology KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78431014?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effects+of+cyclosporine+A+on+T+cell+development+and+clonal+deletion.&rft.au=Jenkins%2C+M+K%3BSchwartz%2C+R+H%3BPardoll%2C+D+M&rft.aulast=Jenkins&rft.aufirst=M&rft.date=1988-09-23&rft.volume=241&rft.issue=4873&rft.spage=1655&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 - 1988-10-24 N1 - Date created - 1988-10-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selective killing of HIV-infected cells by recombinant human CD4-Pseudomonas exotoxin hybrid protein. AN - 78422181; 2843774 AB - It is projected that in the absence of effective therapy, most individuals infected with human immunodeficiency virus (HIV) will develop acquired immune deficiency syndrome (AIDS) and ultimately succumb to a combination of opportunistic microbial infections, malignancies and direct pathogenic effects of the virus. Anti-viral agents, immunomodulators, and inhibitors of specific HIV functions are being tested as potential treatments to alleviate the high morbidity and mortality. An alternative therapeutic concept involves the development of cytotoxic agents that are targeted to kill HIV-infected cells. Here we describe the purification and characterization of a recombinant protein produced in Escherichia coli that contains the HIV-binding portion of the human CD4 molecule linked to active regions of Pseudomonas exotoxin A. This hybrid protein displays selective toxicity toward cells expressing the HIV envelope glycoprotein and thus represents a promising novel therapeutic agent for the treatment of AIDS. JF - Nature AU - Chaudhary, V K AU - Mizukami, T AU - Fuerst, T R AU - FitzGerald, D J AU - Moss, B AU - Pastan, I AU - Berger, E A AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/09/22/ PY - 1988 DA - 1988 Sep 22 SP - 369 EP - 372 VL - 335 IS - 6188 SN - 0028-0836, 0028-0836 KW - CD4-Pseudomonas toxin KW - 0 KW - Exotoxins KW - HIV Envelope Protein gp120 KW - Immunotoxins KW - Receptors, HIV KW - Receptors, Virus KW - Recombinant Proteins KW - Retroviridae Proteins KW - Index Medicus KW - AIDS/HIV KW - Cells, Cultured KW - Humans KW - Escherichia coli -- genetics KW - Pseudomonas KW - Cell Survival KW - Acquired Immunodeficiency Syndrome -- therapy KW - Retroviridae Proteins -- metabolism KW - Recombinant Proteins -- pharmacology KW - Recombinant Proteins -- metabolism KW - Exotoxins -- metabolism KW - Receptors, Virus -- metabolism KW - Immunotoxins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78422181?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Selective+killing+of+HIV-infected+cells+by+recombinant+human+CD4-Pseudomonas+exotoxin+hybrid+protein.&rft.au=Chaudhary%2C+V+K%3BMizukami%2C+T%3BFuerst%2C+T+R%3BFitzGerald%2C+D+J%3BMoss%2C+B%3BPastan%2C+I%3BBerger%2C+E+A&rft.aulast=Chaudhary&rft.aufirst=V&rft.date=1988-09-22&rft.volume=335&rft.issue=6188&rft.spage=369&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-17 N1 - Date created - 1988-10-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Diethylcarbamazine prophylaxis for human loiasis. Results of a double-blind study. AN - 78391810; 3166107 AB - To determine whether infection with Loa loa could be prevented in temporary residents of endemic areas, we conducted a randomized, double-blind, placebo-controlled trial of diethylcarbamazine as a chemoprophylactic agent. Diethylcarbamazine (300 mg) or placebo was taken orally once a week by Peace Corps volunteers serving in Gabon, Cameroon, and the Central African Republic. The participants were assessed clinically and with serologic and parasitologic testing before and yearly during their two years of service. One hundred one persons satisfactorily completed the study. In Gabon (where exposure to the parasite was heaviest), 6 of 20 volunteers (30 percent) in the placebo group had clinical disease, as compared with none of 16 (0 percent) in the diethylcarbamazine-treated group (P less than 0.02). Of those taking placebo, 10 of 20 (50 percent) became seropositive for antifilarial IgG antibody, as compared with 2 of 16 (12 percent) in the drug-treated group (P less than 0.02). Exposure to the parasite appeared to be much lower among the 65 Peace Corps volunteers in Cameroon and the Central African Republic. No volunteer in either group in these countries had overt loiasis; 2 of 40 (5 percent) in the placebo groups in Cameroon and the Central African Republic seroconverted, as compared with none of 25 (0 percent) of those receiving diethylcarbamazine. Occasional nausea was the only symptom significantly associated with the prophylactic drug regimen. We conclude that diethylcarbamazine given orally once weekly can be an effective, acceptable chemoprophylactic agent to prevent loiasis in temporary residents of regions of Africa where Loa loa is endemic. JF - The New England journal of medicine AU - Nutman, T B AU - Miller, K D AU - Mulligan, M AU - Reinhardt, G N AU - Currie, B J AU - Steel, C AU - Ottesen, E A AD - Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Md 20892. Y1 - 1988/09/22/ PY - 1988 DA - 1988 Sep 22 SP - 752 EP - 756 VL - 319 IS - 12 SN - 0028-4793, 0028-4793 KW - Diethylcarbamazine KW - V867Q8X3ZD KW - Abridged Index Medicus KW - Index Medicus KW - Central African Republic KW - Double-Blind Method KW - Random Allocation KW - Humans KW - Adult KW - Middle Aged KW - Gabon KW - Cameroon KW - Male KW - Female KW - Diethylcarbamazine -- adverse effects KW - Diethylcarbamazine -- administration & dosage KW - Loiasis -- prevention & control KW - Diethylcarbamazine -- therapeutic use KW - Filariasis -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78391810?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Diethylcarbamazine+prophylaxis+for+human+loiasis.+Results+of+a+double-blind+study.&rft.au=Nutman%2C+T+B%3BMiller%2C+K+D%3BMulligan%2C+M%3BReinhardt%2C+G+N%3BCurrie%2C+B+J%3BSteel%2C+C%3BOttesen%2C+E+A&rft.aulast=Nutman&rft.aufirst=T&rft.date=1988-09-22&rft.volume=319&rft.issue=12&rft.spage=752&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 - 1988-10-11 N1 - Date created - 1988-10-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cephalotaxine esters: antileukemic advance or therapeutic failure? AN - 78387508; 3045335 AB - Clinical trials conducted in the People's Republic of China and the United States of the antileukemic efficacy of the cephalotaxine esters are reviewed. Harrington has been incorporated into combination regimens for the treatment of newly diagnosed acute nonlymphocytic leukemia (ANLL) in China, and activity with cephalotaxine esters has also been noted in chronic myelogenous leukemia. While the investigational agent homoharringtonine has shown some activity in the United States in ANLL, investigator interest in the United States has waned because of toxicity and inconvenient schedules. The Chinese trials have used different schedules than have U.S. studies and have been associated with less toxicity. These trials provide new information that may lead to further investigations of the cephalotaxine esters in the United States. JF - Journal of the National Cancer Institute AU - Grem, J L AU - Cheson, B D AU - King, S A AU - Leyland-Jones, B AU - Suffness, M AD - Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/09/21/ PY - 1988 DA - 1988 Sep 21 SP - 1095 EP - 1103 VL - 80 IS - 14 SN - 0027-8874, 0027-8874 KW - Alkaloids KW - 0 KW - Harringtonines KW - Index Medicus KW - United States KW - Humans KW - Clinical Trials as Topic KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - China KW - Leukemia -- drug therapy KW - Harringtonines -- therapeutic use KW - Harringtonines -- administration & dosage KW - Alkaloids -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78387508?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cephalotaxine+esters%3A+antileukemic+advance+or+therapeutic+failure%3F&rft.au=Grem%2C+J+L%3BCheson%2C+B+D%3BKing%2C+S+A%3BLeyland-Jones%2C+B%3BSuffness%2C+M&rft.aulast=Grem&rft.aufirst=J&rft.date=1988-09-21&rft.volume=80&rft.issue=14&rft.spage=1095&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 - 1988-10-13 N1 - Date created - 1988-10-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA strand breaks produced by etoposide (VP-16,213) in sensitive and resistant human breast tumor cells: implications for the mechanism of action. AN - 78394813; 2842045 AB - Pleotropic resistant human breast cancer cells (MCF-7), selected for resistance to Adriamycin, were used to study the production of DNA strand breaks by etoposide (VP-16) and its relationship to drug cytotoxicity. It was shown that the resistant MCF-7 cell line was cross-resistant to VP-16, and the degree of resistance was found to be 125-200-fold. Alkaline elution studies indicated that the parental cell line was very sensitive to VP-16 which caused extensive DNA strand breakage. In contrast, little DNA strand breakage was detected in the resistant MCF-7 cells, even at very high drug concentrations, indicating a good agreement between strand breaks and cytotoxicity. Further studies indicated that the nuclei isolated from the parental cell line were more resistant to VP-16-induced DNA strand breaks than the intact cells, while the opposite was found in the resistant cell line. In addition, the alkaline elution studies in isolated nuclei showed only a 2-fold reduction of VP-16-induced DNA breaks in nuclei from the resistant cells. In agreement with this result, it was found that nuclear extract from the resistant cells produced 2-3-fold less VP-16-induced DNA breaks than that from the sensitive cells in 32P-end-labeled SV40 DNA. VP-16 uptake and efflux studies indicated that there was a 2-3-fold decrease in net cellular accumulation of VP-16 in the resistant cells. Although the reduced uptake of VP-16 and decreased drug sensitivity of topoisomerase II appear to contribute to the mechanism of action and the development of resistance to VP-16, they do not completely explain the degree of resistance to VP-16 in this multidrug-resistant MCF-7 cell line indicating that other biochemical factors, such as activation of VP-16, are also involved in drug resistance and suggesting that the resistance is multifactorial. JF - Cancer research AU - Sinha, B K AU - Haim, N AU - Dusre, L AU - Kerrigan, D AU - Pommier, Y AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/09/15/ PY - 1988 DA - 1988 Sep 15 SP - 5096 EP - 5100 VL - 48 IS - 18 SN - 0008-5472, 0008-5472 KW - DNA, Neoplasm KW - 0 KW - Etoposide KW - 6PLQ3CP4P3 KW - DNA Topoisomerases, Type II KW - EC 5.99.1.3 KW - Index Medicus KW - DNA Damage KW - Humans KW - Cell Line -- drug effects KW - DNA Topoisomerases, Type II -- metabolism KW - Drug Resistance KW - Time Factors KW - Female KW - DNA, Neoplasm -- drug effects KW - Breast Neoplasms -- genetics KW - Breast Neoplasms -- pathology KW - Etoposide -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78394813?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=DNA+strand+breaks+produced+by+etoposide+%28VP-16%2C213%29+in+sensitive+and+resistant+human+breast+tumor+cells%3A+implications+for+the+mechanism+of+action.&rft.au=Sinha%2C+B+K%3BHaim%2C+N%3BDusre%2C+L%3BKerrigan%2C+D%3BPommier%2C+Y&rft.aulast=Sinha&rft.aufirst=B&rft.date=1988-09-15&rft.volume=48&rft.issue=18&rft.spage=5096&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 - 1988-10-11 N1 - Date created - 1988-10-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mixing studies during hepatic artery infusion in an in vitro model. AN - 78385978; 2970291 AB - A glass model of the hepatic artery network was used to study the effect of infusion rate on the degree of mixing from an end hole catheter placed in the gastroduodenal artery. Red dye solutions were infused at rates ranging from 1 ml/hour to 20 ml/minute. Effluent samples from each of 16 branch arteries were collected and dye concentrations were analyzed by means of a spectrophotometer. Low infusion rates, e.g., up to 5 ml/minute, showed streaming of the dye solutions and a nonhomogeneous dye distribution in the distal branches. At 20 ml/minute, dye distribution was much more uniform. These experiments are designed to simulate intrahepatic infusion of chemotherapeutic drug solutions. Theoretical considerations suggesting a pharmacokinetic advantage of intraarterial delivery implicitly assume uniform distribution of drug solutions to all perfused tissue. The in vitro data in this study suggests that this assumption may not be operative under certain infusion conditions. Slow infusion can lead to streaming and nonuniform distribution of infused drug solutions, which may in part explain the variability in tumor response in different tissue regions and also some observed toxicities, such as bile duct stricturing and fibrosis after intrahepatic infusions. JF - Cancer AU - Lutz, R J AU - Miller, D L AD - Biomedical Engineering and Instrumentation Branch, National Institutes of Health, Bethesda, MD 20892. Y1 - 1988/09/15/ PY - 1988 DA - 1988 Sep 15 SP - 1066 EP - 1073 VL - 62 IS - 6 SN - 0008-543X, 0008-543X KW - Antineoplastic Agents KW - 0 KW - Coloring Agents KW - Abridged Index Medicus KW - Index Medicus KW - Rheology KW - Chemistry, Physical KW - Humans KW - Chemical Phenomena KW - Cholangitis -- chemically induced KW - Spectrophotometry KW - Catheters, Indwelling KW - Hepatic Artery KW - Antineoplastic Agents -- pharmacokinetics KW - Models, Biological KW - Infusions, Intra-Arterial -- adverse effects KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78385978?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mixing+studies+during+hepatic+artery+infusion+in+an+in+vitro+model.&rft.au=Lutz%2C+R+J%3BMiller%2C+D+L&rft.aulast=Lutz&rft.aufirst=R&rft.date=1988-09-15&rft.volume=62&rft.issue=6&rft.spage=1066&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-03 N1 - Date created - 1988-10-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retroviral activation of a novel gene encoding a zinc finger protein in IL-3-dependent myeloid leukemia cell lines. AN - 78380207; 2842066 AB - Normal hematopoietic stem cells proliferate and differentiate in the presence of growth factors such as interleukin-3 (IL-3). Transformation can alter their growth factor requirements, the ability of the cells to differentiate, or both. To identify genes that are capable of transforming hematopoietic cells, IL-3-dependent cell lines, isolated from retrovirus induced myeloid leukemias, were examined for viral insertions in proto-oncogenes and in common sites of viral integration. Five of 37 cell lines contained proviruses in a common viral integration site termed the ecotropic virus integration 1 site (Evi-1). The integrations were correlated with the activation of transcription from the locus. Sequencing of cDNA clones and genomic clones demonstrated that the integrations had occurred near or in 5' noncoding exons of a novel gene. The sequence of the cDNA clones predicts that the gene product is a 120 kd protein that contains two domains with seven and three repeats of a DNA binding consensus sequence (zinc finger) initially described in the Xenopus transcription factor III A (TFIIIA). This represents the first demonstration of the retroviral activation of a gene encoding a zinc finger protein and the first implication for a member of this gene family in the transformation of hematopoietic cells. JF - Cell AU - Morishita, K AU - Parker, D S AU - Mucenski, M L AU - Jenkins, N A AU - Copeland, N G AU - Ihle, J N AD - NCI-Frederick Cancer Research Facility, Molecular Mechanisms of Carcinogenesis Laboratory, Maryland 21701. Y1 - 1988/09/09/ PY - 1988 DA - 1988 Sep 09 SP - 831 EP - 840 VL - 54 IS - 6 SN - 0092-8674, 0092-8674 KW - DNA-Binding Proteins KW - 0 KW - Interleukin-3 KW - Metalloproteins KW - Transcription Factors KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Base Sequence KW - Interleukin-3 -- physiology KW - Multigene Family KW - DNA -- genetics KW - Molecular Sequence Data KW - Mice KW - Gene Expression Regulation KW - Amino Acid Sequence KW - Cloning, Molecular KW - Leukemia Virus, Murine -- genetics KW - DNA-Binding Proteins -- genetics KW - Metalloproteins -- genetics KW - Transcription Factors -- genetics KW - Leukemia, Experimental -- genetics KW - Cell Transformation, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78380207?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Retroviral+activation+of+a+novel+gene+encoding+a+zinc+finger+protein+in+IL-3-dependent+myeloid+leukemia+cell+lines.&rft.au=Morishita%2C+K%3BParker%2C+D+S%3BMucenski%2C+M+L%3BJenkins%2C+N+A%3BCopeland%2C+N+G%3BIhle%2C+J+N&rft.aulast=Morishita&rft.aufirst=K&rft.date=1988-09-09&rft.volume=54&rft.issue=6&rft.spage=831&rft.isbn=&rft.btitle=&rft.title=Cell&rft.issn=00928674&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-11 N1 - Date created - 1988-10-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Response of canine esophagus to intraoperative electron beam radiotherapy. AN - 85277883; pmid-3138218 AB - Tolerance of esophagus to intraoperative radiotherapy (IORT) was investigated in dogs. Thirteen adult foxhounds were subjected to right thoractomy, mobilization of the intrathoracic esophagus, and IORT to a 6 cm full-thickness esophageal segment using 9 MeV electrons at doses of 0, 2,000, or 3,000 cGy. Dogs were followed clinically and were evaluated at regular intervals after treatment with fiberoptic esophagoscopy, barium swallows, and postmortem histologic evaluations. One sham-irradiated control dog showed no abnormalities during follow-up of 24 months. Seven dogs receiving 2,000 cGy IORT showed transient mild dysphagia and mild esophagitis, but no clinically or pathologically significant complications. Five dogs receiving 3,000 cGy demonstrated severe ulcerative esophagitis within 6 weeks of treatment which progressed to chronic ulcerative esophagitis with stricture formation by 9 months following IORT. One 3,000 cGy dog died at 13 months from an esophageal perforation. On the basis of a pilot experience using 13 experimental animals, it was concluded that intact canine esophagus tolerates IORT well to doses of 2,000 cGy, but doses of 3,000 cGy pose serious and potentially lethal risks. The clinical application of IORT to the treatment of human intrathoracic neoplasms requiring esophageal irradiation should be approached with caution, particularly at doses exceeding 2,000 cGy. JF - International Journal of Radiation Oncology, Biology, Physics AU - Sindelar, W F AU - Hoekstra, H J AU - Kinsella, T J AU - Barnes, M AU - DeLuca, A M AU - Tochner, Z AU - Pass, H I AU - Kranda, K C AU - Terrill, R E AD - Surgery Branch, National Cancer Institute, Bethesda, MD 20892. PY - 1988 SP - 663 EP - 669 VL - 15 IS - 3 SN - 0360-3016, 0360-3016 KW - Deglutition Disorders KW - Esophagus KW - Esophagitis KW - Intraoperative Care KW - Animal KW - Dogs KW - Radiation Tolerance KW - Dose-Response Relationship, Radiation KW - Male KW - Radiotherapy, High-Energy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85277883?accountid=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=International+Journal+of+Radiation+Oncology%2C+Biology%2C+Physics&rft.atitle=Response+of+canine+esophagus+to+intraoperative+electron+beam+radiotherapy.&rft.au=Sindelar%2C+W+F%3BHoekstra%2C+H+J%3BKinsella%2C+T+J%3BBarnes%2C+M%3BDeLuca%2C+A+M%3BTochner%2C+Z%3BPass%2C+H+I%3BKranda%2C+K+C%3BTerrill%2C+R+E&rft.aulast=Sindelar&rft.aufirst=W&rft.date=1988-09-01&rft.volume=15&rft.issue=3&rft.spage=663&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Radiation+Oncology%2C+Biology%2C+Physics&rft.issn=03603016&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Reye's syndrome-like illness in a patient receiving amiodarone. AN - 85223174; pmid-3414648 AB - A 16-yr-old boy who was receiving amiodarone for ventricular arrhythmias developed a Reye's syndrome-like illness several days after an upper respiratory infection. Liver biopsy revealed microvesicular fat and spotty hepatocellular necrosis, typical of Reye's syndrome. Recovery was complete. This case report suggests that medications other than aspirin may predispose to Reye's syndrome, and that children receiving amiodarone should receive prophylaxis against influenza B and chicken pox. JF - The American Journal of Gastroenterology AU - Jones, D B AU - Mullick, F G AU - Hoofnagle, J H AU - Baranski, B AD - Liver Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland. PY - 1988 SP - 967 EP - 969 VL - 83 IS - 9 SN - 0002-9270, 0002-9270 KW - Arrhythmia KW - Human KW - Reye Syndrome KW - Liver KW - Case Report KW - Adolescent KW - Amiodarone KW - Male UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85223174?accountid=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+American+Journal+of+Gastroenterology&rft.atitle=Reye%27s+syndrome-like+illness+in+a+patient+receiving+amiodarone.&rft.au=Jones%2C+D+B%3BMullick%2C+F+G%3BHoofnagle%2C+J+H%3BBaranski%2C+B&rft.aulast=Jones&rft.aufirst=D&rft.date=1988-09-01&rft.volume=83&rft.issue=9&rft.spage=967&rft.isbn=&rft.btitle=&rft.title=The+American+Journal+of+Gastroenterology&rft.issn=00029270&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Erythroproliferation in vitro can be induced by abl, fes, src, ras, bas, raf, raf/myc, erb B and cbl oncogenes but not by myc, myb and fos. AN - 78677866; 3226726 AB - To assess the erythroproliferative effects of a variety of retroviruses in vitro, hemopoietic precursors were incubated with the viruses then plated in methylcellulose. Only replication defective transforming viruses were active in this assay and produced colonies of erythroid cells. The effective transforming viruses were: Friend virus and viruses containing the abl, fes, src, Ha-ras, Ki-ras, bas, raf, raf/myc, erb B and cbl oncogenes. Replication competent viruses and those bearing the myc, myb and fos oncogenes were unable to initiate colony formation. Significant differences were observed in the colonies induced by several of the transforming genes based on (i) colony size, (ii) morphology, (iii) time course of development and (iv) sensitivity to erythropoietin. The oncogene-expressing retroviruses appeared to have the same target cell, which may be less differentiated erythroid precursor than the target cell for Friend virus. JF - Oncogene research AU - Klinken, S P AD - Laboratory of Experimental Carcinogenesis and Immunopathology, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 187 EP - 192 VL - 3 IS - 2 SN - 0890-6467, 0890-6467 KW - Index Medicus KW - Phenotype KW - Animals KW - Mice KW - Colony-Forming Units Assay KW - Oncogenes KW - Erythropoiesis KW - Hematopoietic Stem Cells -- cytology KW - Retroviridae -- genetics KW - Hematopoietic Stem Cells -- microbiology KW - Cell Transformation, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78677866?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+research&rft.atitle=Erythroproliferation+in+vitro+can+be+induced+by+abl%2C+fes%2C+src%2C+ras%2C+bas%2C+raf%2C+raf%2Fmyc%2C+erb+B+and+cbl+oncogenes+but+not+by+myc%2C+myb+and+fos.&rft.au=Klinken%2C+S+P&rft.aulast=Klinken&rft.aufirst=S&rft.date=1988-09-01&rft.volume=3&rft.issue=2&rft.spage=187&rft.isbn=&rft.btitle=&rft.title=Oncogene+research&rft.issn=08906467&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-28 N1 - Date created - 1989-03-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hypothesis: a nicotine-dopamine interaction linking smoking with Parkinson's disease and tardive dyskinesia. AN - 78661586; 3066487 AB - 1. Nicotine, an important pharmacological component of cigarette smoke, is known to have significant effects on central nervous system (CNS) dopaminergic function. Although acute doses of nicotine have been shown to facilitate dopamine release, recent data indicate that chronic nicotine treatment may actually decrease CNS dopamine turnover in the striatum. 2. A number of epidemiological investigations have demonstrated that individuals who are or who have been smokers are less likely to develop idiopathic Parkinson's disease (a disorder involving a deficit in nigrostriatal dopaminergic neurotransmission). In addition, there is preliminary evidence that individuals with tardive dyskinesia (a hyperkinetic movement disorder observed in some cases of chronic neuroleptic treatment and thought by some to be associated with striatal dopamine receptor supersensitivity) are more likely to be smokers. 3. A unitary hypothesis is presented, proposing that smoking in early adult life may decrease CNS catecholamine turnover, thereby protecting against free radical formation from catecholamine oxidation that in turn damages striatal neurons. These individuals are thereby "protected" from the later development of Parkinson's disease. In this hypothetical scheme, individuals who are given neuroleptics and who also are smokers may develop a greater degree of dopamine receptor supersensitivity due to combined receptor blockade by neuroleptics and a decrease in CNS dopamine turnover caused by nicotine, resulting in an increased prevalence of tardive dyskinesia in this group. JF - Cellular and molecular neurobiology AU - Kirch, D G AU - Alho, A M AU - Wyatt, R J AD - Neuropsychiatry Branch, National Institute of Mental Health, Washington, D.C. 20032. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 285 EP - 291 VL - 8 IS - 3 SN - 0272-4340, 0272-4340 KW - Nicotine KW - 6M3C89ZY6R KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Drug Interactions KW - Humans KW - Parkinson Disease, Secondary -- metabolism KW - Dyskinesia, Drug-Induced -- metabolism KW - Nicotine -- metabolism KW - Smoking -- metabolism KW - Smoking -- adverse effects KW - Dopamine -- metabolism KW - Dyskinesia, Drug-Induced -- etiology KW - Parkinson Disease, Secondary -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78661586?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+neurobiology&rft.atitle=Hypothesis%3A+a+nicotine-dopamine+interaction+linking+smoking+with+Parkinson%27s+disease+and+tardive+dyskinesia.&rft.au=Kirch%2C+D+G%3BAlho%2C+A+M%3BWyatt%2C+R+J&rft.aulast=Kirch&rft.aufirst=D&rft.date=1988-09-01&rft.volume=8&rft.issue=3&rft.spage=285&rft.isbn=&rft.btitle=&rft.title=Cellular+and+molecular+neurobiology&rft.issn=02724340&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-29 N1 - Date created - 1989-03-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of a simian virus 40-based shuttle vector to analyze enhanced mutagenesis in mitomycin C-treated monkey cells. AN - 78652944; 2851732 AB - When monkey cells were treated with mitomycin C 24 h before transfection with UV-irradiated pZ189 (a simian virus 40-based shuttle vector), there was a twofold increase in the frequency of mutations in the supF gene of the vector. These results suggest the existence of an enhancible mutagenesis pathway in mammalian cells. However, DNA sequence analysis of the SupF- mutants suggested no dramatic changes in the mechanisms of mutagenesis due to mitomycin C treatment of the cells. JF - Molecular and cellular biology AU - Roilides, E AU - Munson, P J AU - Levine, A S AU - Dixon, K AD - Section on Viruses and Cellular Biology, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 3943 EP - 3946 VL - 8 IS - 9 SN - 0270-7306, 0270-7306 KW - Mitomycins KW - 0 KW - Mitomycin KW - 50SG953SK6 KW - RNA, Transfer KW - 9014-25-9 KW - Index Medicus KW - RNA, Transfer -- drug effects KW - Animals KW - Ultraviolet Rays KW - Base Sequence KW - Genes KW - Base Composition KW - RNA, Transfer -- genetics KW - Cercopithecus aethiops KW - Molecular Sequence Data KW - Kidney KW - Cell Line KW - Transfection -- drug effects KW - Simian virus 40 -- genetics KW - Genetic Vectors -- radiation effects KW - Mitomycins -- pharmacology KW - Mutation KW - Transfection -- radiation effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78652944?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Use+of+a+simian+virus+40-based+shuttle+vector+to+analyze+enhanced+mutagenesis+in+mitomycin+C-treated+monkey+cells.&rft.au=Roilides%2C+E%3BMunson%2C+P+J%3BLevine%2C+A+S%3BDixon%2C+K&rft.aulast=Roilides&rft.aufirst=E&rft.date=1988-09-01&rft.volume=8&rft.issue=9&rft.spage=3943&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 - 1989-03-23 N1 - Date created - 1989-03-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Mol Biol. 1967 Jun 14;26(2):365-9 [4291934] Somat Cell Mol Genet. 1988 Jul;14(4):351-7 [3135602] Exp Cell Res. 1973 Sep;81(1):120-6 [4357029] Photochem Photobiol. 1980 Dec;32(6):823-30 [6450424] Prog Nucleic Acid Res Mol Biol. 1981;25:53-126 [6784186] Proc Natl Acad Sci U S A. 1981 Jul;78(7):4480-4 [6945596] Cell. 1982 May;29(1):11-22 [7049397] Mutat Res. 1982 Nov;105(5):291-8 [6292708] Cell. 1982 Nov;31(1):5-7 [6760987] Genetics. 1984 Mar;106(3):347-64 [6368314] Microbiol Rev. 1984 Mar;48(1):60-93 [6371470] Mol Cell Biol. 1984 Mar;4(3):435-41 [6325877] Cell. 1984 Jun;37(2):675-82 [6373019] EMBO J. 1984 Dec 20;3(13):3117-21 [6098464] Cancer Invest. 1985;3(2):163-74 [2986797] J Mol Biol. 1985 Mar 5;182(1):45-65 [3923204] Mol Cell Biol. 1985 Jul;5(7):1685-93 [2991746] Gene. 1985;38(1-3):233-7 [2998945] Proc Natl Acad Sci U S A. 1985 Dec;82(24):8606-10 [3001711] Proc Natl Acad Sci U S A. 1986 Nov;83(21):8273-7 [3464953] Mol Cell Biol. 1986 Jan;6(1):277-85 [3537686] Mol Cell Biol. 1986 Apr;6(4):1102-7 [3023869] Mol Cell Biol. 1986 Oct;6(10):3349-56 [3540589] EMBO J. 1987 Jan;6(1):63-7 [3034580] Mutat Res. 1987 Jul;179(1):103-14 [3037362] Environ Mol Mutagen. 1987;10(1):97-116 [2826138] Environ Mol Mutagen. 1988;11(1):119-33 [3276505] Mutat Res. 1988 Mar;198(1):199-206 [3127698] J Natl Cancer Inst. 1968 Aug;41(2):351-7 [4299537] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transposon tagging using Ty elements in yeast. AN - 78650624; 2851484 AB - We have used the ability to induce high levels of Ty transposition to develop a method for transposon mutagenesis in Saccharomyces cerevisiae. To facilitate genetic and molecular analysis, we have constructed GAL1-promoted TyH3 or Ty917 elements that contain unique cloning sites, and marked these elements with selectable genes. These genes include the yeast HIS3 gene, and the plasmid PiAN7 containing the Tn903 NEO gene. The marked Ty elements retain their ability to transpose, to mutate the LYS2, LYS5, or STE2 genes, and to activate the promoterless his3 delta 4 target gene. Ty elements containing selectable genes are also useful in strain construction, in chromosomal mapping, and in gene cloning strategies. JF - Genetics AU - Garfinkel, D J AU - Mastrangelo, M F AU - Sanders, N J AU - Shafer, B K AU - Strathern, J N AD - Bionetics Research, Inc., National Cancer Institute-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 95 EP - 108 VL - 120 IS - 1 SN - 0016-6731, 0016-6731 KW - DNA Transposable Elements KW - 0 KW - Index Medicus KW - Genotype KW - Genes, Fungal KW - Crosses, Genetic KW - Nucleic Acid Hybridization KW - Plasmids KW - Saccharomyces cerevisiae -- genetics KW - Mutation KW - Cloning, Molecular UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78650624?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Transposon+tagging+using+Ty+elements+in+yeast.&rft.au=Garfinkel%2C+D+J%3BMastrangelo%2C+M+F%3BSanders%2C+N+J%3BShafer%2C+B+K%3BStrathern%2C+J+N&rft.aulast=Garfinkel&rft.aufirst=D&rft.date=1988-09-01&rft.volume=120&rft.issue=1&rft.spage=95&rft.isbn=&rft.btitle=&rft.title=Genetics&rft.issn=00166731&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-22 N1 - Date created - 1989-03-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Mol Biol. 1970 Oct 14;53(1):159-62 [4922220] Mol Cell Biol. 1988 Apr;8(4):1432-42 [2837641] Proc Natl Acad Sci U S A. 1978 Apr;75(4):1929-33 [347451] J Cell Biol. 1980 Jun;85(3):811-22 [6993497] Cell. 1980 Aug;21(1):239-49 [6250713] Science. 1980 Sep 19;209(4463):1375-80 [6251544] Cell. 1980 Nov;22(2 Pt 2):427-36 [6256080] J Mol Biol. 1981 Feb 5;145(4):619-32 [7021854] Mol Gen Genet. 1981;182(1):159-63 [6267430] J Mol Biol. 1981 Apr 5;147(2):217-26 [6270337] J Bacteriol. 1983 Jan;153(1):163-8 [6336730] Nucleic Acids Res. 1983 Apr 25;11(8):2427-45 [6856467] Methods Enzymol. 1983;100:468-500 [6225933] Anal Biochem. 1983 Jul 1;132(1):6-13 [6312838] Cell. 1983 Dec;35(2 Pt 1):521-9 [6360378] Proc Natl Acad Sci U S A. 1984 Apr;81(8):2431-4 [6326126] Gene. 1984 Feb;27(2):183-91 [6327466] J Bacteriol. 1984 May;158(2):636-43 [6233260] Genetics. 1984 Jun;107(2):179-97 [6329902] Mol Gen Genet. 1984;197(2):345-6 [6394957] Cell. 1985 Mar;40(3):491-500 [2982495] Nucleic Acids Res. 1985 Jun 11;13(11):4097-112 [2989787] Proc Natl Acad Sci U S A. 1985 Aug;82(16):5423-7 [2991922] Proc Natl Acad Sci U S A. 1985 Aug;82(16):5428-32 [2991923] Nucleic Acids Res. 1985 Sep 25;13(18):6679-93 [2997719] Nature. 1985 Dec 12-18;318(6046):583-6 [2415827] Cell. 1985 Dec;43(2 Pt 1):483-92 [3907857] Nucleic Acids Res. 1985 Dec 9;13(23):8587-601 [3001645] Proc Natl Acad Sci U S A. 1986 Feb;83(3):735-9 [3003748] Gene. 1986;42(2):169-73 [3015730] Science. 1986 Dec 19;234(4783):1582-5 [3538420] Mol Cell Biol. 1986 Nov;6(11):3575-81 [3025601] Mol Cell Biol. 1987 Jan;7(1):258-65 [3031464] Genetics. 1987 Jun;116(2):191-9 [3038670] J Virol. 1987 Oct;61(10):3004-12 [3041020] Nucleic Acids Res. 1987 Sep 25;15(18):7309-24 [2821507] J Biol Chem. 1988 Jan 25;263(3):1413-23 [2447089] Science. 1988 Jan 15;239(4837):280-2 [2827308] Mol Cell Biol. 1988 Feb;8(2):978-81 [3280976] Curr Genet. 1986;11(3):193-200 [2834090] J Mol Biol. 1977 Oct 15;116(1):125-59 [338917] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Directed drug distribution: adding controlled brain activity to a drug. AN - 78605810; 3061952 AB - Environmental factors can alter the state of an organism so as to influence the response to drugs. This fact is widely recognized even though the responsible mechanisms are difficult to understand and control. The capacity of environmental influences to alter local drug pharmacokinetics is rarely considered. Drug localization and resulting action within the brain are influenced by vascular blood flow factors, local concentration differences in competing neurohumours, and receptor density. These are all frequently asymmetrically represented in the brain and drug effects are correspondingly laterality dependent. Attention to regional brain pharmacokinetics and the influence of environment on regional blood flow, local neurohumor concentration, and receptor density represents an untapped opportunity to enhance the desired effect of a centrally active drug at its site of action without enhancing general systemic toxicity. Combined pharmacotherapy and psychotherapy may result in superior therapeutic responses. Psychotherapy is a potential tool deliberately to manipulate environmental factors that influence physiological and physical chemical parameters that determine drug disposition. JF - The International journal of neuroscience AU - Myslobodsky, M S AU - Weiner, M AD - NIMH/NIH, Neuropsychiatry Branch, St. Elizabeths Hospital, Washington, DC.20032. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 7 EP - 19 VL - 42 IS - 1-2 SN - 0020-7454, 0020-7454 KW - Central Nervous System Agents KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Tissue Distribution KW - Brain -- drug effects KW - Central Nervous System Agents -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78605810?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+neuroscience&rft.atitle=Directed+drug+distribution%3A+adding+controlled+brain+activity+to+a+drug.&rft.au=Myslobodsky%2C+M+S%3BWeiner%2C+M&rft.aulast=Myslobodsky&rft.aufirst=M&rft.date=1988-09-01&rft.volume=42&rft.issue=1-2&rft.spage=7&rft.isbn=&rft.btitle=&rft.title=The+International+journal+of+neuroscience&rft.issn=00207454&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-14 N1 - Date created - 1989-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Confidence bands for logistic regression with restricted predictor variables. AN - 78589747; 3203128 AB - Confidence bands are constructed for the logistic response function when there is an interval restriction on each of the predictor variables. The construction involves application of a general fitting procedure using Scheffé's S-method, described by Casella and Strawderman (1980, Journal of the American Statistical Association 75, 862-868). Specific details are given for the case of one predictor variable, along with details for a fixed-width alternative to the S-method bands. In the one-predictor case, Monte Carlo results suggest that both bands are conservative for small sample sizes, such as N = 25. By N = 200 the S-method's coverage probabilities are seen to attain their nominal levels while the fixed-width bands remain conservative. The procedures are exemplified with data from a genetic toxicology experiment. JF - Biometrics AU - Piegorsch, W W AU - Casella, G AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 739 EP - 750 VL - 44 IS - 3 SN - 0006-341X, 0006-341X KW - Index Medicus KW - Probability KW - Mutagenicity Tests KW - Dose-Response Relationship, Drug KW - Humans KW - Monte Carlo Method KW - Regression Analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78589747?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Confidence+bands+for+logistic+regression+with+restricted+predictor+variables.&rft.au=Piegorsch%2C+W+W%3BCasella%2C+G&rft.aulast=Piegorsch&rft.aufirst=W&rft.date=1988-09-01&rft.volume=44&rft.issue=3&rft.spage=739&rft.isbn=&rft.btitle=&rft.title=Biometrics&rft.issn=0006341X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-03 N1 - Date created - 1989-02-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tamoxifen and fluoxymesterone versus tamoxifen and danazol in metastatic breast cancer--a randomized study. AN - 78556689; 3058238 AB - A prospective randomized trial of tamoxifen and fluoxymesterone versus tamoxifen and danazol in metastatic breast cancer was conducted from December 1980 to September 1985. Patients were eligible regardless of site of disease, estrogen receptor status, or age. Sixty-two of sixty-three randomized patients were evaluable for response. Overall response for tamoxifen and fluoxymesterone was 11% with 61% stabilization of disease, versus 12% response rate for tamoxifen and danazol with 59% stabilization. Toxicities with tamoxifen and fluoxymesterone were greater with an increase in masculinization. We conclude that the response rates to the combinations of tamoxifen and fluoxymesterone or tamoxifen and danazol reported are equivalent in this study but that the increased toxicity with tamoxifen and fluoxymesterone would make tamoxifen and danazol the treatment of choice if a combination were to be used. JF - Breast cancer research and treatment AU - Swain, S M AU - Steinberg, S M AU - Bagley, C AU - Lippman, M E AD - Medicine Branch, National Cancer Institute, Bethesda, Maryland. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 51 EP - 57 VL - 12 IS - 1 SN - 0167-6806, 0167-6806 KW - Tamoxifen KW - 094ZI81Y45 KW - Fluoxymesterone KW - 9JU12S4YFY KW - Danazol KW - N29QWW3BUO KW - Index Medicus KW - Fluoxymesterone -- administration & dosage KW - Random Allocation KW - Humans KW - Adult KW - Danazol -- administration & dosage KW - Clinical Trials as Topic KW - Aged KW - Middle Aged KW - Tamoxifen -- administration & dosage KW - Menopause KW - Female KW - Breast Neoplasms -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78556689?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Tamoxifen+and+fluoxymesterone+versus+tamoxifen+and+danazol+in+metastatic+breast+cancer--a+randomized+study.&rft.au=Swain%2C+S+M%3BSteinberg%2C+S+M%3BBagley%2C+C%3BLippman%2C+M+E&rft.aulast=Swain&rft.aufirst=S&rft.date=1988-09-01&rft.volume=12&rft.issue=1&rft.spage=51&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 - 1989-01-26 N1 - Date created - 1989-01-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Preclinical antitumor activity of batracylin (NSC 320846). AN - 78545718; 3192381 AB - Batracylin (NSC 320846, BAY H 2049), given ip on days 2 and 9 at a dose 400 mg/kg, inhibited tumor growth completely in 80-100% of mice with early-stage colon adenocarcinoma 38. Therapeutic efficacy against this subcutaneously implanted tumor was retained upon oral administration of Batracylin although, compared to ip treatment, larger doses were required. Batracylin also caused regression of advanced (400 mg) colon 38 tumors. Only modest activity was observed for this compound against P388 leukemia, but P388 sublines with acquired resistance to either adriamycin or cisplatin demonstrated collateral sensitivity. Batracylin currently is undergoing toxicological evaluation by NCI prior to clinical trials. JF - Investigational new drugs AU - Plowman, J AU - Paull, K D AU - Atassi, G AU - Harrison, S D AU - Dykes, D J AU - Kabbe, H J AU - Narayanan, V L AU - Yoder, O C AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 147 EP - 153 VL - 6 IS - 3 SN - 0167-6997, 0167-6997 KW - Antineoplastic Agents KW - 0 KW - Quinazolines KW - batracylin KW - 67199-66-0 KW - Index Medicus KW - Injections, Intraperitoneal KW - Administration, Oral KW - Mice, Inbred Strains KW - Animals KW - Tumor Cells, Cultured -- drug effects KW - Colonic Neoplasms -- drug therapy KW - Mice KW - Drug Evaluation, Preclinical KW - Quinazolines -- administration & dosage KW - Leukemia P388 -- drug therapy KW - Leukemia, Experimental -- drug therapy KW - Quinazolines -- therapeutic use KW - Antineoplastic Agents -- therapeutic use KW - Adenocarcinoma -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78545718?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Investigational+new+drugs&rft.atitle=Preclinical+antitumor+activity+of+batracylin+%28NSC+320846%29.&rft.au=Plowman%2C+J%3BPaull%2C+K+D%3BAtassi%2C+G%3BHarrison%2C+S+D%3BDykes%2C+D+J%3BKabbe%2C+H+J%3BNarayanan%2C+V+L%3BYoder%2C+O+C&rft.aulast=Plowman&rft.aufirst=J&rft.date=1988-09-01&rft.volume=6&rft.issue=3&rft.spage=147&rft.isbn=&rft.btitle=&rft.title=Investigational+new+drugs&rft.issn=01676997&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-12 N1 - Date created - 1989-01-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA alkylation by nitrosobis-(2-oxopropyl)amine in rats of different ages. AN - 78542439; 3142834 AB - We have examined the methylation of liver DNA (O6- and N7-methylguanine) by nitrosobis-(2-oxopropyl)amine (BOP) in male and female rats at various ages, following treatment with 2.5 mg of BOP; this dose given twice weekly for 30 weeks induces tumors in all animals. Except in young rats there was more methylation in female rat liver than in male rat liver, when adjusted for different sizes of the animals. There were differences in the extent of methylation between young (4 weeks) and older rats, but not between young adult (20 weeks) and old adult (65 weeks) males; the latter developed liver tumors when treated with BOP, and the former did not. There was no obvious relation between increased susceptibility to liver tumor induction by BOP and the extent of alkylation of liver DNA. Methylation of DNA was lower in the kidney than in the liver and, here, there was little difference between the sexes. In the testis there was N7-methylation of guanine in DNA, but no O6-methylguanine was detected. JF - Japanese journal of cancer research : Gann AU - Thomas, B J AU - Lijinsky, W AD - NCI-Frederick Cancer Research Facility, BRI-Basic Research Program, MD 21701. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 1039 EP - 1042 VL - 79 IS - 9 SN - 0910-5050, 0910-5050 KW - Nitrosamines KW - 0 KW - nitrosobis(2-oxopropyl)amine KW - 60599-38-4 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Kidney -- metabolism KW - Liver -- metabolism KW - Methylation KW - Male KW - Female KW - Alkylation KW - Nitrosamines -- pharmacology KW - DNA -- metabolism KW - Aging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78542439?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=DNA+alkylation+by+nitrosobis-%282-oxopropyl%29amine+in+rats+of+different+ages.&rft.au=Thomas%2C+B+J%3BLijinsky%2C+W&rft.aulast=Thomas&rft.aufirst=B&rft.date=1988-09-01&rft.volume=79&rft.issue=9&rft.spage=1039&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 - 1989-01-10 N1 - Date created - 1989-01-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Plasma amine metabolites before and after withdrawal from neuroleptic treatment in chronic schizophrenic inpatients. AN - 78522439; 2903509 AB - Plasma catecholamine metabolites were measured in paired blood samples from 22 subjects with chronic schizophrenia. One sample was drawn while patients were on a stable dose of neuroleptic medication; the second was drawn 6 weeks after discontinuation of medication. In comparison with baseline values during neuroleptic treatment, there was a significant increase in the plasma concentration of the norepinephrine metabolite, 3-methoxy-4-hydroxyphenylglycol (MHPG), and a trend toward an increase in the plasma concentration of the dopamine metabolite, homovanillic acid (HVA), in the medication-free subjects. There were no significant correlations between plasma MHPG or HVA concentrations and the corresponding ratings of psychopathology for these patients. JF - Psychiatry research AU - Kirch, D G AU - Jaskiw, G AU - Linnoila, M AU - Weinberger, D R AU - Wyatt, R J AD - Neuropsychiatry Branch, National Institute of Mental Health, St. Elizabeths Hospital, Washington DC. 20032. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 233 EP - 242 VL - 25 IS - 3 SN - 0165-1781, 0165-1781 KW - Antipsychotic Agents KW - 0 KW - Catecholamines KW - Methoxyhydroxyphenylglycol KW - 534-82-7 KW - Homovanillic Acid KW - X77S6GMS36 KW - Index Medicus KW - Homovanillic Acid -- blood KW - Double-Blind Method KW - Methoxyhydroxyphenylglycol -- blood KW - Humans KW - Brain -- drug effects KW - Dyskinesia, Drug-Induced -- blood KW - Adult KW - Clinical Trials as Topic KW - Schizophrenic Psychology KW - Adolescent KW - Male KW - Female KW - Catecholamines -- blood KW - Antipsychotic Agents -- therapeutic use KW - Schizophrenia -- drug therapy KW - Substance Withdrawal Syndrome -- blood KW - Antipsychotic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78522439?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Plasma+amine+metabolites+before+and+after+withdrawal+from+neuroleptic+treatment+in+chronic+schizophrenic+inpatients.&rft.au=Kirch%2C+D+G%3BJaskiw%2C+G%3BLinnoila%2C+M%3BWeinberger%2C+D+R%3BWyatt%2C+R+J&rft.aulast=Kirch&rft.aufirst=D&rft.date=1988-09-01&rft.volume=25&rft.issue=3&rft.spage=233&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 - 1988-12-21 N1 - Date created - 1988-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chronic administration of morphine and naltrexone up-regulate[3H][D-Ala2,D-leu5]enkephalin binding sites by different mechanisms. AN - 78510809; 2847072 AB - Previous studies have demonstrated that chronic administration of morphine up-regulated the lower affinity binding site for [3H][D-ala2,D-leu5]enkephalin, without producing a detectable alteration in the higher affinity binding site for [3H][D-ala2,D-leu5]enkephalin (Rothman et al., Eur. J. Pharmac. 124: 113-119, 1986). The experiments reported in this paper tested the hypothesis that chronic administration of morphine and naltrexone up-regulated the binding sites for [3H][D-ala2,D-leu5]enkephalin by different mechanisms. Rats were given either morphine or naltrexone chronically. Chronic administration of morphine up-regulated the lower affinity site, while chronic administration of naltrexone up-regulated both the higher and lower affinity binding sites for [3H][D-ala2,D-leu5]enkephalin. Unlike the lower affinity binding site for [3H][D-ala2,D-leu5]enkephalin present in membranes prepared from rats treated with placebo pellets, the lower affinity binding sites which were up-regulated by naltrexone and morphine were partially (naltrexone) or completely (morphine) labile to preincubation for 60 min at 25 degrees C in 50 mM Tris-HCl, pH 7.4, containing 0.4 M NaCl. These data suggest that chronic administration of morphine and naltrexone up-regulate binding sites for [3H][D-ala2,D-leu5]enkephalin through different mechanisms, and that the lower affinity binding sites for [3H][D-ala2, D-leu5]enkephalin which are up-regulated by chronic administration of morphine and naltrexone might differ biochemically from the lower affinity binding sites present in membranes treated with placebo. JF - Neuropharmacology AU - Danks, J A AU - Tortella, F C AU - Long, J B AU - Bykov, V AU - Jacobson, A E AU - Rice, K C AU - Holaday, J W AU - Rothman, R B AD - Laboratory of Preclinical Pharmacology, NIMH, St. Elizabeths Hospital, Washington, DC 20002. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 965 EP - 974 VL - 27 IS - 9 SN - 0028-3908, 0028-3908 KW - Receptors, Opioid KW - 0 KW - Sodium Chloride KW - 451W47IQ8X KW - Naltrexone KW - 5S6W795CQM KW - Morphine KW - 76I7G6D29C KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Drug Tolerance KW - Animals KW - Morphine Dependence KW - Male KW - Sodium Chloride -- pharmacology KW - Naltrexone -- administration & dosage KW - Receptors, Opioid -- drug effects KW - Naltrexone -- pharmacology KW - Morphine -- administration & dosage KW - Morphine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78510809?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Chronic+administration+of+morphine+and+naltrexone+up-regulate%5B3H%5D%5BD-Ala2%2CD-leu5%5Denkephalin+binding+sites+by+different+mechanisms.&rft.au=Danks%2C+J+A%3BTortella%2C+F+C%3BLong%2C+J+B%3BBykov%2C+V%3BJacobson%2C+A+E%3BRice%2C+K+C%3BHoladay%2C+J+W%3BRothman%2C+R+B&rft.aulast=Danks&rft.aufirst=J&rft.date=1988-09-01&rft.volume=27&rft.issue=9&rft.spage=965&rft.isbn=&rft.btitle=&rft.title=Neuropharmacology&rft.issn=00283908&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-16 N1 - Date created - 1988-12-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vitro inhibition of human herpesvirus-6 by phosphonoformate. AN - 78496787; 2972736 AB - HSB-2 cell cultures productively infected with human herpesvirus-6 were treated with the antiviral drugs phosphonoformic acid (PFA), acyclovir (ACV), and gancyclovir (DHPG). ACV and DHPG showed significant toxic effects on uninfected HSB-2 cells, yet only incompletely inhibited viral expression upon infection of the cells. PFA, however, showed little direct toxicity on HSB-2 cells while viral replication was inhibited significantly. JF - Journal of virological methods AU - Streicher, H Z AU - Hung, C L AU - Ablashi, D V AU - Hellman, K AU - Saxinger, C AU - Fullen, J AU - Salahuddin, S Z AD - National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 301 EP - 304 VL - 21 IS - 1-4 SN - 0166-0934, 0166-0934 KW - Antiviral Agents KW - 0 KW - Organophosphorus Compounds KW - Foscarnet KW - 364P9RVW4X KW - Phosphonoacetic Acid KW - N919E46723 KW - Ganciclovir KW - P9G3CKZ4P5 KW - Acyclovir KW - X4HES1O11F KW - Index Medicus KW - Acyclovir -- pharmacology KW - Humans KW - Cell Line KW - Acyclovir -- analogs & derivatives KW - Antiviral Agents -- pharmacology KW - Phosphonoacetic Acid -- analogs & derivatives KW - Phosphonoacetic Acid -- pharmacology KW - Organophosphorus Compounds -- pharmacology KW - Herpesviridae -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78496787?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+virological+methods&rft.atitle=In+vitro+inhibition+of+human+herpesvirus-6+by+phosphonoformate.&rft.au=Streicher%2C+H+Z%3BHung%2C+C+L%3BAblashi%2C+D+V%3BHellman%2C+K%3BSaxinger%2C+C%3BFullen%2C+J%3BSalahuddin%2C+S+Z&rft.aulast=Streicher&rft.aufirst=H&rft.date=1988-09-01&rft.volume=21&rft.issue=1-4&rft.spage=301&rft.isbn=&rft.btitle=&rft.title=Journal+of+virological+methods&rft.issn=01660934&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-21 N1 - Date created - 1988-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenesis by nitrosobis-(2-oxopropyl)amine labeled with deuterium and by nitroso-2-hydroxypropyl-2-oxopropylamine in rats and hamsters. AN - 78495729; 3180037 AB - The effects of the labeling with deuterium of the alpha-methylene groups of the carcinogen nitrosobis-(2-oxopropyl)amine (NBOP) on its carcinogenic effectiveness in rats and hamsters have been studied. The greater strength of the C-D bond compared with the C-H bond often leads to slower metabolism and lesser carcinogenic activity. When NBOP and NBOP-d4 were given to male and female rats in drinking water at equimolar doses, the mortality rate from tumors was lower in the rats given the deuterium-labeled compound, although the results were statistically significant (P = 0.012) only in males. The incidences of tumors of several groups was similar for NBOP and NBOP-d4, but there was a marked difference between males and females, females having a high incidence of liver tumors, and males very few. When NBOP and NBOP-d4 were given by gavage to rats or Syrian hamsters at identical doses there was no difference in rate of mortality from tumors, or in the pattern of tumors induced by either compound. In rats, both compounds were given at two dose rates, and in neither was a difference seen. To complement the studies with NBOP, a normal reduction product formed metabolically in vivo, nitroso-(2-hydroxypropyl) (2-oxopropyl)amine (NHPOP) was administered to rats in drinking water at the same dose rate. In male rats, the mortality rate was lower with NHPOP than with NBOP, while with female rats the opposite was the case (P less than 0.01 in both cases) and there was little difference in the pattern of tumors induced in either sex. NHPOP appears to have a quite distinct carcinogenic effect from NBOP, suggesting that the metabolic conversion of one to the other does not play a large role. The weak deuterium-isotope effect of NBOP-d4 given to rats in drinking water, but not detected in rats or hamsters treated by gavage, suggests that alpha-oxidation of NBOP is not likely to be a rate-limiting step in carcinogenesis by NBOP. JF - Cancer letters AU - Lijinsky, W AU - Saavedra, J E AU - Kovatch, R M AD - NCI-Frederick Cancer Research Facility, BRI-Basic Research Program, MD 21701. PY - 1988 SP - 37 EP - 41 VL - 42 IS - 1-2 SN - 0304-3835, 0304-3835 KW - Nitrosamines KW - 0 KW - nitrosobis(2-oxopropyl)amine KW - 60599-38-4 KW - N-nitroso(2-hydroxypropyl)(2-oxopropyl)amine KW - 61499-28-3 KW - Deuterium KW - AR09D82C7G KW - Index Medicus KW - Rats KW - Oxidation-Reduction KW - Animals KW - Sex Factors KW - Mesocricetus KW - Male KW - Isotope Labeling KW - Female KW - Cricetinae KW - Nitrosamines -- toxicity KW - Neoplasms, Experimental -- chemically induced KW - Nitrosamines -- metabolism KW - Neoplasms, Experimental -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78495729?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+by+nitrosobis-%282-oxopropyl%29amine+labeled+with+deuterium+and+by+nitroso-2-hydroxypropyl-2-oxopropylamine+in+rats+and+hamsters.&rft.au=Lijinsky%2C+W%3BSaavedra%2C+J+E%3BKovatch%2C+R+M&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1988-09-01&rft.volume=42&rft.issue=1-2&rft.spage=37&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 - 1988-12-09 N1 - Date created - 1988-12-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Metabolic and renal effects of interleukin-2 immunotherapy for metastatic cancer. AN - 78485036; 3263237 AB - The systemic administration of recombinant interleukin-2 (IL-2) either alone or in combination with lymphokine activated killer cells is a new approach to the immunotherapy of metastatic cancer in man. Renal toxicity is often a dose-limiting side effect of IL-2 administration. This prospective study of 17 consecutive patients receiving parenteral high dose IL-2 documents a reversible syndrome of hypotension, oliguria, fluid retention, azotemia and very low urinary excretion of sodium (median FeNa of 0.04%). The median nadir urinary uric acid to urinary creatinine ratio during IL-2 therapy was 0.2. This IL-2 regimen induces a reversible renal hypoperfusion syndrome (pre-renal azotemia) without evidence of acute uric acid nephropathy. Hypophosphatemia [median serum phosphorus of 1.9 mg/dl (0.61 mmol/l)] prompted further study of tubular function. Urinary excretions of phosphorus, calcium and magnesium were very low. Arterial blood gases revealed hyperventilation without alkalemia. The hypophosphatemia probably reflects increased utilization of inorganic phosphorus by rapidly proliferating lymphoid cells. JF - Clinical nephrology AU - Webb, D E AU - Austin, H A AU - Belldegrun, A AU - Vaughan, E AU - Linehan, W M AU - Rosenberg, S A AD - Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 141 EP - 145 VL - 30 IS - 3 SN - 0301-0430, 0301-0430 KW - Interleukin-2 KW - 0 KW - Lymphokines KW - Phosphates KW - Recombinant Proteins KW - Index Medicus KW - Phosphates -- blood KW - Humans KW - Recombinant Proteins -- adverse effects KW - Natriuresis KW - Middle Aged KW - Recombinant Proteins -- therapeutic use KW - Kidney Neoplasms -- therapy KW - Interleukin-2 -- adverse effects KW - Carcinoma, Renal Cell -- therapy KW - Uremia -- etiology KW - Killer Cells, Natural KW - Interleukin-2 -- therapeutic use KW - Hypotension -- etiology KW - Carcinoma, Renal Cell -- secondary KW - Acute Kidney Injury -- etiology KW - Immunotherapy -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78485036?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+nephrology&rft.atitle=Metabolic+and+renal+effects+of+interleukin-2+immunotherapy+for+metastatic+cancer.&rft.au=Webb%2C+D+E%3BAustin%2C+H+A%3BBelldegrun%2C+A%3BVaughan%2C+E%3BLinehan%2C+W+M%3BRosenberg%2C+S+A&rft.aulast=Webb&rft.aufirst=D&rft.date=1988-09-01&rft.volume=30&rft.issue=3&rft.spage=141&rft.isbn=&rft.btitle=&rft.title=Clinical+nephrology&rft.issn=03010430&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-19 N1 - Date created - 1988-12-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hepatic cholesterol metabolism as a function of carbon disulfide concentration and treatment with phenobarbital. AN - 78473511; 3177220 AB - Male F344 rats were exposed to carbon disulfide (CS2) at 0, 30, 75, 150, 300, or 600 ppm for 6 hr by inhalation in the presence or absence of 0.1% phenobarbital (PB) in the drinking water starting 5 days before exposure to CS2. Exposure to 600 ppm CS2 only resulted in a decrease in hepatic cholesterol synthesis and an increase in the liver-to-body-weight ratio (relative liver weight); however, it caused no histopathological damage and had little or no consistent effect on the concentration of hepatic cholesterol or on hepatic water content. Treatment with PB alone resulted in increases in the concentration of hepatic cholesterol and relative liver weight. Exposure to 300 ppm CS2 + PB or to 600 ppm CS2 + PB resulted in a decrease in hepatic cholesterol synthesis and increases in the concentration of hepatic cholesterol, relative liver weight, hepatic water content, and histopathological damage. A concentration-response relationship was demonstrated between exposure to CS2 only and decreased hepatic cholesterol synthesis. A concentration-response relationship also was demonstrated between exposure to CS2 in rats that had been treated with PB and decreased hepatic cholesterol synthesis, increased hepatic cholesterol concentration, increased relative liver weight, increased hepatic water content, and histopathological damage. Treatment with PB lowered the concentration of CS2 required to alter hepatic cholesterol metabolism. The reported observations are consistent with the theory that oxidative metabolism is involved in the expression of CS2-mediated alterations of hepatic cholesterol metabolism. JF - American Industrial Hygiene Association journal AU - Simmons, J E AU - Sloane, R A AU - Van Stee, E W AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27711. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 427 EP - 433 VL - 49 IS - 9 SN - 0002-8894, 0002-8894 KW - Cholesterol KW - 97C5T2UQ7J KW - Carbon Disulfide KW - S54S8B99E8 KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Drug Interactions KW - Dose-Response Relationship, Drug KW - Male KW - Organ Size -- drug effects KW - Phenobarbital -- pharmacology KW - Liver -- pathology KW - Cholesterol -- biosynthesis KW - Liver -- drug effects KW - Carbon Disulfide -- toxicity KW - Liver -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78473511?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Industrial+Hygiene+Association+journal&rft.atitle=Hepatic+cholesterol+metabolism+as+a+function+of+carbon+disulfide+concentration+and+treatment+with+phenobarbital.&rft.au=Simmons%2C+J+E%3BSloane%2C+R+A%3BVan+Stee%2C+E+W&rft.aulast=Simmons&rft.aufirst=J&rft.date=1988-09-01&rft.volume=49&rft.issue=9&rft.spage=427&rft.isbn=&rft.btitle=&rft.title=American+Industrial+Hygiene+Association+journal&rft.issn=00028894&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-11-21 N1 - Date created - 1988-11-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Oxidation of cyanide to the cyanyl radical by peroxidase/H2O2 systems as determined by spin trapping. AN - 78428373; 2844117 AB - The cyanyl radical was formed during the oxidation of potassium or sodium cyanide by horseradish peroxidase, lactoperoxidase, chloroperoxidase, NADH peroxidase, or methemoglobin in the presence of hydrogen peroxide. The spin adducts of the cyanyl radical with 5,5-dimethyl-1-pyrroline-N-oxide and N-tert-butyl-alpha-phenylnitrone were quite stable at neutral pH. The identity of these spin adducts could be demonstrated using 13C-labeled cyanide and by comparison with the spin adducts of the formamide radical, a hydrolysis product of the cyanyl radical adduct. The enzymatic conversion of cyanide to cyanyl radical by peroxidases should be considered in addition to its well-known role as a metal ligand. Furthermore, since cyanide is used routinely as an inhibitor of peroxidases, some consideration should be given to the biochemical consequences of this formation of the cyanyl radical by the catalytic activity of these enzymes. JF - Archives of biochemistry and biophysics AU - Moreno, S N AU - Stolze, K AU - Janzen, E G AU - Mason, R P AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 267 EP - 271 VL - 265 IS - 2 SN - 0003-9861, 0003-9861 KW - Cyanides KW - 0 KW - Free Radicals KW - Methemoglobin KW - 9008-37-1 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Peroxidases KW - EC 1.11.1.- KW - Potassium Cyanide KW - MQD255M2ZO KW - Sodium Cyanide KW - O5DDB9Z95G KW - Index Medicus KW - Oxidation-Reduction KW - Electron Spin Resonance Spectroscopy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78428373?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Oxidation+of+cyanide+to+the+cyanyl+radical+by+peroxidase%2FH2O2+systems+as+determined+by+spin+trapping.&rft.au=Moreno%2C+S+N%3BStolze%2C+K%3BJanzen%2C+E+G%3BMason%2C+R+P&rft.aulast=Moreno&rft.aufirst=S&rft.date=1988-09-01&rft.volume=265&rft.issue=2&rft.spage=267&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 - 1988-10-21 N1 - Date created - 1988-10-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Exploring relationships between mutagenic and carcinogenic potencies. AN - 78426402; 3419441 AB - Salmonella mutagenic and rodent carcinogenic potencies are calculated for 112 compounds recently studied by the U.S. National Toxicology Program. 28 of the 112 compounds are seen to exhibit simultaneous non-zero mutagenic and carcinogenic potencies. These are combined with an earlier list of mutagenic and carcinogenic compounds (McCann et al., 1988) in order to study possible trends in the data. A significant positive correlation is exhibited between mutagenic and carcinogenic potencies in the combined data, although the observed scatter is too great for the overall result to be predictive. Classification by chemical class further indicates positive correlations near one for chemicals classified as nitroaromatic and related compounds. Patterns in mutagenic and carcinogenic potency over time are also examined. Mean potencies of recently-studied compounds are seen to trend lower than those of compounds studied 10 or more years ago. JF - Mutation research AU - Piegorsch, W W AU - Hoel, D G AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 161 EP - 175 VL - 196 IS - 2 SN - 0027-5107, 0027-5107 KW - Carcinogens KW - 0 KW - Carcinogens, Environmental KW - Environmental Pollutants KW - Mutagens KW - Index Medicus KW - Salmonella -- drug effects KW - Animals KW - Environmental Pollutants -- toxicity KW - Dose-Response Relationship, Drug KW - Mice KW - Carcinogens, Environmental -- toxicity KW - Time Factors KW - Mutagens -- classification KW - Mutagenicity Tests -- methods KW - Carcinogens -- classification KW - Carcinogens -- toxicity KW - Mutagens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78426402?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Exploring+relationships+between+mutagenic+and+carcinogenic+potencies.&rft.au=Piegorsch%2C+W+W%3BHoel%2C+D+G&rft.aulast=Piegorsch&rft.aufirst=W&rft.date=1988-09-01&rft.volume=196&rft.issue=2&rft.spage=161&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 - 1988-10-24 N1 - Date created - 1988-10-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Adjuvant chemotherapy for patients with high-grade soft-tissue sarcomas of the extremity. AN - 78415375; 3047339 AB - We have previously reported the results of a randomized trial that demonstrated the survival benefit of adjuvant chemotherapy in the treatment of patients with high-grade extremity sarcomas compared with no chemotherapy. This regimen included doxorubicin, cyclophosphamide, and methotrexate. This report updates and extends our experience. The median follow-up of this trial is now 7.1 years and reveals a 5-year disease-free survival of 75% and 54% for chemotherapy and no chemotherapy groups, respectively (two-sided P [P2] = .037). The 5-year overall survival for patients in this trial was 83% and 60% for the chemotherapy and no chemotherapy groups, respectively, with a trend towards improved survival in the chemotherapy arm (P2 = .124). Because of doxorubicin-induced cardiomyopathy we performed a subsequent randomized trial comparing this high-dose regimen to reduced cumulative doses of doxorubicin and cyclophosphamide without methotrexate. Eighty-eight patients were entered into this trial which has a median follow-up of 4.4 years. The 5-year disease-free and overall survival for patients treated with the reduced doses of chemotherapy was 72% and 75%, respectively, and was not significantly different from the high-dose regimen. No patients developed congestive heart failure on this study. We conclude that adjuvant chemotherapy improves disease-free survival in patients with extremity soft-tissue sarcomas. The overall survival advantage in patients receiving adjuvant chemotherapy in our initial randomized high-dose chemotherapy trial has diminished though it continues to favor the chemotherapy group. A reduced-dose chemotherapy regimen was found to be comparable to the high-dose regimen. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Chang, A E AU - Kinsella, T AU - Glatstein, E AU - Baker, A R AU - Sindelar, W F AU - Lotze, M T AU - Danforth, D N AU - Sugarbaker, P H AU - Lack, E E AU - Steinberg, S M AD - Surgery Branch, National Institutes of Health, Bethesda, MD. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 1491 EP - 1500 VL - 6 IS - 9 SN - 0732-183X, 0732-183X KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Drug Administration Schedule KW - Random Allocation KW - Combined Modality Therapy KW - Humans KW - Clinical Trials as Topic KW - Follow-Up Studies KW - Doxorubicin -- administration & dosage KW - Time Factors KW - Methotrexate -- administration & dosage KW - Extremities KW - Soft Tissue Neoplasms -- mortality KW - Sarcoma -- mortality KW - Soft Tissue Neoplasms -- drug therapy KW - Sarcoma -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78415375?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Adjuvant+chemotherapy+for+patients+with+high-grade+soft-tissue+sarcomas+of+the+extremity.&rft.au=Chang%2C+A+E%3BKinsella%2C+T%3BGlatstein%2C+E%3BBaker%2C+A+R%3BSindelar%2C+W+F%3BLotze%2C+M+T%3BDanforth%2C+D+N%3BSugarbaker%2C+P+H%3BLack%2C+E+E%3BSteinberg%2C+S+M&rft.aulast=Chang&rft.aufirst=A&rft.date=1988-09-01&rft.volume=6&rft.issue=9&rft.spage=1491&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 - 1988-10-25 N1 - Date created - 1988-10-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Increased angiotensin II receptors in brain nuclei of DOCA-salt hypertensive rats. AN - 78409865; 3414825 AB - We analyzed angiotensin II (ANG II) receptors by in vitro autoradiography in selective brain nuclei of control, salt-treated (1% NaCl in drinking water), deoxycorticosterone acetate (DOCA)-treated (DOCA pivalate, 25 mg/kg sc weekly), and DOCA-salt-treated (DOCA + salt treatments) uninephrectomized male Wistar-Kyoto rats. After 4 wk of treatment, only the DOCA-salt group developed hypertension. ANG II binding increased in median preoptic nucleus and subfornical organ of salt- and DOCA-treated rats. DOCA-treated rats also showed increased ANG II binding in paraventricular nucleus. DOCA-salt-treated rats showed higher ANG II binding in nucleus of the solitary tract and area postrema, as well as in the areas mentioned before. Although salt and/or DOCA treatments alone increased ANG II receptors in some brain nuclei, after combined DOCA-salt treatment there was significantly higher ANG II binding in all areas, except the median preoptic nucleus. These results suggest that increased ANG II receptors in selected brain areas may play a role in the pathophysiology of mineralocorticoid-salt experimental hypertension. JF - The American journal of physiology AU - Gutkind, J S AU - Kurihara, M AU - Saavedra, J M AD - Unit on Preclinical Neuropharmacology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - H646 EP - H650 VL - 255 IS - 3 Pt 2 SN - 0002-9513, 0002-9513 KW - Iodine Radioisotopes KW - 0 KW - Receptors, Angiotensin KW - Sodium, Dietary KW - Angiotensin II KW - 11128-99-7 KW - Desoxycorticosterone KW - 40GP35YQ49 KW - Index Medicus KW - Subfornical Organ -- metabolism KW - Animals KW - Reference Values KW - Brain Stem -- metabolism KW - Rats, Inbred WKY KW - Blood Pressure KW - Organ Specificity KW - Autoradiography KW - Rats KW - Preoptic Area -- metabolism KW - Olfactory Bulb -- metabolism KW - Male KW - Paraventricular Hypothalamic Nucleus -- metabolism KW - Hypertension -- chemically induced KW - Angiotensin II -- metabolism KW - Suprachiasmatic Nucleus -- metabolism KW - Receptors, Angiotensin -- metabolism KW - Brain -- metabolism KW - Hypertension -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78409865?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Increased+angiotensin+II+receptors+in+brain+nuclei+of+DOCA-salt+hypertensive+rats.&rft.au=Gutkind%2C+J+S%3BKurihara%2C+M%3BSaavedra%2C+J+M&rft.aulast=Gutkind&rft.aufirst=J&rft.date=1988-09-01&rft.volume=255&rft.issue=3+Pt+2&rft.spage=H646&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 - 1988-10-12 N1 - Date created - 1988-10-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antisense Myc sequences induce differentiation of F9 cells. AN - 78397809; 2842791 AB - Down-regulation of Myc expression is the earliest documented change in gene expression in retinoic acid-induced differentiation of murine F9 teratocarcinoma cells. F9 cells transfected with plasmids expressing antisense Myc sequences under control of the simian virus 40 (SV40) early promoter exhibit a decrease in Myc protein. The result of this decrease is the spontaneous differentiation into cells that resemble retinoic acid-treated F9 cells as judged by plasminogen activator assays. In contrast, when F9 cells are transfected with a plasmid expressing Myc under control of the SV40 early promoter, resulting cell clones are resistant to differentiation by retinoic acid as shown by the lack of induction of plasminogen activator. These results suggest that down-regulation of Myc is sufficient and necessary for F9 cell differentiation. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Griep, A E AU - Westphal, H AD - Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 6806 EP - 6810 VL - 85 IS - 18 SN - 0027-8424, 0027-8424 KW - Tretinoin KW - 5688UTC01R KW - Index Medicus KW - Phenotype KW - Tretinoin -- pharmacology KW - Animals KW - Transfection KW - Simian virus 40 -- genetics KW - Cell Differentiation KW - Plasmids KW - Cell Line KW - Teratoma -- genetics KW - Oncogenes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78397809?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Antisense+Myc+sequences+induce+differentiation+of+F9+cells.&rft.au=Griep%2C+A+E%3BWestphal%2C+H&rft.aulast=Griep&rft.aufirst=A&rft.date=1988-09-01&rft.volume=85&rft.issue=18&rft.spage=6806&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 - 1988-10-13 N1 - Date created - 1988-10-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Brain Res. 1981 Jul 20;216(2):361-74 [7195765] Cell. 1980 Sep;21(2):347-55 [6250719] Proc Natl Acad Sci U S A. 1982 Apr;79(8):2490-4 [6283530] Exp Cell Res. 1983 Jul;146(2):439-44 [6192006] EMBO J. 1983;2(12):2375-83 [6321164] Cell. 1984 Apr;36(4):1007-15 [6323013] Nature. 1984 Aug 16-22;310(5978):592-4 [6462247] Mol Cell Biol. 1985 May;5(5):1136-42 [3158804] Cell. 1985 Aug;42(1):129-38 [2410135] Cell. 1985 Sep;42(2):519-26 [2992802] EMBO J. 1985 Jun;4(6):1441-7 [2992931] Exp Cell Res. 1986 May;164(1):223-31 [3956593] Nature. 1986 Apr 24-30;320(6064):760-3 [3458027] Proc Natl Acad Sci U S A. 1986 Aug;83(15):5539-43 [3526333] Nature. 1986 Aug 28-Sep 3;322(6082):848-50 [3528863] Mol Cell Biol. 1986 Feb;6(2):518-24 [3785153] Mol Cell Biol. 1987 Feb;7(2):639-49 [3547078] Proc Natl Acad Sci U S A. 1987 Feb;84(4):1040-4 [2434948] J Virol. 1987 May;61(5):1630-8 [3033289] Cell. 1987 Jul 3;50(1):69-78 [3036366] EMBO J. 1987 Aug;6(8):2365-71 [3665880] Nature. 1987 Nov 19-25;330(6145):272-4 [2823151] Nature. 1987 Dec 3-9;330(6147):444-50 [2825025] Nature. 1987 Dec 17-23;330(6149):624-9 [2825036] Proc Natl Acad Sci U S A. 1987 Nov;84(22):7881-5 [2825168] Genes Dev. 1987 Nov;1(9):938-45 [3480843] Mol Cell Biol. 1988 Feb;8(2):963-73 [3280975] Eur J Biochem. 1973 Jul 2;36(1):32-8 [4200179] Cell. 1978 Oct;15(2):393-403 [214238] Dev Biol. 1979 Jun;70(2):515-21 [89977] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] Dev Biol. 1982 Feb;89(2):516-20 [7056445] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A metabolite of the carcinogen 7,12-dimethylbenz[a]anthracene that reacts predominantly with adenine residues in DNA. AN - 78396735; 3136949 AB - Four 7,12-dimethylbenz[a]anthracene--deoxyribonucleoside adducts formed in mouse epidermis in vivo arise from the syn dihydrodiol epoxide metabolite of this carcinogen. With the synthetic syn dihydrodiol epoxide it was possible to identify three of these as deoxyadenosine adducts and to establish their structures. These three adducts account for the large majority of DNA adduct arising from this metabolite in vivo. The in vivo metabolite is unusual, therefore, in that it reacts almost exclusively with adenine residues in DNA while most carcinogen metabolites react preferentially with guanine residues. JF - Carcinogenesis AU - Cheng, S C AU - Prakash, A S AU - Pigott, M A AU - Hilton, B D AU - Lee, H AU - Harvey, R G AU - Dipple, A AD - BRI-Basic Research Program, NCI-Frederick Cancer Research Facility, MD 21701. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 1721 EP - 1723 VL - 9 IS - 9 SN - 0143-3334, 0143-3334 KW - Deoxyadenosines KW - 0 KW - Epoxy Compounds KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - DNA KW - 9007-49-2 KW - Adenine KW - JAC85A2161 KW - Index Medicus KW - Animals KW - Epidermis -- metabolism KW - Circular Dichroism KW - Mice KW - Chromatography, High Pressure Liquid KW - Magnetic Resonance Spectroscopy KW - Deoxyadenosines -- analogs & derivatives KW - 9,10-Dimethyl-1,2-benzanthracene -- analogs & derivatives KW - 9,10-Dimethyl-1,2-benzanthracene -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78396735?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+metabolite+of+the+carcinogen+7%2C12-dimethylbenz%5Ba%5Danthracene+that+reacts+predominantly+with+adenine+residues+in+DNA.&rft.au=Cheng%2C+S+C%3BPrakash%2C+A+S%3BPigott%2C+M+A%3BHilton%2C+B+D%3BLee%2C+H%3BHarvey%2C+R+G%3BDipple%2C+A&rft.aulast=Cheng&rft.aufirst=S&rft.date=1988-09-01&rft.volume=9&rft.issue=9&rft.spage=1721&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-06 N1 - Date created - 1988-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Adriamycin-induced free radical formation in the perfused rat heart: implications for cardiotoxicity. AN - 78394705; 2842038 AB - Adriamycin is an anthracycline drug with a wide spectrum of clinical antineoplastic activity. However, the usefulness of the drug is limited by its dose-dependent cardiotoxicity. Adriamycin-stimulated free radical formation has been suggested as one of the mechanisms for its cardiotoxic effects. In order to evaluate this underlying mechanism, we have perfused rat hearts with Adriamycin, using a modified Langendorf technique, and the free radicals formed were analyzed by electron spin resonance spectroscopy using spin-trapping techniques. Our studies show that Adriamycin stimulated the formation of .OH in the heart, and the maximum .OH was formed with 1 microM of the drug. The addition of superoxide dismutase (600 units/ml) inhibited the hydroxyl radical formation by 2- to 3-fold, while catalase (550 units/ml) abolished it completely, showing the intermediacy of superoxide and H2O2. Furthermore, ICRF-187, an iron chelator and a cytotoxic drug, was also an effective inhibitor of .OH formation in the rat heart. The heart rate was not significantly modified by all the above experiments. This study demonstrates that Adriamycin stimulates the formation of .OH in the isolated rat heart and suggests that this mechanism may be significant in Adriamycin-induced cardiotoxicity. JF - Cancer research AU - Rajagopalan, S AU - Politi, P M AU - Sinha, B K AU - Myers, C E AD - Clinical Pharmacology Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1988/09/01/ PY - 1988 DA - 1988 Sep 01 SP - 4766 EP - 4769 VL - 48 IS - 17 SN - 0008-5472, 0008-5472 KW - Free Radicals KW - 0 KW - Hydroxides KW - Hydroxyl Radical KW - 3352-57-6 KW - Razoxane KW - 5AR83PR647 KW - Doxorubicin KW - 80168379AG KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Razoxane -- pharmacology KW - Superoxide Dismutase -- pharmacology KW - Perfusion KW - Myocardium -- metabolism KW - Male KW - Heart -- drug effects KW - Doxorubicin -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78394705?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Adriamycin-induced+free+radical+formation+in+the+perfused+rat+heart%3A+implications+for+cardiotoxicity.&rft.au=Rajagopalan%2C+S%3BPoliti%2C+P+M%3BSinha%2C+B+K%3BMyers%2C+C+E&rft.aulast=Rajagopalan&rft.aufirst=S&rft.date=1988-09-01&rft.volume=48&rft.issue=17&rft.spage=4766&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 - 1988-09-26 N1 - Date created - 1988-09-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Continuous cell lines with altered growth and differentiation properties originate after transfection of human keratinocytes with human papillomavirus type 16 DNA. AN - 78392813; 2457456 AB - Immortalization of human keratinocytes (HKc) by human papillomavirus type 16 (HPV16) is reproducible at a high frequency, is due directly to the presence of the viral sequences in the cells, and occurs independently from the genetic characteristics of the host cells. Ten human keratinocyte strains, each derived from a different individual, were transfected with pMHPV16d and selected with G418. Eight became established lines. Two strains, which failed to grow shortly after successful G418 selection, were negative for HPV16 DNA. No lines were established following transfection of the same HKc strains with vector sequences only. The immortalized lines maintained a constant number of copies of the viral genome integrated into the cellular DNA. Each line showed a unique integration pattern of HPV16 sequences into the cellular genome, but expressed similar patterns of viral messages. Sublines able to grow in the absence of growth factors (epidermal growth factor and bovine pituitary extract), and others which became resistant to differentiation stimuli (serum and calcium) were obtained by selection in growth factor-free medium and serum-supplemented medium, respectively. The establishment of continuous cell lines is a direct consequence of the presence of viral sequences; however, because none of these lines formed tumors in nude mice, additional events must be necessary for progression of malignancy. HPV16-immortalized human keratinocyte lines can be used to investigate and identify the viral factors involved with the modification of growth and differentiation control by HPV16. JF - Carcinogenesis AU - Pirisi, L AU - Creek, K E AU - Doniger, J AU - DiPaolo, J A AD - Laboratory of Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 1573 EP - 1579 VL - 9 IS - 9 SN - 0143-3334, 0143-3334 KW - DNA, Viral KW - 0 KW - Growth Substances KW - RNA, Viral KW - Keratins KW - 68238-35-7 KW - Index Medicus KW - Aneuploidy KW - DNA, Viral -- analysis KW - Humans KW - Cell Differentiation KW - Genes, Viral KW - Gene Expression Regulation KW - Growth Substances -- physiology KW - Cell Cycle KW - Cell Line KW - RNA, Viral -- analysis KW - Epidermis -- microbiology KW - Epidermis -- cytology KW - Papillomaviridae -- genetics KW - Cell Transformation, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78392813?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Continuous+cell+lines+with+altered+growth+and+differentiation+properties+originate+after+transfection+of+human+keratinocytes+with+human+papillomavirus+type+16+DNA.&rft.au=Pirisi%2C+L%3BCreek%2C+K+E%3BDoniger%2C+J%3BDiPaolo%2C+J+A&rft.aulast=Pirisi&rft.aufirst=L&rft.date=1988-09-01&rft.volume=9&rft.issue=9&rft.spage=1573&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-06 N1 - Date created - 1988-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Relation of changes in amount and type of dietary fat to fecapentaenes in premenopausal women. AN - 78392534; 3412371 AB - Correlation studies suggest that fecal mutagenicity is increased in groups eating high-fat diets, the same groups who are often found to have high colorectal cancer incidence and mortality. The fecapentaenes are the best characterized class of fecal mutagens, but the relationship of dietary fat intake to the excretion of these potent genotoxins is unknown. We studied the effect of changes in amount and type of dietary fat on fecapentaene levels in 31 premenopausal women 20-40 years of age who participated in a controlled feeding study. After a pre-diet free-living period lasting 1 menstrual cycle, women were placed on a high-fat (40% energy from fat) diet for 4 menstrual cycles and then switched to a low-fat (20% energy from fat) diet for an additional 4 menstrual cycles. One-half the subjects were maintained throughout the study at a ratio of polyunsaturated-to-saturated fatty acids (P/S ratio) of 1.0, the other half at 0.3; body weight was constant. All meals during the controlled diet periods were prepared at the Human Study Facility of the Beltsville Human Nutrition Research Center. Fecapentaene and fecapentaene precursor levels were measured in acetone extracts from 3-day pooled stool samples collected during the study. No differences in fecapentaene or precursor levels were observed between the high- and low-fat diets at either P/S ratio. Fecapentaene and precursor levels were higher while on controlled diets than during the pre-diet free-living period, and levels declined again in the post-diet free-living period. We conclude that dietary fat has no significant effect on fecapentaene or precursor levels in acetone extracts of stool in premenopausal women. The effect of other dietary or non-dietary factors on fecapentaenes remains unknown. JF - Mutation research AU - Taylor, P R AU - Schiffman, M H AU - Jones, D Y AU - Judd, J AU - Schatzkin, A AU - Nair, P P AU - Van Tassell, R AU - Block, G AD - Cancer Prevention Studies Branch, NCI, Bethesda, MD 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 3 EP - 9 VL - 206 IS - 1 SN - 0027-5107, 0027-5107 KW - Dietary Fats KW - 0 KW - Fatty Acids, Unsaturated KW - Mutagens KW - Polyenes KW - Index Medicus KW - Fatty Acids, Unsaturated -- metabolism KW - Feces -- metabolism KW - Humans KW - Adult KW - Time Factors KW - Female KW - Dietary Fats -- metabolism KW - Mutagens -- metabolism KW - Polyenes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78392534?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Relation+of+changes+in+amount+and+type+of+dietary+fat+to+fecapentaenes+in+premenopausal+women.&rft.au=Taylor%2C+P+R%3BSchiffman%2C+M+H%3BJones%2C+D+Y%3BJudd%2C+J%3BSchatzkin%2C+A%3BNair%2C+P+P%3BVan+Tassell%2C+R%3BBlock%2C+G&rft.aulast=Taylor&rft.aufirst=P&rft.date=1988-09-01&rft.volume=206&rft.issue=1&rft.spage=3&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 - 1988-10-07 N1 - Date created - 1988-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A theoretical study of the effect of methylation or ethylation at O6-guanine in the structure and energy of DNA double strands. AN - 78392167; 3409460 AB - Quantum and molecular mechanical calculations were employed to examine the effect on binding energies and structure of methylation and ethylation at O6-guanine in double-stranded DNA. Ab initio quantum chemical calculations (STO-3G, 3-21G) were initially used to pseudo-optimize the structure of the 9-methyl derivative of O6-methylguanine. The distal orientation for the O6-methyl group was found to be lower in energy than the proximal orientation. The geometry determined for the distal O6-methyl group was in agreement with recent X-ray work. These results were used in supplementary parameterization of the AMBER molecular mechanics force field necessary for the minimization of DNA double strands containing O6-methylguanosine. Resulting calculations with AMBER on two 5-mer DNA sequences containing the promutagenic G(GM)A subsequence showed that the proximal orientation, while higher in energy in the isolated molecule, is both less disruptive to the DNA double helix and more stable than the distal orientation. Binding energies and degree of destabilization upon methylation were found to be functions of the adjacent bases around a GGA subsequence. Sequence-dependent destabilization could play a role in the repair of alkylated bases. Quantum and molecular mechanics calculations indicate that the O6-methyl and O6-ethylguanines behave energetically in a very similar manner. These calculations suggest that the necessity for the different repair mechanisms for methylation and ethylation lesions cannot be simply explained by energy differences or observed structural differences. JF - Carcinogenesis AU - Pedersen, L G AU - Darden, T A AU - Deerfield, D W AU - Anderson, M W AU - Hoel, D G AD - Biometry Branch, NIEHS, Research Triangle Park, NC 27709. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 1553 EP - 1562 VL - 9 IS - 9 SN - 0143-3334, 0143-3334 KW - 6-ethylguanine KW - 51866-19-4 KW - Guanine KW - 5Z93L87A1R KW - DNA KW - 9007-49-2 KW - O-(6)-methylguanine KW - 9B710FV2AE KW - Index Medicus KW - Base Sequence KW - Computer Simulation KW - Thermodynamics KW - Chemistry, Physical KW - Chemical Phenomena KW - Molecular Conformation KW - Methylation KW - Hydrogen Bonding KW - Structure-Activity Relationship KW - Alkylation KW - Guanine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78392167?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+theoretical+study+of+the+effect+of+methylation+or+ethylation+at+O6-guanine+in+the+structure+and+energy+of+DNA+double+strands.&rft.au=Pedersen%2C+L+G%3BDarden%2C+T+A%3BDeerfield%2C+D+W%3BAnderson%2C+M+W%3BHoel%2C+D+G&rft.aulast=Pedersen&rft.aufirst=L&rft.date=1988-09-01&rft.volume=9&rft.issue=9&rft.spage=1553&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-06 N1 - Date created - 1988-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of cytokines on polymorphonuclear neutrophil infiltration in the mouse. Prostaglandin- and leukotriene-independent induction of infiltration by IL-1 and tumor necrosis factor. AN - 78391646; 3261759 AB - The i.p. injection of mice with highly purified recombinant human rIL-1 alpha or beta resulted in the rapid influx of a large number of polymorphonuclear neutrophils (PMN) into the peritoneal cavity. Significant increases in the number of PMN were induced by doses of IL-1 which ranged from 0.005 to 5 ng/injection. Interestingly the dose response for PMN influx was bell-shaped because 50 ng of IL-1 did not result in a significant increase in peritoneal PMN. IL-1 induced PMN infiltration was detectable by 1 h with peak levels of PMN obtained by about 2 h, followed by a subsequent decline by 24 h. Other cytokines, IL-2, IFN-gamma, IFN alpha beta, granulocyte-CSF, granulocyte-macrophage-CSF, IL-3, TNF-alpha, and TNF-beta were compared to IL-1 for their ability to induce a PMN influx into the peritoneum. Only TNF-alpha or TNF-beta (lymphotoxin) were able to induce a significant influx of PMN within 2 h. However, based on total protein administered, about 100 times more TNF than IL-1 was required to produce a comparable PMN infiltration. Intraperitoneal injection of inhibitors of the cyclooxygenase or lipoxygenase pathways did not inhibit the IL-1-induced influx of PMN. Also, neither IL-1 nor TNF triggered an increase in PG or leukotriene release from peritoneal cells in vitro. Furthermore, direct peritoneal injection of leukotriene B4, a potent PMN chemoattractant in vitro, did not induce any significant increase in PMN in the peritoneal cavity indicating that chemotactic activity alone is insufficient for inducing peritoneal infiltration. These results suggest that the local production of very low levels of IL-1 in vivo would be sufficient to initiate a sequence of events that results in a rapid accumulation of PMN. Because IL-1 was not chemotactic for PMN in vitro, our data suggest that IL-1 induces production of factors that are chemotactic for PMN. Alternatively, IL-1 may act on other stages of the complex sequence of events that regulates the emigration of PMN into tissue sites in vivo. The synergy apparent in PMN influx when suboptimal concentrations of IL-1 and TNF were injected suggests that the local production of very low concentrations of these cytokines in situ could play a critical role in the emigration of PMN during infection. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Sayers, T J AU - Wiltrout, T A AU - Bull, C A AU - Denn, A C AU - Pilaro, A M AU - Lokesh, B AD - Biological Carcinogenesis Development Program, NCI-FCRF, Frederick, MD 21701-1013. Y1 - 1988/09/01/ PY - 1988 DA - 1988 Sep 01 SP - 1670 EP - 1677 VL - 141 IS - 5 SN - 0022-1767, 0022-1767 KW - Interleukin-1 KW - 0 KW - Prostaglandins KW - Recombinant Proteins KW - SRS-A KW - Tumor Necrosis Factor-alpha KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Recombinant Proteins -- pharmacology KW - Peritoneal Cavity -- pathology KW - Kinetics KW - Dose-Response Relationship, Immunologic KW - Mice KW - Mice, Inbred BALB C KW - Drug Synergism KW - Male KW - Prostaglandins -- physiology KW - Neutrophils -- pathology KW - Interleukin-1 -- pharmacology KW - Chemotaxis, Leukocyte -- drug effects KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Neutrophils -- physiology KW - SRS-A -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78391646?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effect+of+cytokines+on+polymorphonuclear+neutrophil+infiltration+in+the+mouse.+Prostaglandin-+and+leukotriene-independent+induction+of+infiltration+by+IL-1+and+tumor+necrosis+factor.&rft.au=Sayers%2C+T+J%3BWiltrout%2C+T+A%3BBull%2C+C+A%3BDenn%2C+A+C%3BPilaro%2C+A+M%3BLokesh%2C+B&rft.aulast=Sayers&rft.aufirst=T&rft.date=1988-09-01&rft.volume=141&rft.issue=5&rft.spage=1670&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 - 1988-09-26 N1 - Date created - 1988-09-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - IL-1 as a co-factor for lymphokine-secreting CD8+ murine T cells. AN - 78389340; 2970506 AB - Immunologically important among the known biologic activities of IL-1 is its ability to function as a co-factor for responses mediated by lymphokine secreting CD4+ Th cells. In contrast to its known effects in CD4+ T cell responses, IL-1 is not known to play a role in CD8+ T cell responses. In the present study, we have assessed the ability of murine recombinant IL-1 to function as a co-factor for stimulating CD8+ T cells to secrete lymphokines such as IL-2. We found that, in conjunction with either Ag or mitogen, IL-1 is able to stimulate lymphokine-secreting CD8+ T cells. Furthermore, we found that, as a consequence of its stimulation of lymphokine-secreting CD8+ T cells, IL-1 is able to reconstitute MHC class I allospecific cytolytic T lymphocyte responses by cell populations depleted of both accessory cells and CD4+ T cells. These results demonstrate that the biologic activity of IL-1 is not restricted to CD4+ cell responses, and suggests that IL-1 can function as a co-factor for the stimulation of lymphokine-secreting Th cells regardless of their CD4/CD8 phenotype. If IL1 acts directly on lymphokine-secreting T cells or on the APC with which they interact is not yet certain. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Mizuochi, T AU - McKean, D J AU - Singer, A AD - Experimental Immunology Branch, National Institutes of Health, Bethesda, MD 20892. Y1 - 1988/09/01/ PY - 1988 DA - 1988 Sep 01 SP - 1571 EP - 1575 VL - 141 IS - 5 SN - 0022-1767, 0022-1767 KW - Antigens, Differentiation, T-Lymphocyte KW - 0 KW - Interleukin-1 KW - Lymphokines KW - Recombinant Proteins KW - Concanavalin A KW - 11028-71-0 KW - Abridged Index Medicus KW - Index Medicus KW - Phenotype KW - Cytotoxicity, Immunologic KW - Animals KW - Recombinant Proteins -- pharmacology KW - Mice, Inbred C57BL KW - T-Lymphocytes, Cytotoxic -- immunology KW - Mice KW - T-Lymphocytes, Helper-Inducer -- metabolism KW - Drug Synergism KW - Concanavalin A -- pharmacology KW - T-Lymphocytes -- classification KW - Lymphokines -- metabolism KW - T-Lymphocytes -- metabolism KW - Interleukin-1 -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78389340?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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-1+as+a+co-factor+for+lymphokine-secreting+CD8%2B+murine+T+cells.&rft.au=Mizuochi%2C+T%3BMcKean%2C+D+J%3BSinger%2C+A&rft.aulast=Mizuochi&rft.aufirst=T&rft.date=1988-09-01&rft.volume=141&rft.issue=5&rft.spage=1571&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 - 1988-09-26 N1 - Date created - 1988-09-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Regulation of Hermissenda K+ channels by cytoplasmic and membrane-associated C-kinase. AN - 78382004; 2457656 AB - Pharmacologic activation of endogenous protein kinase C (PKC) together with elevation of the intracellular Ca2+ level was previously shown to cause reduction of two voltage-dependent K+ currents (IA and ICa2+-K+) across the soma membrane of the type B photoreceptor within the eye of the mollusc Hermissenda crassicornis. Similar effects were also found to persist for days after acquisition of a classically conditioned response. Also, the state of phosphorylation of a low-molecular-weight protein was changed only within the eyes of conditioned Hermissenda. To examine the role of PKC in causing K+ current changes as well as changes of phosphorylation during conditioning (and possibly other physiologic contexts), we studied here the effects of endogenous PKC activation and exogenous PKC injection on phosphorylation and K+ channel function. Several phosphoproteins (20, 25, 56, and 165 kilodaltons) showed differences in phosphorylation in response to PKC activators applied to intact nervous systems or to isolated eyes. Specific differences were observed for membrane and cytosolic fractions in response to both the phorbol ester 12-deoxyphorbol 13-isobutyrate 20-acetate (DPBA) or exogenous PKC in the presence of Ca2+ and phosphatidylserine/diacylglycerol. Type B cells pretreated with DPBA responded to PKC injection with a persistent reduction of K+ currents. In the absence of DPBA, PKC injection also caused K+ current reduction only following Ca2+ loading conditions. However, the direct effect of PKC injection in the absence of DPBA was only to increase ICa2+-K+. According to a proposed model, the amplitude of the K+ currents would depend on the steady-state balance of effects mediated by PKC within the cytoplasm and membrane-associated PKC. The model further specifies that the effects on K+ currents of cytoplasmic PKC require an intervening proteolytic step. Such a model predicts that increasing the concentration of cytoplasmic protease, e.g., with trypsin, will increase K+ currents, whereas blocking endogenous protease, e.g., with leupeptin, will decrease K+ currents. These effects should be opposed by preexposure of the cells to DPBA. Furthermore, prior injection of leupeptin should block or reverse the effects of subsequent injection of PKC into the type B cell. All of these predictions were confirmed by results reported here. Taken together, the results of this and previous studies suggest that PKC regulation of membrane excitability critically depends on its cellular locus. The implications of such function for long-term physiologic transformations are discussed. JF - Journal of neurochemistry AU - Alkon, D L AU - Naito, S AU - Kubota, M AU - Chen, C AU - Bank, B AU - Smallwood, J AU - Gallant, P AU - Rasmussen, H AD - Section on Neural Systems, National Institutes of Health, Bethesda, MD 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 903 EP - 917 VL - 51 IS - 3 SN - 0022-3042, 0022-3042 KW - Ion Channels KW - 0 KW - Leupeptins KW - Nerve Tissue Proteins KW - Phorbol Esters KW - 12-deoxyphorbol-13-isobutyrate-20-acetate KW - 25090-71-5 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Trypsin KW - EC 3.4.21.4 KW - leupeptin KW - J97339NR3V KW - Potassium KW - RWP5GA015D KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Cell Membrane -- enzymology KW - Electric Conductivity KW - Models, Biological KW - Calcium -- metabolism KW - Leupeptins -- pharmacology KW - Phorbol Esters -- pharmacology KW - Phosphorylation KW - Central Nervous System -- enzymology KW - Nerve Tissue Proteins -- metabolism KW - Mollusca KW - Trypsin -- pharmacology KW - Photoreceptor Cells -- ultrastructure KW - Photoreceptor Cells -- enzymology KW - Protein Kinase C -- isolation & purification KW - Protein Kinase C -- physiology KW - Ion Channels -- physiology KW - Cytoplasm -- enzymology KW - Protein Kinase C -- pharmacology KW - Potassium -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78382004?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Regulation+of+Hermissenda+K%2B+channels+by+cytoplasmic+and+membrane-associated+C-kinase.&rft.au=Alkon%2C+D+L%3BNaito%2C+S%3BKubota%2C+M%3BChen%2C+C%3BBank%2C+B%3BSmallwood%2C+J%3BGallant%2C+P%3BRasmussen%2C+H&rft.aulast=Alkon&rft.aufirst=D&rft.date=1988-09-01&rft.volume=51&rft.issue=3&rft.spage=903&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 - 1988-09-26 N1 - Date created - 1988-09-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Increased numbers of N-nitrosodimethylamine-initiated lung tumors in mice by chronic co-administration of ethanol. AN - 78371588; 3409476 AB - Young male strain A mice received 0.5, 1.0 or 5.0 p.p.m. N-nitrosodimethylamine (NDMA) in their drinking water with or without 10 or 20% ethanol. NDMA caused primary tumors of the lung in a dose-dependent manner; these were enumerated after 16 weeks. At the two lower NDMA doses, the ethanol caused a 1.5- to 3-fold increase in the number of lung tumor bearers and a 2-3.5 increase in lung tumor multiplicity. With 5 p.p.m. NDMA concomitant exposure to 10% ethanol resulted in a 2-3.5 increase in multiplicity. In a test for a possible tumor-promoting effect of the ethanol, mice were given 5 p.p.m. NDMA for 4 weeks, followed by ethanol for 12 weeks. There was an insignificant 30% increase in numbers of tumors. By contrast, mice that had received 10% ethanol along with NDMA during the initial 4 weeks experienced a 2.5-fold increase in incidence and 6-fold increase in multiplicity of lung tumors at 16 weeks. Thus, ethanol given simultaneously with chronic oral NDMA greatly enhances tumorigenesis in the lung, by a mechanism probably related to competitive inhibition of NDMA metabolism in the liver and not attributable to promotion of these tumors. JF - Carcinogenesis AU - Anderson, L M AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute-FCRF, MD 21701. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 1717 EP - 1719 VL - 9 IS - 9 SN - 0143-3334, 0143-3334 KW - Ethanol KW - 3K9958V90M KW - Dimethylnitrosamine KW - M43H21IO8R KW - Index Medicus KW - Animals KW - Body Weight -- drug effects KW - Mice KW - Drug Synergism KW - Ethanol -- administration & dosage KW - Lung Neoplasms -- chemically induced KW - Dimethylnitrosamine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78371588?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Increased+numbers+of+N-nitrosodimethylamine-initiated+lung+tumors+in+mice+by+chronic+co-administration+of+ethanol.&rft.au=Anderson%2C+L+M&rft.aulast=Anderson&rft.aufirst=L&rft.date=1988-09-01&rft.volume=9&rft.issue=9&rft.spage=1717&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-06 N1 - Date created - 1988-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - cis- and trans-acting regulation of gene expression of equine infectious anemia virus. AN - 78362164; 2841502 AB - Deletion analysis of the equine infectious anemia virus long terminal repeat revealed that sequences responsive to virus-specific transactivation are located within the region spanning the transcriptional start site (-31 to +22). In addition, an active exon of a trans-acting factor (tat) was identified downstream of pol and overlapping env (nucleotides 5264 to 5461). Activation by tat is accompanied by an increase in the steady-state levels of mRNA directed by the equine infectious anemia virus long terminal repeat. JF - Journal of virology AU - Dorn, P L AU - Derse, D AD - Biological Carcinogenesis Development Program, National Cancer Institute Frederick Cancer Research Facility, Maryland 21701-1013. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 3522 EP - 3526 VL - 62 IS - 9 SN - 0022-538X, 0022-538X KW - Gene Products, tat KW - 0 KW - RNA, Viral KW - Transcription Factors KW - Index Medicus KW - Animals KW - Transfection KW - Exons KW - RNA, Viral -- biosynthesis KW - Repetitive Sequences, Nucleic Acid KW - Plasmids KW - Cell Line KW - Infectious Anemia Virus, Equine -- genetics KW - Transcription, Genetic KW - Gene Expression Regulation KW - Transcription Factors -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78362164?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=cis-+and+trans-acting+regulation+of+gene+expression+of+equine+infectious+anemia+virus.&rft.au=Dorn%2C+P+L%3BDerse%2C+D&rft.aulast=Dorn&rft.aufirst=P&rft.date=1988-09-01&rft.volume=62&rft.issue=9&rft.spage=3522&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 - 1988-09-20 N1 - Date created - 1988-09-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell. 1987 Feb 27;48(4):691-701 [3643816] J Virol. 1987 Mar;61(3):743-7 [3027401] Nature. 1987 Apr 16-22;326(6114):711-3 [3031512] J Virol. 1987 Aug;61(8):2462-71 [3037109] J Virol. 1988 Jan;62(1):120-6 [2824840] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Cell. 1985 Jul;41(3):813-23 [2988790] Science. 1985 Jul 5;229(4708):74-7 [2990041] Science. 1985 Aug 2;229(4712):482-5 [2990051] Nature. 1985 Dec 12-18;318(6046):571-4 [2999613] Virology. 1986 Jan 15;148(1):226-31 [3002031] Science. 1986 May 9;232(4751):755-9 [3008338] Virology. 1986 Oct 15;154(1):1-8 [3750842] J Virol. 1986 Nov;60(2):385-93 [3021973] Virology. 1986 Dec;155(2):309-21 [2431539] Nature. 1987 Apr 16-22;326(6114):662-9 [3031510] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Novel glycosylation pathways of retroviral envelope proteins identified with avian reticuloendotheliosis virus. AN - 78361950; 2841469 AB - Previously, we identified two mature glycoproteins, gp90, the surface glycoprotein, and gp20, the transmembrane protein, from avian reticuloendotheliosis virus and an avian reticuloendotheliosis virus env gene-encoded intracellular polyprotein gPr77env, but the precise relationship of gPr77env to the mature envelope proteins was not determined (W.-P. Tsai, T.D. Copeland, and S. Oroszlan, Virology 155:567-583, 1986). In the present study, using metabolic labeling of viral proteins with [35S]cysteine, radioimmunoprecipitation, and carbohydrate structure analysis, we have identified a higher-molecular-weight endo-H-resistant env gene-encoded polyprotein designated gPr115env in addition to the endo-H-sensitive gPr77env. It appears that gPr77env is the primary polyprotein precursor, modified with mannosyloligosaccharides that are processed into sialic-acid-rich extraordinarily large complex-type carbohydrates (up to 17 kilodaltons for each N-linked site) on the gp90 domain but not on the gPr22 domain. In this process, gPr77env is converted into the apparently endo-H-resistant secondary polyprotein, gPr115env, which is rapidly processed into gp90 and gPr22. The proteolytic processing which occurs only after the appearance of an endo-H resistant precursor is now clearly demonstrated for a retrovirus. Some important aspects of carbohydrate structure, including the site-specific glycosylation, as well as the intracellular location and nature of the potential enzyme involved in the proteolytic cleavage of gPr115env are discussed. JF - Journal of virology AU - Tsai, W P AU - Oroszlan, S AD - Laboratory of Molecular Virology and Carcinogenesis, NCI-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 3167 EP - 3174 VL - 62 IS - 9 SN - 0022-538X, 0022-538X KW - Carbohydrates KW - 0 KW - Glycoproteins KW - Protein Precursors KW - Retroviridae Proteins KW - Viral Envelope Proteins KW - Glycoside Hydrolases KW - EC 3.2.1.- KW - Index Medicus KW - Animals KW - Glycoproteins -- analysis KW - Glycoside Hydrolases -- metabolism KW - Electrophoresis, Polyacrylamide Gel KW - Protein Precursors -- analysis KW - Glycosylation KW - Autoradiography KW - Cell Line KW - Carbohydrates -- analysis KW - Immunoassay KW - Retroviridae -- metabolism KW - Retroviridae Proteins -- metabolism KW - Reticuloendotheliosis virus -- metabolism KW - Viral Envelope Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78361950?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Novel+glycosylation+pathways+of+retroviral+envelope+proteins+identified+with+avian+reticuloendotheliosis+virus.&rft.au=Tsai%2C+W+P%3BOroszlan%2C+S&rft.aulast=Tsai&rft.aufirst=W&rft.date=1988-09-01&rft.volume=62&rft.issue=9&rft.spage=3167&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 - 1988-09-20 N1 - Date created - 1988-09-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1970 Aug 15;227(5259):680-5 [5432063] J Cell Biochem. 1984;24(2):121-30 [6373800] J Virol. 1971 Nov;8(5):778-85 [4332144] Biochem Soc Trans. 1984 Aug;12(4):599-600 [6489589] Anal Biochem. 1984 Sep;141(2):515-22 [6437277] J Cell Biol. 1984 Dec;99(6):2011-23 [6094591] Biochemistry. 1984 Nov 6;23(23):5628-37 [6439245] J Biol Chem. 1985 Jan 25;260(2):1265-70 [3968060] Virology. 1985 Jan 30;140(2):289-312 [2982236] Science. 1985 Aug 23;229(4715):726-33 [4023707] Annu Rev Biochem. 1985;54:631-64 [3896128] Biochemistry. 1985 Aug 13;24(17):4665-71 [4063349] Science. 1986 Mar 28;231(4745):1567-72 [3006247] Virology. 1986 Apr 30;150(2):491-502 [3083581] Cell. 1986 May 9;45(3):375-85 [2421920] J Cell Biol. 1986 Jul;103(1):265-75 [3013899] Science. 1986 Oct 24;234(4775):438-43 [2945253] Virology. 1986 Dec;155(2):567-83 [3024401] Science. 1987 Jan 16;235(4786):348-50 [3541206] Methods Enzymol. 1987;138:169-85 [3298950] Cell. 1987 Aug 14;50(4):523-34 [3038335] Annu Rev Biochem. 1987;56:497-534 [3304143] J Cell Biol. 1987 Sep;105(3):1191-203 [2821009] Nature. 1987 Nov 5-11;330(6143):74-7 [2959866] Proc Natl Acad Sci U S A. 1987 Nov;84(22):8120-4 [2825177] J Virol. 1988 Mar;62(3):1016-21 [2828650] Virology. 1972 Mar;47(3):551-66 [4111052] J Natl Cancer Inst. 1973 Aug;51(2):489-99 [4358134] J Virol. 1975 Jul;16(1):53-61 [166208] Eur J Biochem. 1975 Aug 15;56(2):335-41 [1175627] J Biol Chem. 1975 Nov 10;250(21):8569-75 [389] J Virol. 1976 Mar;17(3):983-90 [56462] J Virol. 1976 Jun;18(3):956-68 [178931] Biochem Biophys Res Commun. 1976 May 3;70(1):139-45 [1275931] Proc Natl Acad Sci U S A. 1976 Jul;73(7):2326-30 [1065881] J Virol. 1977 Feb;21(2):810-4 [189094] Biochemistry. 1977 Feb 22;16(4):710-7 [402147] Virology. 1977 Feb;76(2):539-53 [190766] J Biochem. 1984 Apr;95(4):1209-13 [6430882] J Virol. 1984 Oct;52(1):172-82 [6090694] Proc Natl Acad Sci U S A. 1978 Jun;75(6):2708-12 [208072] Arch Virol. 1978;58(1):61-4 [211992] J Biol Chem. 1979 Feb 25;254(4):1340-8 [216692] J Virol. 1979 Feb;29(2):735-43 [430608] Virology. 1979 Feb;93(1):20-30 [219596] J Virol. 1979 Mar;29(3):1221-5 [87519] J Virol. 1979 May;30(2):508-14 [89204] J Biol Chem. 1979 Dec 25;254(24):12531-4 [500730] Nature. 1979 Nov 29;282(5738):471-7 [503226] J Virol. 1980 Apr;34(1):168-77 [6154804] Nature. 1980 Nov 20;288(5788):236-41 [6985476] Proc Natl Acad Sci U S A. 1980 Nov;77(11):6420-4 [6935656] J Virol. 1981 Aug;39(2):646-50 [6268850] J Virol. 1981 Sep;39(3):845-54 [6169843] Nature. 1981 Oct 15-21;293(5833):543-8 [6169994] Virology. 1981 Dec;115(2):262-71 [6274085] Virology. 1982 May;119(1):122-32 [6280380] J Gen Virol. 1982 Apr;59(Pt 2):329-43 [7077302] Biochim Biophys Acta. 1982 Aug 27;717(3):491-501 [7126644] J Biol Chem. 1982 Dec 10;257(23):14023-8 [6292217] J Virol. 1983 Jun;46(3):920-36 [6304351] J Cell Biol. 1983 Aug;97(2):293-300 [6350314] Virology. 1970 Aug;41(4):631-46 [4319782] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Behavioral evidence for increased acetylcholine receptor sensitivity after nucleus basalis magnocellularis lesions in the rat. AN - 78492889; 3181290 AB - Lesions of the nucleus basalis magnocellularis and the medial septal area have been shown to produce both deficits in memory and decreases in choline acetyltransferase levels. In order to determine whether functional changes in acetylcholine receptor sensitivity also occur, the present experiment examined the ability of acetylcholine, 40 micrograms intraventricularly, to induce motor seizures in nucleus basalis magnocellularis-medial septal area lesioned versus control rats. While choline acetyltransferase activity was only modestly reduced in lesioned rats vs control rats (30%), the seizure scores were considerably higher in lesioned vs. control rats (270%). These results suggest that there is an increased functional response to acetylcholine following bilateral nucleus basalis magnocellularis-medial septal area lesions. JF - European journal of pharmacology AU - Mastropaolo, J AU - Crawley, J N AD - Clinical Neuroscience Branch, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1988/08/24/ PY - 1988 DA - 1988 Aug 24 SP - 301 EP - 304 VL - 153 IS - 2-3 SN - 0014-2999, 0014-2999 KW - Receptors, Cholinergic KW - 0 KW - Choline O-Acetyltransferase KW - EC 2.3.1.6 KW - Acetylcholine KW - N9YNS0M02X KW - Index Medicus KW - Seizures -- chemically induced KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Acetylcholine -- pharmacology KW - Choline O-Acetyltransferase -- antagonists & inhibitors KW - Male KW - Olivary Nucleus -- drug effects KW - Receptors, Cholinergic -- drug effects KW - Receptors, Cholinergic -- physiology KW - Olivary Nucleus -- physiology KW - Behavior, Animal -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78492889?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Behavioral+evidence+for+increased+acetylcholine+receptor+sensitivity+after+nucleus+basalis+magnocellularis+lesions+in+the+rat.&rft.au=Mastropaolo%2C+J%3BCrawley%2C+J+N&rft.aulast=Mastropaolo&rft.aufirst=J&rft.date=1988-08-24&rft.volume=153&rft.issue=2-3&rft.spage=301&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 - 1988-12-21 N1 - Date created - 1988-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prospects for human papillomavirus vaccines and immunotherapies. AN - 78323088; 2840515 JF - Journal of the National Cancer Institute AU - Schreier, A A AU - Allen, W P AU - Laughlin, C AU - Gruber, J AD - Biological Carcinogenesis Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/08/17/ PY - 1988 DA - 1988 Aug 17 SP - 896 EP - 899 VL - 80 IS - 12 SN - 0027-8874, 0027-8874 KW - Papillomavirus Vaccines KW - 0 KW - Viral Vaccines KW - Index Medicus KW - Animals KW - Immunotherapy KW - Humans KW - Disease Models, Animal KW - Viral Vaccines -- immunology KW - Papillomaviridae -- immunology KW - Tumor Virus Infections -- therapy KW - Viral Vaccines -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78323088?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prospects+for+human+papillomavirus+vaccines+and+immunotherapies.&rft.au=Schreier%2C+A+A%3BAllen%2C+W+P%3BLaughlin%2C+C%3BGruber%2C+J&rft.aulast=Schreier&rft.aufirst=A&rft.date=1988-08-17&rft.volume=80&rft.issue=12&rft.spage=896&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 - 1988-09-06 N1 - Date created - 1988-09-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evidence that mouse promotion-sensitivity gene pro1 is transcribed by RNA polymerase III. AN - 78653581; 3146526 AB - The murine gene pro1 confers susceptibility to tumor promoters upon transfection into an insensitive host cell. Nucleotide analysis over a minimally active domain of 1049 bp reveals signals expected for a gene transcribed by RNA polymerase II (RNAPII). Similar analysis of the complementary strand shows intragenic signals characteristic of genes transcribed by RNA polymerase III (RNAPIII). We have previously characterized a small, pro1-homologous transcript that is constitutively expressed at lower levels in promotion-insensitive JB6 epidermal cells as compared to promotion-sensitive and transformed clonal variants. To identify whether the pro1 RNAPII or RNAPIII transcription unit encodes the pro1-homologous RNA, RNA probes specific for each of the predicted transcripts were generated. The RNA probe specific for the pro1 RNAPIII transcription unit was found to detect the pro1-hybridizing RNA. Ligating the pro1 RNAPII 5'-flanking region to an interferon gamma reporter sequence failed to induce synthesis of the reporter protein. In addition, pro1 transcripts generated from the predicted RNAPII and RNAPIII transcription units were untranslatable in rabbit reticulocyte lysates. These data are consistent with pro1 associated tumor promotion occurring not through an RNAPII intermediate, but through an RNAPIII intermediate. JF - Gene AU - Garrity, R R AU - Seed, J L AU - Young, H A AU - Winterstein, D AU - Colburn, N H AD - Biological Carcinogenesis Development Program, Program Resources Inc., NCI-Frederick Cancer Research Facility, MD 21701. Y1 - 1988/08/15/ PY - 1988 DA - 1988 Aug 15 SP - 63 EP - 72 VL - 68 IS - 1 SN - 0378-1119, 0378-1119 KW - Carcinogens KW - 0 KW - Interferon-gamma KW - 82115-62-6 KW - DNA-Directed RNA Polymerases KW - EC 2.7.7.6 KW - RNA Polymerase III KW - Index Medicus KW - Protein Biosynthesis KW - Animals KW - Interferon-gamma -- genetics KW - Transfection KW - Cells, Cultured KW - Genetic Vectors KW - Mice KW - Nucleic Acid Hybridization KW - Plasmids KW - Carcinogens -- pharmacology KW - DNA-Directed RNA Polymerases -- metabolism KW - Genes -- drug effects KW - RNA Polymerase III -- metabolism KW - Transcription, Genetic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78653581?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Evidence+that+mouse+promotion-sensitivity+gene+pro1+is+transcribed+by+RNA+polymerase+III.&rft.au=Garrity%2C+R+R%3BSeed%2C+J+L%3BYoung%2C+H+A%3BWinterstein%2C+D%3BColburn%2C+N+H&rft.aulast=Garrity&rft.aufirst=R&rft.date=1988-08-15&rft.volume=68&rft.issue=1&rft.spage=63&rft.isbn=&rft.btitle=&rft.title=Gene&rft.issn=03781119&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-23 N1 - Date created - 1989-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inter- and intraclonal variability of polypeptides synthesized in a rat hepatoma cell line. Quantitative two-dimensional gel analysis. AN - 78365498; 3403523 AB - To examine the degree of clonal heterogeneity in the synthesis of polypeptides in neoplastic cells, single-cell subclones from the rat hepatoma cell line H4-II-E were isolated. Polypeptides from the clones were resolved on high resolution two-dimensional polyacrylamide gels (PAGE), and quantitatively analyzed with a computerized two-dimensional PAGE analysis system developed in this laboratory. Only four qualitatively different spots were found which were synthesized in one of the subclones in four out of five experiments. In contrast, 5-20% of the spots showed statistically significant quantitative differences when any one subclone was compared to any other. These differences were generally quite small, averaging about 1.5-fold in intensity, although variations of fourfold or more were observed. Different cultures of the same subclone showed quantitative differences of the same order as seen in different subclones, indicating that this variability was primarily intraclonal in nature, i.e. associated with the cultures rather than the subclones. The distribution of quantitatively variable spots indicates that 50% or more of the polypeptides in these cells may display intraclonal variability. Similar results were obtained with a second set of subclones derived from these primary ones. Time course studies were conducted where cells were maintained continuously for 12 weeks, with samples taken for two-dimensional PAGE analysis once a week. The fraction of polypeptides that vary significantly generally increased with time between sampling points. Experiments with independent cultures grown in parallel indicate that about 4% of this variability can be correlated to the age of the culture media, although the majority appears due to uncontrolled and/or random differences that arise between cultures. These results indicate that independent cultures quickly develop detectable quantitative differences in the expression of a large fraction of their polypeptides. These differences cannot, at present, be associated with the observable biology of the cells and probably reflect time-associated variations in the balance of cellular macromolecular synthesis which arise in tissue culture cells. JF - The Journal of biological chemistry AU - Miller, M J AU - Schwartz, D M AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/08/15/ PY - 1988 DA - 1988 Aug 15 SP - 11227 EP - 11236 VL - 263 IS - 23 SN - 0021-9258, 0021-9258 KW - Index Medicus KW - Rats KW - Karyotyping KW - Animals KW - Clone Cells -- metabolism KW - Time Factors KW - Cell Line KW - Peptide Biosynthesis KW - Liver Neoplasms, Experimental -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78365498?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inter-+and+intraclonal+variability+of+polypeptides+synthesized+in+a+rat+hepatoma+cell+line.+Quantitative+two-dimensional+gel+analysis.&rft.au=Miller%2C+M+J%3BSchwartz%2C+D+M%3BThorgeirsson%2C+S+S&rft.aulast=Miller&rft.aufirst=M&rft.date=1988-08-15&rft.volume=263&rft.issue=23&rft.spage=11227&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 - 1988-09-16 N1 - Date created - 1988-09-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenesis by nitroso-2-hydroxyethylurea in splenectomized hamsters. AN - 78343777; 3401843 AB - Several nitrosoalkylureas tested for carcinogenic activity in Syrian hamsters have as their main effect the induction of hemangiosarcomas of the spleen, many of which appear to metastasize to the liver. To investigate whether any of these lesions in the liver might not be metastases, a group of female Syrian hamsters was surgically splenectomized and treated with nitroso-2-hydroxyethylurea (NHEU) dissolved in corn oil/ethyl acetate once a week for 22 weeks. The animals survived much longer (median 45 weeks) than a comparable group of unsplenectomized female hamsters given identical treatment (median 24 weeks). The absence of hemangiosarcomas of the liver in the splenectomized hamsters showed that the presumed metastases seen in intact animals were, in fact, just that. A second interesting conclusion is that the compound did not produce a concomitant increase in tumors of other types. JF - Cancer letters AU - Lijinsky, W AU - Kovatch, R M AU - Thomas, B J AD - NCI-Frederick Cancer Research Facility, Frederick, MD 21701. Y1 - 1988/08/15/ PY - 1988 DA - 1988 Aug 15 SP - 199 EP - 202 VL - 41 IS - 2 SN - 0304-3835, 0304-3835 KW - Carcinogens KW - 0 KW - 1-(2-hydroxyethyl)-1-nitrosourea KW - 13743-07-2 KW - Ethylnitrosourea KW - P8M1T4190R KW - Index Medicus KW - Animals KW - Reference Values KW - Mesocricetus KW - Female KW - Cricetinae KW - Splenectomy KW - Ethylnitrosourea -- toxicity KW - Ethylnitrosourea -- analogs & derivatives KW - Carcinogens -- toxicity KW - Neoplasms, Experimental -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78343777?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+by+nitroso-2-hydroxyethylurea+in+splenectomized+hamsters.&rft.au=Lijinsky%2C+W%3BKovatch%2C+R+M%3BThomas%2C+B+J&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1988-08-15&rft.volume=41&rft.issue=2&rft.spage=199&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 - 1988-09-20 N1 - Date created - 1988-09-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cadmium carcinogenesis in male Wistar [Crl:(WI)BR] rats: dose-response analysis of tumor induction in the prostate and testes and at the injection site. AN - 78336655; 3396014 AB - Carcinogenic dose-response effects of CdCl2 in male Wistar [Crl:(WI)BR] rats were studied over a 2-year period. Groups of rats received a single s.c. injection of CdCl2 at doses of 0, 1.0, 2.5, 5.0, 10.0, 20.0, or 40.0 mumol/kg in the dorsal thoracic midline. Other groups received either four separate s.c. doses of 5 mumol Cd/kg each (at 0, 48, 96, and 168 h), or low dose cadmium (5.0 mumol/kg, s.c., at 0 h) followed by a higher dose (10.0 or 20.0 mumol/kg, s.c., at 48 h). The cadmium treatments resulted in appearance of tumors at the injection site, in the testes, and in the ventral prostate. Injection site tumors (mostly sarcomas) appeared to be strictly related to accumulated dose of cadmium and approached a 45% incidence at the highest cadmium dose (40 mumol/kg). Testicular tumors (mostly Leydig cell adenomas) were found to be highly dependent on testicular degeneration caused by cadmium. The highest Leydig cell tumor incidence occurred in the 40 mumol/kg (83%) and 20 mumol/kg (72%) dosage groups. Low dose pretreatment (5.0 mumol/kg) reduced or prevented the testicular degeneration and tumor formation that would otherwise result from a subsequent higher dose of CdCl2 (20 mumol/kg). Prostatic tumors (mostly adenomas of the ventral lobe) were also found to be associated with cadmium treatment, but in a non-dose related fashion. Prostatic tumor incidence was significantly elevated at the 2.5 mumol/kg dose of CdCl2 (eight tumors/26 rats; 31%) and showed a strong positive correlation between 0.0 and 2.5 mumol/kg in both tumor incidence and multiplicity. At higher doses, including those that caused marked testicular degeneration and induced prostatic atrophy, an elevated incidence of tumors did not occur. The occurrence of hyperplastic foci of the prostate, however, showed a strong positive correlation with increasing dose after single injections of cadmium up to and including 20.0 mumol/kg. Results indicate that CdCl2 can induce preneoplastic lesions of the prostate that appear to develop into tumors only at doses well below those causing marked degeneration of the testes and atrophy of the prostate. JF - Cancer research AU - Waalkes, M P AU - Rehm, S AU - Riggs, C W AU - Bare, R M AU - Devor, D E AU - Poirier, L A AU - Wenk, M L AU - Henneman, J R AU - Balaschak, M S AD - Division of Cancer Etiology, National Cancer Institute, Frederick, Maryland 21701. Y1 - 1988/08/15/ PY - 1988 DA - 1988 Aug 15 SP - 4656 EP - 4663 VL - 48 IS - 16 SN - 0008-5472, 0008-5472 KW - Cadmium KW - 00BH33GNGH KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Dose-Response Relationship, Drug KW - Precancerous Conditions -- chemically induced KW - Pancreatic Neoplasms -- chemically induced KW - Injections, Subcutaneous KW - Male KW - Sarcoma, Experimental -- chemically induced KW - Prostatic Neoplasms -- chemically induced KW - Cadmium -- toxicity KW - Testicular Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78336655?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cadmium+carcinogenesis+in+male+Wistar+%5BCrl%3A%28WI%29BR%5D+rats%3A+dose-response+analysis+of+tumor+induction+in+the+prostate+and+testes+and+at+the+injection+site.&rft.au=Waalkes%2C+M+P%3BRehm%2C+S%3BRiggs%2C+C+W%3BBare%2C+R+M%3BDevor%2C+D+E%3BPoirier%2C+L+A%3BWenk%2C+M+L%3BHenneman%2C+J+R%3BBalaschak%2C+M+S&rft.aulast=Waalkes&rft.aufirst=M&rft.date=1988-08-15&rft.volume=48&rft.issue=16&rft.spage=4656&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 - 1988-09-08 N1 - Date created - 1988-09-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of normal human exocervical epithelial cells immortalized in vitro by papillomavirus types 16 and 18 DNA. AN - 78336235; 2456144 AB - An in vitro system for studying the interaction between human papillomavirus (HPV) 16 and 18 recombinant DNA and normal human exocervical epithelial cells is described. Eight HPV-immortalized human exocervical epithelial cell lines were established; all the lines contained either integrated HPV16 or 18 sequences and expressed HPV mRNAs. Thus, integration and expression appear to be required for immortalization. Immortalized cells (greater than 200 population doublings to date) divided rapidly (doubling time of 30 to 46 h) and morphologically resembled primary cultures of normal human exocervical epithelial cells. They expressed a keratin pattern consistent with their origin from exocervical epithelium. When cultured at high density or in the presence of serum they terminally differentiated. Sublines resistant to terminal differentiation were selected by growth in serum-supplemented medium. Keratin pattern changes suggest they have some properties in common with cervical squamous carcinoma cells. However, HPV-immortalized cell lines were not tumorgenic in nude mice. Thus, HPV16/18 is not carcinogenic by itself. These cell lines represent an appropriate model for studying factors that regulate HPV gene expression in normal cervical epithelial cells and examining the influence of cocarcinogens on neoplastic progression. JF - Cancer research AU - Woodworth, C D AU - Bowden, P E AU - Doniger, J AU - Pirisi, L AU - Barnes, W AU - Lancaster, W D AU - DiPaolo, J A AD - Laboratory of Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/08/15/ PY - 1988 DA - 1988 Aug 15 SP - 4620 EP - 4628 VL - 48 IS - 16 SN - 0008-5472, 0008-5472 KW - DNA, Viral KW - 0 KW - RNA, Messenger KW - Keratins KW - 68238-35-7 KW - Index Medicus KW - Uterine Cervical Neoplasms -- etiology KW - Animals KW - Transfection KW - Epithelium -- microbiology KW - Humans KW - RNA, Messenger -- analysis KW - Mice KW - Keratins -- analysis KW - Female KW - Cell Line KW - Cervix Uteri -- pathology KW - Cervix Uteri -- microbiology KW - DNA, Viral -- analysis KW - Cervix Uteri -- analysis KW - Papillomaviridae -- genetics KW - Cell Transformation, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78336235?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+normal+human+exocervical+epithelial+cells+immortalized+in+vitro+by+papillomavirus+types+16+and+18+DNA.&rft.au=Woodworth%2C+C+D%3BBowden%2C+P+E%3BDoniger%2C+J%3BPirisi%2C+L%3BBarnes%2C+W%3BLancaster%2C+W+D%3BDiPaolo%2C+J+A&rft.aulast=Woodworth&rft.aufirst=C&rft.date=1988-08-15&rft.volume=48&rft.issue=16&rft.spage=4620&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 - 1988-09-08 N1 - Date created - 1988-09-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Malignant pheochromocytoma: effective treatment with a combination of cyclophosphamide, vincristine, and dacarbazine. AN - 78327182; 3395037 AB - To determine the efficacy and toxicity of combination chemotherapy in patients with advanced, malignant pheochromocytoma. Nonrandomized, single-arm trial. Governmental medical referral center. Fourteen patients with malignant pheochromocytoma confirmed by histologic tests. All patients had metastatic disease and elevated urinary catecholamine secretion. After optimization of antihypertensive therapy, patients received cyclophosphamide, 750 mg/m2 body surface area on day 1; vincristine, 1.4 mg/m2 on day 1, and dacarbazine, 600 mg/m2 on days 1 and 2, every 21 days. Combination chemotherapy with cyclophosphamide, vincristine, and dacarbazine produced a complete and partial response rate of 57% (median duration, 21 months; range, 7 to more than 34). Complete and partial biochemical responses were seen in 79% of patients (median duration, more than 22 months; range, 6 to more than 35). All responding patients had objective improvement in performance status and blood pressure. Toxicity included expected hematologic, neurologic, and gastrointestinal effects of chemotherapy without serious sequelae. There were four minor hypotensive episodes and one minor hypertensive episode. Combination chemotherapy with cyclophosphamide, vincristine, and dacarbazine is effective for advanced malignant pheochromocytoma. Urinary catecholamines are useful to ascertain biochemical response to therapy. JF - Annals of internal medicine AU - Averbuch, S D AU - Steakley, C S AU - Young, R C AU - Gelmann, E P AU - Goldstein, D S AU - Stull, R AU - Keiser, H R AD - National Cancer Institute, Uniformed Services, University of the Health Sciences, Bethesda, Maryland. Y1 - 1988/08/15/ PY - 1988 DA - 1988 Aug 15 SP - 267 EP - 273 VL - 109 IS - 4 SN - 0003-4819, 0003-4819 KW - Biomarkers, Tumor KW - 0 KW - Catecholamines KW - Metanephrine KW - 5001-33-2 KW - Vanilmandelic Acid KW - 55-10-7 KW - Vincristine KW - 5J49Q6B70F KW - Dacarbazine KW - 7GR28W0FJI KW - Cyclophosphamide KW - 8N3DW7272P KW - Abridged Index Medicus KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Humans KW - Vincristine -- administration & dosage KW - Adult KW - Biomarkers, Tumor -- analysis KW - Vanilmandelic Acid -- analysis KW - Dacarbazine -- administration & dosage KW - Middle Aged KW - Adolescent KW - Catecholamines -- analysis KW - Female KW - Male KW - Adrenal Gland Neoplasms -- drug therapy KW - Metanephrine -- analysis KW - Pheochromocytoma -- secondary KW - Pheochromocytoma -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Pheochromocytoma -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78327182?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Malignant+pheochromocytoma%3A+effective+treatment+with+a+combination+of+cyclophosphamide%2C+vincristine%2C+and+dacarbazine.&rft.au=Averbuch%2C+S+D%3BSteakley%2C+C+S%3BYoung%2C+R+C%3BGelmann%2C+E+P%3BGoldstein%2C+D+S%3BStull%2C+R%3BKeiser%2C+H+R&rft.aulast=Averbuch&rft.aufirst=S&rft.date=1988-08-15&rft.volume=109&rft.issue=4&rft.spage=267&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 - 1988-08-25 N1 - Date created - 1988-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Biochemistry and clinical activity of N-(phosphonacetyl)-L-aspartate: a review. AN - 78326712; 3293772 JF - Cancer research AU - Grem, J L AU - King, S A AU - O'Dwyer, P J AU - Leyland-Jones, B AD - Investigational Drug Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/08/15/ PY - 1988 DA - 1988 Aug 15 SP - 4441 EP - 4454 VL - 48 IS - 16 SN - 0008-5472, 0008-5472 KW - Antineoplastic Agents KW - 0 KW - Organophosphorus Compounds KW - Aspartic Acid KW - 30KYC7MIAI KW - sparfosic acid KW - 78QVZ7RG8L KW - Phosphonoacetic Acid KW - N919E46723 KW - Index Medicus KW - Drug Evaluation KW - Humans KW - Drug Resistance KW - Organophosphorus Compounds -- therapeutic use KW - Aspartic Acid -- pharmacology KW - Phosphonoacetic Acid -- adverse effects KW - Aspartic Acid -- analogs & derivatives KW - Aspartic Acid -- therapeutic use KW - Phosphonoacetic Acid -- analogs & derivatives KW - Aspartic Acid -- adverse effects KW - Phosphonoacetic Acid -- pharmacology KW - Phosphonoacetic Acid -- therapeutic use KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- pharmacology KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78326712?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Biochemistry+and+clinical+activity+of+N-%28phosphonacetyl%29-L-aspartate%3A+a+review.&rft.au=Grem%2C+J+L%3BKing%2C+S+A%3BO%27Dwyer%2C+P+J%3BLeyland-Jones%2C+B&rft.aulast=Grem&rft.aufirst=J&rft.date=1988-08-15&rft.volume=48&rft.issue=16&rft.spage=4441&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 - 1988-09-08 N1 - Date created - 1988-09-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human repair gene restores normal pattern of preferential DNA repair in repair defective CHO cells. AN - 78405777; 3412890 AB - The pattern of preferential DNA repair of UV-induced pyrimidine dimers was studied in repair-deficient Chinese hamster ovary (CHO) cells transfected with the human excision repair gene, ERCC-1. Repair efficiency was measured in the active dihydrofolate reductase (DHFR) gene and in its flanking, non-transcribed sequences in three cell lines: Wild type CHO cells, a UV-sensitive excision deficient CHO mutant, and the transfected line of the mutant carrying the expressed ERCC-1 gene. The CHO cells transformed with the human ERCC-1 gene repaired the active DHFR gene much more efficiently than the non-transcribed sequences, a pattern similar to that seen in wild type CHO cells. This pattern differs from that previously reported in CHO cells transfected with the denV gene of bacteriophage T4, in which both active and non-transcribed DNA sequences were efficiently repaired (Bohr and Hanawalt, Carcinogenesis 8: 1333-1336, 1987). The ERCC-1 gene product may specifically substitute for the repair enzyme present in normal hamster cells while the denV product, T4 endonuclease V, does not be appear to be constrained in its access to inactive chromatin. JF - Nucleic acids research AU - Bohr, V A AU - Chu, E H AU - van Duin, M AU - Hanawalt, P C AU - Okumoto, D S AD - Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/08/11/ PY - 1988 DA - 1988 Aug 11 SP - 7397 EP - 7403 VL - 16 IS - 15 SN - 0305-1048, 0305-1048 KW - Index Medicus KW - Animals KW - Cell Line KW - Cricetinae KW - Cloning, Molecular KW - DNA Repair UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78405777?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+repair+gene+restores+normal+pattern+of+preferential+DNA+repair+in+repair+defective+CHO+cells.&rft.au=Bohr%2C+V+A%3BChu%2C+E+H%3Bvan+Duin%2C+M%3BHanawalt%2C+P+C%3BOkumoto%2C+D+S&rft.aulast=Bohr&rft.aufirst=V&rft.date=1988-08-11&rft.volume=16&rft.issue=15&rft.spage=7397&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 - 1988-10-05 N1 - Date created - 1988-10-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 1982 Mar;42(3):860-3 [7059984] Cancer Res. 1987 Dec 15;47(24 Pt 1):6426-36 [3315187] Nature. 1983 Nov 10-16;306(5939):206-8 [6417541] Nature. 1984 Aug 2-8;310(5976):425-9 [6462228] Cell. 1985 Feb;40(2):359-69 [3838150] Somat Cell Mol Genet. 1985 Jan;11(1):87-92 [3919454] Proc Natl Acad Sci U S A. 1985 Nov;82(22):7656-60 [3865186] Cell. 1986 Mar 28;44(6):913-23 [2420469] Proc Natl Acad Sci U S A. 1986 Jun;83(11):3830-3 [3459159] Mutat Res. 1986 Jul;166(1):59-69 [2425254] J Biol Chem. 1986 Dec 15;261(35):16666-72 [3023360] Nucleic Acids Res. 1986 Nov 25;14(22):8979-95 [3786142] Proc Natl Acad Sci U S A. 1986 Dec;83(23):8878-82 [3466163] Mutat Res. 1987 Jan;183(1):69-74 [3025723] Cell. 1987 Aug 28;50(5):789-99 [3621344] Carcinogenesis. 1987 Sep;8(9):1333-6 [3621470] Cell. 1987 Oct 23;51(2):241-9 [3664636] Proc Natl Acad Sci U S A. 1983 Sep;80(18):5655-9 [6577448] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - An Hebrew language version of the Stroop test. AN - 85230548; pmid-3211671 AB - We present normative data from a Hebrew language version of the Stroop color-word test. In this sample of college-educated Israeli young adults, 18 women and 28 men with a mean age of 28.4 yr. completed a Hebrew language Stroop test. When compared with 1978 English language norms of Golden, Hebrew speakers were slower on color-word reading and color naming, similar on naming the color of incongruently colored names of colors, and showed less interference. Slowed color-word reading and color-naming may reflect the two-syllable length of the Hebrew names for one-syllable length English language colors; reduced interference may reflect the exclusion of vowels in much Hebrew printing and subjects' ability to provide competing, nonconflicting words while naming the color of words in which the hue and the lexical content do not match. JF - Perceptual and Motor Skills AU - Ingraham, L J AU - Chard, F AU - Wood, M AU - Mirsky, A F AD - Laboratory of Psychology and Psychopathology, National Institute of Mental Health, Bethesda, Maryland 20892. PY - 1988 SP - 187 EP - 192 VL - 67 IS - 1 SN - 0031-5125, 0031-5125 KW - Comparative Study KW - Reading KW - Verbal Behavior KW - Human KW - Adult KW - Israel KW - Female KW - Male KW - Color Perception KW - Language KW - Attention KW - Psychological Tests UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85230548?accountid=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=Perceptual+and+Motor+Skills&rft.atitle=An+Hebrew+language+version+of+the+Stroop+test.&rft.au=Ingraham%2C+L+J%3BChard%2C+F%3BWood%2C+M%3BMirsky%2C+A+F&rft.aulast=Ingraham&rft.aufirst=L&rft.date=1988-08-01&rft.volume=67&rft.issue=1&rft.spage=187&rft.isbn=&rft.btitle=&rft.title=Perceptual+and+Motor+Skills&rft.issn=00315125&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Effects of botulinum toxin injections on speech in adductor spasmodic dysphonia. AN - 85164201; pmid-3399071 AB - Adductor spasmodic dysphonia involves an overadduction of the vocal folds during speech causing uncontrolled voice and pitch breaks and slow, effortful speech. The disorder is resistant to speech therapy and often recurs following initial benefit from unilateral recurrent laryngeal nerve resection. Botulinum toxin injections into multiple sites of the thyroarytenoid muscle on one side were performed in 16 patients. Speech was recorded prior to injection and three times post-injection. Symptoms were measured by two examiners from speech spectrograms without knowledge of speaker identity or recording session. Significant (p less than or equal to 0.03) reductions in pitch and voice breaks, phonatory aperiodicity, and sentence time occurred only when injections resulted in unilateral vocal fold paralysis. Symptoms returned with the restoration of vocal fold movement, 3 months later. Reduction in speed of swallowing without aspiration was reported in 80% of cases. Although speech volume was reduced, there were no instances of aphonia. JF - Neurology AU - Ludlow, Christy L AU - Naunton, R F AU - Sedory, S E AU - Schulz, Geralyn Marie AU - Hallett, M AD - Laryngeal and Speech Section, National Institute of Neurological Disorders and Stroke; Department of Speech and Hearing Sciences, Columbian College of Arts and Sciences, George Washington University PY - 1988 SP - 1220 EP - 1225 VL - 38 IS - 8 SN - 0028-3878, 0028-3878 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85164201?accountid=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=Effects+of+botulinum+toxin+injections+on+speech+in+adductor+spasmodic+dysphonia.&rft.au=Ludlow%2C+Christy+L%3BNaunton%2C+R+F%3BSedory%2C+S+E%3BSchulz%2C+Geralyn+Marie%3BHallett%2C+M&rft.aulast=Ludlow&rft.aufirst=Christy&rft.date=1988-08-01&rft.volume=38&rft.issue=8&rft.spage=1220&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 - Molecular and genetic analysis of cystic fibrosis. AN - 78667420; 3066743 JF - Genomics AU - Dean, M AD - Biological Carcinogenesis Development Program, NCI-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 93 EP - 99 VL - 3 IS - 2 SN - 0888-7543, 0888-7543 KW - Index Medicus KW - Genetic Linkage KW - Humans KW - Chromosomes, Human KW - Restriction Mapping KW - Genes KW - Cystic Fibrosis -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78667420?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+and+genetic+analysis+of+cystic+fibrosis.&rft.au=Dean%2C+M&rft.aulast=Dean&rft.aufirst=M&rft.date=1988-08-01&rft.volume=3&rft.issue=2&rft.spage=93&rft.isbn=&rft.btitle=&rft.title=Genomics&rft.issn=08887543&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-06 N1 - Date created - 1989-04-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evaluation of rodent sperm, vaginal cytology, and reproductive organ weight data from National Toxicology Program 13-week studies. AN - 78652199; 3220212 AB - Sperm morphology and vaginal cytology examinations (SMVCEs), which include evaluations of motility, concentration and head morphology of sperm from the cauda epididymis, and male reproductive organ weight data, were developed by the National Toxicology Program as a screening system for reproductive toxicants. An analysis was conducted of SMVCE studies carried out at the end of fifty 13-week studies (25 for rats, 25 for mice) over a 3-year period. Statistically significant changes in these studies were summarized, as were control data for each male endpoint (mean, SD, 95% confidence limits around the mean, median, and statistical power). Reproductive organ weights (testis, epididymis, cauda epididymis) and sperm motility were the most statistically powerful endpoints evaluated; sperm head morphology may also be a sensitive endpoint for detecting reproductive toxicants. For 24 chemicals tested in both rats and mice, the concordance of results [i.e., no adverse effect in either species, or at least one SMVCE endpoint (not necessarily the same one) adversely affected in both species] was 58%. These data suggest that detection of potential reproductive toxicants might be best when both species are used. Types of sperm head abnormalities and their relative proportion of the total did not differ among control and treatment groups. Estrous cycle data were obtained in the final week of forty-six 13-week studies (23 for mice, 23 for rats). Only 3 chemicals caused an increase in mean cycle length compared with the control group. More data from breeding studies in which female estrous cycle length is measured are needed to assess fully the association of cycle length with reproductive outcome; stages of the estrous cycle are so variable that they may not be useful in assessing potential toxicity. Interlaboratory variability in SMVCE values for many endpoints was documented. Very few of the chemicals that form the basis of this report have been evaluated in definitive reproductive toxicology protocols; a companion paper compares changes in SMVCE endpoints with the outcome of continuous breeding reproduction studies. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Morrissey, R E AU - Schwetz, B A AU - Lamb, J C AU - Ross, M D AU - Teague, J L AU - Morris, R W AD - National Institute of Environmental Health Sciences, National Toxicology Program, Research Triangle Park, North Carolina 27709. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 343 EP - 358 VL - 11 IS - 2 SN - 0272-0590, 0272-0590 KW - Index Medicus KW - Space life sciences KW - Sperm Head -- ultrastructure KW - Body Weight KW - Mice, Inbred Strains KW - Animals KW - Rats, Inbred F344 KW - Sperm Count KW - Reference Standards KW - Sperm Motility KW - Organ Size KW - Male KW - Female KW - Vagina -- cytology KW - Rats -- physiology KW - Mice -- physiology KW - Spermatozoa -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78652199?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Evaluation+of+rodent+sperm%2C+vaginal+cytology%2C+and+reproductive+organ+weight+data+from+National+Toxicology+Program+13-week+studies.&rft.au=Morrissey%2C+R+E%3BSchwetz%2C+B+A%3BLamb%2C+J+C%3BRoss%2C+M+D%3BTeague%2C+J+L%3BMorris%2C+R+W&rft.aulast=Morrissey&rft.aufirst=R&rft.date=1988-08-01&rft.volume=11&rft.issue=2&rft.spage=343&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 - 1989-03-23 N1 - Date created - 1989-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Association of sperm, vaginal cytology, and reproductive organ weight data with results of continuous breeding reproduction studies in Swiss (CD-1) mice. AN - 78651597; 3220213 AB - In continuous breeding reproduction studies in which an adverse effect on fertility was detected over an 18-week treatment period, a crossover mating trial was then conducted to determine the affected sex. Results of 25 crossover breeding studies conducted using Swiss (CD-1) mice were compared with results of sperm morphology and vaginal cytology examinations (SMVCEs) conducted at the conclusion of the mating trial. SMVCE endpoints include sperm concentration, motility, and morphology, vaginal cytology, and male reproductive organ weights. In most SMVCE studies multiple endpoints were adversely affected. For male reproductive toxicants, sperm motility was decreased in 89% of the studies, and absolute right epididymis and right testis weights were affected less frequently (80% each). Among studies with no detectable reduction in male breeding performance, 87% exhibited no detectable decrease in epididymis weight. Eighty-two percent had no change in cauda epididymis weight and 80% had no significant change in sperm concentration. An increase in female cycle length was associated (100%) with an effect on breeding due to female dysfunction. Overall accuracy, defined as correct identification of toxicants and nontoxicants, was highest for epididymis weight (84%), followed by cauda epididymis weight and sperm motility (79% each), and sperm concentration (76%). Female cycle length was so variable that the overall accuracy of the parameter in 13 studies was 69%. With the variety of chemicals used in this analysis, the association of abnormal sperm morphology with reproductive outcome was 71%. Control data (mean, 95% confidence interval around the mean, median, and statistical sensitivity) for each male endpoint (parent, and offspring at 10 weeks of age following a single breeding) were summarized from each of the two laboratories that conducted the studies. For several endpoints, statistical power was dependent on the laboratory conducting the studies. In general, the statistical sensitivity was relatively high for reproductive organ weights, although it was less for smaller organs such as the prostate. On the basis of both the biological and statistical analyses, it is recommended that multiple SMVCE endpoints, including sperm measures, be included in screens for reproductive toxicants. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Morrissey, R E AU - Lamb, J C AU - Schwetz, B A AU - Teague, J L AU - Morris, R W AD - National Institute of Environmental Health Sciences, National Toxicology Program, Research Triangle Park, North Carolina 27709. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 359 EP - 371 VL - 11 IS - 2 SN - 0272-0590, 0272-0590 KW - Index Medicus KW - Sperm Head -- ultrastructure KW - Animals KW - Fertility KW - Testis -- anatomy & histology KW - Sex Factors KW - Reference Standards KW - Reproduction KW - Mice KW - Male KW - Female KW - Pregnancy KW - Organ Size -- drug effects KW - Vagina -- cytology KW - Spermatozoa -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78651597?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Association+of+sperm%2C+vaginal+cytology%2C+and+reproductive+organ+weight+data+with+results+of+continuous+breeding+reproduction+studies+in+Swiss+%28CD-1%29+mice.&rft.au=Morrissey%2C+R+E%3BLamb%2C+J+C%3BSchwetz%2C+B+A%3BTeague%2C+J+L%3BMorris%2C+R+W&rft.aulast=Morrissey&rft.aufirst=R&rft.date=1988-08-01&rft.volume=11&rft.issue=2&rft.spage=359&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 - 1989-03-23 N1 - Date created - 1989-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The acute toxicity of 2,3,4,7,8-pentachlorodibenzofuran (4PeCDF) in the male Fischer rat. AN - 78651039; 3220203 AB - Polychlorinated dibenzofurans are ubiquitous environmental pollutants which have great potential for human exposure. To characterize the toxicity of 2,3,4,7,8-pentachlorodibenzofuran (4PeCDF), male F344 rats were administered a single oral dose of 0, 100, 250, 500, 1000, or 2000 micrograms 4PeCDF/kg. A progressive and dose-dependent loss of body weight was evident by 3 days after treatment. Signs of toxicity included piloerection, hair loss, hypoactivity, morbidity, and death. Death occurred as soon as 14 days after treatment and continued throughout the 35-day observation period. The LD50/35 was estimated to be 916 micrograms/kg with a 95% confidence interval of 565-1484 micrograms/kg. Dose-dependent increases were observed in serum cholesterol, triglyceride, and bile acid concentrations and in sorbitol dehydrogenase and aspartate aminotransferase activities. The hematocrit, hemoglobin, mean corpuscular volume, and mean corpuscular hemoglobin concentrations were depressed in a dose-dependent fashion. Hepatic ethoxyresorufin-O-deethylase (EROD) activity was increased in all treatment groups approximately 25 times above that of control animals. Lymphoid depletion in the thymus and spleen was observed in the three highest doses and thymic atrophy was present at all dose levels. Absolute liver weight and the liver:body weight ratio were significantly increased above controls. Hepatotoxicity was dose-dependent and was characterized by lipid accumulation resulting in hepatocytomegaly. Epithelial hyperplasia and focal ulcerations of the forestomach was observed in animals administered 500 micrograms 4PeCDF/kg. Spontaneous cardiomyopathy was exacerbated by treatment with 2000 micrograms/kg. Since 4PeCDF and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) produce a similar spectrum of toxic effects, the biochemical mechanism(s) of toxicity for these chemicals may be similar. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Brewster, D W AU - Uraih, L C AU - Birnbaum, L S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 236 EP - 249 VL - 11 IS - 2 SN - 0272-0590, 0272-0590 KW - Benzofurans KW - 0 KW - Bile Acids and Salts KW - Triglycerides KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Cholesterol KW - 97C5T2UQ7J KW - Oxidoreductases KW - EC 1.- KW - Cytochrome P-450 CYP1A1 KW - EC 1.14.14.1 KW - 2,3,4,7,8-pentachlorodibenzofuran KW - U4C2RV3124 KW - Index Medicus KW - Triglycerides -- blood KW - Animals KW - Liver -- enzymology KW - Liver -- pathology KW - Cytochrome P-450 Enzyme System -- metabolism KW - Bile Acids and Salts -- metabolism KW - Rats KW - Cholesterol -- blood KW - Rats, Inbred F344 KW - Oxidoreductases -- metabolism KW - Body Weight -- drug effects KW - Lethal Dose 50 KW - Macaca mulatta KW - Male KW - Organ Size -- drug effects KW - Benzofurans -- blood KW - Benzofurans -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78651039?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+acute+toxicity+of+2%2C3%2C4%2C7%2C8-pentachlorodibenzofuran+%284PeCDF%29+in+the+male+Fischer+rat.&rft.au=Brewster%2C+D+W%3BUraih%2C+L+C%3BBirnbaum%2C+L+S&rft.aulast=Brewster&rft.aufirst=D&rft.date=1988-08-01&rft.volume=11&rft.issue=2&rft.spage=236&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 - 1989-03-23 N1 - Date created - 1989-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Developmental characterization and chromosomal mapping of the 5-azacytidine-sensitive fluF locus of Aspergillus nidulans. AN - 78596234; 2463470 AB - In Aspergillus nidulans, a fungus that possesses negligible, if any, levels of methylation in its genome, low concentrations of 5-azacytidine (5-AC) convert a high percentage of the cell population to fluffy phenotypic variants through a heritable modification of a single nuclear gene (M. Tamame, F. Antequera, J. R. Villanueva, and T. Santos, Mol. Cell. Biol. 3:2287-2297, 1983). This new 5-AC-altered locus, designated here fluF1, was mapped as the closest marker to the centromere that has been identified so far on the right arm of chromosome VIII. Of all mutagens tested, only 5-AC induced the fluffy phenotype with a significant frequency. Furthermore, we determined that the wild-type, dominant allele of the fluF gene was primarily accessible to modification by 5-AC at the initial stages of fungal vegetative growth. These results indicated that 5-AC does not act through random mutagenic action but, rather, that fluF constitutes a specific target for this drug during a well-defined period of fungal development. Alteration of fluF by 5-AC resulted in a dramatic modification of the developmental program of A. nidulans. The resulting fluffy clones were characterized by massive, uncontrolled proliferation of undifferentiated hyphae, a drastic delay in the onset of asexual differentiation (conidiation), and colonies with an invasive nature. These features are reminiscent of the malignant properties of tumor cells. We propose that the locus fluF plays a primary role in the control of cell proliferation in A. nidulans and that its alteration by 5-AC produces pleiotropic modifications of the developmental program of this fungus. JF - Molecular and cellular biology AU - Tamame, M AU - Antequera, F AU - Santos, E AD - Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 3043 EP - 3050 VL - 8 IS - 8 SN - 0270-7306, 0270-7306 KW - Azacitidine KW - M801H13NRU KW - Index Medicus KW - Genotype KW - Genetic Variation KW - Cell Nucleus -- ultrastructure KW - Crosses, Genetic KW - Mutation KW - Aspergillus nidulans -- drug effects KW - Azacitidine -- pharmacology KW - Genes, Fungal -- drug effects KW - Aspergillus nidulans -- genetics KW - Aspergillus nidulans -- growth & development KW - Chromosome Mapping UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78596234?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Developmental+characterization+and+chromosomal+mapping+of+the+5-azacytidine-sensitive+fluF+locus+of+Aspergillus+nidulans.&rft.au=Tamame%2C+M%3BAntequera%2C+F%3BSantos%2C+E&rft.aulast=Tamame&rft.aufirst=M&rft.date=1988-08-01&rft.volume=8&rft.issue=8&rft.spage=3043&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 - 1989-02-23 N1 - Date created - 1989-02-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Genetics. 1970 Oct;66(2):267-79 [5512361] Mutat Res. 1969 Sep-Oct;8(2):255-64 [5366006] Biochim Biophys Acta. 1983 Sep 9;740(4):355-61 [6411122] Annu Rev Biochem. 1983;52:93-124 [6311083] J Bacteriol. 1983 Oct;156(1):155-60 [6352675] Mol Cell Biol. 1983 Dec;3(12):2287-97 [6197627] Mutat Res. 1984 Jan;139(1):21-4 [6197648] Cell. 1984 Jun;37(2):359-65 [6722879] Proc Natl Acad Sci U S A. 1984 Jun;81(11):3389-93 [6203119] EMBO J. 1984 May;3(5):961-7 [6203746] J Biol Chem. 1984 Jul 10;259(13):8033-6 [6330093] Cell. 1984 Oct;38(3):791-800 [6207933] Proc Natl Acad Sci U S A. 1984 Nov;81(22):6993-7 [6209710] Cell. 1985 Mar;40(3):485-6 [2578884] J Biol Chem. 1985 Apr 10;260(7):4059-68 [2579944] Nature. 1986 May 15-21;321(6067):209-13 [2423876] Mol Cell Biol. 1986 May;6(5):1698-705 [2431285] Mol Cell Biol. 1986 Aug;6(8):2944-9 [2431295] Cell. 1987 Jan 16;48(1):11-24 [2431792] Mol Cell Biol. 1987 Jun;7(6):2196-200 [2439904] Science. 1987 Oct 9;238(4824):163-70 [3310230] Adv Genet. 1953;5:141-238 [13040135] Mutat Res. 1983 Jul;121(1):47-52 [6191216] Genet Res. 1965 Nov;6(3):352-9 [5848714] Proc Natl Acad Sci U S A. 1983 Aug;80(15):4842-6 [6192443] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of covalent binding from halothane metabolism in hepatic microsomes from phenobarbital-induced and hyperthyroid rats. AN - 78521512; 3188577 AB - 1. Hepatic microsomal suspensions from rats pretreated with saline, phenobarbital or triiodothyronine were incubated with 14C-halothane under aerobic and anerobic conditions. 2. Metabolism of halothane by microsomes from phenobarbital-induced rats under anaerobic conditions resulted in covalent binding of 14C to microsomal lipids, and to a lesser extent, microsomal proteins, as seen in previous studies. Covalent binding was decreased with incubation under aerobic conditions. 3. Metabolism of halothane by microsomal suspensions from hyperthyroid rats produced much less covalent binding to microsomal lipids and proteins, with binding similar to, or less than, that observed with microsomes from saline-treated rats. The covalent binding of halothane to protein of microsomes from hyperthyroid rats was dependent upon metabolism, and was inhibited by SKF 525A, reduced glutathione, or cytosol. 4. The in vitro observations with respect to covalent binding are inconsistent with previous reports on halothane hepatotoxicity in hyperthyroid rats in vivo. This inconsistency and the relatively small extent of covalent binding with microsomes from hyperthyroid rats observed, suggests that covalent binding is not an important mechanism of halothane hepatotoxicity in the hyperthyroid rat model. JF - Xenobiotica; the fate of foreign compounds in biological systems AU - Smith, A C AU - Roberts, S M AU - James, R C AU - Berman, L M AU - Harbison, R D AD - National Cancer Institute, Bethesda, MD. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 991 EP - 1001 VL - 18 IS - 8 SN - 0049-8254, 0049-8254 KW - Proteins KW - 0 KW - Pyridines KW - Triiodothyronine KW - 06LU7C9H1V KW - metapyrone KW - 17286-92-9 KW - NADP KW - 53-59-8 KW - Glutathione KW - GAN16C9B8O KW - Halothane KW - UQT9G45D1P KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Chemical and Drug Induced Liver Injury KW - NADP -- pharmacology KW - Pyridines -- pharmacology KW - Proteins -- metabolism KW - Glutathione -- pharmacology KW - Male KW - Lipid Metabolism KW - Phenobarbital -- pharmacology KW - Halothane -- metabolism KW - Microsomes, Liver -- metabolism KW - Microsomes, Liver -- drug effects KW - Hyperthyroidism -- metabolism KW - Halothane -- toxicity KW - Hyperthyroidism -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78521512?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparison+of+covalent+binding+from+halothane+metabolism+in+hepatic+microsomes+from+phenobarbital-induced+and+hyperthyroid+rats.&rft.au=Smith%2C+A+C%3BRoberts%2C+S+M%3BJames%2C+R+C%3BBerman%2C+L+M%3BHarbison%2C+R+D&rft.aulast=Smith&rft.aufirst=A&rft.date=1988-08-01&rft.volume=18&rft.issue=8&rft.spage=991&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 - 1988-12-07 N1 - Date created - 1988-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chronic silastic central venous catheterization for induction, maintenance and support of persistent granulocytopenia in rabbits. AN - 78513476; 3184859 AB - In order to investigate new approaches in diagnosis, prevention and treatment of infectious complicating chemotherapy-induced granulocytopenia, we developed and prospectively evaluated a method of chronic central venous catheterization for the induction, maintenance and support of persistent granulocytopenia in rabbits. The method entails a central venous silastic catheter with a subcutaneous tunnel and a heparin lock device for repeated non-traumatic sampling of blood and administration of medications. During the course of 10 months, 226 rabbits were studied. Mean duration of catheter placement was 27 days, 17 of which were spent in granulocytopenia. Two-way flow was sustained throughout the duration of placement in 205 rabbits (91%) and for 5,845 (95%) of a total 6,163 catheter-days. All but two catheters could be flushed throughout the duration of their placement. Postoperative infectious complications related to catheter insertion developed in less than 1% of the rabbits. This method of chronic catheterization safely provides long-term venous access for studies requiring frequent venous access, including the painless induction, maintenance, and support of chronic granulocytopenia in rabbits. JF - Laboratory animal science AU - Walsh, T J AU - Bacher, J AU - Pizzo, P A AD - Section of Infectious Diseases, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 467 EP - 471 VL - 38 IS - 4 SN - 0023-6764, 0023-6764 KW - Cytarabine KW - 04079A1RDZ KW - Index Medicus KW - Animals KW - Prospective Studies KW - Rabbits KW - Cytarabine -- administration & dosage KW - Female KW - Catheters, Indwelling KW - Catheterization, Central Venous KW - Disease Models, Animal KW - Agranulocytosis -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78513476?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Chronic+silastic+central+venous+catheterization+for+induction%2C+maintenance+and+support+of+persistent+granulocytopenia+in+rabbits.&rft.au=Walsh%2C+T+J%3BBacher%2C+J%3BPizzo%2C+P+A&rft.aulast=Walsh&rft.aufirst=T&rft.date=1988-08-01&rft.volume=38&rft.issue=4&rft.spage=467&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 - 1988-12-05 N1 - Date created - 1988-12-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ankylosis of hock joints in group caged male B6C3F1 mice. AN - 78511002; 3184849 AB - Enlarged hock joints were observed during 1983 in B6C3F1 mice of chronic toxicity and carcinogenicity studies sponsored by the National Toxicology Program (NTP). Subsequently, approximately 9,500 B6C3F1 mice on 32 NTP chemical toxicity and carcinogenicity studies were evaluated for this condition by clinical examination. Group caged male B6C3F1 mice had thickening and reduced mobility of the hock joints at prevalences of 1.2% up to 6 months of age; 23% at 6 to 12 months of age; and 62% at 13 to 26 months of age. Group caged female B6C3F1 mice had a prevalence of 2% or less. Histologically, affected mice had periarticular exostoses on the bones of the hock joints, with formation of bony bridges around joints and deposition of new bone in joint spaces, resulting in partial or complete ankylosis. Individually caged male and female B6C3F1 mice were not affected. The cause of the ankylosis was not determined, but its occurrence in the NTP studies has been reduced by individual caging. JF - Laboratory animal science AU - Rao, G N AU - Lindsey, J R AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 417 EP - 421 VL - 38 IS - 4 SN - 0023-6764, 0023-6764 KW - Index Medicus KW - Animals KW - Hindlimb KW - Male KW - Ankylosis -- pathology KW - Ankylosis -- epidemiology KW - Joints -- pathology KW - Rodent Diseases -- epidemiology KW - Housing, Animal KW - Ankylosis -- veterinary KW - Mice KW - Rodent Diseases -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78511002?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Ankylosis+of+hock+joints+in+group+caged+male+B6C3F1+mice.&rft.au=Rao%2C+G+N%3BLindsey%2C+J+R&rft.aulast=Rao&rft.aufirst=G&rft.date=1988-08-01&rft.volume=38&rft.issue=4&rft.spage=417&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 - 1988-12-05 N1 - Date created - 1988-12-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Do cage effects influence tumor incidence? An examination of laboratory animal carcinogenicity studies utilizing Fischer 344 rats. AN - 78499681; 3183292 AB - Approximately 125 carcinogenicity studies in Fischer 344 rats conducted by the National Toxicology Program (NTP) were examined to determine the frequency with which cage effects were associated with observed carcinogenic responses. All studies involving groups of 50 rats housed five per cage and showing evidence of chemically-related carcinogenicity were considered. For each of these experiments, two statistical analyses were carried out for each dosed and control group: (i) a test to determine whether or not the occurrence of tumors clustered within cages; and (ii) an evaluation to determine whether or not tumor incidences differed significantly between differing cage shelf levels. These analyses showed that the numbers of statistically significant (P less than 0.05 or P less than 0.01) effects were consistent with the number expected by chance alone. Thus, cage-related factors appeared to have little or no impact upon tumor incidence in these particular studies. Experimental design protocols now used by the NTP (which include random assignment of animals to cages; random assignment of columns of cages to dosed and control groups; and periodic rotation of cage location) further reduce the likelihood that factors associated with the housing of the animals could influence tumor incidence in current studies. JF - Journal of applied toxicology : JAT AU - Haseman, J K AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 267 EP - 273 VL - 8 IS - 4 SN - 0260-437X, 0260-437X KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Neoplasms, Experimental -- etiology KW - Female KW - Housing, Animal KW - Carcinogenicity Tests KW - Animals, Laboratory UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78499681?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+toxicology+%3A+JAT&rft.atitle=Do+cage+effects+influence+tumor+incidence%3F+An+examination+of+laboratory+animal+carcinogenicity+studies+utilizing+Fischer+344+rats.&rft.au=Haseman%2C+J+K&rft.aulast=Haseman&rft.aufirst=J&rft.date=1988-08-01&rft.volume=8&rft.issue=4&rft.spage=267&rft.isbn=&rft.btitle=&rft.title=Journal+of+applied+toxicology+%3A+JAT&rft.issn=0260437X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-21 N1 - Date created - 1988-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A case-referent study of soft-tissue sarcoma and Hodgkin's disease. Farming and insecticide use. AN - 78469982; 3175554 AB - A population-based case-referent study in Kansas examined the relationship between exposure to insecticides and the development of soft-tissue sarcoma (STS) and Hodgkin's disease (HD). Data from telephone interviews for 133 STS cases, 121 HD cases, and 948 referents indicated that STS was associated with use of insecticides on animals, but not on crops. HD was not significantly associated with either use. STS risk was higher among the farmers who themselves mixed or applied insecticides to animals than among farmers who did not. Farmers who failed to use any protective equipment to reduce insecticide exposure were at a significantly elevated risk of STS. Risk rose with early calendar year of first use. The excess risk appeared to be primarily among fibrous and myomatous sarcomas with little association seen for lipomatous or other STS neoplasms. Myomatous sarcomas increased significantly with duration and time since first use of insecticides on animals. If the reported association between STS and insecticides is causal, the data suggest that exposure to the agent(s) responsible may have been reduced in the mid-1950s or the agent(s) have an average latency period for STS of at least 20 years. JF - Scandinavian journal of work, environment & health AU - Hoar Zahm, S AU - Blair, A AU - Holmes, F F AU - Boysen, C D AU - Robel, R J AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 224 EP - 230 VL - 14 IS - 4 SN - 0355-3140, 0355-3140 KW - Hydrocarbons, Chlorinated KW - 0 KW - Insecticides KW - Pesticides KW - Index Medicus KW - Risk Factors KW - Humans KW - Aged KW - Pesticides -- adverse effects KW - Insecticides -- adverse effects KW - Hodgkin Disease -- chemically induced KW - Soft Tissue Neoplasms -- chemically induced KW - Agricultural Workers' Diseases -- chemically induced KW - Sarcoma -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78469982?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+case-referent+study+of+soft-tissue+sarcoma+and+Hodgkin%27s+disease.+Farming+and+insecticide+use.&rft.au=Hoar+Zahm%2C+S%3BBlair%2C+A%3BHolmes%2C+F+F%3BBoysen%2C+C+D%3BRobel%2C+R+J&rft.aulast=Hoar+Zahm&rft.aufirst=S&rft.date=1988-08-01&rft.volume=14&rft.issue=4&rft.spage=224&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 - 1988-11-08 N1 - Date created - 1988-11-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of interleukin 2 and phorbol myristate acetate augmentation of expression of transfected human interferon-gamma genomic DNA. AN - 78444209; 3139787 AB - We have reported that human interferon-gamma (IFN-gamma) genomic DNA is expressed after transfection into a mouse T-lymphoblastoid cell line and expression can be enhanced by both interleukin 2 (IL2) and phorbol myristate acetate (PMA). It can now be shown that PMA rapidly induces new transcription of the IFN-gamma gene and that increased human (Hu) IFN-gamma can be detected by 2 h after the addition of PMA to the mouse cells. Enhancement of IFN-gamma production by IL2 takes place with similar kinetics with increased IFN-gamma production observed at 4-6 h after IL2 addition, although the maximum amount of IFN-gamma produced in response to IL2 was significantly lower than that produced in response to PMA. Furthermore, along with increased levels of cytoplasmic IFN-gamma RNA, we were able to demonstrate increased nuclear transcription at 4 h after IL2 treatment. Stimulation of IFN-gamma mRNA by both PMA and IL2 could occur in the presence of cycloheximide, indicating that protein synthesis was not required for the initial stimulation to occur. However, the functional half-life of IFN-gamma mRNA after actinomycin D treatment was higher in cells that had been treated with PMA when compared with untreated or IL2-treated cells. This data indicates that there are quantitative differences in the ability of PMA or IL2 to augment IFN-gamma production, and that PMA may increase IFN-gamma production in the transfected cell by additional mechanisms, such as increasing mRNA stability. JF - Journal of interferon research AU - Young, H A AU - Birchenall-Sparks, M AU - Kovacs, E AU - Dorman, L AU - Ruscetti, F W AD - Laboratory of Molecular Immunoregulation, NCI-FCRF, Frederick, MD 21701. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 527 EP - 538 VL - 8 IS - 4 SN - 0197-8357, 0197-8357 KW - Interferon Inducers KW - 0 KW - Interleukin-2 KW - RNA, Messenger KW - Receptors, Interleukin-2 KW - Interferon-gamma KW - 82115-62-6 KW - DNA KW - 9007-49-2 KW - Cycloheximide KW - 98600C0908 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Drug Interactions KW - Half-Life KW - Transfection KW - Receptors, Interleukin-2 -- analysis KW - Interferon Inducers -- pharmacology KW - Cells, Cultured KW - Kinetics KW - Humans KW - Cycloheximide -- pharmacology KW - RNA, Messenger -- analysis KW - Radioimmunoassay KW - Cell Division KW - Interleukin-2 -- pharmacology KW - Interferon-gamma -- genetics KW - DNA -- genetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Gene Expression Regulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78444209?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Characterization+of+interleukin+2+and+phorbol+myristate+acetate+augmentation+of+expression+of+transfected+human+interferon-gamma+genomic+DNA.&rft.au=Young%2C+H+A%3BBirchenall-Sparks%2C+M%3BKovacs%2C+E%3BDorman%2C+L%3BRuscetti%2C+F+W&rft.aulast=Young&rft.aufirst=H&rft.date=1988-08-01&rft.volume=8&rft.issue=4&rft.spage=527&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 - 1988-11-23 N1 - Date created - 1988-11-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Changes in cerebral receptors for gamma aminobutyric acid in patients with hepatic encephalopathy. AN - 78423417; 2843723 AB - If the gamma-aminobutyric acid (GABA) inhibitory neurotransmitter system plays an important role in the mediation of hepatic encephalopathy (HE) in man, changes in the status of receptors for GABA in the brain may occur in patients with HE. To test this possibility, brains were obtained at autopsy from 11 patients who had died of causes unrelated to liver disease and from 11 patients who had died with chronic liver disease. Eight of the liver disease group had overt HE at the time of death. The specific binding of GABA to synaptic membranes isolated from frontal cortex was determined. Mean specific binding of GABA for patients with cirrhosis without overt HE was similar to that for control patients. In contrast, corresponding means for patients who had mild HE (stages I-III) and for patients who had severe HE (stage IV) were 45% higher (p less than 0.05) and 43% lower, respectively, than that for control patients. The mean specific binding of GABA was significantly greater for patients with mild HE than in patients with severe HE (p less than 0.025). Scatchard plots of the GABA binding data were curvilinear and consistent with a model of GABA receptors with two independent binding sites. Computer-assisted analysis of the binding data indicated that the altered GABA binding observed in patients with HE is attributable to changes in the affinity rather than the density of both GABA receptors (increased affinities in mild HE, and decreased affinities in hepatic coma). These findings are compatible with the hypothesis that alterations in GABAergic neurotransmission are associated with and contribute to the syndrome of HE in man. JF - Liver AU - Ferenci, P AU - Riederer, P AU - Jellinger, K AU - Schafer, D F AU - Jones, E A AD - Liver Diseases Section, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 225 EP - 230 VL - 8 IS - 4 SN - 0106-9543, 0106-9543 KW - Receptors, GABA-A KW - 0 KW - gamma-Aminobutyric Acid KW - 56-12-2 KW - Index Medicus KW - Liver Cirrhosis, Alcoholic -- metabolism KW - Coronary Disease -- metabolism KW - Aged, 80 and over KW - Humans KW - Aged KW - Middle Aged KW - gamma-Aminobutyric Acid -- metabolism KW - Synaptic Membranes -- metabolism KW - Male KW - Female KW - Receptors, GABA-A -- metabolism KW - Brain -- metabolism KW - Hepatic Encephalopathy -- pathology KW - Hepatic Encephalopathy -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78423417?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Changes+in+cerebral+receptors+for+gamma+aminobutyric+acid+in+patients+with+hepatic+encephalopathy.&rft.au=Ferenci%2C+P%3BRiederer%2C+P%3BJellinger%2C+K%3BSchafer%2C+D+F%3BJones%2C+E+A&rft.aulast=Ferenci&rft.aufirst=P&rft.date=1988-08-01&rft.volume=8&rft.issue=4&rft.spage=225&rft.isbn=&rft.btitle=&rft.title=Liver&rft.issn=01069543&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-27 N1 - Date created - 1988-10-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Testicular toxicity and reduced Sertoli cell numbers in neonatal rats by di(2-ethylhexyl)phthalate and the recovery of fertility as adults. AN - 78395241; 3413790 AB - Neonatal and adult rats (1, 2, 3, 6, and 12 weeks of age) were given five daily oral doses of di(2-ethylhexyl) phthalate (DEHP) (0, 10, 100, 1000, 2000 mg/kg) and histological changes in the testes were examined 24 hr after the last dose. Relative testis weights were reduced at doses of 1000 mg/kg in 1, 2, 3, and 6-week-old but not in 12-week-old rats, while doses of 2000 mg/kg were fatal to suckling rats and caused decreased relative testis weight but not death in 6- and 12-week-old rats. In neonatal rats (1 week old), DEHP (1000 mg/kg) caused a 35% decrease in Sertoli cell numbers while 2- and 3-week-old rats showed losses of spermatocytes but not of Sertoli cells. The 6- and 12-week-old rats showed loss of both spermatids and spermatocytes at 1000 and/or 2000 mg/kg. Total testicular zinc concentrations were decreased in 12-week-old but not in suckling (3-week) or weaned (6-week) rats. The results support the hypothesis that the Sertoli cell is the primary testicular target of phthalate ester toxicity since effects were observed at an age when only Sertoli cells were present. Fertility was assessed in mating trials in adult male rats after neonatal exposure to DEHP on Days 6-10. Although Sertoli cell number was reduced 24 hr after the last dose, the numbers were normal at 6 and 13 weeks of age. However, at 6 weeks there was a dose-related decrease in maturation of the spermatids in the tubules. There were no consistent changes in fertility, implantation rate, or numbers of live fetuses in untreated females mated with the DEHP-treated males. However, there were decreases in testis weight and testicular spermatid numbers at 13 and 19 weeks but not at 11, 12, 16, or 23 weeks of age. Therefore, a loss of Sertoli cells due to DEHP exposure neonatally did not affect the fertility of the rats as adults, but may have caused subtle effects on sperm production. JF - Toxicology and applied pharmacology AU - Dostal, L A AU - Chapin, R E AU - Stefanski, S A AU - Harris, M W AU - Schwetz, B A AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 104 EP - 121 VL - 95 IS - 1 SN - 0041-008X, 0041-008X KW - Phthalic Acids KW - 0 KW - Diethylhexyl Phthalate KW - C42K0PH13C KW - Zinc KW - J41CSQ7QDS KW - Index Medicus KW - Sertoli Cells -- drug effects KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Sperm Count -- drug effects KW - Age Factors KW - Testis -- metabolism KW - Cell Count -- drug effects KW - Zinc -- metabolism KW - Male KW - Organ Size -- drug effects KW - Fertility -- drug effects KW - Testicular Diseases -- pathology KW - Testicular Diseases -- chemically induced KW - Diethylhexyl Phthalate -- toxicity KW - Animals, Newborn -- growth & development KW - Phthalic Acids -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78395241?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Testicular+toxicity+and+reduced+Sertoli+cell+numbers+in+neonatal+rats+by+di%282-ethylhexyl%29phthalate+and+the+recovery+of+fertility+as+adults.&rft.au=Dostal%2C+L+A%3BChapin%2C+R+E%3BStefanski%2C+S+A%3BHarris%2C+M+W%3BSchwetz%2C+B+A&rft.aulast=Dostal&rft.aufirst=L&rft.date=1988-08-01&rft.volume=95&rft.issue=1&rft.spage=104&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 - 1988-09-26 N1 - Date created - 1988-09-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intrauterine radiation exposures and mental retardation. AN - 78390834; 3410697 AB - Small head size and mental retardation have been known as effects of intrauterine exposure to ionizing radiation since the 1920s. In the 1950s, studies of Japanese atomic-bomb survivors revealed that at 4-17 wk of gestation, the greater the dose, the smaller the brain (and head size), and that beginning at 0.5 Gy (50 rad) in Hiroshima, mental retardation increased in frequency with increasing dose. No other excess of birth defects was observed. Otake and Schull (1984) pointed out that the period of susceptibility to mental retardation coincided with that for proliferation and migration of neuronal elements from near the cerebral ventricles to the cortex. Mental retardation could be the result of interference with this process. Their analysis indicated that exposures at 8-15 wk to 0.01-0.02 Gy (1-2 rad) doubled the frequency of severe mental retardation. This estimate was based on small numbers of mentally retarded atomic-bomb survivors. Although nuclear accidents have occurred recently, new cases will hopefully be too rare to provide further information about the risk of mental retardation. It may be possible, however, to learn about lesser impairment. New psychometric tests may be helpful in detecting subtle deficits in intelligence or neurodevelopmental function. One such test is PEERAMID, which is being used in schools to identify learning disabilities due, for example, to deficits in attention, short- or long-term memory, or in sequencing information. This and other tests could be applied in evaluating survivors of intrauterine exposure to various doses of ionizing radiation. The results could change our understanding of the safety of low-dose exposures. JF - Health physics AU - Miller, R W AD - Clinical Epidemiology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 295 EP - 298 VL - 55 IS - 2 SN - 0017-9078, 0017-9078 KW - Index Medicus KW - Radiation Dosage KW - Cephalometry -- instrumentation KW - Nuclear Warfare KW - Humans KW - Brain -- radiation effects KW - Gestational Age KW - Infant, Newborn KW - Brain -- embryology KW - Japan KW - Female KW - Pregnancy KW - Intellectual Disability -- etiology KW - Fetus -- radiation effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78390834?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Intrauterine+radiation+exposures+and+mental+retardation.&rft.au=Miller%2C+R+W&rft.aulast=Miller&rft.aufirst=R&rft.date=1988-08-01&rft.volume=55&rft.issue=2&rft.spage=295&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 - 1988-10-07 N1 - Date created - 1988-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interferon-induced transcription of a major histocompatibility class I gene accompanies binding of inducible nuclear factors to the interferon consensus sequence. AN - 78389205; 2457903 AB - Interferon (IFN) induces transcription of major histocompatibility class I genes by way of the conserved cis-acting regulatory element, termed the IFN consensus sequence (ICS). Binding of nuclear factors to the ICS was studied in gel mobility shift assays with the 5' upstream region of the murine H-2Ld gene. We found that the ICS binds a constitutive nuclear factor present in lymphocytes and fibroblasts regardless of IFN treatment. Within 1 hr after IFN treatment, new ICS binding activity was induced, which consisted of at least two binding activities distinguished by their requirement for de novo protein synthesis. Methylation interference and competition experiments showed that both constitutive and induced factors bind to the same approximately equal to 10-base-pair binding site within the ICS. Site-directed mutagenesis of H-2Ld-chloramphenicol acetyltransferase fusion genes showed that mutations in the binding site, but not in other regions of the ICS, abolish transcriptional activation of class I genes by IFN, providing evidence that specific binding of nuclear factors to the ICS is an essential requirement for transcriptional induction. Finally, we show that IFN-inducible genes of various species share a sequence motif that is capable of competing for the nuclear factors identified here. We propose that specific protein binding to the conserved motif represents a basic mechanism of IFN-mediated transcriptional induction of a number of genes. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Shirayoshi, Y AU - Burke, P A AU - Appella, E AU - Ozato, K AD - Laboratory of Developmental and Molecular Immunity, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 5884 EP - 5888 VL - 85 IS - 16 SN - 0027-8424, 0027-8424 KW - Interferons KW - 9008-11-1 KW - Cycloheximide KW - 98600C0908 KW - Index Medicus KW - Animals KW - Cycloheximide -- pharmacology KW - Binding, Competitive KW - Mice KW - Amino Acid Sequence KW - Methylation KW - Transcription, Genetic -- drug effects KW - Interferons -- pharmacology KW - Genes, Regulator KW - Genes, MHC Class I UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78389205?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Interferon-induced+transcription+of+a+major+histocompatibility+class+I+gene+accompanies+binding+of+inducible+nuclear+factors+to+the+interferon+consensus+sequence.&rft.au=Shirayoshi%2C+Y%3BBurke%2C+P+A%3BAppella%2C+E%3BOzato%2C+K&rft.aulast=Shirayoshi&rft.aufirst=Y&rft.date=1988-08-01&rft.volume=85&rft.issue=16&rft.spage=5884&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 - 1988-10-05 N1 - Date created - 1988-10-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1982 Nov 25;257(22):13169-72 [6183260] Nature. 1982 Oct 28;299(5886):833-6 [6290893] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] Eur J Immunol. 1983 Jun;13(6):495-9 [6190661] Cell. 1984 Oct;38(3):745-55 [6548414] Nature. 1985 Apr 18-24;314(6012):637-9 [3990797] Cell. 1986 Jan 17;44(1):147-58 [3000619] Nucleic Acids Res. 1985 Dec 20;13(24):8765-85 [3001650] Cell. 1986 Jan 31;44(2):261-72 [3510743] Cell. 1986 Aug 1;46(3):389-99 [3755378] Nature. 1986 Aug 21-27;322(6081):743-6 [3748155] Nature. 1986 Oct 16-22;323(6089):640-3 [3095662] Cell. 1986 Dec 26;47(6):921-8 [3096580] Proc Natl Acad Sci U S A. 1986 Dec;83(24):9537-41 [3467324] Interferon. 1986;7:47-87 [2434435] J Cell Physiol. 1987 Feb;130(2):276-83 [3102507] Proc Natl Acad Sci U S A. 1987 May;84(10):3380-4 [3106967] Cell. 1987 Jun 19;49(6):729-39 [3034432] Cell. 1987 Jun 19;49(6):741-52 [3034433] Science. 1987 Jun 5;236(4806):1237-45 [3296191] Nature. 1987 Jun 25-Jul 1;327(6124):727-30 [3600771] Nature. 1987 Jul 9-15;328(6126):175-8 [2885756] Mol Cell Biol. 1987 Jul;7(7):2625-30 [3475569] Annu Rev Biochem. 1987;56:727-77 [2441659] Proc Natl Acad Sci U S A. 1987 Sep;84(18):6394-8 [3476954] Proc Natl Acad Sci U S A. 1988 Feb;85(3):723-7 [3422454] Mol Cell Biol. 1987 Dec;7(12):4498-504 [2830497] Mol Cell Biol. 1987 Dec;7(12):4542-8 [3501825] EMBO J. 1988 Jan;7(1):85-92 [3359997] Nucleic Acids Res. 1983 Mar 11;11(5):1213-26 [6186990] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - New understanding from epidemiology--the next 25 years. AN - 78386359; 3410695 AB - The epidemiology of radiation carcinogenesis is likely to be dominated during the next 25 y by the gradual maturation of major studies of populations exposed to substantial levels of radiation dose. During this period, for example, most of the new information on cancer risk among survivors of the 1945 atomic bombings of Hiroshima and Nagasaki will pertain to persons exposed at ages under 30. From the A-bomb survivor data and from a number of medically and occupationally irradiated populations now under study, it will be possible to construct a fairly complete picture of the temporal distribution of excess cancer risk over the remaining life span following exposure, a major source of uncertainty and controversy in current risk estimates. Provided that the necessary efforts are made, it should be possible to greatly increase our understanding of which organs and tissues are vulnerable to radiation carcinogenesis, variation by age at exposure and sex, and (what is most difficult at the present time) the influence of other risk factors and possible modifying factors on the magnitude of risk associated with radiation exposure. For some sites it may be possible, as it is now for breast cancer, to rule out certain broad classes of simple dose-response models. While the data gathered during the next 25 y will be nearly the last from some very important series, their information content should be extremely high. Thus, there is every reason to improve the resources, e.g., by improving dosimetry, enlarging samples, tapping new sources of case ascertainment, and gathering information on factors other than radiation dose. Modeling in epidemiological investigations depends heavily on work in experimental radiobiology. Thus far, the exchange has been largely in one direction, since epidemiological study design is mostly a matter of extracting information from "experiments" that have already taken place. With more epidemiological information, it seems reasonable to hope that detailed hypotheses, with direct relevance to areas of epidemiological uncertainty, may be generated suitable for experimental investigation. It seems likely that findings from large studies of populations exposed to relatively low levels of radiation, for which the signal-to-noise ratio is low, and for which random error and subtle sources of bias may have more than usual influence on reported results, will continue to generate controversy.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Health physics AU - Land, C E AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, MD 20205. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 269 EP - 278 VL - 55 IS - 2 SN - 0017-9078, 0017-9078 KW - Index Medicus KW - Humans KW - Ukraine KW - Leukemia, Radiation-Induced -- etiology KW - Child KW - Nuclear Reactors KW - Accidents KW - Lung Neoplasms -- etiology KW - Lung Neoplasms -- epidemiology KW - Leukemia, Radiation-Induced -- epidemiology KW - Risk Factors KW - Nuclear Warfare KW - Environmental Exposure KW - Middle Aged KW - Time Factors KW - Female KW - Male KW - Models, Theoretical KW - Neoplasms, Radiation-Induced -- etiology KW - Neoplasms, Radiation-Induced -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78386359?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=New+understanding+from+epidemiology--the+next+25+years.&rft.au=Land%2C+C+E&rft.aulast=Land&rft.aufirst=C&rft.date=1988-08-01&rft.volume=55&rft.issue=2&rft.spage=269&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 - 1988-10-07 N1 - Date created - 1988-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Spontaneous establishment and characterization of mouse keratinocyte cell lines in serum-free medium. AN - 78385939; 2457574 AB - Mouse keratinocytes cultures readily develop into established cell lines without undergoing a "crisis" in a newly-developed serum-free medium, LEP/MK2. LEP/MK2 consists of calcium-free MEM with non-essential amino acids supplemented with 8 factors. Two lines, MK1 and MKDC4, have been isolated and have now doubled more than 400 and 200 times respectively. In MK1 cells, Giemsa banding has revealed significant karyotypic changes as early as the 4th passage, leading to a near-tetraploid karyotype with random loss and gain of individual chromosomes. Minute chromosomes, but no stable markers have been observed. After these initial changes, examination of cultures at several passage levels has shown that the karyotype has remained essentially stable. The MKDC4 line, also sub-tetraploid at the 7th passage, had 4 marker chromosomes by the 47th passage. The rapid increase in chromosome number may have contributed to the "immortalization" of these lines. The response of these established keratinocyte lines to growth factors and serum-derived inhibitors changed with increasing passage level. Most notable of these changes were a reduction in the requirement for bovine pituitary extract (an absolute requirement for growth of secondary MK1 cells) and a decreased sensitivity to serum and serum-derived inhibitors, e.g., transforming growth factor-beta. The established lines, like primary and secondary keratinocytes, remain responsive to calcium-induced terminal differentiation and are non-tumorigenic in athymic, nude mice. This serum-free system is suitable for transformation studies with oncogenes and chemical carcinogens. JF - In vitro cellular & developmental biology : journal of the Tissue Culture Association AU - Kaighn, M E AU - Camalier, R F AU - Bertolero, F AU - Saffiotti, U AD - Laboratory of Experimental Pathology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 845 EP - 854 VL - 24 IS - 8 SN - 0883-8364, 0883-8364 KW - Culture Media KW - 0 KW - Growth Substances KW - Peptides KW - Tissue Extracts KW - Insulin-Like Growth Factor I KW - 67763-96-6 KW - Keratins KW - 68238-35-7 KW - Transforming Growth Factors KW - 76057-06-2 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Karyotyping KW - Animals KW - Pituitary Gland -- physiology KW - Growth Substances -- administration & dosage KW - Dose-Response Relationship, Drug KW - Cell Division -- drug effects KW - Tissue Extracts -- pharmacology KW - Calcium -- pharmacology KW - Mice KW - Mice, Nude KW - Peptides -- pharmacology KW - Neoplasms, Experimental -- pathology KW - Insulin-Like Growth Factor I -- pharmacology KW - Cell Line KW - Epidermis -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78385939?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Spontaneous+establishment+and+characterization+of+mouse+keratinocyte+cell+lines+in+serum-free+medium.&rft.au=Kaighn%2C+M+E%3BCamalier%2C+R+F%3BBertolero%2C+F%3BSaffiotti%2C+U&rft.aulast=Kaighn&rft.aufirst=M&rft.date=1988-08-01&rft.volume=24&rft.issue=8&rft.spage=845&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 - 1988-10-07 N1 - Date created - 1988-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Experimental cardiac allograft survival across major histocompatibility complex barriers in the rhesus monkey following T lymphocyte-depleted autologous marrow transplantation. I. In vitro T lymphocyte depletion studies. AN - 78369721; 3043776 AB - We have developed a rhesus monkey model consisting of myeloablative total-body irradiation and T lymphocyte-depleted autologous bone marrow transplantation followed by MHC-mismatched heterotopic cardiac allograft implantation that has provided an opportunity to study the role of marrow T cells in cardiac allograft rejection. In order to assess quantitatively the effects of low numbers of residual marrow T cells following depletion, methods to deplete rhesus marrow extensively and to detect residual T cells following depletion at levels below the sensitivity of standard assays have been developed. A rhesus marrow limiting dilution assay has been developed that quantifies less than 1 T cell in 10(5) marrow cells and is superior to traditional detection methods by at least 3 logs. In a direct comparison of four T cell depletion methods, effective depletion has been achieved with complement-mediated cytotoxicity (C'MC), erythrocyte rosetting, and counterflow centrifugal elutriation (CCE), the latter with a simplified single-flow rate protocol. Median marrow T cell depletions of 2.1, 1.1, and 3.1 logs, and total nucleated cell losses of 40%, 61%, and 42% respectively, have been observed. A reported use of ricin A-chain-like toxins for the enhancement of C'MC was of low efficacy with rhesus peripheral blood T cell targets. CCE followed by C'MC has resulted in a median 4.8 logs depletion with residual marrow T cell contents less than 0.001%. Thus, C'MC, E-rosetting, and particularly CCE are effective methods of T cell depletion--and, when used in combination, extensively eliminate marrow T cells. A rhesus marrow limiting dilution assay detects residual T cells at these low levels. These techniques provide a basis for the quantitative study of the role of T cells in organ graft rejection following T lymphocyte-depleted autologous marrow transplantation. JF - Transplantation AU - Moses, R D AU - Orr, K S AU - MacVittie, T J AU - Gress, R E AD - Experiemental Immunology, Branches, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 197 EP - 205 VL - 46 IS - 2 SN - 0041-1337, 0041-1337 KW - Immunotoxins KW - 0 KW - Index Medicus KW - Bone Marrow Cells KW - Centrifugation KW - Animals KW - Antibody-Dependent Cell Cytotoxicity KW - Graft Survival KW - Rosette Formation KW - Macaca mulatta KW - Complement Activation KW - Cell Separation -- methods KW - Heart Transplantation KW - T-Lymphocytes -- immunology KW - Bone Marrow Transplantation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78369721?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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&rft.atitle=Experimental+cardiac+allograft+survival+across+major+histocompatibility+complex+barriers+in+the+rhesus+monkey+following+T+lymphocyte-depleted+autologous+marrow+transplantation.+I.+In+vitro+T+lymphocyte+depletion+studies.&rft.au=Moses%2C+R+D%3BOrr%2C+K+S%3BMacVittie%2C+T+J%3BGress%2C+R+E&rft.aulast=Moses&rft.aufirst=R&rft.date=1988-08-01&rft.volume=46&rft.issue=2&rft.spage=197&rft.isbn=&rft.btitle=&rft.title=Transplantation&rft.issn=00411337&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-09-14 N1 - Date created - 1988-09-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ongoing protein synthesis needed for 1,25-(OH)2D3-mediated rapid increase of cyclic GMP in human skin fibroblasts. AN - 78358254; 2456949 AB - Recently we reported that 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) through interaction with its specific receptor rapidly (within 1 min) stimulated intracellular cGMP production in cultured human skin fibroblasts. Here we show that this effect of 100 nM 1,25-(OH)2D3 is prevented by brief (30 min) inhibition of RNA synthesis (with actinomycin D or alpha-amanitin) or by brief inhibition of protein synthesis (with cycloheximide or diphtheria toxin). The protein synthesis inhibitors also blocked stimulation of cGMP by other steroids (testosterone or dexamethasone at 100 nM) but did not block cGMP stimulation by sodium nitroprusside. Since the time for the 1,25-(OH)2D3 receptor to increase cGMP seems too short to require de novo protein synthesis, we conclude that the 1,25-(OH)2D3 receptor acts together with rapidly turning over protein(s) to stimulate cGMP synthesis. JF - FEBS letters AU - Barsony, J AU - Marx, S J AD - Mineral Metabolism Section, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892. Y1 - 1988/08/01/ PY - 1988 DA - 1988 Aug 01 SP - 207 EP - 210 VL - 235 IS - 1-2 SN - 0014-5793, 0014-5793 KW - Amanitins KW - 0 KW - Diphtheria Toxin KW - Nitroprusside KW - 169D1260KM KW - Dactinomycin KW - 1CC1JFE158 KW - Testosterone KW - 3XMK78S47O KW - RNA KW - 63231-63-0 KW - Dexamethasone KW - 7S5I7G3JQL KW - Cycloheximide KW - 98600C0908 KW - Calcitriol KW - FXC9231JVH KW - Cyclic GMP KW - H2D2X058MU KW - Index Medicus KW - Dactinomycin -- pharmacology KW - Transcription, Genetic -- drug effects KW - Testosterone -- pharmacology KW - RNA -- antagonists & inhibitors KW - Cells, Cultured KW - Amanitins -- pharmacology KW - Humans KW - Dexamethasone -- pharmacology KW - Cycloheximide -- pharmacology KW - Diphtheria Toxin -- pharmacology KW - Nitroprusside -- pharmacology KW - RNA -- biosynthesis KW - Protein Biosynthesis KW - Fibroblasts -- drug effects KW - Cyclic GMP -- biosynthesis KW - Fibroblasts -- metabolism KW - Calcitriol -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78358254?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Ongoing+protein+synthesis+needed+for+1%2C25-%28OH%292D3-mediated+rapid+increase+of+cyclic+GMP+in+human+skin+fibroblasts.&rft.au=Barsony%2C+J%3BMarx%2C+S+J&rft.aulast=Barsony&rft.aufirst=J&rft.date=1988-08-01&rft.volume=235&rft.issue=1-2&rft.spage=207&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 - 1988-09-16 N1 - Date created - 1988-09-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Rodent diets for carcinogenesis studies. AN - 78353214; 3404285 AB - An optimal diet for rodents in chemical carcinogenicity studies should be nutritionally adequate for growth and maintenance without excesses of high energy and growth-enhancing nutrients. Purified diets are expensive, and standardized purified diets for long-term studies are not yet established. Purified diets caused periportal lipidosis, hemorrhagic diseases and calcification of tissues in rodents. Diet restriction will result in consumption of most food during the resting phase. This will cause increased activity during the resting phase with a shift of nocturnal cycle and associated changes in physiological processes. Diet restriction may modify the carcinogenic responses to chemicals, and the practice is labor intensive. Decreasing the fat and protein content to adequate levels with a slight increase in fiber content and making the diet available only during the normal feeding period (night) may decrease the energy consumption, slow the growth and lower the body weight gain by 10-20%, with a substantial decrease in the prevalence of spontaneous tumors in the pituitary and mammary glands. We should take advantage of the biological similarities between rodents and humans to enhance the utility of rodent studies; however, mimicking the diet and feeding procedures of humans without a thorough understanding of the physiology of the altered rodent may not be useful. Contaminant concentrations of the diets should be as low as is practical. Each lot of diet should be analyzed for macronutrients and labile micronutrients with complete micronutrient analyses of randomly selected lots. JF - The Journal of nutrition AU - Rao, G N AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 929 EP - 931 VL - 118 IS - 8 SN - 0022-3166, 0022-3166 KW - Index Medicus KW - Animals KW - Nutritive Value KW - Circadian Rhythm KW - Food Contamination KW - Female KW - Neoplasms, Experimental -- etiology KW - Rodentia -- growth & development KW - Diet -- standards UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78353214?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+nutrition&rft.atitle=Rodent+diets+for+carcinogenesis+studies.&rft.au=Rao%2C+G+N&rft.aulast=Rao&rft.aufirst=G&rft.date=1988-08-01&rft.volume=118&rft.issue=8&rft.spage=929&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+nutrition&rft.issn=00223166&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-09-14 N1 - Date created - 1988-09-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human T lymphotropic virus I infection deregulates surface expression of the transferrin receptor. AN - 78352483; 2899599 AB - Human T-lymphotropic virus I (HTLV-I) is an etiologic agent in adult T cell leukemia. In an effort to understand the relationship between HTLV-I infection and malignant transformation, we have examined transferrin receptor expression in HTLV-I-infected cells. Transferrin receptor expression in normal T cells is tightly regulated and essential for cell proliferation. We have used matched T cell sets originating from a normal donor, consisting of tetanus toxoid-specific normal T cell clones (TM3 and TM5) and their in vitro HTLV-I-infected counterparts (TM3H and TM5H). Using these matched sets of virus-infected and normal T cells, we have determined that HTLV-I infection leads to hyperexpression of surface transferrin receptors (five- to six-fold higher than normal counterparts). Although the growth rates of the virus-infected cells did not differ significantly from their normal controls, HTLV-I-infected cells constitutively hyperexpressed surface transferrin receptors, whereas the level of surface receptor expression of normal counterpart cells varied during the cycle of antigenic stimulation. Immunoprecipitation of total (surface plus cytoplasmic) transferrin expression showed that the HTLV-I-infected cells did not possess a greater total number of transferrin receptors than their normal counterparts. This data was supported by Northern blot analysis, which showed equivalent transferrin receptor mRNA expression in HTLV-I-infected and uninfected cells. Functional analysis revealed a marked defect in 59Fe-transferrin internalization in the HTLV-I-infected cells. Furthermore, the HTLV-I-infected cells showed markedly decreased transferrin receptor phosphorylation and internalization in response to active phorbol ester. Thus the data demonstrate that in peripheral blood T cells, HTLV-I infection is accompanied by surface transferrin receptor overexpression secondary to subcellular redistribution and defective internalization. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Vidal, C AU - Matsushita, S AU - Colamonici, O R AU - Trepel, J B AU - Mitsuya, H AU - Neckers, L M AD - Laboratory of Pathology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/08/01/ PY - 1988 DA - 1988 Aug 01 SP - 984 EP - 988 VL - 141 IS - 3 SN - 0022-1767, 0022-1767 KW - Membrane Glycoproteins KW - 0 KW - Receptors, Transferrin KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Lymphocyte Activation -- drug effects KW - T-Lymphocytes -- metabolism KW - Phosphorylation KW - Cells, Cultured KW - Humans KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Membrane -- metabolism KW - T-Lymphocytes -- immunology KW - Receptors, Transferrin -- physiology KW - Deltaretrovirus Infections -- immunology KW - Deltaretrovirus -- physiology KW - Receptors, Transferrin -- drug effects KW - Deltaretrovirus Infections -- metabolism KW - Deltaretrovirus Infections -- etiology KW - Receptors, Transferrin -- metabolism KW - Membrane Glycoproteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78352483?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+T+lymphotropic+virus+I+infection+deregulates+surface+expression+of+the+transferrin+receptor.&rft.au=Vidal%2C+C%3BMatsushita%2C+S%3BColamonici%2C+O+R%3BTrepel%2C+J+B%3BMitsuya%2C+H%3BNeckers%2C+L+M&rft.aulast=Vidal&rft.aufirst=C&rft.date=1988-08-01&rft.volume=141&rft.issue=3&rft.spage=984&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 - 1988-08-31 N1 - Date created - 1988-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Regulation of ornithine decarboxylase activity by IL-2 and cyclic AMP. AN - 78349268; 2840461 AB - IL-2 regulates the expression and activation of the principal rate-limiting enzyme of polyamine synthesis, ornithine decarboxylase (ODC). The apparent activation of ODC occurs by two independent steps. Rapid activation of enzyme occurs within the first 10 min of lymphokine treatment of cloned IL-2-dependent murine cell lines. The initial rapid rise in enzyme activity is insensitive to protein or mRNA synthesis inhibitors. The early rise in ODC activity is followed by a protracted increase in enzyme activity, apparent protein measured by [3H]difluoromethylornithine binding, and by accumulation of steady state ODC mRNA. Stable analogues of cAMP which inhibit IL-2-stimulated proliferation, suppressed only the mRNA-dependent increase in ODC activity. Phorbol esters were shown to increase steady state levels of ODC mRNA whereas cAMP analogue clearly inhibited the growth factor-induced increase in ODC mRNA. These studies show that IL-2 regulates the expression of ODC at multiple levels, including transcription and accumulation of steady state mRNA, and post-translational activation of an enzyme important for DNA synthesis. Furthermore, anti-proliferative signals such as cAMP may effect the regulation of ODC enzyme production at the level of mRNA accumulation and stability. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Farrar, W L AU - Vinocour, M AU - Cleveland, J L AU - Harel-Bellan, A AD - Laboratory of Molecular Immunoregulation, National Cancer Institute, Frederick, MD 21701-1013. Y1 - 1988/08/01/ PY - 1988 DA - 1988 Aug 01 SP - 967 EP - 971 VL - 141 IS - 3 SN - 0022-1767, 0022-1767 KW - Interleukin-2 KW - 0 KW - RNA, Messenger KW - 8-Bromo Cyclic Adenosine Monophosphate KW - 23583-48-4 KW - Cyclic AMP KW - E0399OZS9N KW - Ornithine Decarboxylase KW - EC 4.1.1.17 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Lymphocyte Activation -- drug effects KW - Animals KW - Transcription, Genetic -- drug effects KW - RNA, Messenger -- metabolism KW - Humans KW - Enzyme Activation -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - 8-Bromo Cyclic Adenosine Monophosphate -- pharmacology KW - Cell Line KW - Ornithine Decarboxylase -- metabolism KW - Interleukin-2 -- pharmacology KW - Cyclic AMP -- pharmacology KW - T-Lymphocytes, Cytotoxic -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78349268?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Regulation+of+ornithine+decarboxylase+activity+by+IL-2+and+cyclic+AMP.&rft.au=Farrar%2C+W+L%3BVinocour%2C+M%3BCleveland%2C+J+L%3BHarel-Bellan%2C+A&rft.aulast=Farrar&rft.aufirst=W&rft.date=1988-08-01&rft.volume=141&rft.issue=3&rft.spage=967&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 - 1988-08-31 N1 - Date created - 1988-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Esophageal candidiasis. Managing an increasingly prevalent infection. AN - 78346700; 3041396 AB - Esophageal candidiasis is an opportunistic infection that is being recognized increasingly often in certain patients, including those who have a neoplastic disease, are undergoing protracted antibiotic therapy, or hae acquired immunodeficiency syndrome (AIDS). Impaired cell-mediated immunity may predispose the patient to esophageal mucosal colonization, whereas chemotherapy-induced granulocytopenia may predispose to disseminated candidiasis. Esophageal candidiasis should be suspected in susceptible patients with complaints of substernal odynophagia or dysphagia. The diagnosis is confirmed by endoscopically directed mucosal biopsy. Esophagitis from other causes (eg. herpes simplex virus, cytomegalovirus, or bacterial infection) may develop concomitantly with esophageal candidiasis. Treatment is determined by the clinical and immune status of the patient. Amphotericin B (Fungizone) is administered to immunocompromised patients at risk for disseminated or deeply invasive candidiasis and is indicated in nongranulocytopenic patients whose symptoms prevent reliable administration of oral antifungal agents. Ketoconazole (Nizoral) may be administered to clinically stable nongranulocytopenic patients with esophageal candidiasis limited to the mucosa. Patients with AIDS and a history of esophageal candidiasis usually benefit from long-term suppression with an oral antifungal agent. JF - Postgraduate medicine AU - Walsh, T J AU - Hamilton, S R AU - Belitsos, N AD - Infectious Diseases Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 193 EP - 6, 201-5 VL - 84 IS - 2 SN - 0032-5481, 0032-5481 KW - Antifungal Agents KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Candidiasis, Chronic Mucocutaneous -- complications KW - Acquired Immunodeficiency Syndrome -- complications KW - Drug Interactions KW - Agranulocytosis -- complications KW - Neoplasms -- complications KW - Diagnosis, Differential KW - Risk Factors KW - Humans KW - Adult KW - Esophagoscopy KW - Antifungal Agents -- therapeutic use KW - Esophageal Diseases -- diagnosis KW - Candidiasis -- diagnosis KW - Esophageal Diseases -- therapy KW - Candidiasis -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78346700?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Postgraduate+medicine&rft.atitle=Esophageal+candidiasis.+Managing+an+increasingly+prevalent+infection.&rft.au=Walsh%2C+T+J%3BHamilton%2C+S+R%3BBelitsos%2C+N&rft.aulast=Walsh&rft.aufirst=T&rft.date=1988-08-01&rft.volume=84&rft.issue=2&rft.spage=193&rft.isbn=&rft.btitle=&rft.title=Postgraduate+medicine&rft.issn=00325481&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-09-02 N1 - Date created - 1988-09-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of transfected DNA by primary murine keratinocytes. AN - 78338285; 2456357 AB - Primary murine keratinocytes can be maintained in culture for extended periods in a proliferative, basal cell state under conditions of reduced extracellular Ca2+. In response to increased Ca2+ concentrations, the cells undergo a well-defined program of terminal differentiation, thus serving as a convenient model in which to study the genes involved in regulating this and possibly other differentiation cascades by DNA-mediated gene transfer. However, because of their sensitivity to increased Ca2+ concentrations, the introduction of exogenous genomic DNA into primary keratinocytes by conventional methods is problematic. We have optimized the calcium phosphate DNA transfection procedure by introducing conditions that reduce the potency of Ca2+ as a differentiation signal. Primary epidermal cells were transfected with pSV2CAT, a plasmid that codes for the enzyme chloramphenicol acetyltransferase CAT. Enzyme activity was measured in cell extracts under varying transfection conditions. When the K+ concentration of the medium used for transfection by calcium phosphate precipitation is reduced from 6.5 to 0.01 mM, CAT activity following transfection increases 2-3 times. Exposure to the DNA precipitate for 2-4 h is optimal. By the use of fibroblast conditioned medium following transfection, enzyme activity can be detected in cell extracts for at least 21 d, suggesting that the exogenous gene is integrated. The low K+/Ca2+ transfection method is more effective than SrCl2 used as an alternative for CaCl2 in Ca2+ sensitive cells. Low K+ medium enhances cell survival for Ca2+ mediated transfection but also appears to have a beneficial effect on DNA uptake or expression. JF - The Journal of investigative dermatology AU - Harper, J R AU - Greenhalgh, D A AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 150 EP - 153 VL - 91 IS - 2 SN - 0022-202X, 0022-202X KW - Keratins KW - 68238-35-7 KW - DNA KW - 9007-49-2 KW - Acetyltransferases KW - EC 2.3.1.- KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Potassium KW - RWP5GA015D KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Cells, Cultured KW - Acetyltransferases -- biosynthesis KW - Potassium -- pharmacology KW - Mice KW - Calcium -- pharmacology KW - Acetyltransferases -- genetics KW - Mice, Inbred BALB C KW - Time Factors KW - Fibroblasts -- physiology KW - Transfection KW - Epidermis -- metabolism KW - DNA -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78338285?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Expression+of+transfected+DNA+by+primary+murine+keratinocytes.&rft.au=Harper%2C+J+R%3BGreenhalgh%2C+D+A%3BYuspa%2C+S+H&rft.aulast=Harper&rft.aufirst=J&rft.date=1988-08-01&rft.volume=91&rft.issue=2&rft.spage=150&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 - 1988-08-26 N1 - Date created - 1988-08-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Epidemiologic evidence for early onset of mental disorders and higher risk of drug abuse in young adults. AN - 78336578; 3394882 AB - Data from the National Institute of Mental Health (NIMH) Epidemiologic Catchment Area Program, an epidemiologic survey of five communities, showed that four major disorders commonly begin in late adolescence or young adulthood. The median age at onset for anxiety disorders is 15 years; for major depressive episode, 24 years; for drug abuse or dependence, 19 years; and for alcohol abuse or dependence, 21 years. Findings also suggest that for respondents 18-30 years old, having a major depressive episode or anxiety disorder doubles the risk for later drug abuse or dependence. JF - The American journal of psychiatry AU - Christie, K A AU - Burke, J D AU - Regier, D A AU - Rae, D S AU - Boyd, J H AU - Locke, B Z AD - Division of Clinical Research, National Institute of Mental Health, Rockville, MD 20857. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 971 EP - 975 VL - 145 IS - 8 SN - 0002-953X, 0002-953X KW - Abridged Index Medicus KW - Index Medicus KW - United States KW - Age Factors KW - Risk Factors KW - Humans KW - Adult KW - Adolescent KW - Depressive Disorder -- epidemiology KW - Substance-Related Disorders -- complications KW - Anxiety Disorders -- epidemiology KW - Depressive Disorder -- complications KW - Substance-Related Disorders -- epidemiology KW - Anxiety Disorders -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78336578?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Epidemiologic+evidence+for+early+onset+of+mental+disorders+and+higher+risk+of+drug+abuse+in+young+adults.&rft.au=Christie%2C+K+A%3BBurke%2C+J+D%3BRegier%2C+D+A%3BRae%2C+D+S%3BBoyd%2C+J+H%3BLocke%2C+B+Z&rft.aulast=Christie&rft.aufirst=K&rft.date=1988-08-01&rft.volume=145&rft.issue=8&rft.spage=971&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 - 1988-08-25 N1 - Date created - 1988-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Guanine nucleotide-binding proteins that enhance choleragen ADP-ribosyltransferase activity: nucleotide and deduced amino acid sequence of an ADP-ribosylation factor cDNA. AN - 78326953; 3135549 AB - Three (two soluble and one membrane) guanine nucleotide-binding proteins (G proteins) that enhance ADP-ribosylation of the Gs alpha stimulatory subunit of the adenylyl cyclase (EC 4.6.1.1) complex by choleragen have recently been purified from bovine brain. To further define the structure and function of these ADP-ribosylation factors (ARFs), we isolated a cDNA clone (lambda ARF2B) from a bovine retinal library by screening with a mixed heptadecanucleotide probe whose sequence was based on the partial amino acid sequence of one of the soluble ARFs from bovine brain. Comparison of the deduced amino acid sequence of lambda ARF2B with sequences of peptides from the ARF protein (total of 60 amino acids) revealed only two differences. Whether these are cloning artifacts or reflect the existence of more than one ARF protein remains to be determined. Deduced amino acid sequences of ARF, Go alpha (the alpha subunit of a G protein that may be involved in regulation of ion fluxes), and c-Ha-ras gene product p21 show similarities in regions believed to be involved in guanine nucleotide binding and GTP hydrolysis. ARF apparently lacks a site analogous to that ADP-ribosylated by choleragen in G-protein alpha subunits. Although both the ARF proteins and the alpha subunits bind guanine nucleotides and serve as choleragen substrates, they must interact with the toxin A1 peptide in different ways. In addition to serving as an ADP-ribose acceptor, ARF interacts with the toxin in a manner that modifies its catalytic properties. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Price, S R AU - Nightingale, M AU - Tsai, S C AU - Williamson, K C AU - Adamik, R AU - Chen, H C AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, Bethesda, MD 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 5488 EP - 5491 VL - 85 IS - 15 SN - 0027-8424, 0027-8424 KW - Membrane Proteins KW - 0 KW - DNA KW - 9007-49-2 KW - Cholera Toxin KW - 9012-63-9 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 - Index Medicus KW - Animals KW - Base Sequence KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Cloning, Molecular KW - Cholera Toxin -- metabolism KW - GTP-Binding Proteins -- metabolism KW - DNA -- genetics KW - Membrane Proteins -- genetics KW - Poly(ADP-ribose) Polymerases -- metabolism KW - GTP-Binding Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78326953?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Guanine+nucleotide-binding+proteins+that+enhance+choleragen+ADP-ribosyltransferase+activity%3A+nucleotide+and+deduced+amino+acid+sequence+of+an+ADP-ribosylation+factor+cDNA.&rft.au=Price%2C+S+R%3BNightingale%2C+M%3BTsai%2C+S+C%3BWilliamson%2C+K+C%3BAdamik%2C+R%3BChen%2C+H+C%3BMoss%2C+J%3BVaughan%2C+M&rft.aulast=Price&rft.aufirst=S&rft.date=1988-08-01&rft.volume=85&rft.issue=15&rft.spage=5488&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 - 1988-09-07 N1 - Date created - 1988-09-07 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - J03794; GENBANK N1 - SuppNotes - Cited By: J Mol Biol. 1970 Mar;48(3):443-53 [5420325] Protein Eng. 1986 Oct-Nov;1(1):47-54 [3148932] J Cyclic Nucleotide Res. 1978 Jun;4(3):159-68 [214459] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] J Biol Chem. 1980 Feb 25;255(4):1252-8 [6766444] Biochemistry. 1980 Oct 14;19(21):4871-4 [7426631] Biochim Biophys Acta. 1981 Feb 5;672(3):248-61 [7213814] J Biol Chem. 1981 Aug 10;256(15):7990-7 [7263636] J Biol Chem. 1982 Jan 10;257(1):20-3 [6273425] Biochim Biophys Acta. 1982 Feb 2;714(2):337-43 [7055618] Nature. 1983 Mar 3;302(5903):33-7 [6298635] J Biol Chem. 1983 Oct 10;258(19):11908-14 [6311828] Anal Biochem. 1983 Jul 1;132(1):6-13 [6312838] J Biol Chem. 1984 Jan 25;259(2):696-8 [6582062] J Biol Chem. 1984 May 25;259(10):6228-34 [6327671] J Biol Chem. 1984 May 25;259(10):6235-40 [6327672] Nature. 1984 Aug 16-22;310(5978):583-6 [6087162] EMBO J. 1984 Nov;3(11):2581-5 [6096132] J Mol Evol. 1984-1985;21(2):112-25 [6100188] Science. 1985 Oct 4;230(4721):32-6 [3898365] Science. 1985 Oct 4;230(4721):78-82 [3898366] Cell. 1986 Jan 31;44(2):283-92 [3943125] Annu Rev Neurosci. 1986;9:87-119 [2423011] J Biol Chem. 1986 Jun 15;261(17):7906-11 [3086320] J Biol Chem. 1987 Jan 25;262(3):1030-6 [3100524] Nature. 1987 Jan 29-Feb 4;325(6103):445-7 [2433590] Annu Rev Cell Biol. 1986;2:391-419 [3103658] Proc Natl Acad Sci U S A. 1987 May;84(10):3107-11 [3106961] Proc Natl Acad Sci U S A. 1987 Aug;84(15):5139-42 [3110784] Annu Rev Biochem. 1987;56:615-49 [3113327] Biochem Biophys Res Commun. 1987 Aug 14;146(3):1234-9 [3113429] Proc Natl Acad Sci U S A. 1987 Nov;84(21):7493-7 [3118369] FEBS Lett. 1987 Nov 30;224(2):365-71 [2826231] Nature. 1987 Dec 24-31;330(6150):758-60 [2827032] J Biol Chem. 1988 Feb 5;263(4):1768-72 [3123477] Proc Natl Acad Sci U S A. 1988 Feb;85(4):1015-9 [3277185] Adv Enzymol Relat Areas Mol Biol. 1988;61:303-79 [3128060] Proc Natl Acad Sci U S A. 1977 Aug;74(8):3307-11 [198781] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The gene encoding the nonstructural protein of B19 (human) parvovirus may be lethal in transfected cells. AN - 78316289; 2969055 AB - The B19 parvovirus is a cause of bone marrow failure in humans. B19 is toxic to erythroid progenitor cells in vitro. Viral products possibly responsible for toxicity were explored by transfection of cloned B19 genome into HeLa cells. The nonstructural (NS) protein was detected in cells 30 h after transfection. Plasmids containing the B19 genome were transfected with selectable marker genes in stable transformation assays. Plasmids that contained the left side of the B19 genome, which encodes the NS protein of the virus, inhibited antibiotic-resistant colony formation. Transformation occurred when NS protein expression was blocked by mutation. Suppression of transformation by NS protein was not tissue specific, suggesting a role for NS protein in toxicity for nonpermissive cells without parvovirus replication or virion accumulation. JF - Journal of virology AU - Ozawa, K AU - Ayub, J AU - Kajigaya, S AU - Shimada, T AU - Young, N AD - Cell Biology Section, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 2884 EP - 2889 VL - 62 IS - 8 SN - 0022-538X, 0022-538X KW - Viral Core Proteins KW - 0 KW - Viral Nonstructural Proteins KW - Index Medicus KW - Promoter Regions, Genetic KW - Transfection KW - Transformation, Genetic KW - Transcription, Genetic KW - Gene Expression Regulation KW - Molecular Weight KW - Parvoviridae -- genetics KW - Capsid -- genetics KW - Parvoviridae -- pathogenicity KW - Viral Core Proteins -- genetics KW - Genes, Viral KW - Genes, Lethal UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78316289?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+gene+encoding+the+nonstructural+protein+of+B19+%28human%29+parvovirus+may+be+lethal+in+transfected+cells.&rft.au=Ozawa%2C+K%3BAyub%2C+J%3BKajigaya%2C+S%3BShimada%2C+T%3BYoung%2C+N&rft.aulast=Ozawa&rft.aufirst=K&rft.date=1988-08-01&rft.volume=62&rft.issue=8&rft.spage=2884&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 - 1988-08-19 N1 - Date created - 1988-08-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Blood. 1986 May;67(5):1411-7 [3008891] J Virol. 1985 Sep;55(3):886-9 [4020972] Science. 1986 Aug 22;233(4766):883-6 [3738514] J Virol. 1986 Oct;60(1):251-8 [3018288] Mol Cell Biol. 1986 Aug;6(8):2884-94 [3491293] J Virol. 1987 May;61(5):1448-56 [3033274] J Virol. 1987 Aug;61(8):2395-406 [3599180] J Virol. 1987 Aug;61(8):2627-30 [3599184] Mol Cell Biol. 1987 Apr;7(4):1320-5 [3037312] N Engl J Med. 1987 Jul 30;317(5):287-94 [3037373] Blood. 1987 Aug;70(2):384-91 [3038211] Annu Rev Biochem. 1987;56:317-32 [3113326] Mol Cell Biol. 1987 Aug;7(8):2830-7 [3670295] Lancet. 1981 Mar 21;1(8221):664-5 [6110886] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] J Clin Invest. 1984 Jan;73(1):224-30 [6317715] J Clin Invest. 1984 Dec;74(6):2024-32 [6392340] Mol Cell Biol. 1984 Dec;4(12):2929-31 [6098829] J Virol. 1986 Jun;58(3):921-36 [3701931] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular characterization of gag proteins from simian immunodeficiency virus (SIVMne). AN - 78309633; 3292789 AB - A simian immunodeficiency virus (SIV) designated SIVMne was isolated from a pig-tailed macaque with lymphoma housed at the University of Washington Regional Primate Research Center, Seattle. To better establish the relationship of SIVMne to other immunodeficiency viruses, we purified and determined the partial amino acid sequences of six structural proteins (p1, p2, p6, p8, p16, and p28) from SIVMne and compared these amino acid sequences to the translated nucleotide sequences of SIVMac and human immunodeficiency virus types 1 and 2 (HIV-1 and HIV-2). A total of 125 residues of SIVMne amino acid sequence were compared to the predicted amino acid sequences of the gag precursors of SIV and HIVs. In the compared regions 92% of the SIVMne amino acids were identical to predicted residues of SIVMac, 83% were identical to predicted residues of HIV-2, and 41% were identical to predicted residues of HIV-1. These data reveal that the six SIVMne proteins are proteolytic cleavage products of the gag precursor (Pr60gag) and that their order in the structure of Pr60gag is p16-p28-p2-p8-p1-p6. Rabbit antisera prepared against purified p28 and p16 were shown to cross-react with proteins of 60, 54, and 47 kilodaltons present in the viral preparation and believed to be SIVMne Pr60gag and intermediate cleavage products, respectively. SIVMne p16 was shown to contain covalently bound myristic acid, and p8 was identified as a nucleic acid-binding protein. The high degree of amino acid sequence homology between SIVs and HIV-2 around proven proteolytic cleavage sites in SIV Pr60gag suggests that proteolytic processing of the HIV-2 gag precursor is probably very similar to processing of the SIV gag precursor. Peptide bonds cleaved during proteolytic processing of the SIV gag precursor were similar to bonds cleaved during processing of HIV-1 gag precursors, suggesting that the SIV and HIV viral proteases have similar cleavage site specificities. JF - Journal of virology AU - Henderson, L E AU - Benveniste, R E AU - Sowder, R AU - Copeland, T D AU - Schultz, A M AU - Oroszlan, S AD - Laboratory of Molecular Virology and Carcinogenesis, Bionetics Research, Inc., NCI-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 2587 EP - 2595 VL - 62 IS - 8 SN - 0022-538X, 0022-538X KW - Antigens, Viral KW - 0 KW - Gene Products, gag KW - Protein Precursors KW - Retroviridae Proteins KW - Index Medicus KW - AIDS/HIV KW - Virus Replication KW - Protein Precursors -- metabolism KW - Electrophoresis, Polyacrylamide Gel KW - Chromatography KW - Protein Processing, Post-Translational KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Immunologic Techniques KW - HIV -- analysis KW - Antigens, Viral -- analysis KW - Retroviridae -- analysis KW - Retroviridae -- immunology KW - Retroviridae Proteins -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78309633?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Molecular+characterization+of+gag+proteins+from+simian+immunodeficiency+virus+%28SIVMne%29.&rft.au=Henderson%2C+L+E%3BBenveniste%2C+R+E%3BSowder%2C+R%3BCopeland%2C+T+D%3BSchultz%2C+A+M%3BOroszlan%2C+S&rft.aulast=Henderson&rft.aufirst=L&rft.date=1988-08-01&rft.volume=62&rft.issue=8&rft.spage=2587&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 - 1988-08-19 N1 - Date created - 1988-08-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1986 Jul 18;233(4761):343-6 [2425430] Proc Natl Acad Sci U S A. 1986 Jul;83(14):5286-90 [3014542] J Clin Invest. 1986 Nov;78(5):1229-36 [3771794] J Virol. 1986 Nov;60(2):483-90 [3021982] J Virol. 1987 Apr;61(4):1116-24 [3029406] Nature. 1987 Apr 16-22;326(6114):662-9 [3031510] Cell. 1987 May 8;49(3):307-19 [3646094] Science. 1987 May 15;236(4803):827-31 [3033826] Proc Natl Acad Sci U S A. 1987 Jun;84(12):4298-302 [3035577] Nature. 1987 Aug 6-12;328(6130):539-43 [3497350] Nature. 1987 Aug 6-12;328(6130):543-7 [3649576] Biochem Biophys Res Commun. 1987 Aug 14;146(3):1234-9 [3113429] Proc Natl Acad Sci U S A. 1987 Oct;84(20):7041-5 [2823251] Nature. 1988 Feb 18;331(6157):619-22 [2893293] J Virol. 1988 Jun;62(6):2091-101 [3285032] Biochem Biophys Res Commun. 1967 Sep 7;28(5):815-20 [4861258] Nature. 1970 Aug 15;227(5259):680-5 [5432063] Proc Natl Acad Sci U S A. 1978 Mar;75(3):1404-8 [206897] J Biol Chem. 1981 Aug 25;256(16):8400-6 [6267042] Proc Natl Acad Sci U S A. 1983 Jan;80(2):339-43 [6340098] J Virol. 1983 May;46(2):355-61 [6302307] FEBS Lett. 1983 May 30;156(1):37-40 [6303852] FEBS Lett. 1983 Oct 17;162(2):390-5 [6313426] Virology. 1984 Feb;133(1):137-45 [6322425] J Virol. 1984 Nov;52(2):492-500 [6333515] Cell. 1985 Jan;40(1):9-17 [2981635] Nature. 1985 Jan 24-30;313(6000):277-84 [2578615] Curr Top Microbiol Immunol. 1985;115:221-33 [2983943] Lancet. 1985 Jun 8;1(8441):1330-2 [2860515] Science. 1985 Jun 7;228(4704):1199-201 [3873705] Science. 1985 Jun 7;228(4704):1201-4 [3159089] J Virol. 1985 Sep;55(3):778-87 [3927012] J Virol. 1985 Sep;55(3):870-3 [2991607] Virology. 1985 Sep;145(2):280-92 [2411050] Science. 1985 Oct 4;230(4721):71-3 [2412295] Lancet. 1985 Dec 21-28;2(8469-70):1387-9 [2867393] J Virol. 1986 Mar;57(3):826-32 [3005629] Nature. 1986 May 22-28;321(6068):435-7 [3012358] Int J Cancer. 1986 Oct 15;38(4):563-74 [2428760] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Medicine -- The Art of Humaneness: On Ethics of Traditional Chinese Medicine AN - 60987432; 89V0719 AB - The history of traditional Chinese medical ethics is described, & the Confucian ethics that formed the cultural context of traditional Chinese medicine & medical ethics are outlined. It is argued that the application of Confucian ethics in medicine prescribed the attitudes of physicians toward themselves, patients, & colleagues. 1 Appendix, 37 References. Modified HA JF - The Journal of Medicine and Philosophy AU - Qiu, Ren-Zong AD - Instit Philosophy Chinese Academy Social Sciences, 5 Juanguomen Nei Da Jie Beijing Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 277 EP - 299 VL - 13 IS - 3 SN - 0360-5310, 0360-5310 KW - traditional Chinese medical ethics, Confucian influences KW - Confucianism KW - Ethics KW - Traditional Medicine KW - China KW - article KW - 2045: sociology of health and medicine; sociology of medicine (public health) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/60987432?accountid=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=The+Journal+of+Medicine+and+Philosophy&rft.atitle=Medicine+--+The+Art+of+Humaneness%3A+On+Ethics+of+Traditional+Chinese+Medicine&rft.au=Qiu%2C+Ren-Zong&rft.aulast=Qiu&rft.aufirst=Ren-Zong&rft.date=1988-08-01&rft.volume=13&rft.issue=3&rft.spage=277&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Medicine+and+Philosophy&rft.issn=03605310&rft_id=info:doi/ LA - English DB - Sociological Abstracts N1 - Date revised - 2007-04-01 N1 - Last updated - 2016-09-28 N1 - CODEN - JMPHDC N1 - SubjectsTermNotLitGenreText - China; Traditional Medicine; Ethics; Confucianism ER -